Psychiatry

INTRODUCTION:

People with intellectual disabilities are a heterogeneous group, who can pose a challenge to services in terms of meeting a wide range of needs. Following the closure of large institutions, the optimum means of service provision for people with intellectual disabilities with additional mental illness and challenging behaviour has been a matter of debate.

Challenging behaviour can be defined as a ‘culturally abnormal behaviour of such an intensity, frequency or duration that the physical safety of the person or others is likely to be placed in serious jeopardy, or behaviour which is likely to seriously limit use of, or result in the person being denied access to, ordinary community facilities’ – Emerson, 1995¹. Examples of challenging behaviours include self-injury, aggressive outbursts, destruction of property and socially inappropriate behaviour.

The credit-crunch of recent years has led to an increased use of private sector services delivering care to NHS funded patients. The Winterbourne Scandal unearthed by BBC Panorama in June 2011 (an investigation into the physical abuse and psychological abuse suffered by people with learning disabilities and challenging behaviour at this private hospital in South Gloucestershire), highlighted that whist this maybe an economically viable option, fundamental questions were raised about whether private sector services’ safeguards and monitoring protocols were as robust as the NHS in protecting vulnerable patients. It also reawakened longstanding disputes around the way people with complex needs are cared for in residential settings. The discussions centred around ‘institutional’ versus ‘community’ care styles; specialist intellectual disabilities services versus generic adult psychiatric services; local versus specialist expertise congregated around a single unit; and also financial questions regarding how best to meet the needs of this population at a time of austerity. Opinions vary widely, and at times are even polarised, as a result of several factors including position within this competitive and complex system, personal and cultural politics and also personal experience. As a result of the government review, subsequent to the Winterbourne investigation, a number of recommendations have been made which will affect the future of care of this vulnerable group of patients. These include, “by June 2013, all current placements will be reviewed, everyone in hospital inappropriately will move to community-based support as quickly as possible, and no later than June 2014… as a consequence, there will be a dramatic reduction in hospital placements for this group of people”²

The Department of Health Policy, Valuing People³, set out ‘ambitious and challenging programme of action for improving services’, based on four important key principles – civil rights, independence, choice and inclusion. Government Policy as detailed in both Valuing People and the Mansell Report^{3, 4} recognises that NHS specialist inpatient services are indeed necessary on a short-term basis for some people with intellectual disabilities and complex mental health needs. Inpatient facilities for people with Intellectual Disability have been described as highly specialised services that are a valuable, but also expensive, component of mental health services⁵. The Enfield Specialist Inpatient unit - the Seacole Centre - is one such service.

The Seacole Centre consists of two inpatient units, with a total of 12 inpatient beds, for people with intellectual disabilities with acute mental illness and/or challenging behaviour. It is located within Chase Farm Hospital in Enfield, Greater London. The Seacole Centre has a multidisciplinary team consisting of nurses, psychologists, psychiatrists, a resident GP, occupational therapists, intensive support team staff, physiotherapists, speech and language therapists, a physical exercise coach and administrative staff. Patients are admitted from a variety of sources, including general psychiatric wards, general medical wards and community intellectual disability teams. Since patients are often referred from other boroughs, in addition to this multidisciplinary team, each patient has their own community and social care team based within their own borough. The use of out-of-area units faces similar challenges to out-of-area placements, use of which has been increasing in the UK, and it is important to explore ways in which service users, out-of-area, can be supported effectively⁶.

In 2002, a review of admissions to the unit was completed to describe the management of mental illness and challenging behaviour. Since then there have been several service reconfigurations within the trust, in order to accommodate national, political and financial recommendations. However, despite these changes, it was observed clinically that certain clinical problems including delayed discharges continue to occur. We decided to complete a similar review, to describe current admission trends in further detail, in order to enable us to identify areas of improvement, and also to ascertain the nature and severity of ongoing problems to focus future recommendations.

METHOD:

A retrospective review of the case records of all inpatient admissions to the Seacole Centre was completed over a three-year period – from 1^st January 1999 to 31^st December 2001.

Data collected included age on admission, gender, borough, diagnosis, psychotropic medication on discharge, date of admission and discharge, length of stay, legal status on admission, delays on discharge, and reason for delay, and living arrangements prior to and after discharge

A successful outcome of admission was discharge from hospital to community care. We used the following definition of the delayed discharge:

"A delayed transfer occurs when a patient is ready for transfer from a general and acute hospital bed but is still occupying such a bed. A patient is ready for transfer when:

• a clinical decision has been made that the patient is ready for transfer
• a multi-disciplinary team decision has been made that the patient is ready for transfer
• the patient is safe to discharge/transfer.⁷

The review was repeated during a further three-year period between 1^st January to 2009 and 31^st December 2011.

RESULTS:

Characteristics of 1999-2001 cohort, and comparison with 2009-2011

The basic demographic details can be seen in Table 1.

Table 1 - Demographic details

Trends in Admission Rates

As seen in Tables 1 and 2, there has been a reduction in the total number of admissions between the studies. There has also been a marked reduction in re-admissions. The average length of stay has increased, and although the number of delayed discharges has slightly decreased, it can be seen that this is still a factor in a significant proportion of the admissions.

Table 2 - Trends in admission

Reason for admission

The trends in reason for admission are shown in Figure 1.

Figure 1 – Trends in Reason for Admission, 1999-2001 compared to 2009-2011

In both time periods, the most frequent reason for admission is challenging behaviour (62%, n=37 between 1999-2001; 63%, n=29, between 2009-2011), followed by psychosis (22%, n=13 between 1999-2001; 11%, n=5, between 2009-2011. Social admissions were the third most common reason for admission in the recent study (0% between 1999-2001; 4%, n=2 between 2009-2011). The range of psychiatric presentations was widest during the original time period.

Patterns on discharge

As shown in Figure 2, most patients in the original study were discharged to either the same residential home or back to the family home, where as in the latter time period patients were most frequently discharged to either a different residential home or to supported living. Figure 3 summarises this effect, demonstrating the change in discharging the majority of patients to a different place of residence.

Figure 2 – A graph to show the place of discharge, 1999-2001 compared to 2009-2011

Figure 3 – A Graph to Demonstrate Trends in Place of Discharge – comparing 1999-2001 and 2009-2011

Delayed discharges

The primary cause for delay in both studies was finding appropriate placement, although this was more marked in the recent cohort.

One of the major factors contributing to delayed discharges was lack of identification of suitable placement, which was identified as a major contributing factor to delayed discharges in 69% of cases in 2009-2011 and in 44% in 1999-2001, and apparent delays in the role played by social services (table 2).

DISCUSSION:

Throughout this study spanning 10 years, challenging behaviour followed by psychotic disorder remained the most common cause for admission. Interestingly, by 2008-2011, the third most common cause for admission was related to social reasons (4%). There were no admissions in the original study for this reason. Between 1999 and 2001, there were a wider range of reasons for admission across the mental illness spectrum compared to 10 years on. In previous studies, the largest diagnostic group for all admissions was schizophrenia spectrum disorders^7,8. However, between 2009-2011, more than a quarter of patients admitted to the Seacole Centre did not have any psychiatric diagnosis on admission. It is important to keep in mind that individuals with intellectual disabilities accessing specialist inpatient services are more likely to present with complex clusters of symptoms and behavioural problems that may span several diagnostic categories.

The most significant improvement from the original review and the re-review is that the number of re-admissions significantly reduced from 24% (14 patients) to 2% (1 patient). Of interest to note is that during 1999-2001 a large proportion of patients were discharged to their original place of accommodation (often the family home) whereas in 2009-2011, it was more common for patients to be discharged to a new place of living, more suited to managing increasing complex needs and behaviours. This may account for some of the reduction in re-admission rates.

The length of stay over the 10-year period has slightly increased from an average of 198.6 days up to 244.6 days, which demonstrate that admissions are considerably longer than in more generic medical settings. The findings are in keeping with a number of other studies regarding patients with intellectual disability who are admitted to a specialist unit and continue as inpatients for significantly longer periods. One study showed a mean length of stay 23.2 weeks for a specialist unit versus 11.1 weeks in generic settings ⁸. Another study in South London revealed similar finds of 19.3 weeks compared with generic unit stays of 5.5. weeks⁹. An exploratory national survey of intellectual disability inpatient services in England has shown that 25% of residents had been in the units for more than two years. Only 40% of residents had a discharge plan, and only 20% had both this and the type of placement considered ideal for them in their home area¹⁰. Reasons for length of stay are not fully understood in any of these studies. They may include fear of taking risks, lack of local safe or competent amenities, lack of experience or authority amongst those charged with sourcing bespoke services for complex people with challenging needs, and also a potential lack of such resource in terms of time available to see people, read reports, meet with stake holders and find the right services. The results of another retrospective study comparing the generic and specialist models in two districts in the UK by Alexander et al¹¹ suggested that, within the same district, patients do stay longer in the specialist unit, but they are less likely to be discharged to an out of area placement.

There is no evidence to suggest that comprehensive care for people with intellectual disabilities can be provided by community services alone. Likewise, there is also no clear evidence to suggest that a balanced system of mental health care can be provided without acute beds¹². There is, however, clear evidence that services created by the private sector are used very widely and seen as at time as an economically viable option in the current climate of credit crunches.

The different models of inpatient service provision that have been suggested range from mainstream adult mental health services; alternatively an integrated inpatient scheme whereby people with Intellectual disabilities with additional mental illness or severe challenging behaviour are admitted to adult mental health beds, with provision for extra support from a multidisciplinary learning disabilities team; ranging across to specialist assessment and treatment units^13,14.

Inpatient care is known to consume most of the mental health budget¹⁵ and specialist inpatient units are an expensive component of these services. Cost containment and cost minimisation of inpatient beds within the current economic recession presents a real challenge for those charged with responsibility to provide high-quality, effective, specialist care for adults with intellectual disability. Such cost reduction could be approached in a number of ways, through the reduction of length of stay, optimising drug budgets, reducing rates of re-admissions, and establishment of projects in association with the voluntary and statutory sector to facilitate prompt and safe discharge.

Reducing the average length of stay where possible can reduce the cost, and the resources and budget freed up in this way could be used for other service components¹⁵. However, this single agenda can lead to problems of pressured early discharge to unsuitable placements. It is known that resource consumption is most intense during the early stages of admission. As such, we observe a position whereby reducing length of stay requires proactive planning throughout the whole process of care, as well as active discharge planning, with a need for clearly defined pathways of care.

A crucial aspect of the patient's transition through inpatient placement to life in the community is efficient and regular communication between the relevant professionals and teams who form part of continuity of on-going care back in the community. This can at times be particularly challenging owing to differences in values and perceptions about patient need and problem, and also varying pressures. Understanding and resolving problems for individuals with complex and severe challenging behaviour or mental illness that requires a period of containment in a specialist service also requires specialist on-going work and risk management to ensure that when the problems are contained and understood, they remain contained and understood on discharge and thereafter so long as the individual remains vulnerable to the point of requiring any care giving. Many people from the general population who develop a serious mental illness requiring hospitalisation, have capacity once well, to make decisions for themselves and articulate a need or otherwise for specific care or intervention. This is rarely completely the case for people with Intellectual disabilities. Collaborative approaches together with those involved in community care is crucial to getting the right care at the right financial cost for this relatively small but very complex and vulnerable group of individuals.

Introduction

The global epidemiology of PD varies widely which could be partly accounted for by differences in survival rates.¹ One review paper examined the epidemiology of PD in Austria, the Czech Republic, France, Germany, Italy, The Netherlands, Portugal, Spain, Sweden and United Kingdom. It revealed that the prevalence rates range from 65.6 per 100,000 to 12,500 per 100,000 and annual incidence estimates ranged from 5 per 100,000 to 346 per 100,000.² The wide variation in incidence and prevalence rates of PD across Europe could be due to environmental and genetic factors. Differences in methodologies for case ascertainment, diagnostic criteria, or age distributions of the study populations, could also account for the wide variations.²

Described by James Parkinson in 1817, PD is the second most common neurodegenerative disorder next to Alzheimer’s dementia. Depletion of dopaminergic neurones in the substantia nigra is the main pathology found in PD. Symptoms usually appear when dopamine levels are reduced by 50-80%.³ Noradrenergic, cholinergic and serotonergic pathways are also affected. Clinically PD is characterised by rigidity, tremor (cogwheel, lead pipe, and resting), akinesia, bradykinesia (poverty and slowness of movement), and postural instability (leading to frequent falls).⁴ These symptoms may also be accompanied by a range of non-motor symptoms other than well-known neuropsychiatric syndromes of depression, psychosis, and cognitive impairment.

In essence, a syndrome is a combination of signs and symptoms related to an underlying pathological process. PD may present with neuropsychiatric syndromes of depression, psychosis (usually affective in origin) and cognitive impairment.⁵ These syndromes are not under discussion here as readers are likely to be familiar with them. However, PD may also present with other neuropsychiatric syndromes and for the purpose of this article we have classified them into: 1) Anxiety disorders, 2) Apathy, 3) Involuntary emotional expression disorder, 4) Sleep disorders, and 5) Impulse control disorders.

Drugs used to treat PD themselves are associated with neuropsychiatric side effects. For example, dopamine agonists are well-known to cause sleep disturbance, dizziness (usually due to postural hypotension), hallucinations, hypersexuality, and compulsive gambling. Anticholinergics may cause confusion, hallucinations and impaired memory. Surgery also may cause adverse effects including depression, confusion and cognitive impairment.⁶ Table 1 illustrates the groups of drugs used in PD.

Overlooked neuropsychiatric syndromes in Parkinson’s disease

The prevalence of overlooked neuropsychiatric syndromes found in PD, summarised in Table 2, is generally less common than PD syndromes of depression (up to 50%),psychosis (up to 60%) and dementia (ultimately develops in 80%).^{7, 8, 9}

Anxiety Disorders

Epidemiology

There is a wide range in the reporting of the prevalence of anxiety in patients with PD. Anxiety is significantly more prevalent in PD sufferers compared with age and sex matched non-sufferers. Prevalence is quite high with estimates indicating that up to 40% of PD patients suffer significant anxiety.¹⁰ However, clinicians’ recognition and awareness of anxiety in PD need to be raised because it is likely to be under-diagnosed and untreated.^{11, 12} Consequently the prevalence of anxiety may be even higher. Severity of anxiety is not correlated with severity of parkinsonian symptoms, duration of levodopa use, or current dose of levodopa.

Aetiology and risk factors

Anxiety is an understandable psychological response to the physical symptoms, to the neurochemical changes of the disease itself, or as a side effect of the various medications used to treat the condition.¹⁰ Sleep disturbances and cognitive impairment have been proposed as possible aetiological factors for anxiety in PD.^{11, 12} Depression in PD may manifest in two clinical phenotypes, one ‘anxious-depressed’ and the other ‘depressed’. However, a further large proportion of patients can have relatively isolated anxiety.¹³

Anxiety frequently precedes the development of motor symptoms, suggesting specific neurobiological processes are involved, not merely social and psychological reactions in learning to adapt to PD.¹⁴

Patients with postural instability and gait dysfunction have a higher incidence of anxiety compared with tremor-dominant patients. Younger-onset PD patients are also more likely to experience anxiety. The pathogenesis of anxiety involves noradrenergic, serotonin and dopamine neurotransmitters. GABAergic pathways may also be involved.¹⁴ Right hemisphere disturbances have also been implicated, particularly with panic disorder.Symptom variation in PD may be due to medication, as well as motor fluctuations.¹¹ One study revealed that although the dose of levodopa was not associated with anxiety, the experience of dyskinesia or on-off fluctuations increased the risk of anxiety.^{12, 14, 15}

Presentation and diagnosis

The commonest disorders found in PD are generalised anxiety, panic disorder, and social phobia. Anxiety contributes to the complexity of PD and lowers quality of life. ^{14, 15} The degree of comorbidity between anxiety and depression in PD patients is in excess of that found in patients without PD. While anxiety is significantly associated with depression, some patients show anxiety without depression.¹⁰

The main features of anxiety are inappropriate feelings of apprehension as well as mood, cognitive, and somatic changes. Some symptoms may be common to PD, such as autonomic symptoms, fatigue, muscle tension, insomnia and attention problems. Psychologically, anxiety in PD is understandable because being diagnosed with a chronic disease with no known cure and an inexorable course, would be difficult for anyone to contemplate. Motor signs and changes in appearance could explain social anxiety. However, the frequency of anxiety in PD seems to be higher than in other chronic diseases and unrelated to the severity of motor signs. Even in social phobia the phobic symptoms do not correlate with disease severity and are not restricted to performance situations. Furthermore, anxiety can precede motor signs by several years, suggesting that the neurobiological substrate of PD is responsible for anxiety at least in part.

Treatment

Treatment comprises the use of selective serotonin reuptake inhibitors (SSRIs) such as sertraline, fluoxetine and citalopram as well as other newer antidepressants - serotonin and noradrenaline reuptake inhibitor (SNRIs) for example, venlafaxine, cognitive behavioural therapy (CBT), exercise, the occasional use of atypical neuroleptics, and benzodiazepines.¹⁴ However, benzodiazepines have a tendency to cause sedation, unsteadiness of gait, and even confusion. Antidepressants are useful because they treat both anxiety and depression that often overlap: depression coexists with anxiety in 14% of cases.¹⁵ Low dose tricyclic antidepressants with minimal anticholinergic effects may be useful in those patients who do not respond to benzodiazepines.

Apathy

Epidemiology

Apathy, a state of lethargic indifference and loss of motivation, and fatigue are prominent non-motor symptom in PD with a prevalence of between 16-42%.^{16, 17} Fatigue is a sense of tiredness or exhaustion, due to mental or physical causes. Apathy and fatigue are important because they have significant repercussions for the quality of life in PD.^{18, 19} Apathy can exist without depression but, by definition, patients themselves do not complain of apathy, though are found to be unmotivated to engage in activities. Apathy and fatigue are often difficult to distinguish from low mood and daytime sleepiness, both of which are common to depression.

A four-year prospective longitudinal study of 79 patients found that 13.9% of those with PD had persistent apathy and 49.4% had developed apathy at follow up. The study showed apathy to be a frequent and persistent behavioural feature in PD with a high incidence and prevalence over time, and associated with neurotransmitter deficits.²⁰

Aetiology and risk factors

The dorsolateral, medial and orbital frontal cortices, as well as subcortical structures such as the basal ganglia, thalamus and internal capsule are implicated in the pathogenesis of apathy.The independent risk factors for apathy are dementia at baseline, a more rapid decline in speech, and axial impairment (e.g. poor ability to turn in bed) during follow up.^{20, 21} A more recent study showed that male gender, higher depressive scores, and severe motor symptoms, were significantly associated with apathy, but not with greater cognitive impairment.²² It has been observed that deep brain stimulation (DBS) may contribute to the development of apathy²³ but other studies show conflicting results.²⁴

Presentation and diagnosis

There is a higher incidence of depression and dementia in PD patients with apathy.Therefore differential diagnosis between apathy and cognitive deficits and depression is essential because the therapeutic approaches are different.^{19, 20} It is equally important to differentiate between apathy and depression that are different clinical entitiesalthough both may coexist.The crucial difference is that people with apathy lack serious self-reproach or feelings of guilt. ^{21, 25} The Lille Apathy Rating Scale (LARS), administered as a structured interview, can be a useful tool to distinguish them both²⁶ though further research is needed to differentiate the neurological and neurochemical basis for depression and apathy.

Treatment

Treatment options for apathy are limited. The use of methylphenidate, a stimulant drug related to amphetamine, has been suggested but evidence is scarce and side effects may outweigh its clinical benefit.²⁷ Methylphenidate has been described as effective for both apathy and fatigue²⁸ but more studies are necessary. Antidepressants are not effective, can cause unnecessary side effects and can even aggravate apathy, demonstrating that these syndromes are really independent.²⁹ The association between cognition and apathy, along with the potential benefit of cholinesterase inhibitors on both cognition and apathy, suggests that cholinergic mechanisms take part in the pathophysiology of apathy.^{30, 31} ’Off-time’ refers to periods of the day when the medication is not working well, causing worsening symptoms of fatigue and apathy. ‘Wearing-off’ episodes may occur predictably and gradually, or they may emerge suddenly and unexpectedly. Wearing-off periods may be improved with appropriate changes in the medication regimen. This would mean optimizing dopaminergic agents or using a long-acting levodopa or a catechol-O-methyltransferase (COMT) inhibitor. Wearing off may be also better controlled by shortening the time between medication doses. In a study of 23 PD patients in both the 'on' and 'off' states compared to 28 controls, L-dopa had a positive effect on motivation suggesting striatofrontal loops are involved.³²

Involuntary emotional expression disorder

Epidemiology

Involuntary emotional expression disorder (IEED) has been found to occur in 16.8% of PD patients, and in 15.3% if comorbid depressive disorder was excluded.³³ However, other studies suggest that the symptoms of IEED are present in up 15% of PD patients but the actual IEED disorder occurs in half of these cases.³⁴ This implies that IEED symptoms occur in PD but the condition of IEED is not present although this may depend on the criteria used for the diagnosis. If IEED does develop in PD it is particularly common in the later stages of PD and is likely to be distinct from depressive disorderwhich remains an important differential diagnosis.^{33, 35}

Aetiology and risk factors

IEED can occur in neurological conditions such as stroke, traumatic brain injury, amyotrophic lateral sclerosis, multiple sclerosis, seizure disorders, multiple system atrophy, corticobasal degeneration, and Alzheimer’s disease.³⁵ Injury to the neurological pathways that control the expression of emotion have been implicated in its pathogenesis. Emotional expression involves various pathways within the frontal lobe, limbic system, brainstem and cerebellum, with disruption of regulatory and inhibitory mechanisms in this network implicated.^{36, 37}

Presentation and diagnosis

IEED is described as sudden episodes of laughing or crying that may be spontaneous or disproportionate to the triggering stimuli.The emotional outbursts of IEED may involve laughter, crying or anger. The episodes all share common features in that they are involuntary, uncontrollable, and excessive, not sustained, and usually last from seconds to minutes. Outbursts are often stereotyped though single individuals may have episodes of both laughing and crying.IEED is also known as pseudobulbar affect, pathological laughter and crying, emotional lability, emotionalism, and emotional dysregulation.Despite the various terms used to describe the disorder, IEED is often missed and even sometimes mistaken for depression.^{33, 35} Symptoms of IEED are important because they are associated with an impairment of social and occupational functioning.³⁸ It is hypothesized that neurological disease and injuries affect the excitatory action of glutamate, leading to excessive glutaminergic signalling and increased electrical activity in neurons. As glutamate is the primary excitatory neurotransmitter of the central nervous system, stabilizing or reducing glutaminergic activity could prove useful in the treatment of IEED.³⁹

Treatment

Medication options include the use of SSRIs, tricyclic antidepressants (TCAs) for example, amitriptyline, and less frequently dopaminergic agents.A combination of dextromethorphan and quinidine has also been suggested. ^{35 38}

Sleep disorders

Epidemiology

Sleep disorders have been known to affect 60-98% of patients with PD.⁴⁰

Aetiology and risk factors

The aetiology of sleep disorders includes PD itself or other comorbid conditions such as depression, and cognitive impairment.⁴¹ Nocturnal pain from rigidity or dystonia, restless legs syndrome, and autonomic disturbance leading to nocturnal frequency and urgency, also contribute to insomnia. Degeneration of sleep regulatory centres in the brainstem and thalamocortical pathways, side effects of drugs, motor impairment, and incontinence may affect sleep. Sleep disorders may precede the onset of motor symptoms. Rapid Eye Movement (REM) sleep behaviour disorder (RBD), which occurs in almost a third of PD patients,is often associated with cognitive impairment and hallucinations. This disorder is directly related to the degenerative process of the pedunculopontine nucleus, the locus subceruleus and the retrorubral nucleus. A sudden onset of the disorder is almost always due to the introduction or the withdrawal of drugs, especially antidepressants. Curiously, parkinsonism can disappear during the RBD.⁴²

Sleep fragmentation is the earliest and most common sleep disorder in PD, and gradually worsens as the disease progresses. Vivid dreaming, nightmares and night terrors are common and occur in up to 30% of patients using levodopa for long periods. Dream content is probably altered in PD and many patients vocalize during sleep. Vocalization may vary from incomprehensible sounds to detailed conversations, laughing, cursing or screaming. Excessive daytime sleepiness and 'sleep attacks' affect half of patients with PD and may precede disease onset. The causes are a combination of the disease process, the consequence of other sleep disorders and medication. A sudden onset of sleep during the day is a phenomenon in PD which resembles narcolepsy, and it is commonly associated with dopaminergic drugs. PD patients may be more prone to restless legs syndrome, periodic limb movements and obstructive sleep apnoea.

Sleep disorders in PD are seldom diagnosed and treated. Although an accurate diagnosis of a particular sleep disorder depends on polysomnography, sometimes the diagnosis can be based on clinical observation. Treatment is based on the correct diagnosis and underlying cause of the sleep disorder. Often it is difficult to decide whether excessive daytime sleepiness is cause or consequence of insomnia.⁴³

Presentation and diagnosis

Sleep disorders may manifest as insomnia, excessive daytime sleepiness and sleepwalking.^{44, 45} Sudden attacks of sleepiness are known to occur during stimulating activities such as walking, eating, and even driving a car. These sudden sleep episodes can be associated with medication such as dopamine agonists and levodopa.⁴⁶

RBD is characterised by the loss of the normal atonia during dreaming. In other words, patients act out their dreams as manifested by crying out, kicking or thrashing about during their sleep. RBD can predate the development of motor symptoms by several years and a longitudinal study of a cohort of 26 patients found an association between RBD and the later development of PD. ⁴⁷

Treatment

Management involves the review of medication that may be contributing to the sleep disorder. Treatment of comorbid conditions such as depression and cognitive impairment is essential.

Sleep hygiene is the initial and basic measure applied to all patients. For instance, stimulating patients during the day can decrease the excessive naps and improve sleep at night, thus improving daytime sleepiness. Additional techniques include going to bed only when sleepy, exposure to natural and bright light during day, reduction of light and noise exposure at night as much as possible, and maintenance of a regular schedule.

Long-acting dopaminergic drugs might improve insomnia caused by worsening of motor symptoms at night. Clonazepam, a benzodiazepine, is efficacious and well tolerated by the majority of patients afflicted by RBD and should be considered as initial treatment.⁴⁸ Antidepressants with a sedative effect might be helpful in cases of insomnia with comorbid depression or anxiety. Quetiapine, an antipsychotic which has sedative properties as a side effect, may be a safe and effective treatment for insomnia in PD because it has no untoward effects on motor function.⁴⁹ Small clinical trials with Modafinil for excessive daytime sleepiness had controversial results. An additional remark concerning treatment of sleep disorder in PD is that sleep may provide a short-term benefit on motor symptoms.^{28, 43}

Impulse control disorders

Epidemiology

A large multi-centre investigation (the DOMINION study) of 3,090 patients with PD revealed that impulse control disorder (ICD) was identified in 13.6% of PD patients; specifically, pathological gambling in 5%, compulsive sexual behaviour in 3.5%, compulsive buying in 5.7% and binge-eating disorder in 4.3%.⁵⁰ The prevalence of ICD rises to 14% for patients taking dopamine agonists, compared with 0.7% for patients taking levodopa alone.⁵¹ It is not clear whether these ICD symptoms reflect a primary pathology of PD or whether dopaminergic medication is interacting with an underlying predisposition or vulnerability.⁵² Possible neurobiological explanation centres around dopamine-receptor binding profiles. Dopamine D2 and D1 receptors, abundant in the dorsal striatum, may mediate the motor effects of dopamine replacement therapies, whereas D3 receptors are abundant in the ventral striatum, a brain region associated with addictive behaviour and substance misuse disorders. Second generation non-ergot dopamine agonists (e.g. pramipexole and ropinirole) demonstrate relative selectivity for D3 receptors compared with D2 and D1 receptors.⁵⁰

Aetiology and risk factors

Addiction to dopaminergic medication used in the treatment of PD may explain behaviours such as drug-seeking, gambling, and hypersexuality. The risk of pathological gambling increases if dopamine agonists are used in those with younger age of onset, higher novelty seeking traits, and a personal and family history of alcohol misuse.⁵³

Presentation and diagnosis

In addition to the above PD patients with ICD may present with compulsive shopping, compulsive eating, and compulsive medication use, all of which can have potentially devastating psychosocial consequences because they are often hidden. Complex stereotyped repetitive behaviours (punding) may also be present.⁵⁴Punding behaviour is stereotyped and purposeless and includes hoarding, shuffling papers, sorting labels, assembling and disassembling objects, to name a few.

Treatment

Stopping dopaminergic medication should be considered in the first instance. Further treatment options are limited but one double-blind crossover study demonstrated the use of amantadine in abolishing or reducing pathological gambling.⁵⁵ In addition, one case report suggested the antipsychotic quetiapine to be effective in treating pathological gambling.⁵⁶ Whether other treatments, such as DBS, are effective for these compulsive repetitive behaviours, remains to be seen.

Management of overlooked neuropsychiatric syndromes in PD

Because of the significant disability and impact on quality of life caused by overlooked neuropsychiatric symptoms in PD, it is important for neurologists and psychiatrists to recognise them and develop their clinical skills in order to be aware of their significance. Early detection is crucial. We have shown there is a limited range of treatment strategies available to guide the clinician in treatment choices. Because neuropsychiatric diagnoses in PD are different in phenomenology it is important to remember that treatment with 'psychiatric' drugs will often be insufficient and therefore more consideration should be given to 'antiparkinsonian' medications because the underlying pathology of PD is causing the various syndromes mentioned.

Table 3 provides an overview of the medical treatment of overlooked neuropsychiatric syndromes in PD, although it should be noted that overall very few studies document the effectiveness of the solutions proposed and more controlled studies are needed. Nonetheless, the reader should find the following useful.

Conclusion and implications

The management of PD is often complicated because of the diverse factors underlying its aetiology. Dopaminergic, serotonergic, noradrenergic and cholinergic pathways are involved.⁵⁷ Clinicians are generally competent in recognising the more common disorders such as depression, psychosis and cognitive impairment associated with PD though there is a tendency to focus too much on these at the expense of other nonmotor symptoms. Anxiety, apathy, involuntary emotional expression disorder, sleep disorders, and impulse control disorders cause significant disability and impact heavily on patients and carers.

Before introducing treatment for psychiatric complications it is essential to exclude causes such as antiparkinson’s medication, DBS (implicated in apathy), and underlying medical conditions. Once excluded or treated, subsequent management includes psychotropic pharmacotherapy but there are limited options. With no specific drug designed to treat the overlooked conditions, a wide range of medications (e.g. antidepressants, antipsychotics, benzodiazepines, dopaminergic agents, and psychostimulants) are available to manage the symptoms.

Neurologists and psychiatrists need to work together to manage these syndromes and they must be innovative in setting up joint research ventures into developing treatment options. Simple questionnaires may alert physicians when presenting symptoms are abstruse because many of the nonmotor symptoms predate the motor symptoms⁵⁸ (the presymptomatic phase of stages 1-2 of Braak's classification system).^{59 60} For example, anosmia, constipation and other autonomic symptoms are not considered neuropsychiatric syndromes per se, but are some of the nonmotor problems associated with PD and may give clues that PD is developing.

Despite research highlighting the presence of these disorders in PD, they generally go unrecognised by clinicians, being less common, and therefore psychiatrists in old age and adult psychiatry as well as general neurologists may lack skills to recognise them. Besides, there are no clear treatment guidelines on how to manage the conditions.

Post- graduate medical education in the United Kingdom has seen numerous dramatic changes in the last decade, with the introduction of structured training programmes and changes in assessment of skills driven by Modernising Medical Careers.¹ Overall these new developments emphasise a competency based curriculum and assessments. Alongside and contingent on these wider changes in medical education, psychiatric trainees have faced major transformations in their membership (MRCPsych) examinations.

The MRCPsych examination was first introduced in 1972, a year after the Royal College of Psychiatrists was founded. There have been various modifications in its structure since its inception but a radical change occurred in the last decade with the introduction of an OSCE in 2003 and the CASC, a modified OSCE in June 2008. The CASC is considered as a high- stakes examination as it is now the only clinical and final examination towards obtaining the membership of the College. The MRCPsych qualification is considered as an indicator of achieving professional competence in the clinical practice of psychiatry and has the main aim of setting a standard that determines whether trainees are suitable to progress to higher specialist training.² In his commentary to Wallace et al³ , Professor Oyebode describes the aims, advantages and disadvantages of the various assessment methods used in the MRCPsych examination and conclude that the precise assessment of clinical competence is essential.⁴

Traditionally, assessment of clinical skills involved a long case examination since it was introduced in clinical graduating examination by Professor Sir George Paget at Cambridge, UK in 1842. This has been followed by most of the medical institutions worldwide and remained as the clinical component of the MRCPsych examination until 2003. There are some shortcomings with this assessment method and the outcome can be influenced by several factors such as varying difficulty of the cases, co-operation of the real patient and examiner- related factors. The reliability of assessment of clinical competency with a single long case is low and it is necessary for the candidate to interview at least ten long cases to attain the reliability required for a high stakes examination like MRCPsych.⁵ A fair, reliable and valid examination is necessary to overcome these difficulties. The OSCEs proved to be one of the answers to these difficulties.

One important aspect of assessing the validity and acceptability of assessment methods is asking the opinions of examiners and candidates about their experiences and views about the examination once it has been rolled out. As far as the authors are aware there has been one previous published survey of CASC candidates’ views on this method of examination and this was based at a revision course. Whelan et al⁶ showed that approximately 70% of the candidates did not agree with the statement “there is no longer a need to use real patients in post-graduate clinical psychiatry exams”. In addition, only 50% of the candidates preferred the CASC compared to previous long case and the other 50% remained undecided. This raises doubts about the acceptability of the CASC format and merits further exploration.

Method

We conducted a national on-line survey asking both candidates and examiners about their views on the CASC examination.

Questionnaire development

Two questionnaires (one each for examiners and candidates) based on previously available evidence on this exam format^6,7,8 were developed following discussions among the authors.

The final version of the questionnaire for both groups had the same seven questions with a five point Likert scale. It included questions on whether the exam effectively assessed the competency needed for real life practice, whether there was over testing of communication skills, whether feedback was adequate, respondents’ views on validity and reliability of the method and finally whether the clinical examination should revert to the previous style of long case and viva.

Sampling procedure

The examiners and the candidates who have already appeared in the CASC examination were invited to complete the online survey. The links to the questionnaires were distributed via the Schools of Psychiatry in thirteen deaneries in the United Kingdom (including Wales, Northern Ireland and Scotland). We approached 400 candidates and 100 examiners from different deaneries making sure the wide geographical distribution. The sample size was chosen based on the data that around 500 candidates appear in CASC exam each time and there are approximately 431 examiners on CASC board (personal contact with the College).Participants were assured that their responses were confidential. The survey was open from mid-March to mid-April 2011. Reminders were sent half way through the survey period.

Results

A total of 110 candidates and 22 examiners completed the survey. The response rate was better for candidates (27.5%) compared to the examiners (22%). Albeit the low response rate, the responses showed good geographical spread. Responses were received from most of the deaneries (87%). The London, East and West Midlands deaneries showed higher response rate (14% each) while Scotland, Severn and North Western deaneries showed least response rate (2% each).

Among the 110 candidates, 52% were males and 48% were females and among the examiners, 73% were males and 27% were females. 55% of the examiners were involved in the previous Part 2 clinical exam while only 7% of the candidates had the experience of previous Part 2 clinical exam. The results are summarised in Tables 1 and 2.

Clinical competencies and skills

59% of the examiners and 48% of the candidates have accepted that CASC examines the required competencies to progress to higher training. Strikingly only 18% of the examiners and 15% of the candidates agreed that CASC allows the assessment of all the skills and competencies necessary for the higher trainees in comparison to the previous Part 2 clinical exam.

Content of the CASC

Majority of the examiners (77%) and nearly half of the candidates (48%) agreed that CASC scenarios reflect real life situations faced by clinicians in normal practice. However 60% of the candidates and 48% of the examiners felt that CASC excessively emphasizes communication and interview skills.

Feedback - “areas of concerns”

More than half of the candidates (60%) and half of the examiners (50%) felt that the feedback indicating “areas of concerns”, for the failed candidates was not helpful to improve their preparations before the next attempt.

Validity and reliability of the CASC as a clinical exam

Just over one fourth of the candidates (28%) and less than half of examiners (46%) considered CASC as a valid and reliable method of clinical examination. However, only 36% of the candidates and 32% of the examiners supported replacing CASC with a traditional clinical exam (a long case and a viva). Broadly comparable numbers (39% of the candidates and 27% of the examiners) disagreed with the statement that the CASC should be replaced by the previous examination style.

Discussion

To our knowledge this is the first study of candidate and examiner views since the introduction of the CASC. Its predecessor OSCEs has a good reliability and validity in assessing medical students⁸ and it has become a standard assessment method in undergraduate examinations. Whilst OSCEs have been held to be reliable and valid in a number of assessment scenarios,8 there have been doubts about their ability to assess advanced psychiatric skills,⁹ which was one of the main reasons to retain the long case in MRCPsych Part 2 clinical exam.2 Over the years, most of the Royal Colleges introduced OSCEs into their membership examinations and used simulated patients in some scenarios. However CASC is the first examination with only simulated patients in a combination of paired and unpaired stations. So far there has been no published literature evaluating this method systematically.

In a recent debate paper¹⁰ it has been argued that CASC may have significant problems related to its authenticity, validity and acceptability. The findings of our survey reflect similar doubts about the reliability and validity of the CASC exam amongst both the candidates and examiners. The content validity of CASC has been demonstrated by the College Blueprint¹¹ and the face validity appears to be good. However, as far as we are aware, the concurrent and predictive validity testing data have not been published. Although the global marking system appears to have better concurrent validity than other checklists, it gives the examiners the similar flexibility as the long case in making judgements which may affect CASC transparency and fairness. This may indicate that this new and promising examination method requires further systematic evaluations and modifications before its user’s fully accept it.

According to the results of our study the content of the CASC exam satisfies its purpose of assessing the candidates’ competencies to progress to the higher professional training. However many of the respondents felt that it lacked the completeness of previous traditional clinical examination, which collate skills. Although there were some differences between the candidates and the examiners on how they perceived the CASC exam, most of the respondents agreed that CASC laid more emphasis on communication and interviewing skills rather than overall assessment of the candidate’s competency.

Harden et al,¹² in their paper on OSCEs, criticised the compartmentalisation of knowledge and discouraging candidates from a broader thinking during the clinical examinations. They also suggested using a long case and/or workplace based assessments rather than relying on OSCEs only in assessing trainees. Benning & Broadhurst¹³ expressed similar concerns on the loss of long case in MRCPsych examination. Our findings support the arguments that CASC assesses competencies in a piecemeal fashion rather than being reflective of the demands on senior doctors in real practice which often involve deciding what is and is not important depending on context.

The OSLER¹⁴ (Objective Structured Long Examination Record) method might overcome the shortcomings and improve the objectivity and transparency of long case. In this method, two examiners assess the candidate and grade their skills individually in a ten item objective record. Later they decide together the appropriate grade for each item and agree an overall grade. The ten items include four on history, three on examination and another three covering investigations, management and clinical acumen. The OSLER method is also practical as no extra assessment time is required and it can be used for both norm referenced & criterion referenced exams. The case difficulty can be determined by the examiners and all candidates are assessed for identical items. Thus this method assesses the candidate’s overall clinical competency and eliminates the subjectivity associated with the long case.

Another alternative might be using a combination of assessment methods as suggested by Harden.¹² An 8-10 stations OSCE can be combined with a long case assessment using OSLER method. The OSCE stations might include patient management scenarios along with interview and communication skills scenarios. The final score determining the result could also include marks from work place based assessments as they provide a clear indication of the candidate’s skills and competence in real life situation.

It is also evident from our findings that both candidates and examiners are largely unsatisfied with the extent and usefulness of feedback that is provided to unsuccessful candidates. The feedback system have been criticised for its inability to clarify the specific areas or skills which need to be improved by the unsuccessful candidates. The recent “MRCPsych Cumulative Results Report’’ ¹⁵ states that the pass rate of the candidates declines after the first attempt. Perhaps this could be improved if failed candidates receive more detailed feedback about their performance.

There are a number of limitations to this study. The response rate was low but it was broadly in the range of other online surveys¹⁶ and there was representation from most of the deaneries in the United Kingdom. There could be a number of reasons for low response rate. As far as we are aware few deaneries were not willing to distribute the questionnaire through their School of Psychiatry and we had to contact the individual trusts in the area to distribute the survey. The poor response rate from the examiners could be because of their low interests in participating and lack of time. Also older examiners and those with more experience of CASC may have had particular views which might have had an influence on the responses. But when this was examined further, there were no major differences between respondents who had the experience of previous Part 2 examinations from those who had not. In addition one of the survey questions consisted of two parts (views on validity and reliability) which could have been difficult to answer accurately.

The findings of this preliminary study raise some doubts on acceptability of the CASC by both candidates and examiners. There might be a possibility of subjective bias in the responders’ views, perhaps influenced by other ongoing and controversial changes in the NHS, including the role of GMC and the College in the post- graduate medical education. However on the other hand it might be a signal that it is worthwhile to reconsider the implications of the CASC on education and training and to evaluate systematically this assessment method further.

Introduction

Prolactin is a polypeptide hormone that is secreted by lactotrophs of the anterior pituitary gland. Prolactin secretion shows a circadian rhythm¹, with highest levels occurring during the night and the nadir occurring during the afternoon and eveningThe best known function of prolactin is the stimulation and maintenance of lactation.

Normal basal levels of serum prolactin are approximately 20 to 40 ng/ml in women (depending on the phase of their menstrual cycle), and 15 ng/ml in men. However, these concentrations can also vary with ageHyperprolactinemia is diagnosed when serum prolactin concentrations are >20-25 ng/ml (400-500 mU/l) on two separate occasions³.

Hyperprolactinemia is the most common disorder of the hypothalamic-pituitary-gonadal (HPG) axis⁴ and can have physiological causes - pregnancy, nursing, sleep, stress, sexual intercourse or pathological causes - tumor called prolactinomaMultiple factors are involved in prolactin secretion (Figure 1). However, hyperprolactinemia is also a common side-effect of traditional antipsychotics (e.g. haloperidol) and is associated with the use of some newer second generation agents^{2, 6}.

Figure 1: Factors involved in Prolactin secretion

The prevalence of hyperprolactinemia is low in the general population (0.4%), but it can be as high as 9 to 17 % in women with reproductive disordersThe disease occurs more frequently in women than in men, multiple signs and symptoms associated with hyperprolactinemia (Table 1).

Multiple variables affect probability of development of breast cancer (Table 2) and a number of important factors determine the risk for breast cancer, and the most important of these seem to be related to estrogen and possibly prolactin (Table 3).

Methods

Pubmed.gov searched by using keywords

Antipsychotics and Hyperprolactinemia

Hyperprolactinemia is caused by these agents by blocking D2 receptors on lactotrophs and thus preventing inhibition of prolactin secretion. Furthermore, it has been suggested that the degree of elevation of prolactin correlates with the degree of occupation of D2 receptors in excess of 50%⁸.

Most studies have shown that conventional antipsychotics are associated with a two to tenfold increase in prolactin levels^{9, 10}. In general, second generation antipsychotics produce a lower increase in prolactin than conventional agentsAmong second generation antipsychotics associated with increased prolactin are amisulpride, zotepine and risperidone^{11, 12, 13}.

Antipsychotic induced Hyperprolactinemiaand Breast cancer

Prolactin is known to increase the incidence of spontaneously occurring mammary tumors in mice¹⁴ and increase the growth of established carcinogen-induced mammary tumors in rats¹⁵.

Prolactin and other sex hormones such as, estradiol and progesteroneare important in normal mammary gland growth and developmentas well as lactation. Both animal and in vitro data suggestthat prolactin is involved in tumorigenesis by promotingcell proliferation, increasing cell motility,and improving tumor vascularization. Whereas prolactinand its receptor are found in normal and malignant tissues,concentrations of both are generally higher in malignant tissue¹⁶.

Several studies have linked hyperprolactinemia to an increased risk of breast cancer in women^{17, 18}. Mechanisms that have been suggested to explain this possible action of prolactin include the increased synthesis and expression of prolactin receptors in malignant breast tissue and a prolactin-induced increase in DNA synthesis in breast cancer cells in vivo¹⁸.

One of the hypothesized roles of prolactin in the development of mammary tumors is to create mammary gland conditions favorable for the action of carcinogens through its stimulation of the rate of mammary gland DNA synthesis, a measure of the frequency of mammary gland cell division¹⁹.

Several epidemiological studies have investigated whether female psychiatric patients receiving treatment with antipsychotics have a higher incidence of breast cancer but results have been conflicting. However, the most recent and methodologically strong study, found that antipsychotic dopamine receptor antagonists conferred a small but significant risk of breast cancer. This study had a retrospective cohort design and compared women who were exposed to prolactin-raising antipsychotics with age-matched women who were not²⁰.

Conversely, other studies have shown no correlation between hyperprolactinemia and breast cancer^{21, 22}. Furthermore, as most breast cancers are thought to be fueled by estrogen²³, and hyperprolactinemia causes estrogen deficiency²⁴, it is perhaps surprising that hyperprolactinemia has been linked with an increased risk of breast cancer. Indeed, post-operative hyperprolactinemia in breast cancer patients has been shown to improve disease free and overall survivalObviously, more studies are necessary to define any possible links between hyperprolactinemia and breast cancer.

In view of these problems it would be of interest to go around the contentious issue of possible carcinogenic effects of dopamine antagonists using a classical condition of dopamine loss or attenuation as in Parkinson's disease (PD). Using computerized registers of death data of the National Center of Health Statistics for years 1991 through 1996, estimated 12,430,473 deaths of persons over forty, and extracted 144,364 cases with PDTellingly, PD patients showed a highly significant reduction of overall cancer incidence. PD resistance to breast cancer might conceivably be attributed to dopaminergic treatment antagonizing hyperprolactinemia^{26, 27, 28}.

Another recent study showed that dopaminergic therapy inhibits angiogenesis thereby acting as an anti-tumor agent²⁹.

Epidemiological studies of women who have received prolactin-releasing drugs such as reserpine and perphenazine have not disclosed increased risk³⁰.

Antipsychotic induced Hyperprolactinemia and Other cancers

Antipsychotics have been hypothesized to account for the reduced cancer occurrence observed in patients with schizophrenia in a number of studies. This reduction has been found primarily in men in smoking-related cancers, and in prostate and rectal cancer.

In addition, a study found a reduced risk of rectal cancer in both men and women as well as indications of a reduced risk of colon and prostate cancer in this population-based cohort of neuroleptic users. Reassuringly, they observed no increased risk of breast cancer in female users³¹.

Comments and recommendations

• Hyperprolactinemia results from treatment with any drug that disrupts dopaminergic function on the HPG axis and is not limited to the use of antipsychotics.
• Management of supposed anti-psychotic associated hyperprolactinemia should exclude all other causes, involve regular monitoring of adverse effects and include a regular risk-benefit discussion with patient.
• Switching the patient to prolactin-sparing antipsychotic (i.e. Aripiprazole, Olanzapine, Quetiapine or Clozapine) usually proves effective, though there is also a risk of relapse.
• It seems prudent to avoid prescribing prolactin-raising antipsychotics in patients with past history or family history of breast cancer.
• It is premature to mandate warning patients of an unknown and undemonstrated increase in the risk of developing breast cancer associated with neuroleptic treatment.
• Before initiating antipsychotic treatment a careful examination of patient is necessary.
• One should examine the patient for evidence of sexual adverse events, including menorrhagia, amenorrhoea, galactorrhoea and erectile/ejaculatory dysfunction. If evidence of any such effects is found, then the patient's prolactin level should be measured.
• Patient history, physical examination, pregnancy test, thyroid function test, blood urea and creatinine level can help determine if other etiologies are responsible.
• Presence of headache and visual field defects is suggestive of a sellar space-occupying lesion (MRI indicated), but the absence of these features does not exclude such pathology.
• History of menstrual cycling (duration, amount and intervals of menstruation) as well as lactation and sexual functioning should be taken before antipsychotic medication is initiated.
• Obtain a pretreatment prolactin level, which one can compare with subsequent samples if the patient develops symptoms associated with relatively modest hyperprolactinemia.
• The risk-benefit ratio for treatment of antipsychotic-induced hyperprolactinemia needs to be assessed on an individual basis.
• If there is doubt about the cause of the hyperprolactinemia, patient should be referred to an endocrinologist.

Current recommendation

A rise in prolactin concentration should not be of concern unless complications develop, and until such time no change in treatment is required.²⁰

Conclusions

There is no definitive data suggesting increased risk of breast cancer available at this time, thus author concludes:

• Further prospective studies are needed in this area, with large number of patients, before a more definitive answer can be provided.
• Detection of existing mammary tumor by breast examination or studies (mammogram) is recommended prior to administration of neuroleptics.
• Development of newer antipsychotic drugs that do not increase serum prolactin level may be indicated.

Strengths

• Each article found by search term was reviewed
• Data were extracted from each article to find answer of research question
• Pubmed.gov is a huge database for search.

Limitations

• This literature review has been conducted by a single author, thus bias on part of author cannot be ruled out
• Author was limited by time to review articles available in other databases.

Introduction:

Non adherence to medication is a significant problem for client group in Psychiatry. Between a third and half of medicines that are prescribed for long term conditions are not used as recommended^{2, 3}. In the case of Schizophrenia, studies reveal that almost 76% of the sufferers become non-compliant to the medication within the first 18 months of treatment ⁴.

Non-adherence has consequences for both clients and the Health Care System. If the issues of non-adherence are better identified and addressed actively, it has the potential of improving the mental health of our clients which will reduce the burden of cost to mental health resources. It is estimated that unused or unwanted medications cost the NHS about £300 million every year. This does not include indirect costs which result from the increased likelihood of hospitalization and complications associated with non-adherence⁵.

The WHO identified non-adherence as “a worldwide problem of striking magnitude”. This problem is not only just linked with our psychiatric client groups, but also is prevalent with most chronic physical conditions. It has been reported that adherence to medications significantly drop after six months of treatment⁶.

In broad term compliance is defined as the extent to which the patient is following the medical advice. Adherence on the other hand is defined as the behavior of the clients towards medical advice and their concordance with the treatment plan. Adherence appears to be a more active process in which patients accept and understand the need of their treatment through their own free will and portray their understanding with either a positive or negative attitude towards their medications⁷

Unfortunately there is no agreed consensual standard to define non adherence. Trials suggest a rate of >50% compliance as adequate adherence while other researchers believe it should be at least >95%. As per White Paper of DOH (2010), it has been recommended that clinicians have the responsibility to identify such issues and improve collaborative relationships among multidisciplinary teams to deliver a better clinical and cost effective service⁸.

Methods:

Sampling:

Our cohort included a prospective consecutive sample of 179 patients. The study was conducted in North Essex Partnership NHS Trust which provides general adult services for a catchment area of approximately 147,000 in Tendring area. All these clients were seen at the out patient’s clinic at Clacton & District Hospital. Informed consent was taken as per recommendation of local clinical governance team. The study was conducted during a 2 month period from October to November in 2010. No patient was excluded from the study. Sample consists of clients who were aged 16years and above.

Tools Used:

All the clients were asked questions using a standard questionnaire and MARS (Medication Adherence Rating Scale). MARS was developed by Thompson et al in 1999 as a quick self-reported measure of adherence mainly around psychiatric clients. It was mainly devised from a 30 item Drug Attitude Inventory (DAI) and a 4 item Morisky Medication Adherence Questionnaire (MAQ). The validity and reliability of MARS has been established by Thompson et al and then Fialko et al in 2008 in a large study and has been reported to be adequate^9,10.

The patient questionnaire directly asked clients about their current medications and dosage regimens. It also enquired about various factors leading to non-compliance. It included factors like whether the medication makes them feeling suicidal, causes weight gain, makes them aggressive, causes sleep disturbances, causes sexual side effects, the form and size of tablets, stigma and family pressure, their personal belief about medication or do they feel that they become non adherent because as a direct effect and consequence of the illness.

Medication Adherence Rating Scale focuses both on adherence as well as the patient’s attitudes towards medications. It includes questions about how frequently they forget to take medications or are they careless about taking their medications. It also asks them if they stop taking their medication do they feel well or more unwell. Other aspects include whether they only take medicines when they are sick and do they believe that it is un-natural for their thoughts to be controlled by medications. It also asks about the effect of medication on them, such as; are they able to think clearly, or do they feel like a zombie on them?, or are they tired all the time?. It also checks their belief that if they remain compliant to medication, will it prevent them from getting sick again.

Results:

In total 179 clients were seen in the outpatient clinic during the period of two months. Out of those (54%, n=97) were females whereas nearly half (46%, n=82) were males. Age of the clients ranged from 18 years to 93 years. The mean age of the client group was 55; mode 41 and median was 69.5.

The diagnosis profile was quite varied. As far as the primary diagnosis is concerned, the majority (n=144) of service users were given a primary diagnosis using the ICD 10 criteria. Mood disorders were the most common primary diagnosis whereas personality disorder and anxiety were the most common secondary diagnosis. Table 1 show the number and percentage of the service users who presented with the most common diagnosed conditions:

Table 1: List of primary and Secondary diagnosis

Subjectively 160 (89%) patients reported that they were compliant with medications whereas 19(11%) patients admitted that they have not been adherent to medications. Out of those who said that they were non-adherent, 8 were suffering from Mood disorders, 2 had schizoaffective disorder, 3 had psychotic illness, 3 had organic brain disorder, 2 clients had personality disorder, whereas 1 client had anxiety and 1 had neurological illness.

Prescription rate varied between different types of psychotropic medications. Antipsychotics were the most prescribed medication in our cohort. Table 2 shows data of each individual category.

Table 2: Number and percentage of individual medication category prescribed

Less than half (39%, n=69) of service users had only one type of psychotropic medication whereas the majority (58%, n=104) of patients were on more than one psychotropic medication. A very small number of clients (3%, n=6) were not using any medications at all. When explored further it was revealed that almost two third of the antidepressant prescriptions comprised of SSRI’s (67%, n=55), about one fourth of SNRI (24%, n=21), a small proportion (6%, n=5) of NARI’s and very few (3%, n=3) were given tricyclic antidepressants. Similarly in antipsychotics, 75% of patients were on atypical and 25% were prescribed typical antipsychotics.

Factors leading to non-adherence:

Below is the graphical representation of what clients perceived as the major factors leading to the non adherence to the medication. Weight gain, illness effect, stigma and personal belief appear to be the major factors as displayed in Chart 1.

Chart 1: Number of responses for each individual factor leading to non-adherence:

Attitude towards Medications:

The overall Service users’ attitude towards medication did not appear to be particularly good. They mainly complained of getting tired and forgetting to take medication. Below in Chart 2 is the graphical representation of what overall attitude they had expressed towards psychotropic medications.

Chart 2: Number of responses for each factor indicating attitude towards medication

As far as overall MARS score is concerned, the majority of patients (63%, n=110) scored >6 and about one third of patients (37%, n=63) scored <6. A score of less than 6 is generally considered as a poor level of adherence which means that almost one third of our client group does not comply with medications.

Discussion:

The aim of our study was to highlight the importance of the factors which often lead to non-adherence to medications and to explore patients’ attitudes towards medications. Results are indicating that the problem of non-adherence is much wider and deeper in our clients group. There is a significant gap in between subjective and objective rate of adherence. However we should be mindful that adherence appears to be more of a continuum rather than a fixed entity e.g. some patients can be more adherent than others but still have inadequate adherence and hence arises the concept of partial adherence. It is evident from the results that patients’ attitudes were not encouragingly positive towards psychotropic medications.

Human beings are born potentially non-compliant. It is our tendency to crave and indulge in things which we know might not be good for our health e.g. eating non healthy food, alcohol and substance misuse. We have better compliance to issues which give us the immediate reward like pain relief or euphoria from illicit drugs where as because of lack of this immediate reward, our compliance gradually becomes erratic. Compliance and adherence appears to be a learnt phenomenon which needs to be nurtured throughout our life.

Manifestations of non-adherence:

The consequences of non-adherence are mainly manifested and expressed through clinical and economic indicators. Clinically it means an increase in the rate of relapse and re-hospitalisation. As per one study non-adherent patients have about a 3.7 times high risk of relapse within 6 months to 2 years as compared to patients who are adherent¹¹. In US it was estimated that at least 23% of admissions to nursing homes were happening due to non adherence which meant a cost of $31.3 billion/380,000 admissions per year¹². Similarly 10% of admissions happened for the same reason costing the economy an amount of $15.2 billion/3.5 million patients^13,14. Figures in UK are also not much different where the cost of prescriptions issued in 2007-08 was estimated to be £8.1 billion and it was highlighted that £4.0 billion out of that amount was not used properly¹⁵. Similarly in terms of hospitalization, about 4% admissions happen every year happen because of non-adherenceThe total cost of hospitalization in 2007 was estimated to be £16.4 billion and it was suggested that non-adherence had a burden of costs in the region of £36-196 million¹⁷.

From a clinical aspect it has been suggested that non-adherence causes about 125,000 deaths just in the US every yearMet analysis has suggested significant statistical association between non-adherence and causing depression in certain chronic physical conditions e.g. Diabetes¹⁹.

Dimensional Phenomenon?

We need to be aware that adherence is a multidimensional and a multifaceted phenomenon and is better understood in dimensional rather than categorical terms. It has been widely accepted that if concordance is the process, then adherence will be the ultimate outcome. This was highlighted by WHO guidelines using following diagram:

Chart 3: WHO diagram of the five dimension of adherence:

Therefore any strategy developed to address the issue of non-adherence should be able to consider all these five dimensions; otherwise it will be less likely to have any chance of success.

Measures to improve Compliance:

All the known as clinical and economic indicators suggest that non-adherence issue needs significant attention and special measures which ought to be taken in order to avoid complications. There are already some running campaigns in other countries in order to improve adherence and we need to learn from their experiences such as the National Medication Adherence Campaign in US (March 2011). The campaign is basically a research-based public education effort targeting patients with chronic conditions, their family caregivers, and health care professionals²⁰.

Levine (1998) demonstrated that the following steps may help in increasing adherence:

• To appropriately asses the patient’s knowledge and understanding about the disease process and the need for treatment and to address those issues if there is some dysfunctional belief.
• To link the taking of medication with other daily routines of the life
• To use aids to assist medication adherence e.g. MEMS, ePills, Calendar or Dossette box
• To simplify the dosage regimen
• Flexible Health care team who is willing to support
• Addressing current Psychosocial and environmental issues which might hinder the adherence^21.

It is extremely important for the clinician to take time to discuss in detail with their patients all the possible side effects and indications of the prescribed medications. Unfortunately clinicians may not be able to predict the possibility of having side effects but can certainly educate patients about their psychopathology, indication and rationale for the medication and make them realise how important it is for them to remain adherent to medication. Health education is considered equally effective as compared to any sophisticated adherence therapy and should be used routinely²².Clinicians also have very important role to play in simplifying the dosage regimen and emphasise to the patients that “Medications don’t work in patients who don’t take them”²³.

Various studies have tried to estimate the efficacy of a single factor and the multi factor approaches to improve adherence ²⁴. Studies have showed proven efficacy for education in self management^25,26, pharmacy management programmes^27,28, nursing, pharmacy and other non medical health professional intervention protocols^29,30, counselling^31,32, behavioural interventions^33,34 and follow up^35,36. However multi factor approaches have been found to be more effective than single factor approaches^,38Therefore it has been suggested that we need to address all the five dimensions of adherence (Chart 3) with multiple interventions to improve the adherence in our patients.

One factor potentially of concern leading to non-adherence is the possibility of the current overt or covert misuse of alcohol, illicit substances and over the counter available medications. This issue understandably can lead to partial or complete non adherence as well as worsening of existing psychiatric conditions. Therefore it needs to be explored further in future research projects.

Introduction

Non-attendance in outpatient clinics accounts for a significant wastage of health service resources. Psychiatric clinics have high non-attendance rates and failure to attend may be a sign of deteriorating mental health. Those who miss psychiatric follow-up outpatient appointments are more ill with poor social functioning than those who attend (1). They have a greater chance of drop out from clinic contact and subsequent admission (1). Non-attendance and subsequent loss to follow up indicate possible risk of harm to the patient or to others (2).

Prompts to encourage attendance at clinics are often used and may take the form of reminder letters (3), telephone prompting(4) and financial incentives (5). Issuing a copy of the referral letter to the appointee may prompt attendance for the initial appointment (6). Contacting patients by reminder letters prior to their appointments has been effective in improving attendance rates in a number of settings, including psychiatric outpatient clinics and community mental health centres (3).

Studies investigating the efficacy of prompting for improving attendance have generated contrasting findings and non-attendance remains common in clinical practice. We, therefore, carried out a naturalistic, prospective controlled study to investigate whether reminder letters would improve the rate of attendance in a community-based mental health outpatient clinic.

Design and Methods

The study was carried out at the Community Mental Health Centres based in Runcorn and Widnes in Cheshire, UK. The community mental health team (CMHT) provides specialist mental health services for adults of working age. Both CMHTs are similar in demographics, socio-economic need and, have relatively higher non-attendance rates in the clinic. In the week prior to the appointment, clerical staff from community mental health team sent a standard letter to some patients reminding the date and time of the appointment and name of the consulting doctor.  They recorded whether patient attended, failed to attend or cancelled the appointment irrespective of whether they had received a reminder letter or not.

We compared the attendance rates between experimental group (those who had received the reminder letters) and the control group ( those who had not received the reminder letters) over a period of 18 months. Throughout the study period, the same medical team held the clinics and there had been no major change in the outpatients’ clinic setting or administrative and procedural changes influencing outpatients’ attendance. Care Planning Approach (CPA) was implemented and in operation even before the introduction of reminding letters at both the sites.

Attendance rates for all the clinics held during the study period were obtained from medical records.  For all subjects who failed to attend, age and gender, was obtained from patients’ database. Patients whose appointments were cancelled were also included in the study.

Statistics and Data analysis

The data was analysed using SISA - Simple Interactive Statistical Analysis (7). Chi -squared tests were used to investigate the attendance rates between the groups, new patients and follow-ups, with the P value for statistical significance set at 0.05. Odds ratios were calculated to measure the size of the effect. In addition, we examined how age and gender may have influenced the effect of the text based prompting on attendance.

Results

In the experimental group a total of 114 clinics were booked, with clinic lists totalling 843 patients. Of these, 88 were new referrals and 755 were follow-up appointments.  65 of 114 clinics had full attendance.  A total of 228 patients failed to attend the clinic. Of those who failed to attend, 25 patients were new referrals and 203 were follow-up patients. 28 follow up patients and 2 patients newly referred to the team called to cancel their appointments.

In the control group, a total of 71 clinics were booked amounting to a total of 623 patients. Of these, 86 were new referrals and 537 were for follow-up patients. Only 25 out of 71 clinics had full attendance.  A total of 211 patients failed to attend. Of those who failed to attend, 32 were new referrals and 179 were follow-up patients. 55 follow up patients and 13 patients newly referred to the team called to cancel their appointments.                                        

Of those who failed to attend in the experimental group, 98 (43%) were women. The mean age of non-attendees was 38 years; with a range of 18-76 yrs .Of those who failed to attend in the control group110 (52%) were women. The mean age of non-attendees was 32 years; with a range of 19-70 yrs. 

In our study, failure to attend was not distributed evenly but had seasonal peaks at Christmas and during the summer vacation period.

The outcome from prompting in the experimental group is compared with the control group and displayed in Table 1.

χ^{2 =} Chi square, df = degree of freedom, OR= Odds Ratio, CI= Confidence Interval

The attendance rate in the experimental group was 71.95% (585/813) as opposed to 56.57% (344/555) in the control group (OR=1.57; p=0.0001).

The attendance rate for new patients in the experimental group was 70.9%( 61/88) as opposed to 56.16 %( 41/ 86) in the control group (OR=1.9; p=0.053).

The attendance rate for follow up patients in the experimental group was 72.0%( 524/727) and 62.8% (303/482) in the control group (0R=1.52; p=0.0007).

In addition, there were significantly more (by 22%) number of clinics with full attendance in the experimental group (OR= 2.44, P=0.003).

The observed difference was not influenced by patient’s age or gender.

Discussion

The results from this study confirm previous findings that reminder letters within a week before the appointment can improve attendance rates in community mental health clinics. Our results are similar to those of the Cochrane systematic review, which has suggested that a simple prompt in the days just before the appointment could indeed encourage attendance (8).

Although it has been reported elsewhere(8) that text based prompting increases the rate at which patients keep their initial appointments, our study did not show a similar result for new patients.

It is already demonstrated that new patients and follow-up patients in psychiatric clinics are distinct groups with different diagnostic profiles, degrees of mental illness and with different reasons for non-attendance. Follow-up patients are severely ill, socially impaired and isolated than new patients. (1). Forgetting the appointment and being too unwell are the most common reasons given for non-attendance by follow-up patients, while being unhappy with the referral, clinical error and being too unwell are the most common reasons in the new patient groups (1).  In addition, it has also been observed that increased rate at which patients keep their first appointments is more likely related to factors other than simple prompting (4) This explains our finding that prompting was more beneficial for follow-up patients as opposed to new referrals to the Community Mental Health Team.

We also identified several patients with severe mental illness who ‘did not attend’ for three successive outpatient appointments. Their care plans were reviewed and arrangements made to follow up with their community psychiatric nurses as domiciliary visits at regular intervals.  Such measures should reduce duplication of the services and shorten the waiting times for psychiatric consultation, which are well-recognised factors associated with non-attendance (9).

Non-attendance is an index of severity of mental illness and a predictor of risk (1). In addition to reminder letters, telephone prompts are also known to improve attendance (4). Successful interventions to improve attendance may be labour intensive but they can be automated and, ultimately, prove cost effective (8)

We noticed that there is limited research and lack of quality randomised controlled trials in the area of non-attendance and the effectiveness of intervention to improve attendance in mental health setting. More large, well-designed randomised studies are desirable. We also recommend periodic evaluation of outpatient non-attendance in order to identify high-risk individuals and implement suitable measures to keep such severely mentally ill patients engaged with the services.

There was no randomisation in this study and we relied on medical records.  We have not directly compared the characteristics of non-attendees with those patients who did attend the clinics. We did not evaluate other clinical and socio-demographic factors (e.g. travelling distance, financial circumstances, etc) that are known to influence the attendance rates in mental health setting. Hence, there may be limitations in generalising the results beyond similar populations with similar models of service provision.

The Care Programme Approach (CPA) was introduced in England in 1993 to co-ordinate the care of patients with mental health disorders.¹ Its aim was to ensure that there was a full assessment of the patient’s needs, that a care co-ordinator would see that the care was delivered, regular checks would be carried out to review progress, there would be collaboration between health and social services, and that patients (or the term used to ‘demedicalise’ them in psychosocial Newspeak ²  namely, ‘service users’) and carers (they also use the service) would have a greater say in the written management plan. Targets were set.

What has happened since? Prior to this I recall that most psychiatrists carried out full assessment needs, regular checks reviewed progress (outpatients), social services were involved when necessary, and  patients and their families were nearly always involved in the discussion of after-care, when appropriate. Despite the condescending manner in which patients and carers were treated by the hierarchy, i.e. they would not understand the difference between social services management and other after-care, it was always quite clear to doctors that patients had no difficulty with the concepts of medical intervention (investigations, diagnosis, treatment), psychological therapies, and social help (housing, work, family, finances). 

Rather than simplifying the process we now have two tiers of CPA, namely, standard and enhanced. Where the patient has ‘complex needs’ or is a ‘complicated case’ then you are in the enhanced bracket. For the rest – back to the General Practitioner (GP)! Not enough resources apparently. Not ill enough more likely. Remember – you have to have a severe and enduring mental health disorder – nothing else counts. Nowadays the GP is expected to be a specialist in mental health and run a risk assessment on every ‘psychiatric’ patient. The GP is frowned upon by the ‘experts in living’ should he/she for example, dare refer a mild or moderately (yes - those descriptions again!) ill patient to the Mental Health Services. Because there is no bottomless pit of money, the scenario was changed in 2008 so that those receiving only standard CPA were no longer entitled to it. However, not to appear callous and indifferent to the plight of those suffering from ‘less severe’ mental health problems, the usual lip service was paid to patients, assuring them that they should be respected and supported, and that their carers be also recognised as having ‘needs’. All the buzz words were put in place again – integrated care pathways, working together, reviews about the reviews, good practice, better training, and so forth. Now there is the Supervised Community Treatment Order, (whether you like it or not) and those subject to the new ‘order’ will be entitled to the ‘new’ CPA. Wonderful in theory.

So what happens to a patient who is not on CPA? We are informed that such patients should still be open to secondary mental health services, should continue to receive clinical support, that reviews should take place regularly, and a social assessment should be available under the new guidance to local authorities FACS (Fair Access to Care Services), readily available on the Internet. The truth of the matter is that only those patients on enhanced CPA will receive immediate support, the rest will have to jump through the usual hurdles to prove they have a severe, enduring mental illness (enduring is not enough) in order to gain access to NHS ‘support’ facilities. Some patients are seen as more deserving than others, for example, those admitted to hospital under the Mental Health Act (voluntary admission may count against you), current or potential risk (theoretically, any patient with a mental health disorder, which seems to defeat the purpose of the exercise) or the presence of a dual diagnosis (depression with alcoholism, or is it the other way round?). Anyway, if in doubt, the patient is entitled to a formal reassessment CPA and may be admitted to the ‘new’ CPA list. If all fails, the patient (remember, one with severe, enduring mental health symptoms) may make a complaint to the local authority or even hire a lawyer.

What is the true state of affairs? To begin with, many patients have enduring mental health problems which are not severe, are not life-threatening, and despite the hardship and drudgery endured, manage to trundle through work, relationships, and family life. Years of talking therapies or psychotropic medication, indeed both, may have only taken the edge off their symptoms. Often symptoms resurge and require alterations or adjustments in medication; sometimes a different psychological approach needs to be considered. Such patients are best left to the fountain of all wisdom, the GP, so it seems. Rather akin to telling the GP to treat for example, a ‘minor’ cardiac problem (say, palpitations) because the ‘specialist unit’ only deals with severe arrhythmias, severe pain, severe disability, ‘severe everything’. It is unfair to expect GPs to make informed decisions concerning psychotropic medication (no more than they should about adjusting chemotherapy drugs) and most would be familiar only with specific therapies such as Cognitive Behavioural Therapy (CBT) or Anger Management, where appropriate. The type of patients  described here comprise the majority of those seen in outpatients, yet there is now a growing trend to discharge such patients back to the GP, because he/she is not ‘care co-ordinated’ on enhanced CPA. The burden is on the GP. It does not seem to have registered with politicians or management (doctors included) that chronic schizophrenia is not the same as chronic gastro-oesophageal reflux.

The trend now is for the setting up of Community Clinics (the patient does not necessarily get to see a doctor) where ‘all the other psychiatric problems’ are dealt with. The traditional psychiatric outpatient department is to be abolished, unless of course, GPs do something about this torrid state of affairs now. It could only happen in Psychiatry which seems to me a specialty doomed to oblivion. Family doctors are becoming increasingly irritated by a system or discipline (Psychiatry especially) which seems to ignore their concerns and is more preoccupied with targets (nothing has changed) and outcomes (back to the GP). Even referrals from GPs, who want a medical opinion, are filtered in order to weed out those not worthy to enter the hallowed walls of the Mental Health Institution. Those patients who ‘know the system’ or who are vociferous and make complaints (‘I know my rights’) get to be seen by the Great and Good. Lesser mortals, usually those with serious mental illnesses, do not make any undue demands and are therefore often forgotten or fall by the wayside. A patient with bipolar disorder on lithium is discharged back to a GP who is unsure whether or not the medication needs ‘fine tuning’ at times, should be discontinued, or reinstated were compliance is a problem in one heading for a relapse. As a corollary of that, I am sure most hospital doctors would not know what the acronym ABVD means in the chemotherapy treatment of Hodgkin’s disease. Adjusting psychotropic medication is not quite the same as adjusting an antihypertension regime. Unfortunately, if the patient needs to be referred back into the system the whole Kafkaesque scenario begins again. 

A medical colleague once bemoaned to me that psychiatrists are totally out of touch with Medicine. Alas, it seems they are also now out of touch with their medical colleagues.

Eating disorders are defined as those disorders in which there is excessive concern with the control of body weight and shape, accompanied by grossly inadequate, irregular or chaotic food intake. It is widely accepted that eating disorders occur in young adults and adolescents, however, a number of reports have described series of young patients with eating disorders aged from eight years upwards.^1,2The range of disorders in children includes selective eating, food avoidance emotional disorder, functional dysphagia and pervasive refusal syndrome.  

ANOREXIA NERVOSA.

The DSM IV diagnostic criteria for anorexia nervosa are as follows:

1. Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g weight loss leading to maintenance of body weight less than 85% of expected; or failure to make weight gain during growth period).
2. Intense fear of gaining weight or becoming fat, even though underweight.
3. Disturbance in the way one’s body weight and shape is experienced, undue influence of body weight or shape on self evaluation, or denial of the seriousness of current low body weight.
4. Absence of at least three consecutive menstrual cycles

Subtypes:

Restricting Type: During the current episode of anorexia nervosa, the person has not regularly indulged in binge eating or purging behaviour.

Binge-Eating/Purging Type: During the current episode of anorexia nervosa, the person has regularly indulged in binge eating or purging behaviour.³                       

The above criteria are intended primarily for use with older patients and do not adequately address the problems of anorexia nervosa in children. For example, criterion D in DSM IV applies only to post-menarcheal females and states that there should be an “absence of at least three consecutive menstrual cycles”. This is clearly inapplicable in this age group, where the majority are premenarcheal. Equally unhelpful is the statement that weight should be maintained at less than 85% of that expected, for expected weight can only be calculated on the basis of height and age. Yet growth may also be impaired because of poor nutrition, so further adjustments have to be made. For these reasons, the Eating Disorders Team at Great Ormond Street Hospital for Sick Children in London, U.K, developed a more practical diagnostic criterion for early onset anorexia nervosa.⁴The current criteria is as follows:

Great Ormond Street diagnostic criteria for early-onset Anorexia Nervosa:

1. Determined weight loss (e.g. food avoidance, self-induced vomiting, excessive exercising and abuse of laxatives).
2. Abnormal cognitions regarding weight and/or shape.
3. Morbid preoccupation with weight and/or shape.⁵

Weight loss: Since children should be growing, static weight may be regarded as equivalent to weight loss in adults. Weight loss is a real cause for concern in children, since they have lower total body-fat deposits and therefore do not have much fat to lose. One measurement for weight loss uses the Tanner-Whitehouse Standards⁶ where 100% represents the desired weight for a child’s sex, age and height, and 80% or less is classed as ‘wasting’.

Food avoidance: Children with anorexia nervosa give a variety of reasons for refusing food, the most common of which appears to be a fear of becoming obese. Other reasons include feelings of nausea or fullness, abdominal pain, appetite loss and difficulty swallowing. ⁷

Self-induced vomiting: Fosson et al (1987) reported that at least 40% of the 48 children included in their study of early-onset anorexia nervosa were known to be vomiting at presentation.

Excessive exercising: This is not uncommon in children with anorexia nervosa. Daily exercise workouts may be a feature in these children’s lives. Sometimes exercise may be carried out in secret in the privacy of the bedroom or bathroom.

Laxative abuse: This is not as common as in adult populations partly because children have less access or opportunity to obtain laxatives, but nevertheless, it still occurs.

Abnormal cognitions regarding weight and/or shape: The main beliefs are centred around body image and its distortion, although it must be acknowledged that body image is difficult to assess reliably. Many children with anorexia nervosa will report that they consider themselves fat even when severely underweight, which is similar to the clinical observation seen in adult patients with the same condition.

Preoccupation with weight: Children with anorexia nervosa tend to be preoccupied by their own body weight and are often experts at calorie counting. This preoccupation is closely related to fear of fatness.

Physical Aspects

The majority of physical changes in anorexia nervosa are predominantly related to the effects of starvation and dehydration. This includes slow pulse rate, low blood pressure and poor circulation leading to cold hands and feet. Often there is excess fine hair especially on the back, known as ‘lanugo’. Teeth may be pitted, eroded and decayed from gastric acid during vomiting.

A wide range of biochemical changes have been described in anorexia nervosa, although there is little information specifically relating to children. These include low haemoglobin and white cell count, low levels of potassium and chloride, raised liver enzymes such as alanine transaminase and alkaline phosphatase, and low levels of plasma zinc and serum iron.

A number of endocrine changes appear in anorexia nervosa and evidence suggests that this is due to the secondary effects of starvation. Changes include increased cortisol, growth hormone and cholecystokinin, and decreased luteinizing hormone, follicle stimulating hormone, oestrogen, triodothyronine and thyroid stimulating hormone.

BULIMIA NERVOSA

The DSM IV diagnostic criteria for bulimia nervosa is as follows ⁸ :    

1. Recurrent episodes of binge eating e.g, eating large amounts of food in two hours, and a sense of lack of control during the episode.
2. Regular use of methods of weight control:
3. vomiting
4. laxatives
5. diuretics
6. fasting or strict diet
7. vigorous exercise.
8. Minimum average of two binges a week in three months.
9. Self-evaluation is influenced by body weight or shape.
10. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Sub-types:

Purging Type: During the current episode of bulimia nervosa, the person regularly engages in self-induced vomiting or laxative misuse, diuretics or enemas.

Non-purging Type: During the current episode of bulimia nervosa, the person has used other inappropriate compensating behaviours such as fasting or excessive exercise, but not regularly used purging behaviour. ²

Self-induced vomiting can lead to complications such as fluid and electrolyte disturbance and gastro-intestinal bleeding. Other physical complications include dental erosions, enlargement of the salivary glands, and muscle weakness.

OTHER EATING DISORDERS IN CHILDREN

Food Avoidance Emotional Disorder

This term was first introduced by Higgs et al (1989)⁹, to describe a group of underweight children presenting with inadequate food intake and emotional disturbance who did not meet the criteria for anorexia nervosa.

The operational definition we use has evolved from Higgs and colleagues original description together with clinical experience and is as follows:

1. Food avoidance not accounted for by primary affective disorder.
2. Weight loss.
3. Mood disturbance not meeting criteria for primary affective disorder.
4. No abnormal cognitions regarding weight or shape.
5. No morbid preoccupation regarding weight or shape.
6. No organic brain disease or psychosis.

Selective Eating

Selective eaters are a group of children who present with very restricted eating habits in terms of the range of foods they will accept. Characteristics include:

1. Have eaten a narrow range of foods for at least 2 years.
2. Unwillingness to try new foods.
3. No abnormal cognitions regarding weight or shape.
4. No fear of choking or vomiting.
5. Weight may be low, normal or high.

Pervasive Refusal Syndrome

This term was first described by Lask et al (1991).¹⁰ The main features are:

1. Profound refusal to eat, drink, walk, talk or self-care.
2. Determined resistance to efforts to help.

Initially these children present with features fairly typical of anorexia nervosa, but the food avoidance is gradually followed by a more generalised avoidance with a marked fear response.

Functional Dysphagia

Children with this condition generally present with complaints of difficulty or pain on swallowing. Features include:

1. Food avoidance.
2. Fear of swallowing, choking or vomiting.
3. No abnormal cognitions regarding weight or shape.
4. No morbid preoccupation regarding weight or shape.
5. No organic brain disease or psychosis.

For more information on the above eating disorders in children see Lask & Bryant-Waugh (1999).⁵

INCIDENCE AND PREVALENCE

For a number of reasons, the incidence and prevalence of childhood-onset anorexia are not known. There have been no epidemiological studies which have focussed specifically on this age group and the strict diagnostic criteria used in wider epidemiological studies may lead to a substantial underestimate of the true incidence. ² However studies in adolescent populations estimate the prevalence to be in the order of 0.1-0.2% ^{11, 12} and it is likely to be even lower in children. Although debatable, an increase in actual referral rate of anorexia nervosa in children has been reported.² Gender distribution: Five to ten percent of cases of anorexia nervosa in the adolescent and young adult population occur in males.¹³ However, in children, studies have reported that between 19 and 30% of children with anorexia nervosa have been boys.^7,9,14,15

At present, there is little epidemiological information on the other eating disorders in children.

MANAGEMENT AND INTERVENTIONS¹⁶

Initial assessment

Comprehensive assessment should include physical, psychological and social components. Those with low to moderate risk should be managed as an outpatient. Those who are severely emaciated, with serious risk of self harm, with severe deterioration or with poor response to treatment are deemed high risk and should be considered for inpatient treatment or urgent referral to specialist services.

Anorexia nervosa – outpatient care

Psychological interventions

Psychological interventions are the key element in the management of anorexia.

The delivery of psychological interventions should be accompanied by regular monitoring of a patient’s physical state including weight and specific indicators of increased medical risk.

• When delivering psychological treatment consider, in conjunction with the patient:

– Cognitive analytical therapy (CAT)

– Cognitive behaviour therapy (CBT)

– Interpersonal psychotherapy (IPT)

– Focal psychodynamic therapy

– Family interventions focused explicitly on eating disorders

• Focus of treatment should be on weight gain, healthy eating, and reducing other symptoms related to eating disorders.

• Dietary counselling should not be provided as the sole treatment for anorexia nervosa.

Medication

Pharmacological interventions have a very limited evidence base for the treatment of anorexia nervosa.

• Medication is not effective as sole or primary treatment; caution should be exercised in its use for comorbid conditions such as depression or obsessive–compulsive disorder, as these may resolve with weight gain alone

• Avoid using drugs that affect the heart such as antipsychotics, tricyclic antidepressants, some antibiotics and some antihistamines.

Anorexia nervosa – inpatient care

•Body Mass Index (BMI) is a measure of weight in relation to height. Normal BMI range is 18.5-24.9. BMI below 17 is a concern and GPs should consider referral to specialist services. However, BMI below 15 is serious and inpatient care should be considered.

• Consider inpatient treatment for patients with high or moderate physical risk, who have not improved with appropriate outpatient treatment or have significant risk of suicide or severe self-harm.

• Admit to setting that can provide the skilled implementation of refeeding with careful physical monitoring (particularly in the first few days of refeeding) and in combination with psychosocial interventions

• Consider increased risk of self-harm and suicide at times of transition for patients with anorexia nervosa, especially that of the binge–purging sub-type.

Psychological treatment

• Psychological treatment is a key element of an inpatient stay, but evidence for what kind of treatment or approach to treatment is effective, is limited.

• A structured symptom-focused treatment regimen with the expectation of weight gain should be provided, with careful monitoring of the physical status during refeeding.

• Provide psychological treatment with a focus on both eating behaviour and attitudes to weight and shape, and wider psychosocial issues with the expectation of weight gain

• Do not use rigid behaviour modification programmes.

Feeding against the will of the patient

• Feeding against the will of the patient should be an intervention of last resort in care and should only be done in the context of the Mental Health Act 1983 or Children Act 1989.

Post-hospitalisation treatment in adults

• Following discharge, extend the duration of psychological treatment over that normally provided to those who have not been hospitalised, typically for at least 12 months.

• Offer outpatient psychological treatment that focuses on both eating behaviour and attitudes to weight and shape, and on wider psychosocial issues, with regular monitoring of both physical and psychological risk.

Anorexia nervosa –physical management

Anorexia nervosa carries considerable risk of serious physical morbidity. Awareness of the risk, careful monitoring and, where appropriate, close liaison with an experienced physician, are important in the management of the physical complications of anorexia nervosa.

Managing weight gain

• Aim for an average weekly weight gain of 0.5–1 kg in inpatient settings and 0.5 kg in outpatient settings. This requires about 3500 to 7000 extra calories a week

• Provide regular physical monitoring and consider multivitamin/multimineral supplementation in oral form for both inpatients and outpatients.

• Total parenteral nutrition should not be used unless there is significant gastrointestinal dysfunction.

Managing risk

• Inform patients and their carers if the risk to their physical health is high

• Involve a physician or paediatrician with expertise in the treatment of medically at-risk patients for all individuals who are at risk medically.

• Consider more intensive prenatal care for pregnant women to ensure adequate prenatal nutrition and fetal development.

• Oestrogen administration should not be used to treat bone-density problems in children and adolescents as this may lead to premature fusion of the epiphyses.

• Healthcare professionals should advise people with eating disorders and osteoporosis or related bone disorders to refrain from physical activity that significantly increases the likelihood of falls.

Additional considerations for children and adolescents

The involvement of families and other carers is particularly important.

The right to confidentiality of children and adolescents with eating disorders should be respected.

Family members, including siblings, should normally be included in the treatment of children and adolescents with eating disorders. Interventions may include sharing of information, advice on behavioural management and facilitating communication.

Anorexia nervosa

• Family interventions that directly address the eating disorders should be offered to children and adolescents with anorexia nervosa.

• Offer children and adolescents individual appointments with a health professional separate from those with their family members or carers.

• For children and adolescents, once a healthy weight is reached, ensure increased energy and necessary nutrients are available in the diet to support growth and development.

• Involve carers of children and adolescents in any dietary education or meal planning.

Inpatient care of children and adolescents with anorexia nervosa

• Inpatient care of children and adolescents should be within age-appropriate facilities (with the potential for separate children and adolescent services), which have the capacity to provide appropriate educational and related activities. They should also balance the need for treatment and urgent weight restoration with the educational and social needs of the young person.

• Consider using the Mental Health Act 1983 or the right of those with parental responsibility to override the young person’s refusal to receive treatment that is deemed essential.

• Seek legal advice and consider proceedings under the Children Act 1989 if the patient and those with parental responsibility refuse treatment where treatment is deemed essential.

Bulimia nervosa

Following the initial assessment consider:

• As a possible first step, an evidence-based self-help programme – direct encouragement and support to patients undertaking such a programme may improve outcomes. This may be sufficient treatment for a limited subset of patients.

Psychological treatment should form the key element of treatment, so consider:

• For adolescents: Cognitive behavioural therapy for bulimia nervosa (CBT-BN) adapted as needed to suit their age, circumstances and level of development.

• Where there has been no response to CBT or it has been declined: other psychological treatments,particularly interpersonalpsychotherapy (IPT). (Note: patients should be informed that IPT takes 8–12 months to achieve results comparable with CBT-BN).

Medication may have a role

• Consider a trial of an antidepressant drug as an alternative or additional first step to using an evidence-based self-help programme.

• In terms of tolerability and reduction of symptoms, SSRIs (specifically fluoxetine) are the drug of first choice for the treatment of bulimia nervosa.

• The effective dose of fluoxetine may be higher than for depression.

• Beneficial effects will be rapidly apparent and are likely to reduce the frequency of binge eating and purging, but the long-term effects are unknown.

• No drugs, other than antidepressants, are recommended for the treatment of bulimia nervosa.

Physical management

• Assess fluid and electrolyte balance where vomiting is frequent or there is frequent use of laxatives.

• If electrolyte balance is disturbed, consider behavioural management as the first option

• If supplementation is required, use oral rather than intravenous preparations.

Bulimia nervosa – inpatient or day care

• Consider inpatient treatment for patients with risk of suicide or severe self-harm.

• Admit patients to a setting with experience of managing this disorder.

PROGNOSIS ¹⁷

If untreated, anorexia nervosa carries high mortality rates of

10-15%. If treated, one third have full recovery, one third partial recovery and one third have chronic problems. Poor prognostic factors for anorexia nervosa include: chronic illness, late age of onset, bulimic features such as vomiting and purging, anxiety when eating with others, excessive weight loss, poor childhood social adjustment, poor parental relationships and male sex.

Prognosis for Bulimia nervosa is generally good, unless there are significant issues of low self esteem or evidence of severe personality disorder.

USEFUL RESOURCES

Background:

Loss of a limb for any a reason is a major event with profound implications on the psychological health of an individual involved. It has been seen that 20-60% of the amputees attending surgical or rehabilitation clinics are assessed as being clinically depressed^1-3. Individuals suffering traumatic limb loss at any age are likely to suffer subsequent difficulties with their body image, but these relationships are more striking in the younger age groups who have experienced traumatic injuries. The psychological reactions to amputation are clearly diverse and range from severe disability at one extreme; determined and effective resumption of a full and active life at other end. Indeed, among adults the age at which an individual receives the amputation is also an important factor. The investigation of psycho-social adaptation to amputation has generated a plethora of clinical and empirical studies ^4-7. An amputation is typically equated with loss of once perception of wholeness ⁸, loss of spouse ⁹, symbolic castration and even death ^{10, 11}. The individual’s response to a traumatic event is influenced by personality traits, psychiatric premorbid state, gender, peri-traumatic dissociation, prolonged disability of traumatic events, lack of social support and inadequate coping strategies ^12-15. Even though the previous research on consequences of amputation has focused primarily on relationships among demographic variables, coping mechanisms, and outcome measures; there is lack of literature on prevalence of various specific psychiatric disorders post-amputation ^{16, 17}. Most of the literature and research on prevalence of specific psychiatric morbidity has largely focused on symptoms of depression¹⁸.

1. To study various socio-demographic variables of amputees.
2. To find prevalence of psychiatric disorders in amputees from the out-patient population of the bones and joint surgery hospital, Srinagar which also has an artificial limb rehabilitation centre attached with it.

1. Informed consent from the patients under study
2. Amputation of more than one year duration
3. Age more than 14 years and less than 60 years
4. Patients were included in the study irrespective of their sex

1. Those who do not give consent
2. Those persons who have history of any DSM-IV axis I or axis II disorder before the development of amputation.
3. Presence of disabling medical or neurological conditions like motor neuron disease, Parkinson disease, etc.
4. Age less than 14 years
5. Age more than 60 years

Introduction

The legal high ‘Ivory Wave’, also known as ‘Ivory Coast’, ‘Purple Wave’ or ‘Vanilla Sky’, is a designer drug that has become popular among clubbers in the United Kingdom (UK) after mephedrone was banned in April 2010.¹ Ivory Wave is advertised as a relaxing bath salt and has been freely available on the Internet for about £15 a packet (200mg).² Three different versions have been on the market, namely, Ivory Wave, Ivory Wave Ultra (also known as Ivory Wave 2), and Ivory Wave 3, although their differences are unknown.³ Studies have shown that Ivory Wave contains cathinone-derived stimulants and, when snorted in high doses, bring similar effects to those of amphetamine and ecstasy.⁴ 

Introduction

Figure 1: Pearlin’s stress–process model of stress in carers (adapted from Pearlin et al, 1990)

Risks for carer psychological distress or depression are related to gender, age, health status, ethnic and cultural affiliation, lack of social support, as well as certain other characteristics related to the caregiver (table 2).⁴¹ 

Some of the patient factors related to psychological distress in carers are: behavioural disturbances, functional impairments, physical impairments, cognitive impairments, and fear that their relative may attempt suicide.

'The following article is another in a series of critical essays examining the current status of Psychiatry in the NHS'

In therapy                                          

What is Psychiatry?                                                                     

“The mind is its own place, and in itself can make a heaven of hell, a hell of  heaven” John Milton                                                                                                                                                                                                                                                                                    
The word 'psychiatry' is derived from the Greek for "doctor of the soul" and was first coined in the early 19th century by the German physician and anatomist, Johann Reil (1759-1813), although the treatment of mental disturbances dates back hundreds of years prior to this. The specialty of Psychiatry is regarded as dealing with the prevention, assessment, diagnosis, treatment, and rehabilitation of ‘mind’ illnesses or mental disorders. Diseases of the brain itself, for example encephalitis, tumours, and so forth, fall within the realm of neurology, generally. There are, of course, many overlapping disorders which cause neurological symptoms (paresis, slurred speech, ataxia, to cite a few) and ‘mind’ symptoms (depression, anxiety, psychosis). Disorders which affect several organ systems, for example, the autoimmune diseases, often cause multiple, bewildering neurological and mental symptoms. The primary goal of the psychiatrist is relief of suffering associated with ‘psychiatric’ disorders which include inappropriate anxiety, clinical depression, and psychotic disorders. Attempts have also been made to categorize and ‘treat’ different types of personality disorder. The latter is a contentious issue (perhaps with the exception of antisocial and borderline types) sometimes based on value judgments rather than clear scientific evidence. Treatment for mental health problems nowadays is usually community-orientated for less severe conditions and often hospital-based for more intractable disorders. The vast majority of patients are treated on a voluntary basis, whether in hospital or the community.
 
Medical, biological, social or psychological?                                                            
“ I think we ought always to entertain our opinions with some measure of doubt. I shouldn’t wish people to dogmatically believe any philosophy, not even mine.” Bertrand Russell
 
Psychiatry is sometimes criticized for adopting a ‘too’ medical or biological approach, despite the fact that many physical conditions masquerade initially with ‘mental’ symptoms. It would seem strange, if not irresponsible, were a psychiatrist, who is after all, a qualified medical doctor, not to enquire about a patient’s physical history. What is conveniently overlooked is that in everyday practice psychiatry uses a holistic approach to the patient, taking social and cultural backgrounds into account, as well as the general medical status. Treatment may thus involve medication, various forms of psychotherapy, or both, in addition to practical measures such as help with family problems, debts, housing, residential placements and so forth. In recent years, particularly in the UK, there has been a much greater emphasis on psychological treatments and social interventions. The ‘medical’ approach has taken a definitive back seat. Psychotropic drugs are frowned upon because of their side-effects, or perceived as a form of control used by psychiatrists towards their patients. Sweeping statements are made about their lack of efficacy and selective abstraction of the research is used to support such statements. Psychiatrists are denigrated for being in the grip of Big Pharma and are further demoralized by the being perceived as ‘drug pushers’. They are perceived by mostly non-medical ‘therapists’ as not being in touch with the psychological and sociological issues which are cited as underlying and perpetuating psychiatric disorders. Electroconvulsive therapy is considered barbaric; it is banned in some states in the USA. Complementary or ‘alternative’ therapies, regardless of whether or not they stand up to scientific scrutiny, are proliferating, and prescribed drugs are being replaced by ‘natural’ herbal products, despite the inherent dangers of the latter (1). Psychiatry is in decline and is becoming obsolete, a victim of its own psychobabble and increasingly mind-numbing research, understandable to the elite few. The profession is in danger of being ‘psychologised’ in order to appear acceptable and user-friendly, advocating therapies which in themselves do not stand up to scientific scrutiny. Outcome studies are quoted as favourable, when the very tenet of their foundations is very shaky, to say the least.
 
Perhaps there is not much reason for surprise when one considers not very long ago psychiatry advocated behaviour therapy for the treatment of homosexuality, orgone energy accumulators for neuroses, and insulin coma for schizophrenia. In hindsight such practices were totally unsound, unacceptable, and in the case of insulin coma therapy, dangerous; fortunately, they are now obsolete. Yet the history medicine is replete with such ‘cures’: mercury was once used to treat syphilis, and in surgery trepanation was widely used in ancient times for the treatment of seizures. In retrospect these procedures could be also be considered outrageous and barbaric, though with the development of scientific knowledge it is easy now to understand, reflect, and accept, that no other effective treatments were available at the time. Not so the case for psychiatry. Psychiatrists and other mental health professionals, who by and large genuinely have empathy and sympathy for their patients and want them to get better quickly, discharge them from hospital or outpatient clinics, and reunite them with their families whenever possible, are still unjustly accused of wanting to exert social control. There is no doubt that abuse of psychiatric practice does occur in some institutions and that political regimes throughout the world have used and still use powerful neurotropic drugs to subdue and control individuals who challenge the authority of the State. It is common knowledge that psychiatry was used by some totalitarian regimes as part of a system to enforce political control, for example in Nazi Germany, the Soviet Union, and the apartheid system in South Africa. Whether such abusive practices, which no doubt still exist, will ever be abolished will depend on the will of Governments and pressure from Human Rights campaigners such as Amnesty International. 
                                                                  
 
What is madness?
“ Madness is rare in individuals - but in groups, parties, nations, and ages it is the rule” Friedrich Nietzche
 
It is not possible to delineate the boundary between sanity and insanity. Broad definitions of mental disorder have been attempted and an individual might be said to be ‘mentally disordered’, or as formerly described, ‘of unsound mind’, when there is a more than temporary impairment of cognitive functions such as memory, orientation and comprehension, an alteration of mood leading to a delusional appraisal of one’s situation, abnormal perceptions and disordered thinking. However, this concept is criticised for being overinclusive and precise definitions of mental illness remain elusive. It is probably easier to envisage mental health problems as being on a continuum from normal to abnormal for example, from a relative sense of well-being and contentment to a state of distress and unhappiness. Further exacerbations or stressors lead to a disintegration of oneself and that sense of oneness with the environment. Loss of reality ensues with further anxiety and perplexity, disordered and confused thinking or delusions, and perceptual disturbances (usually auditory hallucinations), in some cases. The same symptoms can be caused by drugs such as cocaine or amphetamines. It is known that these drugs alter the effects of dopamine, serotonin, noradrenaline, and perhaps other transmitters, leading to the assumption that anxiety, depression and psychoses are biologically driven, the often cited chemical imbalance approach. In the case of dopamine, implicating this neurotransmitter as a sole trigger factor in psychoses is simplistic and naïve. Likewise, depression and anxiety may have other biological causes such as hormone irregularities or fluctuating glucose levels. The dopamine hypothesis alone has largely been discredited in the aetiology of psychoses. Dopamine as an causative factor is only one small part of a much wider as yet unknown picture: for example, psychosis occurs in Parkinson’s disease where dopamine is actually deficient.
 
The ‘psychologised’ individual                                                           
 ‘Common sense is not so common’   Voltaire
 
One major criticism of psychiatry concerns the endless diagnostic categories or disorders which set out to describe and define the whole range of normal human expression, from the histrionic to the shy. No wonder then that psychiatry and allied specialties, for example, psychology and sociology, are accused of a sweeping disregard for the extraordinary complexity and richness of human behaviour. Whole subsets of psychiatric specialties have mushroomed over the last 30 or more years, to include substance misuse, forensic issues, autistic spectrum disorders and many others(2). Many disorders have variants, for example schizoaffective or schizomanic subtypes for schizophrenia, without any real scientific basis for such assertions. The eccentric individual becomes ‘schizotypal’; the individual who is detached from others and prefers his/her own company, is labelled ‘schizoid personality disorder’. Some would question whether many psychiatric descriptions are indeed ‘disorders’. There are very few ‘mental’ conditions which really could be regarded as disorders, save for example, severe clinical depression, bipolar disorder, obsessive compulsive states, and the psychoses, the latter often drug-induced. The diagnostic categories become bewildering and meaningless when subtypes are used, for example schizoaffective, bipolar I and bipolar II, depression with or without psychotic symptoms, and so forth; all have their supporters and detractors. Objectively, the symptoms are merely variations on a theme and cannot be accurately rated scientifically, unlike the gradings of say, Hodgkins or non-Hodgkins lymphoma. The distinction between normal and abnormal is blurred and varies among cultures. This is particularly pertinent when describing or defining personality disorder. For example, when does narcissistic behaviour become an illness? Why should it be seen as a disorder?  Indeed, high self-esteem is encouraged in today’s’ climate and we are told to ‘love themselves more’. The usual response to the questioning of such behaviour is that it is ‘inappropriate’ or ‘out of proportion’ to the individual’s circumstances, or that ‘the patient is suffering’. Yet the entire media business, arts and entertainment, modelling and fashion industry is engaged in a narcissistic mind set, and the public love it! In other scenarios words are used interchangeably such that a psychopath, say, is perceived as a cold-blooded killer without conscience or feeling for his victim, or considered a creative genius, or indeed admired as a successful politician. The list of descriptions in the psychiatric disorders classification is wearisome and meaningless in many respects.
 
Much research in psychiatric journals nowadays is organic-based with ever intensive searches for newer receptors or transmitters, with increasing emphasis on the neurological basis for psychiatric conditions. In the past, emphasis was placed on the positive outcomes of drug trials, though this, fortunately, is now changing and reputable medical journals are now prepared to publish the results of negative findings. On the other hand, other researchers attempt to prove one type of psychotherapy is more effective than drug therapy, or that both together are better than either alone. Psychiatry has become polarized, with the ‘organic camp’ advocating a neurobiological basis and reductionist paradigm for psychiatric disorders, while the ‘psychotherapy model’ emphasizes the individual’s part in his/her illness with the development of strategies to defeat and overcome irrational beliefs and counterproductive emotions. There are problems with both approaches.  A great deal of criticism is now being targeted against the psychology industry with its claims of treating serious illnesses through talking cures, and using labels to categorize almost every aspect of human behaviour (3). For example, how does one account for biological symptoms which are pervasive in severe depression without considering the role of neurotransmitters and regulatory hormones? How does one measure the complexity of suffering in any one individual and translate that into a rating scale for myriads of others whose problems have different origins? Are two people with severe depression really the same if they score identical marks on a depression scale? Whole books are written on the use of rating scales for research into psychological/psychiatric disorders. Yet there are over 250 different psychotherapy treatment approaches, which inevitably leads one to question the overall value of psychotherapy (4). In Epstein’s view, the whole field of psychotherapy is ‘pseudoscientific, an elaborate mysticism only differentiated from religion by a seemingly modern orientation and the cant of science (5). Research in psychotherapy is in any event notoriously difficult because of sample sizes, control groups, placebo effects and the nature of the therapeutic intervention itself (cognitive therapy, family therapy, psychoanalytic therapy). Besides, even when some patients show a moderate improvement, nonspecific factors are always operating in the period between therapy sessions and follow-up. Patients may have had a better social adjustment because of a new job, an increase in salary, or a change in a relationship and so forth, while others may have had a general decrease in life stresses, for example, through improved physical health (recovery from surgery, better control of diabetes). Some patients will deteriorate, despite ‘cognitive restructuring’, because of redundancy from a job, or ending of a relationship and so forth.
 
What next?                                                   
“Just trust yourself and you’ll learn the art of living”  Goethe      
                                                                                                                        
Although many of the psychological treatments available nowadays were initially propounded by psychiatrists, psychotherapy and behavioural management are now more often carried out by psychologists, nurse practitioners and counsellors. Psychiatrists tend to deal with more severely affected individuals, ironically, those deemed to need psychotropic medication or where ‘counselling’ has failed. It could be argued that talking to a stranger for a fixed number of sessions (ranging from 10–12 one-hour slots) actually impedes the normal process of recovery and that a patient would benefit more from using his/her own social networks including family, friends, general practitioner and others, who are better placed to view the patient’s problems in context. Research claiming that depressed people are most likely to benefit from cognitive therapy, or that the majority of people suffering from panic attacks will recover with anxiety management, is deceptive and naively optimistic. Too many nonspecific factors are at play. The notion that a psychologist/counsellor/psychiatrist could turn a patient’s life around in 10 hours or so (10 sessions) is difficult to sustain when such problems have accumulated over that person’s lifetime, no matter how long or short-lived. The human mind is too complex and the human condition too intricate to be hoodwinked into such quick-fix solutions. Perhaps the best way forward is, ironically, to revert to an holistic approach with better education and training of both psychiatrists and psychologists. The former need further training in neurology (they already receive extensive training in psychology) and time spent in GP surgeries, the latter should be required to gain more experience of patients with severe types of psychiatric disorders (many hospital-affiliated psychologists already do), and general exposure to medicine via an acute emergency department or at a GP surgery (say, one year in total), preferably both, in order to broaden their horizons. The author appreciates the inherent, perhaps, unfortunately, insurmountable difficulties in setting up such a system involving the various disciplines. All ‘therapists’ should have a grounding in philosophy and sociology. It needs to be made clear that many patients simply feel better by talking to someone, though this ‘feeling better’ is not often sustained, and that knowing the cause of one’s problems does not equate with ‘cure’. Many patients have intractable conditions which are not amenable to ‘talking therapies’, and such individuals do not fit the category of the ‘worried well’, the usual ‘clients’ of counsellors and other therapists.

The significance of disturbed subjective sleep quality in the general population is important because of high prevalence rates (of up to 30%)¹ and the association with decreased quality of life.² Poor sleep affects cognitive and physical functioning, and insomnia is associated with a greater risk of falls and accidents,³ higher rates of absenteeism⁴ and increased health care utilization.⁴

Insomnia is commonly encountered in primary and secondary care settings, and can be symptomatic of many medical, neurological, substance abuse or primary sleep disorders.

Epidemiological and clinic-based studies consistently demonstrate high rates of psychiatric comorbidity.^5,6 Sleep disturbance is an important clinical construct in psychiatry. It represents formal diagnostic criterion in mental illnesses such as affective and anxiety disorders.^7,8

Insomnia is broadly defined as the subjective experience of poor or unrefreshing sleep, with some objective evidence of reduced time asleep or delayed sleep-onset. The subjective nature of such complaints remains key, because sleeping is a private event, and there is often no informant history. Furthermore, it is the perceptual aspects of sleep that influence patients’ help-seeking behaviour, such as consultation requests, demands for night sedation, and medication and substance use. It is noteworthy that despite the wide-ranging implications and subjectively distressing nature of this phenomenon, it remains arguably one of the least satisfying symptoms to treat. Seeking a better understanding of the extent and nature of patients’ sleep perception can help optimise appropriate therapeutic strategies.

This is the first study assessing the subjective sleep quality of a sample of psychiatric disordered in-patients in a UK psychiatric hospital setting, using the Pittsburgh Sleep Quality Index (PSQI).⁹ This study is framed in the context of increasing the awareness of the significance of patients’ complaints of insomnia and addressing the wider psychosocial issues that this raises.

Method

Design: This was a cross-sectional survey of the self-reported quality of sleep in a population of psychiatric in-patients on the acute adult wards of a London psychiatric hospital.

Participants and Procedure:Participants consisted of psychiatric in-patients (ages 18-65) on all five of the acute adult open psychiatric wards of the Highgate Mental Health Centre, London, currently admitted for the assessment or treatment of mental illness. Financial compensation was not provided for any subject.

Subjects were approached on the ward by a member of nursing staff and asked if they were interested in participating in a study about sleep. The researcher was then introduced to explain further details with the aid of the participant information sheet. After a minimum of 24 hours, patients were approached again by the researcher and asked if they were willing to participate. Recruitment of subjects took place if the patient was agreeable to take part and did not meet any of the exclusion criteria (listed below). A scheduled time and date was made with participants in order to obtain written informed consent and to administer the questionnaire. Questionnaire data was collected from each subject by the researcher in a private interview room located on the patient’s psychiatric ward. Demographic and clinical data required from the patient’s medical notes was recorded on the day of sampling. Exclusion criteria were: the presence of severely disturbed behaviour, or having received rapid tranquilisation for such behaviour on the day of sampling; a significant impairment in physical condition (e.g. infection, trauma); a history of a sleep disorder (e.g. obstructive sleep apnoea); the presence of organic illness including dementia; and lack of capacity to give informed consent.

Quality of Sleep:Subjects' quality of sleep was assessed by the administration of the Pittsburgh Sleep Quality Index (PSQI).⁹ This is one of the most widely used questionnaires employing standardised measures to assess subjective sleep quality in clinical and research settings. It assesses sleep quality and disturbances over a 1-month time interval. 19 individual items are used to generate 7 component scores (with a range of possible subscale scores from 0 to 3): 1) overall subjective sleep quality; 2) sleep latency; 3) sleep duration; 4) habitual sleep efficiency; 5) sleep disturbances 6) use of hypnotic or sedative medication; 7) daytime dysfunction. Higher scores indicate greater sleep disturbances. The sum of the component scores yields a global score (ranging from 0 to 21), which was used as the primary outcome measure in this study. A global PSQI score cut off score of 5 discriminates between good and bad sleepers and the PSQI gives acceptable measures of internal homogeneity, consistency (test-retest reliability) and validity.^9,10

Other Variables:Demographic and clinical data recorded concurrently from participant's medical notes included: sex (male/female); age (years); ethnicity (Asian/Black/Mixed//Other); body mass index (BMI) (calculated as the ratio between weight [kilograms] and squared height [metres]); primary psychiatric diagnosis (based on ICD-10 criteria); duration of psychiatric illness (years); past medical history; number of currently prescribed medications; length of admission to date (days); current admission status (informal/detained under Section 2 of the Mental Health Act (MHA) (1983) (this is for a maximum period of 28 days for further assessment)/detained under Section 3 MHA (1983) (this is for a maximum period of 6 months for psychiatric treatment). A further category (detained under another type of section) was dropped as this did not apply to any of the subjects.

Ethics Committee Approval:Ethical and research governance authorisations were granted from Camden and Islington Community Local Research Ethics Committee, and from the North Central London Research Consortium, respectively.

Statistical Analysis:The aim was to compare clinical, demographic and PSQI data between the poor sleepers and good sleepers. The prevalence (%) of poor sleep was determined by the proportion of subjects with global PSQI score of 5 or more. Statistical analyses were predominantly performed using the software package Stata, version 9.2.

Results

Sample Characteristics

77 patients were initially identified as potentially eligible subjects. Of these, 31 (40%) were excluded due to: the presence of disturbed behaviour (n=1); inability to give informed consent (n=9); unwillingness to participate (n=19); absence from ward (either on leave or absent without leave) (n=2).

This left a total of 46 patients who were enrolled in to the study. Subject characteristics are given in Table 1.
Table 1: Demographic and clinical characteristics of study subjects

s.d.: standard deviation

As defined by ICD-10 criteria, the most common subdivisions of patients’ psychiatric diagnoses in descending order were: paranoid schizophrenia, F20.0, (n=16); emotionally unstable personality disorder, F60.3, (n=6); depressive disorder, F32, (n=6); bipolar affective disorder, F31 (n=5). Other subdivisions of subjects’ diagnoses included: organic mood disorder, F06.3 (n=1); organic personality disorder, F07, (n=1); residual and late onset psychotic disorder due to alcohol use, F10.7, (n=1); persistent delusional disorder, F22, (n=1); acute and transient psychotic disorder, F23, (n=1); unspecified non-organic psychosis, F29, (n=1); post traumatic stress disorder, F43.1, (n=1). One patient was undergoing psychiatric evaluation and therefore had no formal diagnosis.

Medications prescribed regularly were: antipsychotics (for 40% of the total sample of patients), mood stabilizers (16%), antidepressants (14%) and benzodiazepines (7%). In terms of regular night time sedation, two patients out of a total of 46 were prescribed zopiclone and diazepam respectively. Zopiclone was prescribed on an “as required” basis for 15 patients (33% of the total sample).

Overall sleep quality evaluated by the PSQI revealed a mean score of 9.74 (standard deviation= 5.11). Poor sleep quality (defined as a global PSQI score of 5 or more) was present in 36 out of the total of 46 subjects (78% of the sample).

Comparison between good and poor sleepers

Comparison of numerical measurements between the two sleep groups is presented in Table 2. For the normally distributed variables the figures reported for each group are the mean (standard deviation) and the p-value from the t-test. For the non-normally distributed variables the figures reported are the median (inter-quartile range) and the p-value from the Mann-Whitney test.

Table 2: Comparison of demographic and clinical data between good and poor sleepers.

(total PSQI <5)

Mean (SD)

Poor sleepers

(total PSQI ≥5)

Mean (SD)

P-value

Age (years)41.0 (12.1)37.2 (10.9)0.34BMI (kg/m²)23.0 (2.5)26.7 (5.2)0.15Duration of psychiatric illness (years) ^(*)10 (8, 12)9.5 (3, 12)0.70Duration of admission (days) ^(*)44 (13, 111)15 (5, 41)0.06Medications ^(*)2 (1, 3)2 (1, 4)0.55Psychiatric medications ^(*)1.5 (1, 2)2 (1, 2)0.68

(*) Median (Inter-quartile range) reported. Analysis performed using Mann-Whitney test

The results indicate that there was no strong evidence of a statistically significant difference between good and poor sleepers for any of the variables examined. However, there was a possible difference for duration of admission, although this result was only of borderline statistical significance (p=0.06). The results indicate a median duration of admission of 44 days for good sleepers and 15 days for poor sleepers.

The difference between sleep groups for the categorical variables was examined using Fisher’s exact test. Results, presented in Table 3, show the number (and percentage) of subjects falling into each category, with the p-value indicating the significance of the results.

Table 3: Comparison of categorical data between good and poor sleepers

There was a significant difference between sleep groups with regard to their admission status. Almost all (90%) of the good sleepers were detained under Section 3 MHA (1983), whilst this applied to only half of those in the poor sleepers group. Being detained under Section 2 MHA and informal admission were more commonly found amongst those categorised as poor sleepers.

There was no significant difference between groups in terms of sex or the presence of physical comorbidities.

The final set of analyses compared the differences between groups for the PSQI measures, and the results are summarised in Table 4. The figures reported are the mean (standard deviation) score for each group. For the individual components the Mann-Whitney test was used to compare between groups, and the p-values from this analysis are reported. For the PSQI total score, the unequal variance t-test was used to compare between groups.

Table 4: Comparison of PSQI measures between the good and poor sleepers

(*) Analysis performed using Mann-Whitney test

There was a statistically significant difference between good and poor sleepers for all PSQI components and for the PSQI total. The PSQI component values and PSQI total scores for poor sleepers were significantly higher than for good sleepers.

A profile of the mean PSQI individual component scores between the two groups (good sleepers versus poor sleepers) is displayed in Figure 1.

Figure 1: Mean component PSQI scores of good and bad sleepers

Profiles of the PSQI represent group differences of individual component scores. Mann-Whitney test, *p<0.05).

Subjective Patient Comments

The PSQI also comprises an open ended question, providing subjects with the opportunity to cite “other” (subjective) reasons for difficult sleep. The most common response was anxiety (n=8). Other examples included: medication alterations (n=3); environmental noise (n=2); “thinking excessively” (n=1); “a desire to be creative” (n=1); hard mattress (n=1); “food eaten” (n=1); “sedentary lifestyle” (n=1); alcohol (n=1); hunger (n=1); asthma (n=1); symptoms of the menopause (n=1); and “voices”(n=1).

Discussion

Main Results

This is the first study to examine the subjective quality of sleep among a population of psychiatric in-patients in the UK. The prevalence of poor sleep, as defined by a cut off PSQI score of 5 or more, was present in 78% of the patients sampled. Patients detained under Section 3 MHA (1983) were more likely to report sleeping well when compared to informal patients or those detained under section 2 MHA (1983). There was some evidence of good subjective sleep quality being related to a longer duration of admission, but this requires further investigation.

There were no significant differences between good and poor sleepers for any of the other demographic and clinical variables studied, including age, body mass index, duration of psychiatric illness, number of prescribed medications, sex, and physical comorbidities.

Individual PSQI component scores and global scores were significantly lower for good sleepers compared to poor sleepers. This would be expected given that higher scores indicate more severe sleep complaints, and this supports the consistency of the PSQI as a research instrument.

Factors Affecting Sleep

In-patients’ disturbed sleep may be caused by a variety of exogenous factors such as unfamiliar surroundings, environmental noise, bright lighting and staff interactions or monitoring. Physical and psychological factors, such as the side-effects of medication and substance use, may also have a detrimental effect on sleep quality. In the added presence of a psychiatric disorder, each of these factors may act synergistically on the relationship between mental illness and sleep. Despite substantial research supporting the robust associations between insomnia and comorbid conditions, specific mechanisms linking sleep, medical and psychiatric factors have not been well established.

Sleep complaints may represent early symptoms and risk factors for new episodes of mental illness rather than simply representing phenomena secondary to experience of mental illness. For example, longitudinal studies have found insomnia to be a substantial risk factor for the development of a depressive disorder^5,11,12 and the risk for developing new anxiety disorders and alcohol abuse is also greater for insomniacs.⁶

Stepanski & Rybarczyk¹³ present research arguing against the more traditional conceptualisation of insomnia as simply a consequence of another disorder. They propose the need for a revised model to understand insomnia that is comorbid with medical and/or psychiatric illness. Abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis may represent the underlying pathophysiological process in many chronic insomnia patients.¹⁴ This may signify a common risk factor for insomnia and depression, thus predisposing the individual to a vulnerability to both conditions.¹⁵

In this study, detained patients (under Section 3 MHA (1983)) were significantly more likely to be classified as good sleepers. A suggestion for this finding could be that these patients may be less resisting of remaining and sleeping on the ward due to the involuntary nature of their admission. Alternatively these patients may represent the group with the most severe mental illnesses and with the least insight, and therefore less able to accurately recall their (poor) sleeping habits over the previous month.

There was also a potential association between longer admission status and better sleep quality. Explanations for this observation might include: patients’ acceptance over time of their admission and the consequent conditioning to, and familiarisation with, the ward environment; achievement of stability in mental state over time; or the adaptation of the perception of sleep quality to the sleep disturbances that accompany mental illness.

Limitations

This study is based on cross-sectional data and the relationship between the course of mental illness and sleep perception cannot be determined. In order to verify the direction of causality, it is necessary to demonstrate longitudinally that improvement in symptom severity is accompanied by an increase in subjective sleep quality.

This study was not designed to look at the prevalence of poor sleep across the different classes of psychiatric illnesses and dual diagnoses were not considered. It did not measure psychopathology or self-reported psychological distress. Possible confounding factors were not taken in to account, such as concurrent use of caffeine, alcohol, nicotine, illicit substances, hypnotics or other medications known to affect sleep.

The PSQI measures sleep quality averaged over the previous month. In cases where patients had only very recently been admitted to hospital, measurements would have been unlikely to accurately reflect the perspective of an in-patient’s experience. The mean length of admission for this population however was longer than one month (42 days).

These results were drawn from a small sample, with a fairly high proportion of excluded patients (40%). This may explain why this study did not identify factors previously found to more frequently affect sleep adversely such as female gender, the elderly and those with chronic medical conditions.¹⁶ In addition the population sample has little ethnic diversity which limits the generalisability of the results.

Implications

This study found that the prevalence of poor sleep quality was more common than previously reported in the general population¹⁷ and more comparable to the higher rates reported in similar patient populations. Two previous studies investigating subjective sleep quality using the PSQI, found prevalence rates of poor sleepers to be 45.5%¹⁸, and 91.22%¹⁹ among a population of schizophrenia patients and psychiatric in-patients respectively.

Complaints of poor sleep are important for diagnostic purposes and also raise the need to address the adequacy of therapeutic strategies, given the consequent adverse impact on patients’ mental state, physical health, daytime function and quality of life.

Improving Sleep

Hypnotics such as benzodiazepines and benzodiazepine receptor agonists can be efficacious for the treatment of insomnia.^20,21 However the clinical benefits must be weighed against well known adverse effects, such as daytime sedation, agitation, memory impairment, confusion and ataxia. This, together with the recommendation that hypnotics should only be used for short periods of time because of the risk of drug tolerance and dependence,²² highlights the need for suitable non-pharmacological alternatives.

Recent reviews support the notion of the effectiveness of Cognitive Behavioural Therapy for insomnia in the treatment of people with psychiatric or medical conditions.^13,23 Modified, lower cost education initiatives to promote good sleep could be employed by utilising the skills of the mental health professionals caring for patients on the ward, supplemented by the provision of clear written material.

Environmental variables to consider include adherence to regular ward routines including bedtime and awakening times, attention to ward layout and design (including the provision individual bedrooms), lighting, ambient noise, temperature, and the provision of comfortable mattresses and appropriate bed linen. Medication scheduling times, regular medication reviews, and avoidance of non-prescribed substances such as caffeine, alcohol and illicit substances are also important. Physical health problems, pain and psychological distress should be optimally managed. Moderate intensity exercise programs have also been found to bring about significant improvements in self-rated sleep quality.²⁴ Finally, increased staff awareness and sensitivity to the sleep problems on the ward, supplemented with objective recording of such disturbances, would be informative in gaining a further understanding of patients’ insomnia experiences.

Future Directions for Research

The PSQI is simple and inexpensive to perform. Results could be followed longitudinally in order to examine the course of sleep problems throughout an episode of acute mental illness, or to examine the effects of specific therapeutic interventions for sleep disorders. Sleep diaries have been shown to provide reliable estimates of subjective sleep parameters²⁵ and could be used as an adjunct to the PSQI. Ideally, concomitant objective measures such as polysomnography or wrist actigraphy (which detects physical motion), as well as cognitive and behavioural measures could be used to provide additional data.

This study represents the first attempt to examine the degree of self-reported poor sleep quality in a UK-based population of psychiatric in-patients and results suggest unsatisfactory sleep is a common finding. Large prospective longitudinal studies of sleep quality with control for confounding factors are needed to confirm the high prevalence rates in psychiatric in-patients. Studies comparing psychiatric patients with healthy controls, and also with insomniacs without psychiatric comorbidity, would further clarify the role of psychopathology in sleep disturbance.

References

1. Ancoli-Israel S, Roth T. Characteristics of insomnia in the United States: results of the 1991 National Sleep Foundation Survey. I. Sleep 1999;22 Suppl 2:S347-53.

2. Leger D, Scheuermaier K, Philip P, et al. SF-36: Evaluation of quality of life in severe and mild insomniacs compared with good sleepers. Psychosom Med 2001;63:49-55.

3. Roth T. Prevalence, associated risks, and treatment patterns of insomnia. J Clin Psychiatry 2005;66 suppl 9:10-13.

4. Leger D, Guilleminault C, Bader G, et al. Medical and socio-professional impact of insomnia. Sleep 2002;25(6):625-629.

5. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA 1989;262:1479-84.

6. McCall WV. A psychiatric perspective on insomnia. J Clin Psychiatry 2001;62 Suppl 10:27-32.

7. World Health Organisation. The ICD-10 Classification of Mental and Behavioural Disorders: Diagnostic Criteria for Research. Geneva: World Health Organisation, 1993.

8. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: American Psychiatric Association, 1994.

9. Buysse DJ, Reynolds CF 3rd, Monk TH, et al. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res 1989;28:193-213.

10. Doi Y, Minowa M, Uchiyama M, et al. Psychometric assessment of subjective sleep quality using the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J) in psychiatric disordered and control subjects. Psychiatry Res 2000;97:165-172.

11. Breslau N, Roth T, Rosenthal L, et al. Sleep disturbance and psychiatric disorders: a longitudinal epidemiological study of young adults. Biol Psychiatry 1996;39:411-418.

12. Chang PP, Ford DE, Mead LA, et al. Insomnia in young men and subsequent depression. The Johns Hopkins Precursors Study. Am J Epidemiol 1997;146:105-114.

13. Stepanski EJ, Rybarczyk B. Emerging research on the treatment and etiology of secondary of cormorbid insomnia. Sleep Med Rev 2006;10:7-18.

14. Richardson GS, Roth T. Future directions in the management of insomnia. J Clin Psychiatry 2001;62 suppl 10:39-45.

15. Roth T, Roehrs T. Insomnia: Epidemiology, Characteristics, and Consequences. Clin Cornerstone 2003;5(3):5-15.

16. Morin CM, Hauri PJ, Espie CA, et al. Nonpharmacologic treatment of chronic insomnia: an American Academy of Sleep Medicine review. Sleep 1999;22:1134-56.

17. Doi Y, Minowa M, Uchiyama M, et al. Subjective sleep quality and sleep problems in the general Japanese adult population. Psychiatry Clin Neurosci 2001; 55(3): 213-215.

18. Ritsner M, Kurs R, Ponizovosky A, et al. Perceived quality of life in schizophrenia: Relationships to sleep quality. Qual Life Res 2004;13:783-791.

19. Prieto-Rincón D, Echeto-Inciarte S, Faneite-Hernández P, et al. [Quality of sleep in hospitalized psychiatric patients]. Invest Clin 2006;47:5-16.

20. Nowell PM, Mazumdar S, Buysse DJ, et al. Benzopdidazepines and zolpidem for chronic insomnia: a meta-analysis of treatment efficacy. JAMA 1997;278:2170-7.

21. Holbrook AM, Crowther R, Lotter A, et al. Meta-analysis of benzopdiazepine use in the treatment of insomnia. CMAJ, 2000; 162: 225-233.

22. National Institute for Health and Clinical Excellence. Guidance on the use of zaleplon, zolpidem and zopiclone for the short-term management of insomnia. London: NICE, 2004. (Technology Appraisal 77.) Available from: URL: http://www.nice.org.uk/TA077guidance

23. Smith MT, Huang MI, Manber R. Cognitive behavior therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clin Psychol Rev 2005;25:559-92.

24. King AC, Oman RF, Brassington GS, Bliwise DL, Haskell WL. Moderate-Intensity Exercise and Self-rated Quality of Sleep in Older Adults. A Randomized Controlled Trial. JAMA 1997;277:32-37.

25. Coates TJ, Killen JD, George J, et al. Estimating sleep parameters: A multitrait-multimethod analysis. J Consult Clin Psychol 1982;50:345-52.

"Those who can, do; those who can't, bully" ¹

Bullying in the workplace is emerging as a problem over the past decade. Despite the tendency for incidents of bullying to be underreported ² it is widespread in all sectors of the workforce including healthcare in the United Kingdom (UK) ³. The culture of bullying in medicine contributes to this pattern of bullying behaviour that can adversely affect any aspect of working life from an employees health ⁴ to the reputation of the organisation ⁵. Therefore immediate changes are required to increase the recognition of this problem and take further steps to a solution.

Bullying and harassment

There are different ways to understand the terms bullying and harassment but considerable overlap exists with similar patterns of behaviour (figure 1).

The essential difference between bullying and harassment is that the latter is usually a single incident that relates to ones social identity and is therefore viewed as discriminatory in nature e.g. racial or sexual harassment. In legal terms harassment refers to a course of conduct directed at a specific person, which causes substantial emotional distress, and can be identified by equality laws in the relevant country.

On the other hand workplace bullying is generally not covered by specific legislation. The exception to this is found in such as Sweden and Norway ⁷. Indeed it is in Scandinavia where extensive research into bullying in the workplace originated ⁷.

Bullying

Bullying in the workplace is known internationally by terms such as mobbing, workplace harassment, employee abuse, mistreatment at work, and petty tyranny ⁸. There is no generally accepted definition of workplace bullying but it is summed up well by the following:

Persistent, offensive, abusive, intimidating or insulting behaviour, abuse of power or unfair penal sanctions which makes the recipient feel upset, threatened, humiliated or vulnerable, which undermines their self-confidence and which may cause them to suffer stress ⁹.

It is important to distinguish between bullying, which is always undermining and destructive, and constructive supervision that is developmental and supportive ⁸. The three essential elements of bullying are that it has a negative impact on the victim, it is persistent and, crucially, bullying is subjective ¹⁰. If a person feels bullied then he/she is being bullied ¹¹. This last point may be controversial because it is dependent on the bullied persons views and not based on objective evidence. Nevertheless workplace bullying exists as a problem. According to the Chartered Institute of Personnel and Development (CIPD) there has been a shift of perception in organisations from denying it happens to accepting that bullying is a problem ³.

How common is bullying?

The Silent Epidemic ⁷

Workplace bullying affects up to 50 per cent of the UK workforce at some time in their working lives and has an annual prevalence nearly 40 per cent ⁷. One in 10 callers to the UK National Bullying Advice Helpline are health care professionals ³. A questionnaire survey ¹² revealed that 38% of staff in a community healthcare trust were subject to workplace bullying in the previous year and that 42% had witnessed bullying of others. The British Medical Association (BMA) has acknowledged that bullying rates are higher in healthcare organisations and stated that 1 in 7 National Health Service (NHS) staff reported being bullied by other staff ¹³.

The scale of the problem has been widely highlighted as a problem in the nursing profession ¹⁰ with increased rates of bullying reported in Black and Minority Ethnic (BME) groups ¹⁴. In doctors bullying may occur in the clinical, educational ⁸ and research environment ¹⁵. One survey of doctors in the UK revealed that 37% of junior doctors had been bullied and 84% had experienced at least one bullying behaviour in the preceding year¹⁶. Higher rates have been reported in non-European Union (non-EU) doctors practicing in westernised countries ¹⁷ who are also less likely to take action against bullying ¹⁸.

Despite the growth of literature in this area the problem of workplace bullying is obscured by underreporting which has numerous causes (figure 2).

The greatest fear is that of reprisals from the employer, associates of the bully, and powerful professionals, who may close ranks and compromise the career of the whistle blower ¹.

Why do people bully in medicine?

The antecedents to bullying have undergone considerable debate in the psychology literature. Bullies may be attracted to the caring professions to take advantage of the vulnerability embedded in them in relation to clients and employees ¹. However in most cases the bullying in medicine is likely to be unintentional and could be shaped by the power inequality in relationships (e.g. consultant Vs junior doctor) in the field.

Moreover the traditional hierarchy within medicine and the teaching by intimidation and humiliation may foster a culture of bullying ¹⁸. Studies in the United States ¹⁹ and UK ¹³ have suggested that bullying commences with medical student and that this sets up a transgenerational legacy ⁷ as the behaviours of bullying are passed down. The BMA urges for a stop to the cycle of bullying and argue further that the target ethos in the health service with the survival of the fittest culture adds to bullying ¹³.

How do you know if you are being bullied?

If you are being bullied early warning signs may be present. These include the perception that your working relationship is different, that you are being persistently got at, that your work is being unfairly criticised, or you begin to question whether these mistakes you are supposed to have made really are your fault ²⁰. In addition to feelings of being undermined, or humiliated, bullying may also be associated with symptoms (figure 3).

Why does bullying matter?

It is clear from the physical and psychological effects that bullying affects people in their personal health. Workplace bullying can also contribute to problems of staff retention and economy. Estimates suggest that in the UK bullying cost employers 80milion lost working days and up to 2-30 billion in lost revenue each year ⁷. It costs the NHS more than 325 million a year and accounts for around 50 per cent of stress-related workplace illnesses ⁵.

Other effects of bullying at work include poor morale, poor employee relations, loss of respect for managers or supervisors, poor performance, lost productivity, absences, resignations, damage to organisations reputation and potential costs in tribunal and other court cases ⁶. Ultimately if the culture of bullying results in demoralized staff working, in a caring profession, it is the patients who will suffer.

What is currently being done about it?

In the UK the BMA has called for zero tolerance on bullying ¹³ and have provided a report on bullying and harassment in the workplace ²¹. Most NHS trusts disseminate anti-bullying policies, in connection with Dignity at Work, but the effective implementation of these policies has been questioned with the criticism that it is only for show ¹⁸. The information on guidance and policy, in relation to workplace bullying, is not widely publicised and the question is whether bullying is being systematically played down?

Recommendations

Although organisations such as the health service have taken steps to deal with bullying it is clear that problems persist. Heenan ⁵ states that an all-singing all-dancing policy is worthless without a culture that believes in and supports it and recommends steps employers need to consider (figure 4).

Awareness of bullying needs to be raised and the problem dealt with at an organisational and individual level. The authors suggest that bullying should be incorporated into teaching programmes and induction of junior doctors. Heenan ⁵ recommends training for managers and supervisors so that they have the confidence to deal with a situation, and deal with it at an early stage, rather then allowing the problem to accumulate and end up in the courts. Therefore it is in the healthcare trusts interests to take these steps to monitor and manage this problem.

In addition employees in healthcare need to be better informed of what steps to take if they find themselves as victims of a bully at work. NHS employers provide options available to deal with bullying and provide support for it (figure 5).

Conclusion

The late Tim Field, founder of the National Workplace Bullying Helpline, warns that everyone is at risk of becoming a target of bullying ¹. However the bully in healthcare organisations may not often realise what they are doing, so do both parties require help? There are conflicting views for the solution to bullying in the workplace regarding whether educational ²² or punitive ¹⁷ measures are appropriate. This will continue to be a matter of debate. Whichever approach is adopted, identification and increased awareness of bullying is the first step to the solution.

Bullying is an old problem that keeps re-emerging without a clear solution ³

Useful UK online resources

• http://www.acas.org.uk - Advisory, Conciliation and Arbitrary Service

• http://www.andreaadamstrust.org - Non-political non-profit making charity focussing on problems caused by workplace bullying.

• http://www.dignityatwork.org - A website for the Dignity at Work Partnership the worlds largest anti-bullying project.

• http://www.jfo.org.uk - Just Fight On is a non-profit making anti-bullying organisation.

• http://www.workplacebullying.co.uk - a non-profit site providing legal resources to those fighting against workplace bullying.

References

1. Field T, Becker K, Mackenzie GM, and Crossan L. Bullying in medicine. BMJ. 2002; 324: 786.

2. NHS Employers. Bullying and harassment staff guidance. 2007. Available from: http://www.nhsemployers.org/HealthyWorkPlaces/BullyingAndHarassment/Pages/Staffguidance.aspx

3. Al-Daraji WI. An old problem that keeps re-emerging without a clear solution. Medico-Legal Update. 2008; 8(2), 24-30.

4. Kivimki M, Elovaino M and Vahtera J. Workplace bullying and sickness absence in hospital staff. Occup Environ Med. 2000; 57: 656-660.

5. Heenan R. How to beat the workplace bully. Health Service Journal. 12^th February 2009: 25-27.

6. ACAS advice leaflet. Bullying and harassment at work: guidance for employees. 2008.

7. McAvoy B and Murtagh J. Workplace bullying the silent epidemic. BMJ. 2003; 326: 776-777.

8. Hicks B. Time to stop bullying and intimidation. Hosp Med. 2000; 61 (6): 428-431.

9. Lyons R, Tivey H, and Ball C. Bullying at work: how to tackle it. A guide for MSF representatives and members. London: MSF. 1995.

10. Quine L. Workplace bullying in nurses. J Health Psych. 2001; 6: 73-84.

11. Macpherson W. Stephen Lawrence inquiry: report of an enquiry by Sir William Macpherson of Cluny. London: Stationary Office. 1999.

12. Quine L. Workplace bullying in NHS community trust: staff questionnaire survey. BMJ.1999; 318: 228-232.

13. BMA Newswire article. BMA calls for zero tolerance on bullying and harassment in the Workplace. 19 May 2006.

14. Giga S, Hoel H, and Lewis D. A review of Black and Minority Ethnic (BME) employee experiences of workplace bullying. University of Bradford, (Research commissioned by the Dignity at Work Partnership). May 2008.

15. Stebbing J, Mandalia S, Portsmouth S, Leonard P, Crane J, Bower M, Earl H and Quine L. A questionnaire survey of stress and bullying in doctors undertaking research. Postgrad Med J. 2004; 80: 93-96.

16. Quine L. Workplace bullying in junior doctors: questionnaire survey. BMJ. 2002; 324: 878-879.

17. Cheema S, Ahmad K, Giri SK, Kaliaperumal VK, Naqvi SA. Bullying of junior doctors prevails in Irish health system: a bitter reality. Ir Med J. 2009; 98(9):274-5.

18. Hoosen A and Callaghan R. A survey of workplace bullying of psychiatric trainees. Psych Bull. 2004. 28: 225-227.

19. Frank E, Carrera JS, Stratton T, Bickel J, and Nora LM. Experiences of belittlement and harassment and their correlates among medical students in the United States: longitudinal survey. BMJ. 2006; 333:682

20. Andrea Adams Trust. Factsheet on workplace bullying. 1997. Available online from: http://www.andreaadamstrust.org/live/factsheet.html

21. BMA report. Bullying and harassment of doctors at work in the workplace, 17 May 2006. Available online from: http://www.bma.org.uk/employmentandcontracts/morale_motivation/bullying2006.jsp

22. Paice E, Aitken M, Houghton A, and Firth-Cozens J. Bullying among doctors in training: cross sectional questionnaire survey. BMJ. 2004. 329: 658-659.