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BJMP March 2011 Volume 4 Number 1


BJMP March 2011 Volume 4 Number 1 

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Research Articles

Community-acquired urinary tract infection in the elderly
Mahesh E, Medha Y, Indumathi V A, Prithvi S Kumar, Mohammed Wasim Khan and Punith K
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Review Articles

Eating Disorders in Children and Adolescents
Fayyaz Khan and Uttom Chowdhury
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Diffuse Alveolar Haemorrhage with ANCA associated vaculitis-review of Literature
Fadi Hammoudeh, Muhammad K. Perwaiz, Setu Patolia, Frances M. Schmidt, Narayan Neupane, Neerja Gulati, Danilo Enriquez, Joseph Quist, Mehjabeen Zahir and Eneh Kennedy.
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Case Reports/Series
An Unusual Cause of Chronic Dyspnoea
Fadi Seif and Lamia H. Ibrahim
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Theophylline Toxicity – A Forgotten Entity
N Altaie, S Malik and S Robertson
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Painless aortic dissection presenting with congestive heart failure
Usman Ali, Wai Hang Cheung and Ashis Banerjee
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Clinical Practice



BJMP December 2010 Volume 3 Number 4

BJMP December 2010 Volume 3 Number 4
Full Issue Booklet
John Agens
Research Article
Imtiyaz Mansoor, Mushtaq A Margoob, Nasseer Masoodi, Huda Mushtaq, Tayzeen Younis, Arshad Hussain, Shabir Dhar, , Parvez Chowdary
S.M. Coughlin , I. Walker, W.S. Wassif
Hyder Z, Dewer P
Review Article
Jayprakash Gopall , Wen Huang , Yu Zhao
Rakesh Kumar Jha , Yanli Zou, Jin Li, Bing Xia
Vinoth Sankar, Steven Close, Stephen J Leslie
Case Report/Series
Ciaran Clarke , Norbertas Skokauskas
Hye Seon Kim, Ambreen Aftab, Mehraj Shah , Jitendra Nayar
Education & Training
Ovais Wadoo, Aadil Jan Shah, Aamer Sajjad, Dave Fearnley
Clinical Practice
Daljit Singh Sura, Stephen Newell
Francis J Dunne
Suhail Y Hakim, Gursimran Singh Kundan, Sofia Gani Rah

To ‘D’ or not to ‘D’ in the older person, that is the question.

John Agens
Article Citation and PDF Link
BJMP 2010;3(4):a352

In anticipation of new recommendations from the Institute of Medicine and others, it behooves physicians and healthcare providers to review their knowledge base concerning adequate vitamin D intake for fall and fracture prevention in the elderly. There is enough new data for the Institute of Medicine to consider a new Dietary Reference Intake, or DRI, for vitamin D.1 A recent review by Bischoff-Ferrari et al, of numerous randomized controlled trials of vitamin D supplementation in older persons, concluded that both falls and fractures could be prevented. In addition, a dose-response relationship suggested that the optimal supplementation dose is 700 IU to 1000 IU per day.2 Epidemiologic associations between low vitamin D status and various cancers has led some to recommend balancing risk and benefit of moderate ultraviolet light (UV) exposure against complete UV protection for prevention of skin cancer.3 Others have reviewed the epidemiologic evidence for vitamin D supplementation in treatment of hypertension and prevention of cardiovascular disease.4 These epidemiologic studies are tantalizing, yet the evidence is not sufficient to support a causal relationship in making decisions about vitamin D supplementation for the prevention of cancer and cardiovascular disease. I will limit my editorial comments to preventing falls and fractures.

I would suggest looking at potential short- and long-term risks as well as the benefits of any intervention. What evidence do we have for the risks of vitamin D use for prevention? One recent study using a single dose of 500,000 IU of vitamin D daily showed an increased relative risk of fractures,5 but the dose of vitamin D in that study was far higher than other randomized controlled trials. Bischoff-Ferrari et al reviewed documented cases of hypercalcaemia in the randomized controlled trials;2 those authors add that only one trial reported nephrolithiasis, the Women’s Health Initiative.6 It is noteworthy that only the self-reported vitamin D and calcium dose was determined in that study, not the vitamin D status of the subjects. My opinion is that hypercalcaemia is uncommon and its complications are rare.
Many interventions that are routinely recommended for the older person probably have higher risks than the 700 IU to 1000 IU of vitamin D per day suggested by the evidence. Medications for hyperlipidaemia are one case in point; antihypertensives are another. Both are considered relatively safe and effective in primary and secondary prevention of cardiovascular disease. The long-term risks of the supplementation of 700 IU to 1000 IU of vitamin D are not well known compared to those long-term risks associated with lipid-lowering drugs or antihypertensives. On the other hand, some older persons at increased fall risk have more immediate threats to their health from a fall or fracture than any long-term risks of vitamin D supplementation. Given the detrimental consequences of falls and fractures in the elderly, the risks of vitamin D supplementation may be worth it. 




Acknowledgements / Conflicts / Author Details
Competing Interests: 
None declared
Details of Authors: 
JOHN AGENS MD, FACP. Associate Professor Geriatrics, Florida State University College of Medicine, 1115 West Call Street Suite 3140- H, Tallahassee, Florida 32306-4300
Corresponding Author Details: 
JOHN AGENS MD, FACP. Associate Professor Geriatrics, Florida State University College of Medicine, 1115 West Call Street Suite 3140- H, Tallahassee, Florida 32306-4300
Corresponding Author Email: 
[email protected]

1.  Yetley EA, Brulé D, Cheney MC et al. Dietary reference intakes for vitamin D: justification for a review of the 1997 values. The Am J Clin Nutr. 2009 Mar;89(3):719-727.

2.   Bischoff-Ferrari HA, Shao A, Dawson-Hughes B et al. Benefit-risk assessment of vitamin D supplementation. Osteoporosis Int. 2010 Jul;21(7):1121-1132.
3.   Zeeb H, Greinert R. The role of vitamin D in cancer prevention: does UV protection conflict with the need to raise low levels of vitamin D? Dtsch Arztebl Int. 2010;107(37):638-643.
4.   Holick MF. The D-bate: do calcium and vitamin D affect cardiovascular health? Menopause. 2010;17(4):667-668.
5.   Sanders KM, Stuart AL, Williamson EJ et.al. Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial. JAMA. 2010;303(18):1815-1822.
6.   Jackson RD, LaCroix AZ, Gass M et.al. Women's Health Initiative trial of calcium plus vitamin D supplementation and the risk of fractures. NEJM. 2006;354:669-683.



Vertigo- Diagnosis and management in primary care

Daljit Singh Sura and Stephen Newell
Article Citation and PDF Link
BJMP 2010;3(4):a351

General Information 

  1. Vertigo is the hallucination of movement of the environment around the patient, or of the patient with respect to the environment 1. It is not a fear of heights.
  2. Vertigo is not necessarily the same as dizziness
  3. Dizziness is a non-specific term which can be categorised into four different subtypes according to symptoms described by the patients:
    1. Vertigo
    2. Presyncope: the sense of impending faint, caused by a reduced total cerebral perfusion
    3. Light-headedness: often described as giddiness or wooziness 2
    4. Disequilibrium: a feeling of unsteadiness or imbalance when standing 2

Classification Vertigo may be classified as:

    1. Central - due to a brainstem or cerebellar disorder
    2. Peripheral - due to disorders of the inner ear or the Vestibulocochlear (VIIIth) cranial nerve

Incidence/Prevalence: Most patients who complain about dizziness do not have true vertigo:

    1.    5 community based studies into dizziness indicated that around 30% of patients were found to have vertigo,     rising to 56.4% in an older population 3
    2.   A postal questionnaire study which examined 2064 patients, aged 18-65, 7% described true vertigo in the       previous year 3
    3.   A full time GP can therefore expect between 10-20 patients with vertigo in one year 3
    4.   93% of primary care patients with vertigo have either benign paroxysmal positional vertigo (BPPV), acute         vestibular neuronitis, or Ménière's disease 4. These conditions are highlighted in Table 2 

Causes A wide range of conditions can cause vertigo, and identifying whether deafness or CNS signs are present, can help narrow the differential diagnosis, as shown in Table 1. 

Table 1 Causes of vertigo
Vertigo with deafness Vertigo without deafness Vertigo with intracranial signs
Ménière’s disease Vestibular neuronitis Cerebellopontine angle tumour
Labyrinthitis Benign positional vertigo Cerebrovascular disease : TIA / CVA
Labyrinthine trauma  Acute vestibular dysfunction  Vertebro-basilar insufficiency and thromboembolism:- lateral medullary syndrome- subclavian steal syndrome- basilar migraine
Acoustic neuroma  Medication induced vertigo e.g. aminoglycosides  Brain tumour:- e.g. ependymoma or metastasis in the fourth ventricle
Acute cochleo-vestibular dysfunction Cervical spondylosis Migraine
Syphilis (rare) Following flexion-extension injury Multiple sclerosis
    Aura of epileptic attack – especially temporal lobe epilepsy
    Drugs – e.g. phenytoin, barbiturates


  1. Vertigo may be due to central lesions or peripheral lesions. Vertigo may also be psychogenic or occur in conditions which limit neck movement, such as vertigo caused by cervical spondylosis, or following a “whiplash” flexion-extension injury.
  2. It is essential to determine whether the patient has a peripheral or central cause of vertigo 1.
  3. Information obtained from the history that can be used to make this distinction includes 1
    1. The timing and duration of the vertigo
    2. Provoking or exacerbating factors
    3. Associated symptoms such as
      1. Pain
      2. Nausea
      3. Neurological symptoms
      4. Hearing loss
  4. Central vertigo:
    1. The vertigo usually develops gradually
    2. Except in: an acute central vertigo is probably vascular in origin, e.g. CVA
    3. Central lesions usually cause neurological signs in addition to the vertigo
    4. Auditory features tend to be uncommon.
    5. Causes severe imbalance
    6. Nystagmus is purely vertical, horizontal, or torsional and is not inhibited by fixation of eyes onto an object
  5. The duration of vertigo episodes and associated auditory symptoms will help to narrow the differential diagnosis 5. This is illustrated for various pathologies that cause vertigo, in Table 2
    Table 2 Timing of symptoms
    Pathology Duration Of Episode Associated Auditory Symptoms Peripheral or Central Origin
    Benign Paroxysmal Positional Vertigo Seconds No Peripheral
    Vestibular Neuronitis Days No Peripheral
    Ménière's Disease Hours Yes Peripheral
    Perilymphatic Fistula Seconds Yes Peripheral
    Transient Ischemic Attack Seconds / Hours No Central
    Vertiginous Migraine Hours No Central
    Labyrinthitis Days Yes Peripheral
    Stroke Days No Central
    Acoustic Neuroma Months Yes Peripheral
    Cerebellar Tumour Months No Central
    Multiple Sclerosis Months No Central

    It is important to differentiate vertigo from non-rotatory dizziness (presyncope, disequilibrium, light-headedness). Patients can be asked whether they “felt light headed or felt as if the world was spinning around” during a dizzy spell 3.

  6. Important points in the history:
    1. Onset - specific provoking events such as flying or trauma
    2. Duration:
      1. Seconds - Benign positional vertigo
      2. Hours - Ménière's Disease
      3. Weeks - Labyrinthitis, Post-head trauma, Vestibular neuronitis
      4. Years - may be psychogenic
    3. Associated auditory symptoms - rare in primary CNS lesion
    4. Other associated symptoms
      1. Nausea and vomiting in a vestibular cause
      2. Neurological symptoms such as visual disturbance, dysarthria in a central lesion


  1. Examination of ear drums (Otoscopy/ Pneumatic otoscopy) for:
    1. Vesicles (Ramsay Hunt syndrome)
    2. Cholesteatoma
  2. Tuning fork tests for hearing loss – Rinne/Weber tests
  3. Cranial nerve examination. Cranial nerves should be examined for signs of :
    1. Nerve palsies
    2. Sensorineural hearing loss
    3. Nystagmus 3 
  4. Hennebert's sign 1
    1. Vertigo or nystagmus caused by pushing on the tragus and external auditory meatus of the affected side
    2. Indicates the presence of a perilymphatic fistula.
  5. Gait tests:
    1. Romberg's sign (not particularly useful in the diagnosis of vertigo 1)
    2. Heel-to- toe walking test
    3. Unterberger's stepping test 1 (The patient is asked to walk on the spot with their eyes closed – if the patient rotates to one side they have labyrinth lesion on that side
  6. Dix-Hallpike manoeuvre 1
    1. The most helpful test to perform on patients with vertigo1
    2. If rotational nystagmus occurs then the test is considered positive for BPPV. During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the ear closest to the ground.
  7. Head impulse test/head thrust test
    1. Useful in recognizing acute vestibulopathy 6
  8. Caloric tests
    1. Cold or warm water or air is irrigated into the external auditory canal
    2. Not commonly used

Investigations/Testing to consider:

  1. Special auditory tests
    1. Audiometry helps establish the diagnosis of Ménière's disease
  2. The history is most important and may give a quite good indication of the cause of vertigo. General medical causes such as anaemia, hypotension and hypoglycaemia may present with dizziness, and therefore should be investigated.
  3. If features of CNS causes is suspected from the history or examination:
    1. CT/MRI Brain imaging as appropriate


  1. Treatment should ideally aim at the cause of the vertigo 7:
    1. Medical management – as described below.
    2. Vestibular rehabilitation exercises – e.g. Cawthorne-Cooksey exercises 5.
      1. These exercises aim to help the patient return to normal activity more quickly.
      2. Moving the eyes from side to side and up and down while in bed or sitting down - then moving the head, first with your eyes open and then closed
      3. Other forms use gaze and gait stabilising exercises. Most exercises involve head movement
  1. For most patients the main priority is effective control of the symptoms.
    1. For acute attacks, treatments include 5,8: -
      1. Betahistine hydrochloride 8-16mg upto TDS
      2. Cinnarizine, 15-30 mg TDS or
      3. Prochlorperazine should be reserved for rapid relieve of acute symptoms only 8,12 - tablets 5-10 mg or buccal 3mg TDS or injection 12.5 mg IM or 25mg PR suppository - if vomiting
    2. Preventive measures for recurrent attacks include:
      1. Restrict salt and fluid intake - stop smoking and restrict excess coffee or alcohol 9,10
      2. Betahistine hydrochloride 16mg regularly TDS seems most effective in Ménière's
      3. Cinnarizine 15-30 mg TDS
    1. Points to consider
      1. Warn patients when drugs may sedate 10.
      2. Prochlorperazine is less sedating than some other recommended antihistamines, but may cause a dystonic reaction (particularly in children and young women) 11.
      3. Benzodiazepines are not recommended 9.
    2. Recurrent vertigo
      1. The most important first step in the management of recurrent vertigo is to distinguish vertigo from 'dizziness'.
      2.  In attacks of vertigo there is a sense of mobile disequilibrium ("the room spinning") which, if severe, results in uncontrolled staggering in one direction which may be only prevented by grabbing a solid object 10.
    3. Epley's manoeuvre

          a.     Aims to remove debris from the semicircular canals and deposit it in the utricle where hair cells are not                     stimulated 11      b.     Contraindications include 10:                                         i.     Severe carotid stenosis                                         ii.     Unstable heart disease                                         iii.    Severe neck disease (cervical spondylosis with myelopathy)                                         iv.    Advanced rheumatoid arthritis Consultation and referral:

    1. Refer to secondary care if 10 :
      1. Recurrent separate episodes
      2. Neurological symptoms e.g. dysphasia, paraesthesiae or weakness
      3. Associated sensorineural deafness
      4. If there is an inadequate visualisation of the entire tympanic membrane or an abnormality (e.g. cholesteatoma)
      5. Atypical nystagmus e.g. non-horizontal, persisting for weeks, changing in direction or differing in each eye
      6. Positive fistula sign: pressure on the tragus reproducing symptoms (suggests endolymphatic fistula
    2. If the patient has hearing problems in addition to vertigo then referral should be made to an ENT specialist. Other cases should be referred to a neurologist 10.
    3. While awaiting referral:
      1. Consider symptomatic drug treatment  for no longer than 1 week because prolonged use may delay vestibular compensation
      2. It is important that the person stops symptomatic treatment 48 hours before seeing a specialist, as it will interfere with diagnostic tests such as the Dix-Hallpike manoeuvre.
      3. If the person's symptoms deteriorate, seek specialist advice.

    When to consider hospitalization

    1. Admit the patient to hospital if they have severe nausea and vomiting, and are unable to tolerate oral fluids 9.
    2. Admit or urgently refer the person to a neurologist if they have:
      1. Very sudden onset of vertigo (within seconds) that persists.
      2. Acute vertigo associated with neurological symptoms or signs (e.g. new type of headache - especially occipital, gait disturbance, truncal ataxia, numbness, dysarthria, weakness) which may suggest CVA, TIA, or multiple sclerosis 9.
    3. Admit or refer the person as an emergency to an ENT specialist if they have acute deafness without other typical features of Ménière’s disease (tinnitus and a sensation of fullness in the ear). Sudden onset unilateral deafness would suggest acute ischaemia of the labyrinth or brainstem, but can also occur with infection or inflammation.
      1. Emergency treatment may restore hearing. The person should be seen within 12 hours of the onset of symptoms 9
    4. The urgency of referral depends on the severity of symptoms (e.g. requirement for intravenous fluids because of excessive vomiting) and the suspected diagnosis 9.

     Patient InformationThe Ménière's Society www.menieres.org.ukwww.patient.co.uk/doctor/Vertigo.htm


Acknowledgements / Conflicts / Author Details
Competing Interests: 
None declared
Details of Authors: 
Daljit Singh Sura, GP ST3 Registrar, North Street Medical Care, RM1 4QJ, UK Stephen Newell, General Practitioner, North Street Medical Care, RM1 4QJ, UK
Corresponding Author Details: 
Dr Daljit Singh Sura, GP ST3 Registrar, North Street Medical Care, RM1 4QJ, UK
Corresponding Author Email: 
[email protected]

1.     Ronald H. Labuguen. Initial Evaluation of Vertigo. Am Fam Physician 2006;73:244-51, 254

2.     Kuo CH, Pang L, Chang R. Vertigo - part 1 - assessment in general practice. Aust Fam Physician.                       2008;37(5):341-73.     Barraclough K, Bronstein A. Vertigo. BMJ. 2009;339:b34934.     Hanley K, O'Dowd T, Considine N. A systematic review of vertigo in primary care. Br J Gen Pract.                       2001;51(469):666-715.     Randy Swartz. Treatment of vertigo. Am Fam Physician 2005;71:1115-22, 1129-306.     Information from your family doctor. Vertigo-A Type of Dizziness. Am Fam Physician 2005;71: 67.     Hanley, K. and O'Dowd, T. (2002) Symptoms of vertigo in general practice: a prospective study of                   diagnosis. British Journal of General Practice 52(483), 809-812.8.     British National Formulary9.     NHS Clinical Knowledge Summaries10.   GP Practice Notebook11.   Swartz R. Treatment of vertigo. Am Fam Physician 2005;71:1115-22, 1129-30 12.    Hamid M. Medical management of common peripheral vestibular diseases. Curr Opin Otolaryngol Head Neck          Surg. 2010 Oct;18(5):407-12.

Interview with Professor Richard D Griffiths

Article Citation and PDF Link
BJMP 2010;3(4):a349

Richard D Griffiths BSc, MD, FRCP, FHEA

Prof Griffiths is a Professor of Medicine (Intensive Care), Dept of Musculoskeletal Biology, Institute of Ageing & Chronic Disease, Faculty of Health & Life Sciences University of Liverpool, and Honorary Consultant Physician in Intensive Care Medicine, Whiston Hospital, UK.
He obtained a BSc in Physiology during undergraduate training in medicine (MBBS) at University College London during the ‘70s. During the early ‘80s in London obtained a research MD studying muscle energetics in the early days of human Magnetic Resonance Spectroscopy. Became a consultant in adult Intensive Care Medicine in 1985 following a move to Liverpool in 1984 and continued research interests in muscle and expanded these into nutrition (glutamine) and the critically ill. Since then has been a pioneer of the rehabilitation of the post-ICU patient. He extensively involved over the last two decades in undergraduate curriculum reform and as the Director of the Final Year has pioneered a fully portfolio based professional learning programme.
How long have you been working in your speciality?
I have been a consultant intensive care physician for more than 25 years.
Which aspect of your work do you find most satisfying?
To be able to improve patient care through clinical research and the training of medical students.
What achievements are you most proud of in your medical career?
Raising the awareness of the physical, psychological and cognitive challenges ICU patients and relatives face during recovery and contributing to the evidence base guiding rehabilitation.Clinical nutrition research on glutamine and identifying the need to use six month mortality outcomes in the critically ill. Creating a final year of undergraduate medical training that fosters professionalism and critical self awareness based upon a clinical portfolio and appraisal process that produces graduates fit for practice.  
Which part of your job do you enjoy the least?
Very little, but perhaps the ever increasing bureaucracy of regulation in practice and research.
What are your views about the current status of medical training in your country and what do you think needs to change?
In the UK most medical schools have radically reformed their curriculum to meet the needs of modern medicine and life- long learning. In Liverpool our students are recognized to be well prepared with the skills to ensure patient safety and start foundation training following a course commended by clinicians, hospitals, examiners and GMC alike. Post-graduate changes have paralleled these developments and while the training structures and closer observations are to be commended the restrictions on working time remains a concern for the acquisition of real “shop floor” experience. Our trainees simply don’t get enough “flying hours” as in the past.
How would you encourage more medical students into entering your speciality?
Intensive care medicine is popular. The problem for students is to understand how to get there. The new Faculty of Intensive Care medicine, that has just starte, brings an independent speciality out from under the umbrella of its various parent specialities and hopefully will provide the focus to make the career pathway clearer in the future.
What qualities do you think a good trainee should possess?
All those attributes that the GMC expect of a practitioner! In particular I like to see enthusiasm, self awareness and measured confidence, an enquiring and questioning mind and a degree of professional flexibility mixed with the ability to ask for help and advice. I need to trust them just as their patients need to as well.
What is the most important advice you could offer to a new trainee?
Stay calm, be professional and follow the basic principles of good medical practice doing the simple things well, and don’t be afraid to ask for help.
What qualities do you think a good trainer should possess?
Maintain professionalism and be a role model at all times with the ability to listen, support and recognize the strengths as well as being firm with those things that need developing.
Do you think doctors are over-regulated compared with other professions?
No, while regulation does not itself prevent bad medicine it does prevent it being ignored.
Is there any aspect of current health policies in your country that are de-professionalising doctors? If yes what should be done to counter this trend?
De-professionalising only occurs when doctors avoid taking leadership roles. I think this was a fear in the recent past but in the last 10 years in the UK there has been a strong drive to redefine professionalism and the role of the doctor for the 21st century and it is central now to modern undergraduate and post graduate training with the importance of Consultants and GPs taking leadership roles in planning health care delivery.
Which scientific paper/publication has influenced you the most?
Huxley AF 1957 A theory of muscular contraction” Prog. In Biophys. And Biophys. Chem; 7:255.
Professor Sir Andrew Huxley was awarded the Nobel prize in medicine in 1963 with AL Hodgkin for nerve conduction but my personal memory is in muscle physiology (as one of my tutors) for his work on the theory of muscle contraction and the role of cross bridges. His clarity of thought was demonstrated in his ability to always ask the question everyone else wished they had asked! He was a kind and gentle teacher that gave time even for a simple medical student.
What single area of medical research in your speciality should be given priority?
The brain is the forgotten organ in multiple organ failure. We now recognize that acute brain dysfunction is a serious problem but we know little about its pathology, how to prevent it or recover from it.
What is the most challenging area in your speciality that needs further development?
There has been a rush towards ill conceived large scale pragmatic clinical effectiveness studies of various therapies few of which have shown much to change practice. Rather there is a need for more detailed scientific research to better define efficacy of therapies by exploring the pathological processes and the genetic and environmental influences of common disorders that result in multiple organ failure.
Which changes would substantially improve the quality of healthcare in your country?
Addressing the challenge of an ageing population and in particular the community medical and non-medical support of the aged infirm so that modern medicine does not grind to a halt.
Do you think doctors can make a valuable contribution to healthcare management? If so how?
By showing leadership and making the changes happen and not leaving it to others perhaps less informed to direct change.
How has the political environment affected your work?
I have tried to ignore it as much as possible. Politics is a business best left to politicians while the rest of the world gets on with life.
What are your interests outside of work?  
I treasure my family, a marriage of 28 years, with two undergraduates in medicine and one in architecture and doing all the jobs they ask of a father. When not escaping to the south of France or walking I become a generalist handyman so it can be a gardener, electrician, plumber, decorator, carpenter, car mechanic………and the Sunday Roast!
If you were not a doctor, what would you do?
With the exception of playing a musical instrument anything that combines academia, teaching and its practical application, but with preference in the natural world.


BJMP September 2010 Volume 3 Number 3


BJMP Sept 2010 Volume 3 Number 3
Full Issue Booklet (All articles)

Cervicogenic headache: It is time to call for more attention Full Text PDF
Yili Zhou

Research Article
Effects of Lornoxicam on the Haemodynamic and Catecholamine Response to Laryngoscopy and Tracheal Intubation Full Text PDF
M. Daabiss , M. Hashish , R. AlOtaibi , R. AlDafterdar
Seroprevalence of Co-infection of Hepatitis B and Hepatitis C Genotypes among Adult Female Population of Karachi, Pakistan Full Text PDF
Shazia Tabassum Hakim, Samina Noorali, Meaghen Ashby, Anisah Bagasra, Shahana U. Kazmi , Omar Bagasra

Review Article
Psychological Distress in Carers of People with Mental Disorders Full Text PDF
Aadil Jan Shah , Ovais Wadoo , Javed Latoo
Vitiligo Management: An Update Full Text PDF
Imran Majid
Psychological aspects of infertility Full Text PDF
Prasanta Kumar Deka, Swarnali Sarma

Case Report/Series
Coronary vasospasm in a patient with respiratory failure: A case report and a brief review. Full Text PDF
Mujeeb Sheikh , Satjit Adlakha , Steven Bruhl , Shaffi Kanjwal
Elevated pancreatic enzymes within the content of liver abscess in a patient with a history of chronic pancreatitis. Full Text PDF
Muhammad Z Bawany , Thomas Sodeman
Giant Cerebral Hydatid Cyst in a Child- A Case Report and Review of Literature Full Text PDF
Ali Nemati , Ahmad Kamgarpour , Murtaza Rashid , Sahar Sohrabi Nazari

Education and Training
Post MTAS: A Survey of the first MMC Surgical Trainees in the Oxford Deanery Full Text PDF
Khurram K Khan , Karen A Eley, Bettina Lieske, and Mr Bob Soin

Clinical Practice
Female urinary incontinence - primary care management Full Text PDF
Anita Sharma

Online Interview with Dr David Fearnley Full Text PDF

BJMP Sept 2010 Volume 3 Number 3

Welcome to this issue of the BJMP

Giant Cerebral Hydatid Cyst in a Child- A Case Report and Review of Literature

Ali Nemati, Ahmad Kamgarpour, Murtaza Rashid and Sahar Sohrabi Nazari
Article Citation and PDF Link
BJMP 2010;3(3):a338
Abstract / Summary
Cystic hydatidosis is a rare disease which mainly involves the liver and lungs, and rarely the brain. Cysts may be single or multiple. A 6-year-old boy presented with the chief complaint of ataxia. Brain imaging revealed a huge cystic structure involving the right side of the brain. A diagnosis of brain hydatid cyst was made and the patient was operated on. A large cyst was successfully delivered without rupture. Antihelminthic medication was started and the patient was discharged with full recovery of neurological function. Hydatid cysts must be considered as a differential diagnosis in patients with cystic lesions of the brain, especially in children. Surgery remains the standard method of treatment, and care must be taken in order to recover the cyst without rupture to avoid severe complications and recurrence.
Hydatid cyst; Brain; Imaging; Surgery

Introduction  A hydatid cyst is the larval stage of a small tapeworm, Echinococcus granulosus. This is an emerging zoonotic parasitic disease throughout the world, thought to cause an annual loss of US $193,529,740.1 Hydatid cysts are more prevalent in Australia, New Zealand, South America, Russia, France, China, India, the Middle East and Mediterranean countries.2,3,4 They are most commonly (about 50-75%) seen in children and young adults.4,5,6 The liver is the most common organ involved (77%), followed by the lungs (43%).7,8,9,10 However, some researchers report that the lung is the most common organ involved in children, possibly due to bypass of the liver by lymphatics, and higher incidental findings in the lungs when children are assessed for other respiratory infections.8,11,12,13 Hydatid cysts have been reported in the brain (2%),3,4,5,7,8,14,15 heart (2%),8,10,13,16 kidneys (2%),9,10,11 orbit (1%),17,18 spinal cord (1%),3,19 spleen,4 spine,3,8 spermatic cord20 and soft tissues.8 However, in the Mediterranean region, the incidence of brain hydatid cysts have been reported higher (7.4-8.8%).21 Surgery remains the treatment of choice, although recently some new modalities have been described.5,8,22 Careful removal of the lesion is of considerable importance, otherwise fatal complications are inevitable.23,24,25 We describe the case of a 6 year old boy who came to our department with various neurological manifestations. The main purpose of this study is to demonstrate the unusual symptoms of the patient and the enormity of the operated cyst, which was fully resected without rupture. Case Report A 6-year-old boy was referred to our Neurosurgery Department with a four week history of ataxia and left sided weakness. His vital signs were normal and his Glasgow Coma Scale (GCS) was 15. The symptoms had started about six months ago with numbness and parasthesia of the toes. Subsequently he developed intermittent nausea and vomiting. He then started to develop left sided weakness and finally ataxia. He also had a few focal convulsions but did not complain of headache. Fundoscopy revealed bilateral frank papilloedema. On examination, the patient had nystagmus and a positive Romberg’s test. Laboratory data showed mild leucocytosis without any significant rise in eosinophils, and liver enzymes were normal. The enzyme-linked immunosorbent assay (ELISA) for hydatid cysts was negative. Plain chest X-ray and ultrasound scan of the abdomen and pelvis were also normal. Brain computed tomography (CT scan) of the frontal and parietal lobes demonstrated a single large, spherical, well-defined, thin-walled homogenous cyst, with an inner density similar to that of cerebrospinal fluid (CSF), and a wall which did not show enhancement [fig 1(a)]. This cystic structure caused a mass effect and a midline shift towards the left, as well as hydrocephalus, possibly due to obstruction. Magnetic resonance imaging (MRI) of the brain showed cystic signal intensity similar to that of CSF, without ring enhancement or oedema [fig 2].   Fig 1 (a): Pre-operative unenhanced CT scan which shows a large CSF density cystic lesion on the right side causing mass effect and midline shift to the left. There is no peri-lesional oedema. Fig 1 (b): Post-operative CT scan of the lesion shows a large void which can lead to dangerous collapse. Mild haematoma is also seen. Fig 2 (a): T1-weighted axial MRI of the brain demonstrates a cyst density similar to CSF. Fig 2 (b): T2-weighted MRI shows no ring enhancement or oedema. The periventricular hyperintensity of the left side is probably due to obstructive hydrocephalus. Fig 3: This shows the cyst removed in toto after operation. The cyst appears creamy and smooth. After summation of all the above data, the diagnosis of a hydatid cyst was made and a right frontotemporoparietal craniotomy was performed. A large cystic structure (14×14×12 cm) was delivered with utmost care to avoid rupture and spillage [fig 3]. A hydatid cyst was confirmed by pathology reports.  A post-operative CT scan showed a large space without any residual matter [fig 1(b)]. Post-operatively, albendazole 15 mg/kg was started and continued for four weeks. The patient showed marked improvement in his neurological deficit and was discharged after one week with close follow-up. Discussion/Review Of Literature Life CycleHydatidosis is caused by Echinococcus granulosus, which occurs mainly in dogs. Humans who act as intermediate hosts get infected incidentally by ingesting eggs from the faeces of the infected animal. The eggs hatch inside the intestines and penetrate the walls, entering blood vessels and eventually reach the liver where they may form cysts or move on towards the lungs. Even after pulmonary filter, a few still make it to the systemic circulation and can lodge in almost any part of the body, including the brain, heart and bones.2,3,8,14,16,26 Brain hydatid cysts are relatively rare and only account for up to 2% of total cases.4,5,7  The actual percentage may be higher than what we have in literature, due to under-reporting. Brain hydatid cysts can be primary (single) or secondary (multiple).2,3,4,5,7 The latter are thought to arise from the multiple scolices released from the left side of the heart following cyst rupture in the heart2,3,5,27 or due to spontaneous, traumatic or surgical rupture of a solitary cranial cyst.3,5 Cysts mostly involve the territory of the middle cerebral artery4,7 but other regions like intraventricular, posterior fossa and the orbit have also been reported.15,17,18,28 The wall of the cyst consists of an inner endocyst (germinal layer) and outer ectocyst (laminated layer). The host reacts to the cyst forming a pericyst (fibrous capsule), which provides nutrients to the parasite. In the brain, due to minimal reaction, the pericyst is very thin. The endocyst produce scolices which bud into the cyst cavity and may sediment within the hydatid cavity, commonly known as hydatid sand.3,14,29,30 Presentation and DiagnosisMost hydatid cysts are acquired in childhood and are manifested during early adulthood.8,29 Cysts develop insidiously, usually being asymptomatic initially, and present with protean clinical and imaging features.3,5,6 In previous studies the most common presenting symptoms were headache and vomiting.4,5,7,14,15,28 Also in the literature, patients reported ataxia, diplopia, hemiparesis, abducens nerve palsy and even coma.5,7,15,28 Surprisingly, in the present study the patient did not have a headache and presented with parasthesia and numbness of the toes. Later he developed left sided weakness, convulsions and finally ataxia, which correlate with previous studies. Diagnosis of a hydatid cyst can sometimes be confused with other space occupying lesions of the brain, especially abscesses, neoplasms and arachnoid cysts.14,31  In this study the patient had bilateral frank papilloedema which is also mentioned in earlier reports.4,28  The Casoni and Weinberg tests, indirect haemagglutination, eosinophilia and ELISA are used in diagnosing hydatid cysts, but as brain tissue evokes minimal response many results tend to be false negatives.2,5,8,25  In our case also, serology for hydatid cyst was negative. CT scan and MRI are used frequently in diagnosing the cystic lesions.3,8,14,23,32,33  However, MRI is considered superior in demonstrating the cyst rim.5,8,11,21,32,34  On CT scan, a solitary cyst appears as well-defined, spherical, smooth, thin-walled and homogeneous, with an inner density similar to CSF, and non-enhancing walls.11,29,32The wall may appear iso-dense to hyper-dense on CT scan3,8, and rarely, may become calcified.11,29,32 There is usually no surrounding brain parenchymal oedema, which if exists along with ring enhancement, indicates inflammation and infection. 7,11,32,33,34,35 Ring enhancement and peri-lesional oedema differentiates brain abscesses and cystic neoplasms from uncomplicated hydatid cysts.3,8 These findings can in fact sometimes cause dilemma and misdiagnosis and lead to catastrophic events.14 The cyst shows low signal intensity on T1-weighted, and high signal intensity on T2-weighted MRI.2 MRI may also show peri-lesional oedema not seen on regular CT scan imaging.7 MRI may prove superior in determining exact cyst location, presence of super-added infections and cystic contents, and also in surgical planning and ruling out other diagnostic possibilities.14,33 We strongly recommend MRI for better evaluation of cystic brain lesions. Spontaneous cystic rupture can lead to different appearances depending on which layers have been obliterated, and produce some specific signs.3 When only the endocyst ruptures, cyst contents are held by the outer pericyst giving a peculiar water lily sign, which is pathognomic.3,8 TreatmentThough still in infancy, medical therapy for small or inoperable brain hydatid cysts has been promising. Albendazole alone or in combination with other compounds, such as praziquantel, has been reported with favourable results as an adjunct and, in certain circumstances, as the primary mode of treatment.2,36,37,38 It is reported that albendazole results in the disappearance of up to 48% of cysts and a substantial reduction in size of the cysts in another 28%.2 The duration of the treatment is four weeks or more, and recently many authors have favoured a prolonged therapy. The change in levels of cyst markers such as alanine, succinate, acetate and lactate, measured before and during treatment on Proton Magnetic Resonance Spectroscopy (MRS), correlate well with shrinkage and resolution of cyst findings on conventional MRI and help in evaluating the efficacy of chemotherapy.39 Cysts may drain into ventricles or rupture completely, causing spillage of contents into the subarachnoid space, leading to fatal anaphylactic shock, meningitis or local recurrence.3,5,22,25 Surgery is the mainstay for treating intracranial hydatid cysts and the aim is to excise the cysts entirely without rupture, which can otherwise lead to catastrophic events as described earlier 2,3,14,25. The Dowling-Orlando technique remains the preferred method, in which the cyst can be delivered by lowering the head of the operating table and instilling warm saline between the cyst and the surrounding brain.40 Even minimal spillage can cause deleterious effects (1 ml of hydatid sand contains 400,000 scolices).14 The thin cyst wall, periventricular location and micro-adhesions to the parenchyma are the main problems encountered during the surgical procedure.1,22 The large cavity remaining after the cystic removal can lead to many serious complications, such as cortical collapse, hyperpyrexia, brain oedema and cardio-respiratory failure.5 Recurrence remains a major concern, which is managed by both antihelminthic chemotherapy and surgery. In a study conducted by Ciurea et al, 25% of the patients had recurrence, which highlights the need for long term follow up.23 In the present study, due to the huge size of the cyst and progressive neurological deficit, it was not wise to completely rely on medical therapy. Surgery was performed and post-operatively albendazole was started as an adjunct. We recommend that for treating brain hydatid cyst, the size of the cyst, multiplicity, location and neurological deficit must all be taken into consideration. 

Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
ALI NEMATI MD; Chief Resident, Department Of Neurosurgery, Shiraz Medical School AHMAD KAMGARPOUR MD; Associate Professor, Department Of Neurosurgery, Shiraz Medical School MURTAZA RASHID MD; House Officer, Department Of Neurosurgery, Shiraz Medical School SAHAR SOHRABI NAZARI MD; House Officer, Department Of Neurosurgery, Shiraz Medical School
Corresponding Author Details: 
MURTAZA RASHID MD,Department of Neurosurgery, Shiraz University of Medical Sciences, Iran. P.O. Box: 71455-166 Tel: +98 917 910 5372
Corresponding Author Email: 
[email protected]

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Cervicogenic headache: It is time to call for more attention

Yili Zhou
Article Citation and PDF Link
BJMP 2010;3(3):a337
Cervicogenic headache (CH) refers to head pain originating from the pathology in the neck.1 However, the diagnosis of CH is still controversial 2,3 and it is often misdiagnosed. The author was called to consult a patient in a university hospital not so long ago. The patient was a 28-year-old female with a history of headache for six months. Her headache was described as continuous, dull and achy. It was mainly in the right side occipital and parietal areas. Sometimes she felt a headache behind the eyes. Her headache got worse periodically, several times a month, with nausea, photophobia, and phonophobia. She had no previous history of headache until a whiplash injury six months before. She had been diagnosed as having ‘migraine’ and ‘post-traumatic headache.’ She had used all anti-migraine medications. ‘Nothing was working.’ The patient was admitted into hospital because of ‘intractable headache.’
On the day when the author saw the patient, she was lying on the bed, with the room light turned off and a bed sheet covering her head and eyes. She was given Dilaudid, 2mg/h continuous intravenous (IV) drip, for the headache. The patient had normal results from magnetic resonance imaging (MRI) of the brain and lumbar puncture. According to the patient, no doctors had touched the back of her head and upper neck since admission. The author examined the patient and found a jumping tenderness over the right greater occipital nerve. The patient was given 2ml of 2% lidocaine with 40mg of Kenalog for the right greater occipital nerve (GON) block. Her headache was gone within five minutes and the Dilaudid drip was immediately discontinued. At follow-up four weeks later, the patient was headache-free. This was a typical missed case of CH (occipital neuralgia).
The concept of CH was first introduced by Sjaastad and colleagues in 1983.4 The International Headache Society published its first diagnostic criteria in 1998 which was revised in 2004.5 Patients with CH may have histories of head and neck trauma. Pain is often unilateral. Headache is frequently localized in the occipital area. However, pain may also be referred to the frontal, temporal or orbital regions. Headaches may be triggered by neck movement or sustained neck postures.6 Headache is constant with episodic throbbing attacks, like a migraine. Patients may have other symptoms mimicking a migraine such as nausea, vomiting, photophobia, phonophobia, and blurred vision. Due to the fact that there is a significant overlap of symptoms between CH and migraine without aura, CH is often misdiagnosed as migraine. CH is commonly found in patients after whiplash injuries, especially in the chronic phase.7
Anatomical studies have provided a basis for the pathogenesis of CH. The suboccipital nerve (dorsal ramus of C1) innervates the atlanto-occipital (AO)joint and dura matter over in the posterior fossa. Therefore, a pathologic condition of AO joint is a potential source for occipital headache. It has been reported that pain from the C2-3 and C3-4 cervical facet joints can radiate to the occipital area, frontotemporal and even periorbital regions. Even pathology in C5 or C6 nerve roots have been reported to cause headache.8 The trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibres in the descending tract of the trigeminal nerve (trigeminal nucleus caudalis) are believed to interact with sensory fibres from the upper cervical roots. This functional convergence of upper cervical and trigeminal sensory pathway sallows the bidirectional referral of painful sensations between the neck and trigeminal sensory receptive fields of the face and head.
Clinicians should always put CH in the list of differential diagnoses when they work up a headache patient. A history of head/neck injury, and detailed examination of the occipital and upper cervical area, should be part of the evaluation. Patients with CH may have tenderness over the greater or lesser occipital nerve, cervical facet joints and muscles in the upper or middle cervical region. Diagnostic imaging such as X-ray, computerized tomography (CT) and MRI cannot confirm CH, but can lend support to its diagnosis.
Treatment of CH is empirical. This headache does not respond well to migraine medications. Treatment should be focused on the removal of the pain source from the occipital-cervical junction. Initial therapy should be directed to non-steroidal anti-inflammatory drugs (NSAIDs) and physical therapy modalities.9 GON block is easy and safe to perform in office.10 It is effective for the treatment for occipital neuralgia and CH.11 The author followed a group of patients after GON block. The pain relief effects of GON block lasted an average of 31 days (unpublished data). If patients do not respond to GON block, diagnostic medial branch block and radiofrequency (RF) denervation of the upper cervical facet joints can be considered. Early studies have reported positive results.12 A subsequent randomized study found no benefit of RF. However, there were only six cases in each group,13 which significantly limited the power and validity of the conclusion from that study. Surgical treatment of cervical degenerative disc disease may offer effective pain relief for CH. Jansen14 reported 60 cases of CH patients treated mainly with C4/5, C5/6 and C6/7 nerve root decompression. More than 63% patients reported long lasting pain freedom or improvement (> 50%).
CH is common, with a prevalence of 0.4% and 2.5% in the general population. However, compared with other common pain conditions, CH is less studied. A Medline search found 6818 abstracts for migraine in 2009, whereas only 86 abstracts on CH were found. CH has not been well studied and it is often misdiagnosed. It is time to call for more attention.
Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
Dr YILI ZHOU MD PhD. Comprehensive Pain Management of North Florida,6830 NW 11th Place, Gainesville, Fl 32608 USA www.cmpnf.com
Corresponding Author Details: 
Dr YILI ZHOU, Comprehensive Pain Management of North Florida 6830 NW 11th Place, Gainesville, Fl 32608 USA www.cmpnf.com
Corresponding Author Email: 
[email protected]
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