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.
Brain tumour:- e.g. ependymoma or metastasis in the fourth ventricle
Acute cochleo-vestibular dysfunction
Following flexion-extension injury
Aura of epileptic attack – especially temporal lobe epilepsy
Drugs – e.g. phenytoin, barbiturates
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.
It is essential to determine whether the patient has a peripheral or central cause of vertigo 1.
Information obtained from the history that can be used to make this distinction includes 1:
The timing and duration of the vertigo
Provoking or exacerbating factors
Associated symptoms such as
The vertigo usually develops gradually
Except in: an acute central vertigo is probably vascular in origin, e.g. CVA
Central lesions usually cause neurological signs in addition to the vertigo
Auditory features tend to be uncommon.
Causes severe imbalance
Nystagmus is purely vertical, horizontal, or torsional and is not inhibited by fixation of eyes onto an object
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
Duration Of Episode
Associated Auditory Symptoms
Peripheral or Central Origin
Benign Paroxysmal Positional Vertigo
Transient Ischemic Attack
Seconds / Hours
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.
Important points in the history:
Onset - specific provoking events such as flying or trauma
Associated auditory symptoms - rare in primary CNS lesion
Other associated symptoms
Nausea and vomiting in a vestibular cause
Neurological symptoms such as visual disturbance, dysarthria in a central lesion
Examination of ear drums (Otoscopy/ Pneumatic otoscopy) for:
Vesicles (Ramsay Hunt syndrome)
Tuning fork tests for hearing loss – Rinne/Weber tests
Cranial nerve examination. Cranial nerves should be examined for signs of :
Sensorineural hearing loss
Hennebert's sign 1
Vertigo or nystagmus caused by pushing on the tragus and external auditory meatus of the affected side
Indicates the presence of a perilymphatic fistula.
Romberg's sign (not particularly useful in the diagnosis of vertigo 1)
Heel-to- toe walking test
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
Dix-Hallpike manoeuvre 1
The most helpful test to perform on patients with vertigo1
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.
Head impulse test/head thrust test
Useful in recognizing acute vestibulopathy 6
Cold or warm water or air is irrigated into the external auditory canal
Not commonly used
Investigations/Testing to consider:
Special auditory tests
Audiometry helps establish the diagnosis of Ménière's disease
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.
If features of CNS causes is suspected from the history or examination:
CT/MRI Brain imaging as appropriate
Treatment should ideally aim at the cause of the vertigo 7:
Medical management – as described below.
Vestibular rehabilitation exercises – e.g. Cawthorne-Cooksey exercises 5.
These exercises aim to help the patient return to normal activity more quickly.
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
Other forms use gaze and gait stabilising exercises. Most exercises involve head movement
For most patients the main priority is effective control of the symptoms.
For acute attacks, treatments include 5,8: -
Betahistine hydrochloride 8-16mg upto TDS
Cinnarizine, 15-30 mg TDS or
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
Preventive measures for recurrent attacks include:
Restrict salt and fluid intake - stop smoking and restrict excess coffee or alcohol 9,10
Betahistine hydrochloride 16mg regularly TDS seems most effective in Ménière's
Cinnarizine 15-30 mg TDS
Points to consider
Warn patients when drugs may sedate 10.
Prochlorperazine is less sedating than some other recommended antihistamines, but may cause a dystonic reaction (particularly in children and young women) 11.
Benzodiazepines are not recommended 9.
The most important first step in the management of recurrent vertigo is to distinguish vertigo from 'dizziness'.
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.
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 arthritisConsultation and referral:
Refer to secondary care if 10 :
Recurrent separate episodes
Neurological symptoms e.g. dysphasia, paraesthesiae or weakness
Associated sensorineural deafness
If there is an inadequate visualisation of the entire tympanic membrane or an abnormality (e.g. cholesteatoma)
Atypical nystagmus e.g. non-horizontal, persisting for weeks, changing in direction or differing in each eye
Positive fistula sign: pressure on the tragus reproducing symptoms (suggests endolymphatic fistula
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.
While awaiting referral:
Consider symptomatic drug treatment for no longer than 1 week because prolonged use may delay vestibular compensation
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.
If the person's symptoms deteriorate, seek specialist advice.
When to consider hospitalization
Admit the patient to hospital if they have severe nausea and vomiting, and are unable to tolerate oral fluids 9.
Admit or urgently refer the person to a neurologist if they have:
Very sudden onset of vertigo (within seconds) that persists.
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.
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.
Emergency treatment may restore hearing. The person should be seen within 12 hours of the onset of symptoms 9
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
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.
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 LiteratureLife 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.3,14,29,30Presentation 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.3,8TreatmentThough 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.
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.