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Neurology

Neurology Letters 20 August 2012 Free

A screening program to detect aminoglycoside- induced ototoxicity

To the Editor: We note Ahmed and colleagues’ extensive case series of patients with severe vestibulopathy due to aminoglycosides. We attempted to develop a hospital-based screening program to detect vestibulopathy in inpatients that may be informative for others considering similar programs. We established a pilot project involving student pharmacists. Patients who received more than a single dose of any aminoglycoside antibiotic were identified by therapeutic drug ...

Maryam Teimoori · Gina Mistry · Carmela Corallo · Allen C Cheng

Neurology Letters 6 August 2012 Free

Headache sufferers need to be heard too

To the Editor: The 2 April issue of the Journal contained several articles on pain, but no mention of patients who suffer with head pain. Headache is one of the commonest acute and chronic pain conditions. Studies have shown that episodic migraine affects 18% of women and 8% of men.1 Daily headache afflicts 4% of people worldwide, and half have chronic migraine.2 According to data from ...

Alessandro S Zagami

Neurology Letters 6 August 2012 Free

The need to tackle concussion in Australian football codes

To the Editor: I read with interest the recent article on concussion in Australian football by Gilbert and Partridge, and although it is well written, and I agree with virtually all that was said, there is a significant glaring error. In discussing the guidelines on return to play after concussion, they give the impression that the National Rugby League (NRL) is somehow lagging behind the ...

Ron Muratore

Letters20muratore
Neurology Letters 6 August 2012 Free

Terson syndrome: the need for fundoscopy in subarachnoid haemorrhage

To the Editor: Patients who survive subarachnoid haemorrhage (SAH) are at significant risk of visual impairment, further complicating their recovery. This may arise as a result of Terson syndrome,1 which is the phenomenon of intraocular haemorrhage associated with any intracranial bleed and raised intracranial pressure. We report a case of missed Terson syndrome at a tertiary referral centre. A 36-year-old previously well woman presented with a ...

Akbar N Ashrafi · Rahul Chakrabarti · John Laidlaw

One GP’s take on neurology

THE COMPLEXITY of neurology is both alluring and intimidating — rather like learning Ancient Greek or a Bach five-part fugue. Attempts at popularisation often fail because of either persistent obscurity or oversimplification. In this book, Professor Roy Beran, from the School of Medicine, Griffith University, Queensland, has produced a practical overview which aims to be approachable without dumbing down.To this task he is eminently suited, ...

Timothy J Kleinig

Neurology Letters 18 June 2012 Free

First-person neuroscience and the understanding of pain

To the Editor: At first, Thacker and Moseley appear to do an about-turn on much of their published work by de-emphasising the role of the brain and nervous system in the human pain experience.1 However, on closer scrutiny, their reflection encapsulates key messages for health professionals about pain not being located in the tissues, while exposing the inadequacy of non-person-centred approaches to their practice and ...

Lester E Jones · Laura Y Whitburn

Gentamicin ototoxicity: a 23-year selected case series of 103 patients

Objective: To review patients with severe bilateral vestibular loss associated with gentamicin treatment in hospital. Design and setting: A retrospective case series of presentations to a balance disorders clinic between 1988 and 2010. Main outcome measures: Relationship between vestibulotoxicity and gentamicin dose or dosing profile; indications for prescribing gentamicin. Results: 103 patients (age, 18–84 years; mean, 64 years) presented with imbalance, oscillopsia or both, but none had vertigo. Only three noted some hearing impairment after having gentamicin, but audiometric thresholds for all patients were consistent with their age. In all patients, the following tests gave positive results: a bilateral clinical head-impulse test, a vertical head-shaking test for vertical oscillopsia, and a foam Romberg test. In 21 patients, imbalance occurred during gentamicin treatment (ignored or dismissed by prescribers in 20) and in 66 after treatment; the remaining 16 could not recall when symptoms were first noticed, except that it was after gentamicin treatment in hospital. Total gentamicin dose range was 2–318 mg/kg (mean, 52 mg/kg), daily dose range was 1.5–5.6 mg/kg (mean, 3.5 mg/kg), and duration was 1–80 days (mean, 17 days). Six patients had only a single dose; 26 had five or fewer doses. Serum gentamicin levels, measured in 82 patients, were in the recommended range in 59. Time to diagnosis ranged from 4 days to 15 years. Nephrotoxicity developed in 43 patients. Gentamicin dosage complied with contemporary or current Australian antibiotic guidelines in under half the patients. Conclusions: Gentamicin ototoxicity is vestibular, not cochlear, producing permanent loss of balance, but not of hearing. Gentamicin can be vestibulotoxic in any dose, in any regimen, at any serum level.

Rebekah M Ahmed MB BS, FRACP · Imelda P Hannigan RN · Hamish G MacDougall PhD · Raymond C Chan MB BS, FRACP, FRCPA · G Michael Halmagyi MD, FRACP

Neurology Editorial 21 May 2012 Free

Does football cause brain damage?

Available evidence suggests anecdotal media reports need to be assessed carefullyThe critical issues in the clinical management of sports concussion include confirming the diagnosis, excluding structural abnormality and determining when players can be safely returned to competition. Despite the apparent simplicity of this process, the management of this one injury seems to provoke more debate ...

Andrew H Kaye MB BS, MD, FRACS · Paul McCrory PhD, FRACP, FACSP

The need to tackle concussion in Australian football codes

A call for systematic and comprehensive investigation into the long-term effects of football-related head trauma. Postmortem evidence of chronic traumatic encephalopathy (CTE) in the brains of American National Football League players who suffered concussions while playing have intensified concerns about the risks of concussion in sport. Concussions are frequently sustained by amateur and professional players of ...

Frederic Gilbert PhD · Bradley J Partridge BPsych(Hons), PhD

Perspectives20gilbert
Neurology Clinical focus 21 May 2012 Free

Sudden limb weakness

Stroke is a common neurological emergency and may occur in patients of all ages. Rapid assessment is crucial for patients with acute neurological symptoms suggestive of stroke because the opportunity for a positive outcome from thrombolytic treatment diminishes rapidly within the first few hours. Although plain non-contrast computed tomography of the brain is ...

Bill O’Brien FRACP, MRCP · Mark W Parsons BMed, PhD, FRACP · Craig S Anderson MB BS, PhD, FRACP

Cardiovascular diseases Case reports 7 May 2012 Free

Brain abscess due to Propionibacterium propionicum in Eisenmenger syndrome

Clinical record A 33-year-old man with Eisenmenger syndrome due to a congenital ventricular septal defect presented with a 3-week history of headache, blurred vision and expressive dysphasia, and unintentional weight loss of 10% of his body weight. His medications included sitaxsentan sodium (a sulfonamide endothelin-receptor antagonist, recently withdrawn because of hepatotoxicity) for pulmonary arterial hypertension. He ...

Anthony M T Chau MB BS(Hons) · Lileane L Xu · Jacob M Fairhall MB BS, FRACS · Joga Chaganti FRANZCR · Brendan J McMullan BMed(Hons), DTMH, DCH

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Neurology Clinical focus 16 April 2012 Free

Upper limb tremor

Tremor is a common clinical problem in middle-aged and older patients, and Parkinson disease (PD) is one of the commonest causes. Careful history-taking and physical examination is usually sufficient for diagnosis of PD; extensive ...

Thomas E Kimber MB BS(Hons), PhD, FRACP · Philip D Thompson MB BS, PhD, FRACP

Hematologic diseases Case reports 16 April 2012 Free

Endovascular therapy after stroke in a patient treated with dabigatran

This is the first report of endovascular therapy for acute ischaemic stroke in a patient with atrial fibrillation who was taking the direct thrombin inhibitor dabigatran for stroke prevention. As more of these agents will ...

Andrew W Moey MB BS · Simon A Koblar MB BS, FRACP, PhD · Steve Chryssidis MB BS, RANZCR · Martin Robinson MB BS, FRACP · Jim Jannes MB BS, FRACP, PhD

Neurocysticercosis in Australia: still free of autochthonous cases?

To the Editor: I have read two recent reports on neurocysticercosis in the Journal.1,2 After performing a literature search for Australian cases of neurocysticercosis (PubMed search, using the terms “cysticercosis”, “neurocysticercosis” and “Australia”), I found reports of 39 patients, and the reports of 33 of these patients were published in the past two decades. This suggests that the prevalence of neurocysticercosis in Australia is rising, or that it has been increasingly recognised and reported in recent years. As expected in a developed country, more than three-quarters of the patients were immigrants from neurocysticercosis endemic areas, and the remainder were Australian residents who had travelled to endemic regions. So, although it appears that Australia is free of locally acquired neurocysticercosis, it is possible that some immigrants who developed the disease while living in Australia were not infected overseas, because some of them developed the disease more than 10 years after they migrated from their home countries. The occurrence of neurocysticercosis among people returning from endemic areas to cysticercosis-free countries shows that cysticerci may remain asymptomatic for a long time in the nervous system or may become symptomatic years (or even decades) after infection.3 Indeed, certain forms of neurocysticercosis, including calcifications, chronic arachnoiditis, subarachnoid cysts and even spinal cysticerci may manifest a long time after infection. However, the single cysticercus granuloma causes symptomatic disease in the first few months after infection;4 this form of the disease occurs mainly in people who have not had previous infection and involves an acute inflammatory reaction to the implantation of one cysticercus in the brain parenchyma. At least seven of the immigrants to Australia with neurocysticercosis had this form of the disease, and some of them developed symptoms up to 3 years after arrival, suggesting local acquisition of the disease from a contact infected with Taenia solium. Unfortunately, case reports and case series of neurocysticercosis diagnosed in Australia do not include information on whether household contacts of diagnosed patients had been tested for carriage of Taenia. Increased awareness of the mechanisms of disease transmission for neurocysticercosis will help to reduce further spread of this zoonosis.

Oscar H Del Brutto

Neurology Clinical focus 20 February 2012 Free

Practical neurology Part 7 - Recurrent headaches with visual disturbance

Abstract: Headache, particularly migraine, is the commonest neurological problem with which patients present to general practitioners and neurologists. Episodic migraine affects up to 18% of women and 6% of men. Acute migraine attacks can be severely disabling and chronic migraine is even more disabling. Of the mental and neurological disorders, migraine ranks eighth worldwide in terms of disability....

Alessandro S Zagami MB BS, MD, FRACP · Sian L Goddard BSc, MB BS

Neurology Clinical focus 6 February 2012 Free

Memory loss

Most older people with memory loss do not have dementia. Those with mild cognitive impairment are at increased risk of progressing to dementia, but no tests have been shown to enhance the accuracy of assessing this risk.

Leon A Flicker MB BS, PhD, FRACP · Andrew H Ford MB ChB, FRANZCP · Christopher D Beer MB BS, PhD, FRACP · Osvaldo P Almeida MD, PhD, FRANZCP

Neurology Reflections 6 February 2012 Free

Understanding whiplash

Whiplash: evidence base for clinical practice. Michele Sterling, Justin Kenardy. Sydney: Elsevier 2011 (xv + 197 pp, $77.25). ISBN 9780729639463. WHIPLASH is a controversial, but widely accepted, “diagnostic” term that describes a putative causal mechanism for a constellation of symptoms that are generally not underpinned by recognisable pathology. This reference book has the stated aim: “to bring together current knowledge of the whiplash condition that will allow all stakeholders involved in the management of patients with whiplash, from clinicians to policy makers, to gain greater understanding of this condition”. Whiplash research is important, as up to 50% of people with this condition do not recover fully and up to 30% remain moderately to severely disabled. The editors of this book, Michele Sterling (associate professor of physiotherapy) and Justin Kenardy (professor of psychology), are both from the University of Queensland, and have both made significant contributions to the university’s Centre of Clinical Research Excellence in Spinal Pain, Injury and Health. They are well positioned, therefore, to comment on contemporary work in their fields, particularly as considerable research concerning whiplash arises from their institution. They have also attracted contributors from a spectrum of disciplines including neurosurgery, psychology, physiotherapy, rehabilitation, epidemiology, engineering, economics and law. The book comprehensively elucidates contemporary research, particularly in the fields of physiotherapy and psychology. However, as it observes, there is little or no evidence to guide the clinician who is managing the whiplash patient. There is virtually no evidence that confirms a link between symptoms and pathology, and there is also very little established evidence-based management. The chapters on law, compensation and insurance are worthwhile reading for medical practitioners involved in the medicolegal aspects of whiplash. A series of case studies is also included. The book is recommended for scientists involved in physical and psychological rehabilitation research into whiplash. It confirms the paucity of evidence related to the whiplash construct. However, it does not assist the clinician who is interested in providing evidence-based whiplash management.

David G Vivian

Neurology Editorials 16 January 2012 Free

Late mortality after severe traumatic brain injury

The first Australian report is welcome and should help inform policy Traumatic brain injury (TBI) continues to be a significant public health issue in Australia. Despite advances in acute medical care and decreases in mortality, those affected experience long-term morbidity and have an increased late mortality rate. TBI is the leading cause of death and disability among young people, and the incidence of severe TBI is higher in men than women at a ratio of 3.5 : 1.1 The leading causes of TBI include: motor vehicle accidents (50%); falls (21%); violence (12%); and sports and recreation (10%).2 In Australia in 2008, there were 2493 new cases of TBI (about 1000 of these were severe),2 and the estimated total cost of care was $8.6 billion. Across Australia, lifetime cost per incident case of severe TBI was estimated at $4.8 million.2 In 2007, more than 16 000 patients were admitted to hospitals with TBI,3 with an average length of stay of 6.1 days in acute care, 64.2 days in rehabilitation and 84.1 days in other care. These patients characteristically have multiple disabilities and, in addition to health care services, they frequently receive other disability support services (eg, case management, individual therapy support, life skills development). Many factors affecting outcomes after TBI are modifiable, and influenced by medical management. Multidisciplinary assessments early in the course of the disease guide medical care and provide predictive information about the potential for recovery. Rehabilitation interventions have documented benefit in patients with TBI.4 Research into rehabilitation in severe TBI is challenging because of: the heterogenous manifestations of sequelae of severe TBI; the unpredictable course of the disease; the range and variety of rehabilitation services; and inconsistent use of appropriate outcome measures.4 Few studies tackle long-term outcomes in this population, so evidence is insufficient for establishing optimum integrated care, agreement on a minimum clinical dataset for effective communication between clinicians, and incorporation of patient and caregiver perspectives. The multicentre study by Baguley and colleagues in this issue of the Journal5 adds clarity by describing the long-term mortality pattern in adults with severe TBI, and identifies the risk factors associated with mortality. Among their 2545 patients with severe TBI discharged from tertiary rehabilitation units of the New South Wales Brain Injury Rehabilitation Program, with a mean follow-up period of 10 years, there were 258 recorded deaths. The authors report an increased risk of death up to 8 years after discharge from rehabilitation services that was 3.2 times greater than that for the general population, and higher than rates in previous reports (range of long-term mortality estimates, 1.1–3.1).6 The mortality rates remained higher than for the general population for up to 5 years after discharge from rehabilitation. True mortality rates may be underestimated; similar data for late mortality after TBI in children and Indigenous people are needed. The findings of Baguley and colleagues have implications for health service use and health modelling. The study by Baguley et al is the first long-term mortality report of Australian data, and shows an increased risk of death among patients with more severe TBI, greater functional dependence, previous drug and alcohol misuse, epilepsy before their TBI and older age at injury; these findings are consistent with those of other studies.7,8 Compared with the general population, those with severe TBI had a particularly high risk of death from respiratory disorders, and a high risk of death from nervous system, mental and behavioural, and digestive disorders. Discharge to an aged care facility was identified as a risk factor independent of functional dependency at discharge from rehabilitation, and needs further investigation. Older patients are considered at risk because of an altered pathophysiological response in the ageing central nervous system. Further, health, lifestyle and social deprivation have been linked with survival.9 Other reports suggest that TBI itself provokes lifestyle and behavioural changes, or defines a subgroup in the population at higher risk of death for other reasons.7 Future research should target interventions for general preventive measures to maintain health, and social and lifestyle changes in people discharged to the community after a TBI.7 The important elements of service provision for patients with TBI are similar to those in other conditions requiring neurorehabilitation:10 involvement and support of primary health practitioners; education of doctors, patients and caregivers about mortality, declining health and high-risk behaviours for targeted intervention; clinical guidelines to include routine postdischarge follow-up over a longer time, and a flexible health care delivery system that prioritises the rehabilitation needs of patients with TBI; and a clear plan of action and compliance, including indications for referral to specialised multidisciplinary services. Policy recommendations to establish services for continuity of care (acute to subacute and community care) for patients with TBI include:4,10,11 develop rehabilitation services (including infrastructure and personnel) for patients with severe TBI; provide services to meet the complex needs of those with severe TBI, to identify unmet needs for assistance and reduce reliance on informal assistance; link TBI rehabilitation programs with the existing Australian Rehabilitation Outcomes Centre dataset for long-term collection of clinical data, using standardised common data elements; computerise national monitoring systems in real-time to document mortality and morbidity in TBI, and monitor patterns of recovery; review policy and implement rigorous assessment of the impact of quality care to decrease mortality rates and harm from ineffective or insufficient treatment; expand national insurance schemes to fund non-compensatable TBI rehabilitation; and maintain a sustained public health information campaign to publicise issues and promote strategies for implementation in patients with TBI.

Fary Khan MB BS, MD, FAFRM

Neurology Letters 16 January 2012 Free

Tools to inform general practitioners’ decision making on driving following a stroke

To the Editor: Return to driving following a stroke is a complex issue. Austroads provides general guidelines1 and the National Stroke Foundation recommends a process including off-road and on-road driving tests.2 On-road assessments conducted by occupational therapists are considered the gold standard for decision making on return to driving following a stroke. Limited access is available to off-road and on-road tests across Australia, with few occupational therapists qualified to assess driving ability. Additionally, a range of off-road assessments are used for patients who have had a stroke. General practitioners, who are instrumental in managing return to driving, often base their decisions on limited information regarding functional status, particularly in terms of vision, cognition and perception. Rehabilitation physicians generally have access to more detailed information from allied health staff on which to base their decisions on driving ability. I investigated whether rehabilitation physicians’ recommendations on driving following a stroke were associated with patients’ performance on two objective tools, which could be used in general practice to assist with decision making. Participants were recruited at two rehabilitation services in Adelaide, South Australia, using the following inclusion criteria: had been diagnosed with stroke; had driven before the stroke; were aged over 18 years; and had provided written informed consent. I performed two assessments. The first was the Useful Field of View (UFOV) assessment;3 this is a computer-administered assessment that analyses processing speed, divided attention and selective attention, and takes 20 minutes to complete. The second was the Stroke Drivers Screening Assessment (SDSA);4 this consists of three tests conducted at a table — dot cancellation, compass recognition and road sign recognition — and takes 45–60 minutes to complete. Both assessments have been validated in patients who have had a stroke by comparison to on-road assessment.5 Treating rehabilitation physicians, blinded to assessment results, were contacted to obtain their recommendations on driving ability based on their clinical assessment and feedback from allied health staff at a case conference. A total of 123 participants (98 men [80%]) were recruited, and diagnoses included 53 right hemisphere strokes (43%), 63 left hemisphere strokes (51%) and 7 other strokes (6%). The participants’ mean age was 67.3 years (SD, 13.5 years), median period since injury was 42 days (range, 7–2190 days) and mean amount of driving experience was 48 years (SD, 14.9 years). Results of the SDSA (n = 120) and UFOV assessment (n = 123) were significantly associated with rehabilitation physicians’ recommendations on driving (Box). This suggests that referring patients who have had a stroke for one of these assessments would provide GPs with objective information to guide decision making on driving. With the introduction of Medicare Locals, resources that allow GPs to refer patients for standardised off-road driving tests should be considered. Rehabilitation physicians’ recommendations on driving for patients with a stroke diagnosis and results of two off-road assessments Rehabilitation physicians’ recommendations (number of patients) Not medically fit to return to driving On-road assessment required Return to driving — no on-road assessment required P SDSA results Pass (n = 61) 5 36 20 0.001* Fail (n = 59) 24 29 6 UFOV results Processing speed Pass (n = 97) 18 55 24 0.02* Fail (n = 26) 13 11 2 Divided attention Pass (n = 59) 10 33 16 0.22 Fail (n = 62) 19 33 10 Selective attention Pass (n = 82) 11 49 22 0.001* Fail (n = 39) 18 17 4 Overall risk category Pass (n = 80) 12 46 22 0.007* Fail (n = 41) 17 20 4 SDSA = Stroke Drivers Screening Assessment. UFOV = Useful Field of View. * P values of < 0.05 were considered significant and indicate an association between rehabilitation physicians’ recommendations and results of off-road assessments.

Stacey R George

Neurology Research 16 January 2012 Free

Late mortality after severe traumatic brain injury in New South Wales: a multicentre study

Objectives: To determine the long-term mortality pattern of adults with severe traumatic brain injury (TBI), and to identify the risk factors associated with death in this group.Design, patients and setting: Inception cohort study of 2545 adults consecutively discharged from one of three metropolitan tertiary, post-acute inpatient rehabilitation services of the New South Wales Brain Injury Rehabilitation Program from 1 January 1990 to 1 October 2007 after inpatient rehabilitation for primary TBI.Main outcome measure: Survival status at 1 October 2009.Results: 258 deaths were recorded in this sample, yielding a standardised mortality ratio of 3.19 (95% CI, 2.80–3.60). Risk of death remained elevated above societal norms for at least 8 years after discharge from rehabilitation. Mortality risk was increased by: functional dependence at discharge; age at injury; pre-injury drug and alcohol misuse; pre-injury epilepsy; and discharge to an aged care facility. The risk of death from external causes, and respiratory system and nervous system disorders was six to seven times higher, and the risk of death from disorders of the digestive system, and mental and behavioural disorders was five times higher in adults with severe TBI than in the general population.Conclusions: People who survive to discharge from inpatient rehabilitation following a severe TBI were found to have a sustained increase in risk of death for eight years post discharge. Various demographic and injury-related variables selectively increase mortality risk and may be modifiable in order to reduce the observed increase in mortality.

Ian J Baguley MB BS, FAFRM, PhD · Melissa T Nott BAppSc(Hons), PhD · Alison A Howle BSpPath · Grahame K Simpson BSocStud, MA, PhD · Stuart Browne MB BS, MD, FAFRM · A Clayton King MB BS, MD, FAFRM · Rachel E Cotter BA(Hons) · Adeline Hodgkinson MB BS, FAFRM

Neurology Clinical focus 21 November 2011 Free

Practical Neurology Part 5: Recurrent unresponsive episodes and seizures

Janice’s story: Janice, who is 23 years old, presented to her general practitioner with a history of stereotyped episodes that her partner had observed every 1–2 weeks over the previous year. She described the episodes as starting with “butterflies in the stomach”(rising up to her throat and lasting about 20 seconds) and intense deja vu.

Melissa A DeGruyter BM BS, BA(Physio) · Mark J Cook MB BS, MD, FRACP

Neurology Research 21 November 2011 Free

Ischaemic stroke among young people aged 15 to 50 years in Adelaide, South Australia

Objectives: To report risk factors, aetiology and neuroimaging features among a large series of young Australian patients who were admitted to hospital for a first-ever occurrence of ischaemic stroke; to analyse the effect of age, sex and ethnicity on the presence of risk factors; and to compare Australian and overseas data.Design, setting and patients: Retrospective evaluation of data for all patients aged from 15 to 50 years who were admitted to a public hospital in Adelaide, South Australia, from January 2006 to June 2010 with a primary diagnosis of ischaemic stroke.Results: Among 326 patients (184 males), the most frequent stroke risk factors overall were dyslipidaemia (187), smoking (161), hypertension (105) and obesity (92). Fifty-one patients used illicit drugs, mostly comprising marijuana and amphetamines. The most frequent stroke aetiologies overall were cardioembolism (85), arterial dissection (49), and small-vessel occlusion (31). Cardioembolism was highly prevalent among our study population compared with patients in other countries. Neuroimaging showed that more patients in our study had strokes that involved both vascular territories concurrently (9%) compared with patients in other countries.Conclusions: Risk factors, aetiology and features of ischaemic stroke among young people in Adelaide differ significantly from published data for young patients around the world. Patients in Adelaide are more likely to be obese, to be misusing marijuana and amphetamines, to suffer a cardioembolic event and to have a stroke that concurrently affects both the anterior and posterior cerebral circulation.

Matthew C L Phillips MB BS · James M Leyden MB BS, FRACP · Woon K Chong MB BS, FRANZCR · Tim Kleinig MB BS(Hons), PhD, FRACP · Philippa Czapran MB BS · Andrew Lee MB BS, FRACP · Simon A Koblar BM BS, FRACP, PhD · Jim Jannes MB BS, FRACP, PhD

Neurology Editorials 7 November 2011 Free

NSAIDs and stroke risk

Recent studies build a strong case to suggest that there is a clear risk Clearly, stroke prevention is preferable to the currently available treatments, particularly for haemorrhagic stroke. The burden of stroke is substantial, so all strategies to reduce risk must be considered. The traditional risk factors, especially hypertension, are well recognised, but there is also increasing interest in identifying and modulating novel risks1 and precipitant causes. In this issue of the Journal, an important article by Caughey and colleagues2 adds to the growing literature concerning the risk of stroke related to the use of non-steroidal anti-inflammatory drugs (NSAIDs), particularly those with selective cyclooxygenase (COX)-2 inhibition. If the use of these agents is a clear and substantial risk, then avoiding such medications, particularly in high-risk patients, may be an important preventive strategy. But is the risk clear and substantial, or are other factors involved? Is there a potential for abandoning useful medications and also creating undue anxiety for patients currently using them to treat painful chronic conditions? The lessons regarding the cardiovascular risk of rofecoxib must be heeded,3 and the pharmacological basis for increased risk of thrombosis and elevation of blood pressure (and thus haemorrhagic stroke risk) is well founded. Surprisingly, recent guidelines4 pertaining to patients with extracranial large arterial stenosis, who are at high risk of stroke, made no specific comment for or against the use of NSAIDs because of a lack of evidence. This was based on some earlier studies5 that did not show increased stroke risk. Two more recent studies6,7 from different populations demonstrated an increased stroke risk, especially for haemorrhagic stroke. Combined with the results of Caughey et al,2 these studies build a strong case to suggest that there is a clear risk. There are consistencies across the studies, including the observation that adverse outcomes seem to vary with different NSAID classes. The population studied by Caughey et al2 was elderly, with comorbidities and, frequently, a combination of arthritis and vascular disease. This is precisely the group of patients where the dilemma commonly arises, making the study clinically valuable. The data appear robust, and feature a sensitivity analysis that strengthens the initial findings. It should be remembered, however, that the conclusions do not apply to younger and healthier populations. Additionally, the absolute stroke risk is small, and may be exceedingly small, particularly if NSAID exposure is brief. What is not clear from these studies is the role of confounding variables. The use of a prescription medication database and hospitalisation codes might suggest an association, but will not provide all the answers to a complex clinical scenario. Although the crude sequence ratio is robust to confounders that are stable within individuals over time, cardiovascular and stroke risk are unlikely to be stable over time and probably fluctuate. Intercurrent infection, inflammation, immune response and blood pressure variability are dynamic factors that may precipitate vascular events, particularly in predisposed individuals. Blood pressure variability8 is under increasing scrutiny as a provoking factor for stroke events. Given the important impact of COX-2 inhibition on increased blood pressure,9 this may be the true link in the relationship. The reasons for NSAID prescription would be of great interest. Suppose, for example, that an NSAID is prescribed for analgesia in an older patient with vascular disease who has a painful arthritic condition. The NSAID may well raise blood pressure, and fluctuations in pain may result in blood pressure fluctuations; thus providing two risks for stroke. Several NSAIDs were shown by Caughey and colleagues2 to carry stroke risk similar to the cardiovascular risk of the now-withdrawn rofecoxib. Low-dose preparations of several NSAIDs are available in Australia without prescription. The findings of Caughey and colleagues further emphasise the need for great care in the use of these agents in patients with hypertension and other stroke risks.

David J Blacker MB BS, FRACP

Neurology Clinical focus 7 November 2011 Free

Practical Neurology Part 4: Dizziness on head movement

Benign positional vertigo (BPV) is the most common cause of episodic vertigo. It results from activation of semicircular canal receptors by the movement of calcium carbonate particles (otoconia) which dislodge from the otolith membranes. During changes in head position, the otoconia either float freely within the semicircular canal duct (canalithiasis) or adhere to and move with the cupula of the canal (cupulolithiasis). BPV from canalithiasis evokes brief spells of vertigo lasting seconds and can be diagnosed at the bedside by provoking paroxysmal vertigo and nystagmus on tilting the head in the plane of the affected canal. The nystagmus has a unique rotational axis perpendicular to the affected canal. The Dix–Hallpike test is a simple means of confirming the diagnosis in patients presenting with episodic vertigo or imbalance. Audiovestibular tests are only indicated if a symptomatic primary underlying inner ear disease is suspected. In over 80% of patients, BPV can be treated successfully with a single bedside Epley (particle-repositioning) manoeuvre, which can be performed by any medical practitioner.

Miriam S Welgampola MB BS, PhD, FRACP · Andrew Bradshaw BE, BSc · G Michael Halmagyi MB BS, MD, FRACP

Neurology Research 7 November 2011 Free

Stroke risk and NSAIDs: an Australian population-based study

Objective: To determine the risk of stroke associated with non-steroidal anti-inflammatory drug (NSAID) use.Design, setting and participants: Retrospective cohort study of 162 065 Australian veterans with incident dispensing of an NSAID between 1 January 2001 and 31 December 2008, using prescription event sequence symmetry analysis.Main outcome measures: Hospitalisation for stroke, ischaemic stroke or haemorrhagic stroke.Results: The absolute risk of stroke was low: 7.1/1000 people/year. Incident use of NSAIDs was associated with a 1.88 times increased risk (95% CI, 1.70–2.08) of hospitalisation for stroke (ischaemic or haemorrhagic) following first ever dispensing of an NSAID. This equates to an increased absolute risk of 13.4 strokes/1000 people/year. Significant positive associations between starting an NSAID and having a hospitalisation for stroke were found for most NSAIDs, with adjusted sequence ratios ranging from 1.44 (95% CI, 1.16–1.80) for indomethacin to 1.80 (95% CI, 1.59–2.04) for rofecoxib.Conclusions: Incident use of NSAIDs was associated with an increased risk of stroke. Increased awareness of the potential for serious adverse cardiovascular events, together with individual assessment of cardiovascular risk, careful deliberation of the balance between risk and benefits and appropriate supervision, is required when initiating NSAID therapy.

Gillian E Caughey BSc(Hons), PhD · Elizabeth E Roughead BPharm, MAppSc, PhD · Nicole Pratt BSc, PhD · Graeme Killer AO, MB BS, MSc · Andrew L Gilbert BPharm, DipAppPsych, PhD

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