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Dive into the research topics where Colin Chalk is active.

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Featured researches published by Colin Chalk.


Neurology | 2009

Is there a higher risk of restless legs syndrome in peripheral neuropathy

Erin Hattan; Colin Chalk; Ronald B. Postuma

Objective: Associations between peripheral neuropathy and restless legs syndrome (RLS) have been described, but have not been consistently reproduced. If RLS prevalence is truly increased by neuropathy, this has important implications for RLS pathophysiology. Methods: In a case-control design, 245 patients with peripheral neuropathy and 245 age- and sex-matched controls were screened for RLS using a standardized phone questionnaire based on international RLS diagnostic criteria. All persons who answered yes to three of four criteria were considered screen-positive. All screen-positive patients underwent a confirmatory diagnostic evaluation by a movement disorders specialist blinded to the neuropathy status of the patient. RLS prevalence was calculated and compared using Fisher exact test. Results: A total of 65 (26.5%) patients with neuropathy screened positive compared to 25 (10.2%) controls (p < 0.0001). However, the diagnosis was confirmed in only 46% of screen-positive patients with neuropathy, vs 80% of controls (p = 0.005). Cramps and paresthesia without true diurnal variation or rest exacerbation were the commonest causes of false-positive screens. After diagnostic confirmation, the overall prevalence of RLS did not differ between neuropathy patients and controls (12.2% vs 8.2%, p = 0.14). However, when classified by etiology, RLS was found in 14/72 (19.4%) patients with hereditary neuropathy, a prevalence higher than found in controls (p = 0.016) and acquired neuropathy (9.2%, p = 0.033). Among patients with neuropathy, those with RLS more commonly had a family history of RLS (37% vs 15%, p = 0.007) and were younger (49.9 vs 61.4, p = 0.0003). Conclusions: Restless legs syndrome is more prevalent among patients with hereditary neuropathy, but not in those with acquired neuropathies. CIDP = chronic inflammatory demyelinating polyneuropathy; GBS = Guillain-Barré syndrome; HMSN = hereditary motor sensory neuropathy; HSAN = hereditary sensory and autonomic neuropathy; IRLSSG = International Restless Legs Study Group; MGUS = monoclonal gammopathy of uncertain significance; NCS = nerve conduction studies; PPV = positive predictive value; RLS = restless legs syndrome.


Neurology | 2009

THE ESSENTIAL NEUROLOGIC EXAMINATION: WHAT SHOULD MEDICAL STUDENTS BE TAUGHT?

Fraser Moore; Colin Chalk

McKeon, Pittock, and Lennon for their comments on our recent article.1 It is understood that a large majority of patients with antibody-associated stiffperson syndrome will have antibodies to GAD65, and that for the most part, testing for these relevant antibodies is no longer performed using immunocytochemistry. The data of Dr. McKeon et al. may be constrained by the presence of ascertainment bias.4 For the data they have presented, the ascertainment of cases is through a laboratory test that is offered for all neurologic syndromes with suspected comorbid cancer. The acquisition of cases in this manner necessarily limits the application of such data to more general clinical scenarios. In our case, study inclusion criteria sought to examine patients who were referred with symptoms suggestive of stiff-person syndrome. This is reflected in the high probability of a positive result associated with our (GAD65) antibody testing, which approached 25%.5 In the case of our amphiphysin antibody testing, probability was still relatively high at 2%, compared with an estimated 0.01% for the Mayo group. One additional point is that McKeon et al. are describing the neurologic accompaniments of amphiphysin antibodies, findings that are first of interest to those working in serologic testing laboratories or conducting research on amphiphysin, and secondarily of interest to clinicians who may order paraneoplastic antibody testing as part of “casting a wide net.” Our report focused on the clinical characterization of stiff-person syndrome associated with these antibodies, information that we believe will be of great utility to clinicians at the bedside of patients with this often devastating disorder. Our study represents a significant advance in the understanding of stiff-person syndrome that we have previously described more broadly.6 Beth B. Murinson, MS, MD, PhD, Baltimore, MD; Joseph B. Guarnaccia, MD, New Haven, CT


Canadian Journal of Neurological Sciences | 2004

The academic half-day in Canadian neurology residency programs.

Colin Chalk

BACKGROUNDnThe academic half-day (AHD) appears to have become widespread in Canadian neurology residency programs, but there is little published information about the structure, content, or impact of the AHD.nnnMETHODSnA written questionnaire was sent to the directors of all active Canadian adult and child neurology residency programs.nnnRESULTSnAll 21 program directors responded. An AHD was operating in 15/15 adult and 5/6 child neurology programs. The AHD typically lasts three hours, and occurs weekly, 10 months per year. Most of the weekly sessions are lectures or seminars, usually led by clinicians, with about 90% resident attendance. Course-like features (required textbook, examinations) are present in many AHDs. There is a wide range of topics, from disease pathophysiology to practice management, with considerable variation between programs.nnnCONCLUSIONSnAlmost all Canadian neurology programs now have an AHD. Academic half-days are broadly similar in content and format across the country, and residents now spend a substantial portion of their training attending the AHD. The impact of the AHD on how residency programs are organized, and on the learning, clinical work, and professional development of residents merits further study.


Muscle & Nerve | 2003

Clinical significance of complex repetitive discharges: A case-control study

Lesley K. Fellows; Bethany J. Foster; Colin Chalk

Complex repetitive discharges (CRDs) are a striking, infrequent finding on needle electromyography (EMG), but their significance is debated. This retrospective case‐control study of 486 patients evaluated in a general hospital–based EMG laboratory examined the association of CRDs with specific diagnostic categories, duration of symptoms, and comorbid diabetes mellitus. No CRDs were identified in patients without other evidence of neuromuscular disease. Myopathy was associated with an increased risk of CRDs (adjusted odds ratio, 5.98; 95% confidence interval, 2.38 to 14.99). In general, neuropathic conditions were not associated with either an increased or decreased risk of CRDs compared with other neuromuscular diseases, although confidence intervals were wide. Similarly, neither the chronicity of symptoms nor the presence of diabetes yielded odds ratios that differed significantly from unity. In clinical populations similar to the one we studied, the positive predictive value of CRDs for any of the diagnoses we evaluated is low. However, the absence of CRDs can be of diagnostic value in that it reduces the likelihood of myopathy or motor neuron disease. The likelihood of finding CRDs in acute conditions is the same as that in chronic conditions. Muscle Nerve 28: 504–507, 2003


Canadian Journal of Neurological Sciences | 2012

Improving the neurological exam skills of medical students.

Fraser Moore; Colin Chalk

OBJECTIVEnDetermine if distributed practice of of neurological exam (NE) skills in first year medical school produces sustained improvements in the skills of second year students.nnnMETHODSnA prospective, controlled, non-blinded study conducted at McGill University (class size = 180 students). Expanded teaching of muscle stretch reflexes was provided to first year medical students. A structured examination of muscle stretch reflexes (max score = 100) was administered in second year medical school after a required two week rotation in Neurology. Results for class A (received the intervention in first year) were compared to the results for the preceding class B (had not received the intervention).nnnRESULTSn77 of 177 (44%) eligible in class A and 69 of 166 (42%) eligible students in class B participated. Results were analyzed separately for each of the two examiners. Mean (SD) scores were 95.2 (5.6) for class A (intervention) and 81.7 (11.1) for class B (control) for the first examiner and 90.4 (8.2) for class A and 83.8 (11.7) for class B for the second examiner. Results were statistically significant (Mann-Whitney test z = 5.27, p<0.0001 first examiner and z = 2.67, p<0.0038 second examiner).nnnCONCLUSIONSnDistributed practice of muscle stretch reflexes during first year medical school results in improved performance by second year medical students after their mandatory clinical rotation in neurology, even when examined up to 14 months after the intervention. This finding has implications for the teaching of the NE.


Neurology | 2008

Making the lame walk?: Transplantation for POEMS

Colin Chalk

The acronym POEMS, coined by Bardwick et al. in 1980,1 summarizes the features of a rare peripheral nerve syndrome characterized by polyneuropathy, organomegaly, endocrinopathies, monoclonal gammopathy, and skin lesions. Although there is debate about precise limits of the syndrome, most now agree that the defining features of POEMS are polyneuropathy and a monoclonal plasma cell dyscrasia, and that two or more other features (e.g., sclerotic bone lesions, hyperpigmentation or hypertrichosis, endocrine dysfunction) are necessary to confidently distinguish POEMS from related conditions such as monoclonal protein-associated (MGUS) neuropathy.2nnAlthough rare, POEMS has features that are of interest to all neurologists. POEMS is fundamentally a paraneoplastic syndrome, but its pathophysiology is distinctive. Unlike most paraneoplastic neurologic syndromes (e.g., Lambert-Eaton myasthenic syndrome, sensory neuronopathy), which are accidental consequences of a host’s immune response to a neoplasm, the manifestations of POEMS appear to be caused by overproduction of a cytokine, vascular endothelial growth factor (VEGF), by the neoplastic plasma cells themselves.3 Most patients with POEMS …


Canadian Journal of Neurological Sciences | 2011

Not just numbers: qualitative research and the clinical neurosciences.

Mary Ellen Macdonald; Colin Chalk

nerve decompression, and then living with the consequences – good or bad – of the surgery. Qualitative inquiry is not a monolith. It is an umbrella term that encompasses numerous approaches to health research. 3 Khu and colleagues have chosen an exploratory descriptive design using semi-structured interviews to better understand patient satisfaction with entrapment neuropathy surgery. Other data collection and analytic approaches for exploring issues relevant to such disorders and their treatments could also be employed. For example, grounded theory – a sociological methodology to understand social processes – could use face-to-face interviews and focus groups to understand the process of adapting to a condition such as CTS. Phenomenology – a philosophically-based methodology to better understand human experience – using in-depth interviewing could explore the everyday experience of living with a disability. Ethnography – an anthropological methodology to investigate socio-cultural phenomena – using participant observation could be employed to understand how our socio-cultural values and practices influence the provision of services for disabled members of our society. Qualitative approaches can also be used in other complex areas of neurological health care. Kaptchuk and colleagues, 4 for example, use a qualitative methodology to demonstrate how conventional theories of placebo inadequately attend to the myriad factors (physiological, embodied, social and cultural) that co-mingle to create what we call, in shorthand, the placebo effect. Similarly, Thorne and colleagues 5 demonstrate with interpretive description the intricacies of good communication between health care providers and MS patients, and the iatrogenic effects of poor communication. Critiques of qualitative inquiry as an approach to health research are often located in a debate about objective versus subjective engagement with data. In qualitative inquiry, the researchers themselves are the tools for the collection of data, given that they are embedded in the research contexts where they talk to and observe patients, health care providers and even policy makers. While subjectivity is indeed an important element of quality inquiry, this should not be taken to mean a lack of a rigorous research process. On the contrary, standards of rigor and critical appraisal are essential to qualitative inquiry, ensuring that research is conducted with the sophistication and precision one would expect from expert quantitative sciences. 6 The careful development of the Cochrane Qualitative Research Methods Group, for example, is a case in point. Furthermore, quantitative and epidemiological research is not immune to subjectivity; Shrier and colleagues, for example, demonstrate how the …


Canadian Journal of Neurological Sciences | 2018

Autoantibodies to Low-Density Lipoprotein Receptor-Related Protein 4 in Double Seronegative Myasthenia Gravis: A Systematic Review

Stephen Bacchi; Philippe Kramer; Colin Chalk

BACKGROUNDnMyasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction in which a clinical diagnosis may be confirmed with serological testing. The most common autoantibodies used to support a diagnosis of MG are anti-acetylcholine receptor antibodies and anti-muscle-specific tyrosine kinase antibodies. In cases in which both of these autoantibodies are negative (termed double-seronegative [dSNMG]), other autoantibodies such as low-density lipoprotein receptor-related protein 4 (LRP4) may be used to aid in diagnosis.nnnMETHODSnWe have undertaken a systematic literature review to identify studies that have assessed the frequency of anti-LRP4 antibodies in dSNMG patients and the characteristics of anti-LRP4+ dSNMG patients (epidemiology, clinical features, electromyographic findings, or management). PubMed, EMBASE, Medline, and Scopus were searched on January 14, 2017, using the medical subject headings myasthenia gravis and low-density lipoprotein receptor-related protein 4 or LRP4.nnnRESULTSnThe initial search identified 367 articles. Fourteen publications met the inclusion criteria. There were ten cross-sectional research studies, three were case series, and one was a case report. The majority of studies were limited by small sample sizes of LRP4+ dSNMG. There has been a wide range of frequencies of anti-LRP4 antibodies detected in different MG patient populations, some involving different laboratory techniques.nnnCONCLUSIONSnLRP4+ dSNMG is more likely than LRP4- dSNMG to have a younger onset of disease and occur in females. LRP4+ dSNMG most often is mild in severity and often involves isolated ocular weakness. It typically responds well to pyridostigmine or prednisone.


Canadian Journal of Neurological Sciences | 2018

Mycophenolate Mofetil-Induced Status Epilepticus

David Pellerin; Kelita Singh; Thomas Maniatis; Colin Chalk; Laurence Green

Mycophenolate mofetil (MMF) has become a widely used immunosuppressive agent owing to its potent cytostatic effect on lymphocytes. It is commonly used to prevent graft rejection in transplant patients and as a steroid-sparing therapy for a variety of autoimmune conditions, including connective tissue diseases and inflammatory myopathies. Mycophenolate mofetil has the advantage over other immunosuppressants of having a favorable safety profile, lacking nephrotoxicity and hepatotoxicity. Its main adverse effects relate to gastrointestinal disturbances, such as diarrhea and nausea, occurring in as many as 30% of patients. Of particular note, MMF is traditionally considered one of the least neurotoxic immunosuppressive drugs, occasionally causing tremor and mild psychiatric symptoms. Serious neurological adverse effects of MMF, such as progressive multifocal leukoencephalopathy and central nervous system (CNS) lymphoproliferative disorders, have nonetheless been recognized. Post-marketing surveillance data additionally suggest that encephalopathy and seizures might be related to MMF use in transplant patients concomitantly treated with corticosteroids and cyclosporine. An observational study of neurological complications following liver transplant also reported on frequent occurrence of encephalopathy and seizures in patients on combined MMF and calcineurin inhibitor (CNI) therapy. It must nonetheless be emphasized that CNIs are highly neurotoxic drugs, such that the potential contribution of MMF to the development of those adverse CNS effects remains unclear. There is also one case report of a patient who suffered generalized tonic–clonic seizures while on MMF and acyclovir following a penetrating keratoplasty. Acyclovir has an independent neurotoxic potential, and when co-administered with MMF the pharmacokinetics of both drugs are altered such that their serum concentrations increase simultaneously, which was the presumed causative mechanism of seizures in that case. Herein, we report a patient with probable MMF-induced encephalopathy and status epilepticus. A 61-year-old Inuit female from a northern Québec community was transferred to our institution for assessment of altered mental status. She had been diagnosed with statin-associated necrotizing autoimmune myopathy at our center 5 weeks earlier, based on positive serum anti-3-hydroxy-3-methylglutarylcoenzyme A reductase (HMGCR) antibodies and a compatible muscle biopsy. For 6 weeks before the diagnosis, she had been treated with high-dose corticosteroids for presumed polymyositis. When the diagnosis of necrotizing autoimmune myopathy was made, MMF (1 g twice daily) and monthly intravenous immunoglobulins (IVIg) were added. The patient was also known to have insulin-dependent diabetes mellitus type 2, hypertension, dyslipidemia and non-alcoholic fatty liver disease without cirrhosis. Three weeks after MMF was started, the patient developed behavioral changes, confusion and psychiatric symptoms, including visual hallucinations and delusional thoughts, over a 2-week period. There were no other neurological or systemic symptoms, nor any history of preceding febrile illness or of toxin use. On arrival at our center, the neurological examination was remarkable for decreased alertness, psychomotor retardation, confused verbal responses, eye opening to speech and inconsistency in following simple motor commands. The remainder of the examination was essentially normal. The initial workup revealed no metabolic, toxic or infectious abnormalities. The patient was subsequently admitted for further investigation. Preliminary CSF analysis, including Gram stain, was unremarkable, except for mildly elevated protein at 0.61 g/L (normal 0.15-0.45 g/L). Subsequent CSF bacterial culture was negative, as were syphilis, tuberculosis and human immunodeficiency virus testing. Gadolinium-enhanced head MRI showed only non-specific microvascular changes. On the second day of admission, the patient’s neurological status worsened, with no localization to noxious stimuli, no eye opening to speech and absent verbal responses. We opted to start empiric therapy with acyclovir and to discontinue MMF. Later during the night she experienced two episodes of brief generalized tonic–clonic seizures, which were treated with intravenous lorazepam and phenytoin. An emergent electroencephalogram (EEG) performed while the patient was not clinically seizing showed bifrontally predominant generalized epileptiform activity, consistent with non-convulsive status epilepticus (Figure 1A). She was then urgently transferred to the neurological intensive care unit for sedation with propofol and continuous EEG telemetry. Levetiracetam was subsequently added for persistent electrographic epileptiform activity. Further testing for infectious and immunological causes was negative, including CSF anti-N-methyl-D-aspartate receptor antibodies, anti-neuronal cell surface antibodies, herpes simplex virus and enterovirus assays, as well as serum anti-onconeuronal antibodies. A whole-body CT scan did not reveal evidence of an underlying malignancy. Following titration of the antiepileptic agents, the patient steadily improved, and after 4 days she was transferred back to the ward on a regimen of phenytoin and levetiracetam. She experienced no recurrence of clinical seizures, and a repeat EEG a week later showed only mild-to-moderate diffuse persistent slowing (Figure 1B). After this event, she did not suffer any residual neurological deficit. She was eventually discharged home on levetiracetam and high-dose corticosteroids. Monthly IVIg was continued for treatment of her myopathy. Two months after discharge, the patient returned to her previous level of functioning without recurrence of seizures. The absence of an alternative explanation for our patient’s condition prompted us to consider the possibility of a neurological complication induced by MMF. Our hypothesis is further supported by previous data suggesting a neurotoxic potential of MMF, by the temporal relationship between the introduction of MMF and the onset of her encephalopathy, and her clinical improvement after its withdrawal. Several features of this case argue against a diagnosis of idiopathic new-onset refractory status epilepticus, including


Neurology | 1995

Pathology of the Peripheral Nerve (Major Problems in Pathology, Vol. 32)

Colin Chalk

by EDWARD P. RICHARDSON, JR., and UMBERTO De GIROLAMI, 176 pp., ill., Philadelphia, W.B. Saunders, 1995.

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Fraser Moore

Jewish General Hospital

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Lesley K. Fellows

Montreal Neurological Institute and Hospital

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