Access to multiple sclerosis (MS) diagnosis in Canada has never been assessed. This study was designed to examine the pattern of MS diagnosis in Canada, including neurologists' diagnostic approach and waiting times for investigations.

A mail survey was forwarded to every registered neurologist in Canada (n = 479) in late 1996. Questions included their diagnostic approach to MS including perceived waiting times for various investigations including MRI. Actual MRI waiting periods were separately obtained from booking clerks or neuroradiologists from every MRI unit in Canada.

153 responses were received. Neurological assessment is obtained, on average, 1 month after referral. MRI is routinely ordered by 92% of neurologists for suspected MS followed by evoked potentials (EP) (36%) and lumbar puncture (LP) (17%). The perceived waiting period for EP and LP is less than one month but 3 months for MRI. This is very similar to the actual waiting periods obtained from the MRI units surveyed (mean of 101 days). There is a trend for longer waiting periods as one moved east to west (Eastern provinces — mean of 62 days, Ontario — 95 days, Quebec — 102 days and 122 days in the Western provinces). Private MRI units have appeared in the Western provinces and have the shortest waiting periods (2 weeks maximum). The current MRI/million population ratio in Canada is 1.8, far below the ratios of other developed nations.

Canadian neurologists prefer MRI of the brain to confirm an MS diagnosis and desire greater access to it. Access to neurological assessment, EP and LP is probably adequate but the average wait for MRI of 3 months is relatively long. The perceived average waiting period for MRI is similar to the actual waiting times of 3 months, with the Western provinces of Canada having the longest waits. Canada continues to have one of the lowest MRI/population ratios in the developed world.

Guillain-BarrÈ syndrome (GBS) classically presents with a subacutely evolving areflexic paralysis, with typical laboratory findings of elevated cerebrospinal fluid protein and abnormal nerve conduction studies. There is now an increasing recognition of GBS variants that differ in clinical presentation, prognosis, electrophysiology and presumed pathogenesis. Fulminant cases of GBS have been reported in which a rapid deterioration evolves to a clinical state resembling ìbrain deathî.

A retrospective analysis of two such cases of fulminant neuropathy are described, that includes the clinical course, electrophysiology and neuropathology where available.

We describe two patients that presented with a rapid course of neurological deterioration, lapsing into what resembled a ìclinically brain-deadî state that was subsequently ascribed to a fulminant polyneuropathy. Investigations (electrophysiological, pathological) and the clinical course suggested an axonal neuropathy.

A fulminant neuropathy can result in a clinical state resembling ìbrain deathî through diffuse de-efferentation. Although generally attributed to aggressive demyelination with secondary axonal degeneration, a primary axonopathy can also lead to a similar clinical presentation.