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• Clinical neurology in practice
  Abhijit Chaudhuri
  Published on: 14 April 2016

• Published on: 14 April 2016

  Clinical neurology in practice

  • Abhijit Chaudhuri, Consultant Neurologist

  Dear Editor,

  I felt rather uncomfortable with some of the articles in the August 2006 issue of the Practical Neurology and it was not because I was reading the journal in a sultry afternoon of Indian summer.

  Andrew Chancellor was wrong in invoking a clinical diagnosis of multiple sclerosis in his fourth problem (Test Yourself, p260). The diagnosis of multiple sclerosis (MS) cannot be made without objecti...

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  Dear Editor,

  I felt rather uncomfortable with some of the articles in the August 2006 issue of the Practical Neurology and it was not because I was reading the journal in a sultry afternoon of Indian summer.

  Andrew Chancellor was wrong in invoking a clinical diagnosis of multiple sclerosis in his fourth problem (Test Yourself, p260). The diagnosis of multiple sclerosis (MS) cannot be made without objective clinical findings, even if objective paraclinical findings are in place (1). In the given case, one would only suspect the possibility of demyelination or a "clinically vague syndrome" (1).

  We should be aware of the inherent pitfall of overdiagnosis of MS and its consequences. In their commentary, Gold and Hohfield (2) avoided the key issue of selection of MS patients for monoclonal antibody based interventions in clinical practice. Given the unknown risks of long-term therapy, the benefit would seem less certain in patients with low disability and relatively stable disease (3). However, nearly two-thirds of recruited patients in natalizumab trials (1801 and 1802) had low disability (Kurtzke’s EDSS score 0-2.5), only a minority had serious clinical relapses during treatment (7 and 13% in the treated and placebo arms respectively in the monotherapy trial), and absolute reduction of disease progression was rather modest (between 6 and 12%). I am uncertain if the trial data can be extrapolated to the general population of the MS clinic notwithstanding the regulatory approval of the drug.

  My disappointment did not get any better with the review of ulnar neuropathy by John Stewart (4). Worldwide, probably the commonest cause of ulnar neuropathy -and its disabling serious motor complication-is leprosy, not habitual elbow leaning. Leprosy only appears at the tail of Table 2, with no mention about its clinical diagnosis and management, and the fact that leprosy is possibly the only example of peripheral (ulnar) nerve abscess. A picture of Hansen, rather than the sculpture of Rodin would have been more appropriate, but I have enclosed a picture (courtesy: World Health Organisation) of an ulnar neuropathic hand of leprosy after reconstruction surgery. Maybe the editor would commission an article on this topic in the future to rectify the omission. As one of the junior colleagues has written it, I would prefer not commenting on some of the misconceptions regarding the immunity of Guillain-Barre syndrome (GBS)(5).

  Passive transfer of anti-ganglioside antibodies has never capitulated the nerve pathology of GBS and anti-GQ1b antibody does not explain the known pathology of cerebellar ataxia in Miller Fisher syndrome. It may also be important to draw the attention of the readers to the not-so-infrequent findings of liver function test abnormalities and the commonly overlooked association of GBS with acute glomerulonephritis(6-10). Plasma exchange or human intravenous immunoglobulin should be started in an eligible patient once the diagnosis is clinically secure and treatment must not be delayed for peripheral nerve electrophysiology (Figure 3, p214). The risk of relapsing GBS is also higher in treated patients but the relapses respond well to treatment.

  Rather than writing individual responses, I thought it might not be inappropriate to write a jobbing neurologist’s feedback to the editor and I hope to be excused if my response falls outside the rules of the book.

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  References

  1. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the "McDonald criteria". Ann Neurol 2005; 58: 840-6.

  2. Gold R, Hohlfield R. Multipe sclerosis therapy: new agents carry new risks. Practical Neurology 2006; 6: 248-51.

  3. Chaudhuri A. Lessons for clinical trials from natalizumab in multiple sclerosis. BMJ 2006; 332: 416-419. 4. Stewart J. Ulnar neuropathies: where, why and what to do. Practical Neurology 2006; 6: 218-229.

  5. Pritchard J. What’s new in Guillain-Barre syndrome? Practical Neurology 2006; 6: 218-217.

  6. Behan PO, Lowen stein LM, Stilmant M, Sax DS. Landry-Guillain- Barre-Strohl syndrome and immune-complex nephritis. Lancet 1973; 1: 850-4.

  7. Talamo TS, Borochovitz D. Membranous glomerulonephritis associated with the Guillain-Barre syndrome. Am J Clin Pathol 1982; 78: 563-6.

  8. Bettinelli A, Giani M, Rossi L, et al. Ex novo episodes of acute glomerulonephritis and Guillain-Barre syndrome: a case report. Clin Nephrol 1989; 31: 269-73.

  9. Olbricht CJ, Stark E, Helmchen U, Sculze M, Brunkhorst R, Koch KM. Glomerulonephritis associated with inflammatory demyelinating polyradiculoneuropathy: a case report and review of the literature. Nephron 1993; 64: 139-41.

  10. Emsley HC, Molloy J. Inflammatory demyelinating polyneuropathy associated with membranous glomerulonephritis and thrombocytopenia. Clin Neurol Neurosurg 2002; 105: 23-6.

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  Conflict of Interest:
  None declared.

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