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  • Differential diagnosis of acute flaccid paralysis  return to main page

    Acute anterior poliomyelitis
    – caused by poliovirus
    – caused by other neurotropic viruses
    Acute myelopathy
    – space occupying lesions
    – acute transverse myelitis
    Peripheral neuropathy (all except GBS usually have axonal neurophysiology)
    – Guillain-Barrι syndromes
    – post-rabies vaccine neuropathy
    – diphtheritic neuropathy
    – heavy metals, biological toxins or drug intoxication
    – acute intermittent porphyria (usually pure motor neuropathy)
    – vasculitic neuropathy
    – critical illness neuropathy
    – lymphomatous neuropathy
    – infections (HIV, Borrelia)

    Disordersof neuromuscular transmission
    – myasthenia gravis
    – biological or industrial toxins—for example, botulism

    Disordersof muscle
    – hypokalaemia
    – hypophosphataemia
    – inflammatory myopathy
    – acute rhabdomyolysis
    – trichinosis
    – periodic paralyses

    Cerebrospinal fluid examination is needed largely to exclude alternative diagnoses, such as infectious (for example, Borreliaor poliomyelitis) or lymphomatous polyradiculitis. The CSF protein is classically elevated as a result of albumin leakage fromthe blood, but may be normal within the first week. The CSF leucocyte count is usually normal but the diagnostic criteriaallow up to 50 cells/΅l. Pleocytosis is more likely incoexistent HIV infection.
    GBS is preceded in two thirds of cases by an infection such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus or Mycoplasma pneumoniae.4 The infection is usually cleared before development of neurological symptoms. Identification of serum IgM antibodies to one of these agents demonstrates recent infection but is not clinically useful. Stool culture occasionally isolates C jejuni, but antibiotics probably donot influence outcome (level 4 evidence; box 2). The risk of developing GBS after C jejuni enteritis is less than 1 in 2500.

    Serum antibodies to many peripheral nerve antigens have been found in GBS, but the majority of GBS patients have no identified autoantibodies so the pathogenesis of the disease is still debated. The antibodies that are found may also be present in other neurological diseases or occasional normal controls, and may be an epiphenomenon. Nevertheless, some antibodies do correlate with clinical sub types of GBS . Their presence does not influence treatment.

    Neurophysiological abnormalities are often very mild or occasionally normal in early GBS, and do not correlate well with clinical disability.The earliest consequence of acute demyelination is focal axonal conduction block, and it takes several days before slowing of conduction develops. Unfortunately for the purposes of diagnosis, conduction block is most common in the proximal nerve roots at sites that are awkward to test,at distal sites that mimic axonopathy, and at sites of compression,so it is often difficult or impossible to distinguish between axonal and demyelinating GBS in the early stages. Axonal degeneration may occur as a consequence of primary autoimmune attack on the axon or as a bystander phenomenon secondary to a primary attack on the myelin. It becomes evident after a few weeks as muscle wasting and electromyographic features of denervation, which signify a poor outcome. In the early stages, axonal neurophysiology may represent reversible axonal dysfunction rather than degeneration.