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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-Barré 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 toxinsfor example, botulism
Disordersof muscle
- hypokalaemia
- hypophosphataemia
- inflammatory myopathy
- acute rhabdomyolysis
- trichinosis
- periodic paralyses
Functional/non-organic
Investigations
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/µl.
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.
Neurophysiology
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.