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Neurology
Mental Retardation

Investigations

Investigations

Diagnosis usually is made on clinical grounds.

Laboratory studies are useful to rule out other diagnoses and to better assess functional status and prognosis:

  • Lumbar puncture and spinal fluid analysis
  • Elevated or rising protein levels on serial lumbar punctures and 10 or fewer mononuclear cells/mm2 strongly support the diagnosis.
  • Most, but not all, patients have an elevated level of CSF protein ( 400 mg/L), with no elevation in CSF cell counts.
  • Normal CSF protein does not rule out GBS because the level of CSF protein remains normal in 10% of cases and because any rise in the CSF protein may not be observed until 1-2 weeks after the onset of weakness.
  • CSF pleocytosis is well recognised in HIV-associated GBS.
  • Biochemical screening
    • Biochemical screening includes electrolytes levels; liver function tests (LFTs); CPK level; erythrocyte sedimentation rate (ESR); antiganglioside antibodies; and antibodies to C. jejuni, cytomegalovirus, Epstein-Barr virus, herpes simplex virus (HSV), HIV, and M. pneumoniae.
  • MRI
    • MRI is a sensitive but nonspecific test.
    • Spinal nerve root enhancement with gadolinium is a non-specific feature seen in inflammatory conditions and caused by disruption of the blood-nerve barrier.
    • Selective anterior nerve root enhancement appears to be strongly suggestive of GBS.
    • The cauda equina nerve roots are enhanced in 83% of patients.
  • Forced vital capacity
    • Forced vital capacity (FVC) is very helpful in guiding disposition and therapy.
    • Patients with an FVC less than 15-20 mL/kg, maximum inspiratory pressure less than 30 cm H2O, or a maximum expiratory pressure less than 40 cm H2O, generally progress to require prophylactic intubation and mechanical ventilation.
  • Nerve conduction studies
    • A delay in F waves is present, implying nerve root demyelination.
    • Nerve motor action potentials may be decreased. This is technically difficult to determine until the abnormality is severe.
    • Compound muscle action potential (CMAP) amplitude may be decreased.
    • Frequently patients show evidence of conduction block or dispersion of responses at sites of natural nerve compression. The extent of decreased action potentials correlates with prognosis.
    • Prolonged distal latencies
    • Rarely, neurophysiologic testing is normal in patients with GBS. This is believed to be due to the location of demyelinating lesions in proximal sites not amenable to study.
  • Muscle biopsy may help to distinguish GBS from a primary myopathy in unclear cases.
  • Many different abnormalities may be seen on an ECG, including second-degree and third-degree atrioventricular (AV) block, T-wave abnormalities, ST depression, QRS widening, and a variety of rhythm disturbances.
  • Lumbar puncture and spinal fluid analysis.

Investigations

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