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Chapter 7: Infections of the nervous system 307

exercise early in the illness; trauma, surgery, or intra- Post-polio syndrome management is non-specific,
muscularinjectionwhichlocalisestheparalysis,recent withthetreatmentoflimbandjointdeformities,man-
tonsillectomy (bulbar poliomyelitis). agement of pain, and maximisation of function and
i Afteraninitialfebrileillness,symptomssubsidefor strength by not overworking muscles. Sleep disor-
4–5 days. ders, including nocturnal hypoventilation, need to be
ii Symptoms then reoccur with greater severity and treated with non-invasive ventilation.
signs of meningeal irritation and muscle pain, fol- Prophylaxis: Live attenuated (Sabin) or killed (Salk)
lowed by paralysis typically affecting one arm and polio vaccine.
the opposite leg.
iii Bulbar poliomyelitis is characterised by cranial
nerve involvement commonly with palsies of the Abscesses of the nervous system
soft palate, pharyngeal and laryngeal muscles. Dys-
phagia and dysarthria result, with the risk of aspi- Cerebritis and cerebral abscess
ration pneumonia.
Definition
iv Respiratory involvement may lead to the need for
Afocal infection within the parenchyma of the brain –
ventilatory support.
cerebritis–canleadtotheformationofacerebralabscess.
Complications
Post-polio syndrome – this is progressive, often painful Aetiology
weakness in the territories originally affected by the Often the causative organism cannot be identified, or
acute illness which can occur many years later (usually a mixed growth of bacteria is found. Bacteria that
20–40 years) in about a quarter of patients. More suffer cause cerebral abscesses include various Streptococci,
from pain, but without progressive weakness. It appears Bacteroides, Staphylococci and Enterobacteria. Immuno-
to be a failure of the compensatory mechanisms which suppressed patients are predisposed to fungal abscesses
occur to bring about the original recovery – those with such as Candida, Aspergillus and Toxoplasma.
agreater original recovery tend to have the greatest de-
cline, and those who were younger at the age of acute
Pathophysiology
polio appear to be relatively protected.
The organism may enter the brain by direct exten-
sion from meningitis, otitis media or sinusitis, or
Investigations
by haematogenous spread, e.g. from infective endo-
Diagnosis is clinical but laboratory confirmation is by
carditis. Surgery or trauma may also inoculate organ-
viral culture. In post-polio syndrome, polio virus is not
isms directly through an open wound. Multiple lesions
found in the CNS, but muscle EMG and biopsy show
suggest haematogenous seeding.
evidence of motor unit loss.
Clinical features
Management
Acute treatment is supportive with bed rest, respira-
The onset of symptoms is usually insidious, with
tory support where indicated. headache as the most common symptom, variable neck
Post-infection:
stiffness, fever, and possible focal signs, seizures or con-
i Occupational and physical therapy should be used fusion.
to maximise function.
ii Splinting and even tendon transfer or arthrodesis Macroscopy/microscopy
may be required for weakness or joint deformity. In the first 1–2 weeks, there is inflammation and oedema
iii Shortening: Leg length inequality of up to 3 cm (cerebritis). Later, necrosis and liquefaction lead to for-
may be treated by built up shoes, larger differences mation of a cavity filled with pus. There are acute in-
may require leg lengthening (or shortening of the flammatory cells (neutrophils), surrounded by gliosis
opposite leg) procedures. and fibroblasts.