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Neurological Alterations and Management 467

neural cell damage, as well as the apoptosis of astrocytes. Guillain–Barré Syndrome
The disruption of the blood–brain barrier progresses to Guillain–Barré syndrome (GBS) is an immune-mediated
the systemic cytokine storm, resulting in septic shock, disorder resulting from generation of autoimmune anti-
disseminated intravascular coagulopathy (DIC) and mul- bodies and/or inflammatory cells which cross-react with
tiorgan failure (MOF).
epitopes on peripheral nerves and roots, leading to demy-
elination or axonal damage or both, and autoimmune
Clinical features and diagnosis insult to the peripheral nerve myelin. In Australia,
Encephalitis may present with progressive headache, fever Guillain–Barré has an average incidence of about 1.5 per
and alterations in cognitive state (confusion, behavioural 100,000, in men slightly higher than in women. Of all
106
change, dysphasia) or consciousness. Focal neurological patients, 85% recover with minimal residual symptoms;
signs (paresis) or seizures (focal or generalised) may also severe residual deficits occur in up to 10%. Residual defi-
occur. Upper motor signs (hyperreflexia and extensor– cits are most likely in patients with rapid disease progres-
plantar responses) are often present, but flaccid paralysis sion, those who require mechanical ventilation, or those
and bladder symptoms may occur if the spinal cord is 60 years of age or over. Death occurs in 3–8% of cases,
involved. Associated movement disorders or the SIADH resulting from respiratory failure, autonomic dysfunc-
secretion may be seen. In northern Australia, it may be tion, sepsis or pulmonary emboli. 107
desirable to distinguish MVE from Japanese encephalitis
clinically. Both conditions often affect the brainstem and Aetiology
basal ganglia, but MVE often involves the spinal cord,
while Japanese encephalitis may produce striking menin- The diagnosis of GBS is confirmed by the findings of
geal signs, with or without thalamic involvement. Both cytoalbuminological dissociation (elevation of the CSF
have high mortality (25–33%) and high rates of chronic protein without concomitant CSF pleocytosis), and by
sequelae in survivors (~50%). 101 neurophysiological findings suggestive of an acute
(usually demyelinating) neuropathy. These abnormalities
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The most sensitive type of imaging for diagnosis of may not be present in the early stages of the illness.
encephalitis is MRI; in HSV encephalitis, CT scans may There are two forms of GBS. The demyelinating form, the
initially appear normal, but MRI usually shows invol- more common one, is characterised by demyelination
vement of the temporal lobes and thalamus. 103,104 Exa- and inflammatory infiltrates of the peripheral nerves and
mination of CSF can assist in differential diagnosis. roots. In the axonal form the nerves show Wallerian
Electroencephalography is less sensitive but may be degeneration with an absence of inflammation. Discrimi-
helpful if it shows characteristic features (e.g. lateralising nation between the axonal and demyelinating forms
periodic sharp and slow-wave patterns). Refer to Table relies mainly on electrophysiological methods. There is a
17.6 for CSF profiles. close association between GBS and a preceding infection,
suggesting an immune basis for the syndrome. The com-
Collaborative management monest infections are due to Cambylobacter jejuni, cyto-
Support in an ICU is often required in encephalitis to megalovirus and Epstein–Barr virus.
maintain ventilation, protect the airway and manage
complications, such as cerebral oedema. The man- Pathophysiology
agement of acute viral encephalitis includes aggressive GBS is the result of a cell-mediated immune attack on
airway, ventilation, sedation, seizure, haemodynamic, and peripheral nerve myelin proteins. The Schwann cell is
fluid and nutritional support. Clinical deterioration in spared, allowing for remyelination in the recovery phase
encephalitis is usually the result of severe cerebral oedema of the disease. With the autoimmune attack there is an
with diencephalic herniation or systemic complications, influx of macrophages and other immune-mediated
including generalised sepsis and multiple organ failure. agents that attack myelin, cause inflammation and
The use of ICP monitoring in acute encephalitis remains destruction and leave the axon unable to support nerve
controversial but should be considered if there is a conduction. This demyelination may be discrete or
rapid deterioration in the level of consciousness, and if diffuse, and may affect the peripheral nerves and their
imaging suggests raised ICP. Prolonged sedation may be roots at any point from their origin in the spinal cord to
necessary. Decompressive craniotomy may be successful the neuromuscular junction. The weakness of GBS results
in cases where there is rapid swelling of a non-dominant from conduction block and concomitant or primary
temporal lobe, as poor outcome is otherwise likely. 105 axonal injury in the affected motor nerves. Pain and par-
aesthesias are the clinical correlates of sensory nerve
NEUROMUSCULAR ALTERATIONS involvement.

Generalised muscle weakness can manifest in several
disorders that require ICU admission or complicate the Clinical manifestations
course of patients. These may involve motor neuron Onset is rapid, and approximately 20% of cases lead to
disease, disorders of the neuromuscular junction, peri- total paralysis, requiring prolonged intensive therapy
pheral nerve conduction and muscular contraction. with mechanical ventilation. The therapeutic window for
These disorders manifest as Guillain–Barré syndrome, GBS is short, and the current optimal treatment with
myas thenia gravis, and critical illness polyneuropathy whole plasma exchange or IV immunoglobulin (IVIg)
and myopathy. therapy lacks immunological specificity and only halves