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446 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

supratentorial pressure, by infratentorial pressure, and by of a partial seizure patient is the preepileptic event, the
intrinsic brainstem lesions. Supratentorial lesions produce aura. The patient will describe the aura as a virtually
impaired consciousness by enlarging and displacing identical sensation every time.
tissue. Lesions that affect the brainstem itself damage the
reticular activating system directly. Aetiology of seizures
Seizures may either prompt the patient’s admission to ICU
Aetiology of altered cognition (because of status epilepticus) or develop as a complica-
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Recently gained confusion, severe apathy, stupor or coma tion of another illness. Seizures can be due to vascular,
implies dysfunction of the cerebral hemispheres, the infectious, neoplastic, traumatic, degenerative, metabolic,
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diencephalon and/or the upper brainstem. Focal lesions toxic or idiopathic causes. Factors influencing the develop-
in supratentorial structures may damage both hemi- ment of posttraumatic epilepsy include an early post-
spheres, or may produce swelling that compresses the traumatic seizure, depressed skull fracture, intracranial
diencephalic activating system and midbrain, causing haematoma, dural penetration, focal neurological deficit
transtentorial herniation and brainstem damage. Primary and posttraumatic amnesia (PTA) over 24 hours with the
subtentorial (brainstem or cerebellar) lesions may com- presence of a skull fracture or haematoma. Seizures in
press or directly damage the reticular formation anywhere critically ill patients are most commonly due to drug
between the level of the midpons and, (by upward pres- effects; metabolic, infectious or toxic disorders; and intra-
sure), the diencephalon. Metabolic or infectious diseases cranial mass lesions although they may be due to trauma
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may depress brain functions by a change in blood com- or neoplasm. Conditions producing seizures tend either
position or the presence of a direct toxin. Impaired con- to increase neuronal excitation or to impair neuronal
sciousness may also be due to reduced blood flow (as inhibition. A few generalised disorders (e.g. non-ketotic
in syncope or severe heart failure) or a change in the hyperglycaemia) may produce partial or focal seizures.
brain’s electrical activity (as in epilepsy). Concussion,
anxiolytic drugs and anaesthetics impair consciousness ALTERATIONS IN MOTOR AND
without producing detectable structural changes in the SENSORY FUNCTION
brain.
Alterations of motor and sensory function include skeletal
Many of the enzymatic reactions of neurons, glial cells, muscle weakness and paralysis. They result from lesions
and specialised cerebral capillary endothelium in the in the voluntary motor and sensory pathways, including
brain must be catalysed by the energy-yielding hydrolysis the upper motor and sensory neurons of the corticospinal
of adenosine triphosphate (ATP) to adenosine diphos- and corticobulbar tracts, or the lower motor and sensory
phate (ADP) and inorganic phosphate. Without a con- neurons that leave the CNS and travel by way of the
stant and generous supply of ATP, cellular synthesis slows peripheral nerve to the muscle and sensory receptors.
or stops, neuronal functions decline or cease, and cell Muscle tone, which is a necessary component of muscle
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structures quickly fall apart. The brain depends entirely movement, is a function of the muscle spindle (myotatic)
on the process of glycolysis and respiration within its system and the extrapyramidal system, which monitors
own cells to provide its energy needs. Even a short inter- and buffers input to the lower motor neurons by way of
ruption of blood flow or oxygen supply threatens tissue the multisynaptic pathways. Upper motor neuron lesions
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vitality.
produce spastic paralysis, and lower motor neuron lesions
produce flaccid paralysis. Damage to the upper motor
Seizures and sensory neurons of the corticospinal, corticobulbar
A seizure is an uninhibited, abrupt discharge of ions from and spinothalamic tracts is a common component of
a group of neurons resulting in epileptic activity. The stroke. Polyneuropathies involve multiple peripheral
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majority of patients experiencing seizures in the ICU do nerves and produce symmetrical sensory, motor, and
not have preexisting epilepsy, and their chances of devel- mixed sensorimotor deficits:
oping epilepsy in the future are usually more dependent
on the cause than on the number or intensity of seizures ● Lesions of the corticospinal and corticobulbar tracts:
that they experience. However, because of other deleteri- result in weakness or total paralysis of predominantly
ous neuronal and systemic effects of seizures, their rapid distal voluntary movement, Babinski’s sign (i.e. dorsi-
diagnosis and suppression during a period of critical flexion of the big toe and fanning of the other toes in
illness is necessary. response to stroking the outer border of the foot from
heel to toe), and often spasticity (increased muscle
Seizures are classified depending on how they start as (a) tone and exaggerated deep tendon reflexes).
partial or focal seizures, (b) generalised or full body sei- ● Disorders of the basal ganglia: (extrapyramidal dis-
zures involving both cerebral hemispheres, or (c) partial orders) do not cause weakness or reflex changes.
seizures with secondary generalisation. A patient may still Their hallmark is involuntary movement (dyskinesia),
be conscious during a partial seizure whereas in gener- causing increased movement (hyperkinesias) or
alised seizures they are not. As partial seizures may not decreased movement (hypokinesia) and changes in
always progress to tonic-clonic movement or alteration muscle tone and posture.
in consciousness, partial seizure represents one of the ● Cerebellar disorders: cause abnormalities in the range,
most elusive diagnoses in neurology and is often misdi- rate and force of movement. Strength is minimally
agnosed. One of the most helpful points in the history affected.