Emergency Medicine

ACUTE NEUROLOGICAL CONDITIONS

General Medical Emergencies 93

(c) cerebral hypoxia

(d) drug toxicity, e.g. theophylline.

(iii) Subtle generalized convulsive status epilepticus.

(iv) Non-convulsive status epilepticus:

(a) complex–partial (temporal lobe) seizures

(b) petit mal status.

Transient ischaemic attack

DIAGNOSIS

1 TIAs are episodes of sudden transient focal neurological deficit, maximal at
the outset and lasting for <24 h, usually <10 min.
(i) They may recur and are important in that they are part of a
spectrum that can progress to a full-blown stroke.
(ii) Thus they may be followed by a major ischaemic stroke or other
serious vascular event:
(a) 2.5–5% at 2 days
(b) 5–10% at 30 days
(c) 10–20% at 90 days.

2 The causes may be considered in three groups.
(i) Embolic
(a) extracranial vessels – carotid stenosis, narrowed vertebral
artery
(b) cardiac – post-myocardial infarction, AF, mitral stenosis,
valve prosthesis.
(ii) Reduced cerebral perfusion
(a) hypotension from hypovolaemia, drugs or a cardiac arrhythmia
(b) hypertension (especially in hypertensive encephalopathy)
(c) polycythaemia, paraproteinaemia, or a hypercoagulable state
such as protein C, protein S or antithrombin III deficiency,
and with antiphospholipid antibodies
(d) vasculitis, e.g. temporal arteritis, SLE, polyarteritis nodosa, or
syphilis.
(iii) Lack of nutrients
(a) anaemia
(b) hypoglycaemia.

3 TIAs present clinically as:
(i) Carotid territory dysfunction causing hemiparesis,
hemianaesthesia, homonymous hemianopia, dysphasia,
dysarthria and amaurosis fugax (transitory monocular
blindness).
(ii) Vertebrobasilar territory dysfunction (posterior circulation) causing
combinations of bilateral limb paresis, crossed sensory symptoms,
diplopia, nystagmus, ataxia, vertigo and cortical blindness.