This unsatisfactory term is reserved for seizures that start in close temporal association to a sudden acute precipitant, in people who had not had prior seizures. If the epilepsy can be attributed to a pre-existing non-acute or static cause, it is referred to as remote symptomatic epilepsy, but clearly there is a grey area in which the distinction between acute and remote symptomatic epilepsies is rather arbitrary. The boundary is similarly blurred in some cases of reflex epilepsy or cases in which seizures have acute precipitants such as sleep deprivation or alcohol. Furthermore, if seizures continue after the acute phase, and if the cause remains present (e.g. post-stroke, post-trauma, tumoural, post-infectious epilepsy), seizures that were initially categorized as acute symptomatic are reclassified as remote symptomatic. This makes rather a nonsense of the classification scheme, the utility of which is best reserved for epidemiologically based incidence studies. Even in cases where the cause is reversible (e.g. acute metabolic disturbance or intoxication), there is a higher incidence of subsequent unprovoked seizures than in control populations, and classification as acute symptomatic even in these cases makes little sense. For all these reasons the term has fallen from common usage in research practice, although it remains useful shorthand to describe acute de novo seizures presenting in the context of sudden cerebral dysfunction, particularly where this is due to reversible factors such as metabolic or endocrine disturbance or exposure to alcohol, toxins or drugs (these factors are discussed below).
Acute symptomatic seizures usually take the form of tonic-clonic convulsions or tonic-clonic status epilepticus. Some causes of acute symptomatic seizures are given in Table 1.34. In epidemiological studies, the most common causes in a typical Western country are found to be: cerebral trauma (15%), cerebral infection (15%), cerebrovascular disease (15-30%), drugs, toxins and alcohol (15-20%), and metabolic disturbances (10%).
The age-adjusted incidence rate of symptomatic seizures, reported in an old study from the record-linkage system in Rochester, Minnesota, was about 40 per 100,000 person-years. In adults, acute symptomatic seizures are more common in men than in women (52 vs. 29 per 100,000 per year). The highest rate is in the first year of life due to metabolic, infectious and encephalopathic aetiologies. The rate decreases in childhood and early adulthood, with a nadir at 25-34 years, and then increases, producing a second peak at age 75 and older, accounted for mostly by cerebrovascular disorders. The cumulative incidence of acute symptomatic seizures has been estimated to be about 4% up to the age of 80 years.
The emergency treatment of acute seizures is described on p. 211.
Table 1.34 Some causes of acute symptomatic seizures.
Acute cerebral infections—encephalitis, meningitis, abscess Acute para-infectious encephalopathies—acute disseminated encephalomyelopathy Acute metabolic disturbance—hypoglycaemia, hypocalcaemia, hyponatraemia, hypernatraemia, hypomagnesaemia Acute hypoxia/ischaemia—stroke, cardiac arrest, acute hypotension, asthma, perinatal Acute renal or hepatic failure, uraemic encephalopathy, dialysis disequilibrium syndrome and dialysis encephalopathy Acute traumatic brain injury Acute intoxication with drugs or toxins Acute drug or alcohol withdrawal
Acute hypertension—hypertensive encephalopathy, eclampsia Acute haemorrhage
Acute vasculitis—Henoch-Schonlein purpura, SLE, polyarteritis nodosa (PAN)
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