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Editor—Alpha coma (AC) is the combination of coma and an electroencephalographic (EEG) pattern of synchronous, rhythmic 8–13 Hz activity which has been described in certain severe neurological conditions such as post anoxic or ischaemic encephalopathy, head trauma, brain stem infarcts and drug overdoses.1-3 In neonates AC has been associated with chromosomal abnormalities and inborn errors of metabolism and α rhythms have been described transiently during seizure activity.4 5 Most reported cases have been associated with a poor outcome
A boy weighing 4080 g was born by vaginal delivery following prolonged fetal distress and meconium stained amniotic fluid to non-consanguineous parents. Cesarean section had been refused. Apgar scores were 1,6, and 7 at 1, 5, and 10 minutes, respectively. At one hour, arterial pH was 7.29, bicarbonate 20 mmol/l, and base deficit 6 mmol/l. The infant developed mild meconium aspiration syndrome that required mechanical ventilation.
Increased tone, fisting of both hands, and blank staring were noted shortly after birth. When 6 hours old, coma and convulsions appeared. Treatment with phenobarbital and subsequently phenytoin was partially effective, with serum concentrations in the therapeutic range. The convulsions diminished and the coma resolved over several days.
Blood count, blood glucose, serum electrolytes, calcium and magnesium and urinary amino and organic acids were normal. Metabolic acidosis was not detected throughout the hospital course. Karyotype was normal.
The EEG on day 3 showed continuous 10–11 Hertz α activity with amplitude of 15–40 uV localised over the left parasagittal and temporal regions, with sporadic generalised short bursts of mixed frequencies and sharp waves not associated with clinical correlates. Marked suppression of cortical activity was recorded over the right hemisphere with occasional 10–11 Hertz α of 10 uV amplitude. (fig1). The EEG showed burst–suppression pattern on day 4 (fig 2) and prolonged polymorphic delta activity of low to medium amplitude when the child was 3 months old.
A computed tomography scan showed severe bilateral cortical atrophy, basal ganglia infarcts, and periventricular cystic leucomalacia. At 3 years of age, the child had severe spastic quadriplegic cerebral palsy, pseudobulbar palsy, and psychomotor retardation.
In spite of the relatively mild evidence of asphyxia at birth, the intrapartum history, the course of the encephalopathy and the absence of appropriate abnormalities on metabolic or imaging studies make any diagnosis other than HIE unlikely.
The α rhythm in this infant was consistent, non-reactive, and not associated with a clinical seizure correlate, as described in AC in other settings. This description of AC in HIE adds to the usual EEG findings of initial voltage suppression followed most often by burst-suppression pattern.6
Poor prognostic indicators in HIE include the presence of seizures, the duration of the EEG abnormalities, and the severity of the clinical syndrome.7 The burst–suppression pattern in HIE is of ominous clinical significance. Although we have presented only one case of AC in HIE with poor neurodevelopmental outcome, this may represent an additional poor prognostic indicator.
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