The electroencephalogram in pernicious anaemia and subacute combined degeneration of the cord

Abstract

Eighty cases of pernicious anaemia in relapse, of which 24 had subacute combined degeneration of the cord (one with optic atrophy), 41 mild neurological involvement and 15 none, have been studied by means of the EEG. Seven cases showed mild organic reactions and in all of these the pre-treatment record was abnormal. The pre-treatment record was also abnormal in 60 per cent of the remaining patients who showed no significant mental abnormality. In some cases abnormality was severe (delta activity, generalised, paroxysmal or focal), in some slight (slight or moderate excess of theta activity), but the degree of abnormality bore no relationship to the severity of the anaemia, the age of the patient or the degree of neurological involvement. Ten cases of anaemia of miscellaneous type were also studied before treatment; although in 3 of these the haemoglobin level was less than 40 per cent, only in one case did the EEG show a significant abnormality and this patient had severe hypertension and atherosclerosis. Seventy-six of the cases of pernicious anaemia were re-examined after treatment with vitamin B 12. In 14 of the 29 cases which gave normal records before treatment there was a significant increase in mean frequency of the alpha rhythm and diminution in overall amplitude. Forty-two of the remaining 47 cases in which the initial record was abnormal s showed a satisfactory clinical response to treatment and in 31 (74 per cent) the EEG returned to normal, so that 60 of the 76 cases (79 per cent) eventually gave normal records. Improvement in the record began as a rule 7–10 days after the beginning of treatment and was often complete within a month, although some cases showed further improvement after intervals varying from 3–16 months. In the other 11 cases (26 per cent) who responded, persisting abnormalities consisted of a slight excess of generalised theta activity, a finding which in some could possibly be accounted for by age or constitution. Another 50 cases of pernicious anaemia (including 37 with subacute combined degeneration of the cord, 8 with mild neurological involvement and one with optic atrophy) were first studied after treatment had been in progress for between 3 months and 8 years (average 18 months). Excluding 5 cases showing epileptic discharges, 38 (84 per cent) of the other 45 patients had normal records; the remaining 7 cases (16 per cent) were restudied and in all EEG showed further improvement 5 months to 3 years after the beginning of treatment. The final total of normal records was 42 (93 per cent). Eight (6 per cent) of the 130 cases of pernicious anaemia studied gave records showing epileptic discharges (usually temporal spikes or sharp waves) and of these 4 (3 per cent) gave a personal or family history of fits or faints. It is suggested that the EEG changes in pernicious anaemia are due not to the anaemia but to a specific defect in cerebral metabolism, presumably related to the deficiency state responsible for the anaemia. Though not as sensitive as studies of cerebral metabolism by the blood flow method, the EEG is a useful tool in the investigation of these cases and reveals that maximum improvement may be delayed for up to 3 years after treatment has begun. The possible relationship of the EEG changes to alterations in glucose and pyruvate metabolism is discussed.