Charles E. Wells

Cerebral toxicity associated with massive intravenous penicillin therapy

THE EPILEPTOGENIC POTENTIAL of penicillin is well recognized and has restricted its subarachnoid and intraventricular administration.1-4 This epileptogenic effect has not previously significantly limited its use by other routes of administration. In recent years, however, extremely high doses of penicillin intravenously have been advocated for subacute bacterial endocarditis and for gram-negative bacillary infections.5 In patients with renal tubular dysfunction, this may produce serious neural toxicity. Two patients who developed generalized seizures and other signs of nervous system dysfunction associated with high doses of penicillin have recently been observed. Both had renal tubular malfunction.

Cerebellar dysfunction associated with chronic alcoholism.

ALTHOUGH GREEN FIELD^ has stated that no differential diagnosis is possible during life between different forms of cerebellar and spinocerebellar disease, we have recently observed a group of patients whose history, signs, and clinical course are similar enough to set them aside from the mass of these disorders. During the past three years, 10 patients with cerebellar system disease associated with chronic alcoholism have been observed at Bellevue Hospital. These patients were free of other nervous system diseases which might interfere with a clinical diagnosis of cerebellar disease. The striking features are the long duration of alcoholism prior to onset of symptoms, absence of extreme nutritional deprivation, the much greater involvement of the lower extremities, the improvement with abstinence and hospital care, and the tendency for relapse to occur. No similar disorders had occurred in the family of any patient. Symptoms of cerebellar system disease in this group were classic-a wide based, reeling gait; decomposition of compound movements of the extremities including dysmetria on point-to-point tests and breakdown of rapid alternating movements; impaired check movements and overactive rebound; and hypoactive deep tendon reflexes. All patients had these signs to varying degrees. Omitted from this series were patients with signs of dysfunction of the corticospinal tracts, evidence of sensory loss other than minimal impairment of vibration perception in the feet, hereditary tendency to neuromuscular disease, previous trauma associated with the onset of cerebellar symptoms, and evidence on physical examination or laboratory studies of other diseases known to cause central nervous system dysfunction. MATERIAL

The electroencephalogram during administration of 100% oxygen and of 5% carbon dioxide in patients with cerebral infarction

CEREBRAL INFARCTION is often associated in man with the appearance of slow waves in the electroencephalogram. Study of these alterations through serial electroencephalograms shows that, after an initial worsening of the record during the period immediately after onset of an infarction, there is a delayed but significant diminution in this slow activity, so that in only a relatively small percentage of patients are focal abnormalities present a year after the onset of the infarction.1.2 Gibbs, Williams, and Gibbs,s using the Grass method for the Fourier transform of the electroencephalogram, reported that increase in the carbon dioxide content in the internal jugular blood was accompanied by a shift in the electroencephalographic activity toward the fast side of the spectrum. It was later demonstrated that breathing 5 to 7% carbon dioxide produced a significant increase in cerebral blood flow in normal subjects4 and a less constant augmentation in patients with cerebral arteriosclerosis,:’ observations which suggested its therapeutic use in cerebral vascular occlusive disorders. The question therefore arose as to whether inhalation of carbon dioxide affected slow wave activity appearing in the electroencephalogram following cerebral infarction. This problem was studied in a small group of patients by Waltz, von Weiss, and Stevens,s who concluded that the inhalation of 7% carbon dioxide “was accompanied by a statistically significant decrease in focal cerebral slow wave activity in 50% of +he caser qt-tidied.” The aim

Chronic hypoventilation in an epileptic patient.

SINCE THE EFFECTS of hyperventilation were first described by Rosettl and Foerster,2 it has been known that the epileptic patient is profoundly sensitive to changes i n respiration, especially to hyperpnea. A search of the Iiterature fails to reveaI any case report in which a chronic respiratory abnormality has been found in a patient subject to seizures. For this reason the present case is considered to be of interest.

Discussion of “The Electroencephalogram in Cerebrovascular Diseases”

U’E ARE GREATLY INDEBTED to Professor Gastaut and the school of Marseille for their endeavors over the past several years which have so expanded our knowledge of the electrophysiology of cerebral anoxia. I should like to examine Professor Gastaut’s paper today in respect to what he has left unsaid, as well as to what he has said, and to pose the question: “Can we now, by combining earlier observations with those just presented, evaluate the clinical role of electroencephalography in cerebrovascular diseases as a whole?” Professor Gastaut has not dealt in any detail with the electroencephalographic changes in structural alterations such as cerebral hemorrhage or infarction. It is pertinent to ask whether such an omission is justifiable-justifiable, that is, not because of the limited time available for these presentations but justifiable by its lack of clinical significance. For electroencephalography to be of value clinically in structural or functional cerebrovascular disease, it must fulfill 3 criteria: [I] the electroencephalogram must show alteration when functional or structural abnormality is demonstrated clinically; [ 21 the electroencephalogram must differentiate dysfunction secondary to vascular disease from dysfunction due to other causes such as tumor or epilepsy; [3] the electroencephalographic abnormality should not occur with any significant frequency in a patient free of clinical signs and symptoms of disease. Since the first systematic studies of the electroencephalogram in cerebrovascular disease published in 1948 by Strauss and Greenstein’ and Cohn and associates,z it has been known that cerebrovascular lesions, whether hemorrhagic, embolic, or thrombotic, may be associated with changes in the electroencepha-