Nonepileptic Subjects Research Articles

Electroencephalographic changes in man during use and withdrawal of barbiturates in moderate dosage

1. 1. In contrast to doses of over 0.6 g. per day, the withdrawal of 0.4 g. daily of seconbarbital or pentobarbital after three months was not followed by psychotic or convulsive manifestations in any of 18 nonepileptic subjects. 2. 2. Seven of 13 individuals demonstrated some evidence of EEG tolerance to 0.4 g. daily of secobarbital or pentobarbital during 90 days. 3. 3. During withdrawal from this same barbiturate regimen, 5 of 18 subjects developed paroxysmal EEG discharges which later disappeared and were not associated with observable clinical abnormalities.

Experimentally induced epilepsy in the cat with injury of cornu Ammonis.

Seizures originating in the temporal lobe have been associated with the pathological findings of scars in the cornu ammonis (hippocampus) since 1825, when, according to Gastaut, 1 Bouchet and Cazauvielh 2 first noticed macroscopically detectable lesions in this area. It has been argued in the past ( a ) that such lesions may be secondary to the epileptiform attacks, ( b ) that the hippocampus is not concerned with motor activities and, consequently, is not likely to be concerned in motor fits, and ( c ) that similar lesions may be found in nonepileptic subjects. Nevertheless, seizure discharges were evoked upon stimulation of the hippocampus by Kaada, 3 Green and Morin, 4 and Morin and Green 5 ; and motor fits have been seen by Kaada, Jansen, and Andersen, 6 Green and Shimamoto, 7 and others. Such discharges, spreading to the rest of the brain apparently via the temporal lobe more readily than via the fornix, 7,8

Effects of chlorpromazine on the electroencephalogram with report of a case of chlorpromazine intoxication

All these observations including our own show that the clinical and electroencephalographic effects of chlorpromazine are extremely complex. Chlorpromazine has: (1) an effect similar to that seen in many sedative drugs; (2) effects similar to that of Metrazol which has been shown to provoke localized spikes in patients with focal seizures (Kaufman et al. 1947) and diffuse spike and wave patterns in nonepileptic subjects (Strauss et al. 1952). The fact that the provocation of focal spikes by chlorpromazine is not associated with clinical or electroencephalographic signs of sleep makes its activating effect very similar to that of Metrazol. According to the literature, it seems to be even more promising in the provocation of focal spikes. We cannot make any statement as to the amount of chlorpromazine necessary to produce diffuse spike and wave patterns either in normals or epileptics, but can state that such patterns can be produced in normals. The question of the quantity is open for further investigation. So also is the question of the point of attack of chlorpromazine on the central nervous system, on which several assumptions have been made, none of which, however, explains all the observed facts.

The EEG effect of metrazol and photic stimulation in 682 normal subjects

1. 1. Six hundred and eighty-two normal air force applicants, ages 17–24, were examined electroencephalographically at rest and during provocation with hyperventilation, photic stimulation and Metrazol. Electroencephalograms were classified as normal (84.9 per cent); borderline (5.1 per cent); slightly abnormal, non-paroxysmal (3.8 per cent); markedly abnormal, non-paroxysmal (2.6 per cent); questionably paroxysmal (0.9 per cent); and paroxysmal (2.6 per cent). 2. 2. Clinical information included personal history of head injury (11), birth injury (2), fainting (2), and meningitis (1); family history of convulsions (10), and questionable (12) or definite neurological (36) findings. Seventy-seven subjects had one or a combination of these findings suggesting neurological involvement. 3. 3. The incidence of Metrazol-induced paroxysms was correlated both with the appearance of the EEG at rest, and with the neurological status as indicated by the personal and family history and neurological findings. 4. 4. Metrazol-induced paroxysms occurred in 15 per cent of subjects with a normal EEG; 32 per cent of those with a borderline; 40 per cent of those with a slightly, non-paroxysmally abnormal; 47 per cent of those with a questionably paroxysmal; 50 per cent of those with a paroxysmal pre-Metrazol EEG; and in 27 per cent of those with a markedly but non-paroxysmally abnormal EEG. 5. 5. The “neurologically involved” subjects had eight times the incidence of paroxysmal abnormalities and about two times the incidence of other abnormalities as in the non-involved group. Fifty-three per cent of the “neurologically involved” subjects developed Metrazol-induced paroxysms as compared with 15 per cent of subjects with no such evidence. Neurologically involved subjects with a normal pre-Metrazol EEG had a high incidence (51 per cent) of Metrazol-induced paroxysms. 6. 6. Of the 682 applicants, 30 per cent were rejected, and of these, 16.3 per cent had paroxysmal or markedly abnormal EEGs at rest and with hyperventilation and photic stimulation, and 30.2 per cent Metrazol-induced paroxysms. Twenty-five per cent were dismissed after admission, and of these, 9.6 per cent had paroxysmal or markedly abnormal EEGs, and 16.9 per cent Metrazol-induced paroxysms. Of the 46 per cent who completed training successfully, 8.7 per cent had paroxysmal or markedly abnormal, and 14.2 per cent Metrazol-induced paroxysms. 7. 7. Compared with 682 normals, with an 82.3 per cent incidence of normal EEGs and a 2.9 per cent incidence of paroxysmal EEGs, 100 patients with grand mal epilepsy had a 37 per cent incidence of normal or borderline EEGs and a 36 per cent of paroxysmal abnormalities. Of subjects in both groups with a normal EEG, 15 per cent of normals and 80 per cent of grand mal epileptics developed paroxysms with Metrazol. Corresponding figures for the effect of photic stimulation, indicate that 1.4 per cent of normals and 15 per cent of epileptics develop paroxysmal abnormalities with photic stimulation. An estimate is given for the diagnostic efficacy of Metrazol and photic stimulation in cases of grand mal epilepsy with a normal EEG. 8. 8. Metrazol provocation in this normal group thus confirms the diagnostic value of this method in epilepsy, and also confirms the validity of the usual interpretation of EEG abnormalities in non-epileptic subjects as probably representing acquired or inherent lowered convulsive threshold; and it suggests similarly the presence of such factors in individuals with a normal EEG who develop Metrazol-induced convulsions.

Activation of EEG disturbances with metrazol (pentazol) in epileptics, normals and patients with syncopal attacks

A short survey is given of the methods available at present to provoke EEG changes in cases of epilepsy or suspected epilepsy with a normal resting EEG. It is shown that while only one of 63 (1,6 per cent) non-epileptic subjects exhibits characteristic EEG disturbances (“cerebral paroxysm”) after 350 mg. Pentazol (Metrazol) administered by intravenous injection, these EEG changes are seen after≦ 350 mg. Pentazol in 79 of 96 (82 per cent) patients suffering from epilepsy and in 51 of 75 (68 per cent) patients suffering from syncopal spells (excluding 17 cases with syncope attributable to vascular or other demonstrable etiological factors). The idiopathic cases of both groups were more likely to show cerebral paroxysms (after a smaller mean dose) than the symptomatic ones.

ELECTROENCEPHALOGRAPHIC CLASSIFICATION OF EPILEPTIC PATIENTS AND CONTROL SUBJECTS

The clinical application of electroencephalography is complicated by the wide range of individual patterns encountered in the most carefully selected control groups and by the fact that almost all patterns which might be used for diagnosis can be found in the electroencephalograms of symptom-free persons. 1 Nevertheless, a relation has been shown between abnormalities in the electroencephalogram and clinical epilepsy, and specific relationships have been reported between different types of clinical seizures and the electroencephalographic patterns that accompany them. It seemed likely that if the routine electroencephalograms of a large group of epileptic patients were compared with those of a large group of nonepileptic subjects, certain wave forms and frequencies would be encountered so rarely among the nonepileptic subjects and so commonly among epileptic subjects that they could be given diagnostic significance. It was also considered possible that differences might appear between the routine electroencephalograms of patients with contrasting types

The pH and the CO2 Content of Cerebrospinal Fluid in Epilepsy.

Although considerable work has been done on the acid-base relationships in epilepsy, the evidence presented thus far has been conflicting and indecisive. Because of the importance of this phase of the problem, we have determined the pH and CO2 content of the cerebrospinal fluid in 125 epileptics and 30 non-epileptic control subjects by procedures which eliminate errors due to loss of CO2.1, 2The colorimetric method of McQuarrie and Shohl1 used for determining the pH may be briefly described as follows: The clear fluid is drawn into a special glass sampling burette over clean mercury after all air in the connecting tubes has been eliminated by means of a 3-way stop-cock. In preparation for taking the sample a number of tenths of a cc. of 0.0075% phenol red equal to the number of cc. of fluid to be taken is measured into the apparatus. After the spinal fluid is mixed with the dye in this concentration, it is read directly at 38°C. against the bicolor standards of Hastings and Sendroy in a simple comparator ...