Machine detection of spike-wave activity in the EEG and its accuracy compared with visual interpretation.

Machine detection of epileptiform activity in the EEG is useful in seizure monitoring because of its inherent consistency and the rapid data reduction it can provide. Devices based on a few detection criteria have lacked reliability of detection and those with more complex algorithms have sacrificed operating speed and portability. This paper describes a largely analog device which detects irregular as well as classic spike and wave activity. It is portable and it can process the accelerated playback of 24 h tape recorders as well as real-time EEG. It recognizes spikes by their shape and waves by their frequency. It makes inter-channel comparisons to identify trains of bilateral synchronous spikes, generalized waves, and coincidence of spikes and waves and furnishes a limited description of each event in terms of these characteristics. The device was tested against the judgment of 3 experienced and certified electroencephalographers in 18 h of EEG containing 769 bursts of spike-wave activity from 6 patients. It detected 96.5% of the consensus spike and wave activity (i.e., activity identified by all 3 electroencephalographers). Only 0.56% of the machine's detections were false positives (i.e., activity identified by none of the electroencephalographers), though the false positive rate was higher in the presence of chewing artifact. It measured burst duration with an average error of 0.43 sec/burst. While reader-machine agreement varied somewhat by patient, in general, the machine disagreed with the consensus no more than the readers disagreed with each other. In a second reading session after 6 months, the amount of activity identified by the readers changed by an amount ranging from 2.4% to 57% while the machine was consistent within a few tenths of 1%. Hence, this paper demonstrates that by implementing a multi-criteria detection algorithm in special purpose circuitry, a cost-effective solution to the problem of reliable machine detection of spike and wave activity can be obtained.

Status epilepticus. The role of intravenous phenytoin.

The treatment of status epilepticus can be improved by using recent developments in the pharmacokinetics and method of intravenous (IV) administration of phenytoin sodium. While diazepam, administered IV, remains the drug of choice for the short-term control of seizures associated with compromised respiratory exchange, phenytoin is effective in preventing recurrence of such seizures and in treating most other forms of status epilepticus. A loading dose of 18 mg/kg given by IV infusion in either 0.45% or 0.9% sodium chloride at a rate no greater than 50 mg/min results in therapeutic serum levels for up to 24 hours in most patients. Maintenance therapy with phenytoin should start at 4 to 7 mg/kg/day and be adjusted to both clinical response and serum levels.

Postural reflex gelastic seizures.

A 26-year-old man had gelastic seizures ("laughing attacks") preceded by an aura of sexual pleasure. They were reflexly induced by volitional hyperextension of his neck and trunk. His EEGs showed a right temporal spike focus. We discuss the characteristics of this unique case.

Cerebellar degeneration due to chronic phenytoin therapy.

Five patients developed cerebellar degeneration while being treated with phenytoin. All had high plasma levels of the drug, and none was having seizures of a type that could have caused systemic hypoxia at the time the cerebellar syndrome appeared. Cerebellar degeneration was confirmed by the finding of atrophy on CT scan and by persistence of cerebellar signs when plasma phenytoin levels were decreased. We suggest that chronic phenytoin therapy can cause cerebellar degeneration. The question of whether phenytoin or the cumulative effect of hypoxia from repeated convulsions causes cerebellar degeneration should not be posed as one of exclusive alternatives, since hypoxia is a well-known cause of cerebellar atrophy. Instead, the question should be whether or not phenytoin can also be responsible. The cases reported here suggest that it can.

The pregnant epileptic: a review and recommendations.

The major concerns in the pregnant epileptic patient are loss of seizure control and the teratogenic effects of antiepileptic drugs on the fetus. Loss of seizure control is usually caused by a progressive decline of antiepileptic plasma levels throughout pregnancy. This decline can be prevented by monthly dose adjustments based on plasma level determinations. Although infant malformations are a more prevalent outcome of the pregnancies of epileptics than of nonepileptics, the role of antiepileptic drugs in teratogenicity is not fully established. Only trimethadione has been convincingly linked to fetal malformation. Recommendations for the management of epilepsy in pregnancy are made.

A direct hepatotoxic effect of valproic acid.

Nine patients treated with valproic acid had low plasma fibrinogen concentration and other liver function abnormalities. Several patients also had a low platelet count and prolonged bleeding time. The abnormal values returned promptly to normal when the drug therapy was discontinued or the dosage reduced. The liver function abnormalities are consistent with a direct, dose-related hepatotoxicity.

Computed tomography in cerebellar atrophic processes.

Forty-six patients with cerebellar atrophy were identified by review of CT scans of 7,500 patients. Independent examination of a separate file of the same group disclosed 49 patients whose history indicated cerebellar degeneration. Forty-three patients were in both groups indicating excellent correlation between CT abnormality and clinical cerebellar signs. Three patients with CT cerebellar atrophy failed to show clinical cerebellar signs, and 6 had clinical signs without evidence of changes on CT. Specific anatomic correlation was suggested in 10 of 13 patients with predominantly midline cerebellar CT abnormalities, and in 3 with olivopontocerebellar degeneration clinically who showed brainstem and cerebellar atrophy.

Neurotoxicity in uremia.

The dialysis patient is aware that his behavior evokes reciprocal and complicating responses from important people in his environment. These interactions are perceived and conducted by neurochemical mechanisms which may be impaired in the abnormal chemical environment imposed in renal failure. It is the behaviors we comprehend as indicators of disordered nervous mechanisms. Therefore, it is logical that neurophysiological and neurobehavioral phenomena should be measured quantitatively in order 1) to estimate objectively the patients' success in achieving the goal of maintenance dialysis treatment, 2) to assess the comparative adequacy of dialysis regimens and 3) to provide objective endpoint measures which are relevant to uremia for further investigations of the etiology and pathogenesis of these critically significant uremic manifestations. Our experimental results illustrate that: 1) measures of conduction velocity, distal latency and response amplitudes, as employed by us, were relatively insensitive in the patients and circumstances studied; 2) several neurophysiological measures, i.e., the spontaneous EEG, VER latency and, perhaps, photic stimulation, on the other hand, are highly correlated with the severity of renal failure; 3) behavioral measures of sustained attention and alertness (TMT), of short-term memory (ASTM) and of cognitive manipulation of symbols (AR) are also highly correlated with the severity of renal failure; 4) some measured abnormalities improve following dialysis, but not always to normal--three residual impairments may indicate dialysis in adequacy; 5) several of these measures can provide objective evidence for adequacy of dialysis and other clinical and treatment effects in patients with renal failure.