Language function following subdural grid-directed temporal lobectomy.

The purpose of the study was to determine the extent to which a temporal resection may be undertaken without producing risk to temporal language areas. Patients undergoing craniotomy and placement of a subdural electrode array (SEA) for evaluation of intractable epilepsy were studied to determine the variability of distance of temporal language cortex from the temporal pole. Hemisphere dominance was determined by intracarotid sodium amytal injection. Temporal lobe speech arrest (SA) was mapped with a 64 contact point SEA. Thirty-one patients had left dominant hemisphere SEAs. Thirty had SA 5 cm to 9 cm from the temporal pole (median 7 cm). One had SA at 3 cm. Twenty-one patients subsequently had temporal lobectomy (TL). Mean extent of resection was 5.7 cm (range 3 to 9 cm). In 18 TL patients who had neuropsychometric evaluation of language function pre- and post-surgery, there was no significant deterioration. Thirty-nine patients had right non-dominant SEAs placed. Eighteen had TL. Thirteen of these had pre- and post-surgery language evaluation and there was no significant change. Comparison of preoperative scores showed significant superiority of the right non-dominant group over the left dominant group for naming. TL up to 5 cm without stimulation mapping of language areas would be safe in the majority of cases, but one subject (3%) had SA mapped anterior to this and a small number of cases may therefore be at risk to language function following a 5 cm TL. Extensive lateral resections up to 9 cm are possible with preservation of language function with stimulation cortical mapping.

Outcome of resective surgery for intractable partial epilepsy guided by subdural electrode arrays.

The aim of this paper was to evaluate the outcome and the factors predictive for a good prognosis of resective surgery for intractable partial epilepsy guided by subdural electrode arrays (SEA's) and operative electrocorticography. Sixty-four patients, aged 8-52 years, were evaluated with chronic SEAs in order to record interictal and ictal activity and delineate speech and motor areas by functionally mapping. Resection were individualized to each patient's SEA recorded electrocorticogram and operative electrocorticogram and functional mapping results (tailored resection). The follow-up time was a minimum of one year. Good seizure outcome was defined as seizure free from complex partial and secondary generalized seizures. After one year 70% of the patients with a temporal ictal focus was seizure free compared to 55% of the patients with an extra-temporal focus. Complete resection of interictal or ictal fields as mapped with SEAs, gave better prognosis than partial resection. Patients with no postresection spikes had a better prognosis than patients with residual postresection spikes evaluated with operative electrocorticography. Sex, age, duration of epilepsy prior to surgery, extent of temporal lobe resection and structural abnormalities determined by MRI were not associated with a favorable seizure outcome after surgery. We conclude that complete resection of the interictal and ictal field mapped with SEA's and absence of postresection spikes on operative electrocorticography are associated with an excellent seizure outcome.

Longitudinal neurophysiologic studies in a patient with metachromatic leukodystrophy following bone marrow transplantation.

We describe a girl with late infantile metachromatic leukodystrophy. The patient has been followed up with serial neurologic and neurophysiologic examinations for 8 years following bone marrow transplantation, which she underwent when she was 4 3/4 years old. Her older sister died from metachromatic leukodystrophy at the age of 8 years, whereas our patient has retained significant cognitive and motor skills. Serial neurophysiologic studies initially demonstrated continued deterioration after the bone marrow transplantation, but since then, most results have remained stable or improved. Although, to our knowledge, there have been no previous serial studies of metachromatic leukodystrophy, individual case studies suggest that these findings in our patient are very unusual. With the advent of possible treatment for this condition, there is a need for further serial neurophysiologic studies to characterize the natural progression and the possible detection of progression or reversal with treatment.

EEG and seizures in children with hemolytic-uremic syndrome.

The EEG results of 11 children, ages 1-15 years, who presented with hemolytic-uremic syndrome complicated by seizures 3-10 days after the prodrome were studied. In four children who experienced generalized tonic-clonic seizures, the EEGs demonstrated diffuse delta slowing with no focality. All recovered without neurological deficit or a residual seizure disorder. Of seven children who experienced partial seizures, six had structural lesions on cranial computed tomography and residual focal neurological deficits with epilepsy. The EEGs in two patients revealed focal spikes and slowing consistent with the lateralization of the partial seizures, in four it was characterized by atypical "burst suppression," and in one showed epochs of high-amplitude delta slowing alternating with generalized suppression. Although episodic and generalized burst suppression is usually regarded as a grave prognostic indicator, all four subjects recovered.

Lack of pathologic changes in human temporal lobes after transcranial magnetic stimulation.

Most animal studies have failed to demonstrate pathologic changes in the brain after transcranial magnetic stimulation (TMS). Nevertheless, vacuolar lesions in the cortex of rats after TMS have been reported. We report the first histopathologic studies of human brains after TMS in 2 patients with epilepsy who underwent temporal lobectomies. They had been involved in a study to determine the speech-dominant hemisphere by TMS and had received approximately 2,000 stimuli centered over the resected temporal lobe. Histologic study of the surgical specimens did not show any lesions attributable to TMS in these 2 patients.

Chronic, habitual cocaine abuse and kindling-induced epilepsy: a case report.

Kindling has been suggested as a possible mechanism for cocaine-induced seizures in chronic cocaine abusers, even though no convincing examples have been reported. We report a 37-year-old woman who initially experienced generalized tonic-clonic seizures (GTC) only immediately after "crack" use. She had a normal examination, negative family or past history for seizures, and normal cranial computed tomography and EEG. After she had abused cocaine almost daily for 2 years, her EEG demonstrated bitemporal slowing with independent spikes, and seizures were no longer temporally associated with acute cocaine use. Thereafter, despite complete abstinence from cocaine and treatment with phenytoin, she continued to experience four to six GTC a month. In light of the lack of other predisposing factors for epilepsy, this case may represent an example of cocaine-induced kindling in humans.

Cocaine-related vascular headaches.

The records of 21 patients admitted to hospital from January 1985 to December 1988 for acute headache associated with cocaine intoxication were reviewed. Fifteen patients were identified who experienced headaches with migrainous features in the absence of neurological or systemic complications. None of them had a history of cocaine-unrelated headaches or a family history of migraine, and all had a favourable outcome. Three possible mechanisms of cocaine-related vascular headaches are discussed which depend on the interval between cocaine ingestion and development of the headache. We postulate that acute headaches following cocaine use may relate to the sympathomimetic or vasoconstrictive effects of cocaine, while headaches following cocaine withdrawal or exacerbated during a cocaine "binge" may relate to cocaine-induced alteration of the serotoninergic system.

Transcranial magnetic stimulation in patients with epilepsy.

We studied the effects of transcranial magnetic stimulation (TMS) applied in trains of 8- to 25-Hz stimuli on electroencephalographic epileptiform activity on eight patients being evaluated for epilepsy surgery. We performed the stimulation with a round water-cooled stimulation coil held flat on the scalp and centered over different positions of the International 10-20 System. We were unable to trigger seizures or induce epileptiform discharges arising from the epileptic focus in any of the eight patients with any of the stimulation protocols. However, we induced a partial motor seizure from the contralateral hemisphere to the exclusive temporal focus in the only patient stimulated with 100% maximal intensity. Precautions have to be taken when applying rapid TMS to patients because of the risk of seizure induction. Our results do not support the view that TMS specifically activates the epileptic foci.

Induction of speech arrest and counting errors with rapid-rate transcranial magnetic stimulation.

Six adult epileptic patients underwent rapid-rate transcranial magnetic stimulation (rTMS) at stimulation rates of up to 25 Hz with an 11-cm water-cooled round coil held flat on the scalp, centered over 15 different positions on each side of the scalp. The trains of stimuli were for 10 seconds while the patients counted aloud. rTMS centered over D5 or D7 induced reproducible speech arrest in all patients and counting errors in three when applied at lower intensities. There were no such speech disturbances by rTMS centered over the different positions on the right side. Intracarotid amobarbital test (IAT) demonstrated left hemispheric language dominance in all patients. Lateralization of speech arrest induced by rTMS correlated with the IAT results and may be helpful for noninvasive determination of hemispheric language dominance.

Exacerbation of partial seizures and onset of nonepileptic myoclonus with carbamazepine.

A child had two to three generalized tonic-clonic (GTC) seizures per week unresponsive to phenobarbital (PB) and valproate (VPA). Interictal EEG demonstrated left occipital spikes. When carbamazepine (CBZ) therapy was started, he developed very frequent (4-6/day) complex partial seizures (CPS) characterized on ictal EEG by focal right temporal lobe discharges. The seizure exacerbation, which was associated with development of nonepileptic, multifocal myoclonus, resolved 24 h after CBZ was discontinued. The exacerbation occurred with therapeutic CBZ serum levels, but may have been related to the toxic levels of carbamazepine-10, 11-epoxide (CBZE).

Cerebral atrophy in habitual cocaine abusers: a planimetric CT study.

We compared cranial CTs of 35 habitual cocaine abusers, 16 self-reported 1st-time users, and 54 headache patients using linear planimetric measures. All patients met the following criteria: age 20 to 40 years, no polydrug abuse (including alcohol), HIV seronegativity, normal albumin level, and no history of any other neurologic disease. The sex ratios and ages were not significantly different in the 3 groups. The planimetric measurements and calculated indices of cerebral atrophy were significantly different in the habitual cocaine abusers compared with the 2 other groups of patients. There were no differences between 1st-time cocaine users and controls. Among the habitual cocaine abusers there was a positive correlation between the approximate duration of cocaine abuse and the calculated atrophy indices. The findings suggest that cerebral atrophy develops in chronic cocaine abusers, and the severity correlates with the duration of abuse.

Longterm neurological complications of chronic, habitual cocaine abuse.

We review and expand the results of several previously published studies on computed tomographic and electroencephalographic correlates of chronic, habitual cocaine abuse in order to present a complete spectrum of the longterm neurological complications of cocaine abuse. We argue that prolonged and frequent cocaine abuse leads to biochemical and vascular cerebral insults that eventually may cause functional and structural abnormalities affecting predominantly the fronto-temporal areas.

Epileptogenic properties of cocaine in humans.

Ninety-eight of 945 patients admitted to Hennepin County Medical Center with acute medical complications of cocaine intoxication presented with seizures within 90 min of cocaine ingestion. Cocaine-related seizures were most frequently single, generalized convulsions, and these individuals all had normal cranial CT and EEG. Of the 945 patients, 18.4% of the women presented with seizures, compared with only 6.2% of the men. All subjects who presented with new onset focal seizures following cocaine ingestion had acute cocaine-related cerebral strokes or hemorrhages. Individuals with a history of cocaine-unrelated seizures, had their typical convulsions precipitated with "recreational" doses of cocaine. All four subjects with status epilepticus had ingested massive doses of cocaine, were resistant to medical treatment, and had significant morbidity and mortality. We were able to characterize four subgroups of subjects at risk for cocaine-related convulsions. First, individuals who had ingested massive doses of cocaine (2-8 gms) in whom cocaine induced seizures by its direct, dose-related convulsant effects. Second, individuals with a history of epilepsy had their typical seizures precipitated by lowering the seizure threshold. Third, females are at greater risk for cocaine-related compared to males. Fourth, years of chronic, habitual cocaine abuse may result in "chemical" kindling of epilepsy.

EEG correlation of improvement in hemolytic-uremic syndrome after plasma infusion.

We report a previously undescribed electroencephalographic pattern of epochs of diffuse delta background (85-240 sec) alternating with epochs of classic "burst suppression" (90-270 sec) in a 13-month-old girl with hemolytic-uremic syndrome. A dramatic electroencephalographic improvement was evident on continuous monitoring of cerebral function 3 hours after initiating fresh frozen plasma infusion, well before any clinical improvement was apparent. This patient, in addition to the unusual electroencephalographic findings, illustrates the role of continuous electrophysiologic monitoring of cerebral function and supports the use of fresh frozen plasma in hemolytic-uremic syndrome.

Cocaine-associated multifocal tics.

Of 4 patients with cocaine-induced multifocal tics, 2 had Tourette's syndrome and had a severe exacerbation of their symptoms. One of these 2 patients experienced the exacerbation following her 1st exposure to the drug; the 2nd, a habitual cocaine snorter, after smoking "crack" for the 1st time. The other 2 patients were habitual cocaine abusers who, following a binge with high doses of cocaine, experienced new-onset tics.

Cocaine-induced seizures.

We retrospectively studied 474 patients seen at Hennepin County Medical Center because of medical complications related to acute cocaine intoxication. Of the 474, 403 had no history of seizures. Seizures within 90 minutes of cocaine use was the primary diagnosis in 32 (7.9%) of the 403. The majority of seizures were single, generalized, induced by intravenous or "crack" cocaine, and not associated with any lasting neurologic deficits. Most that were focal, multiple, or induced by nasal cocaine were associated with an acute intracerebral complication or concurrent use of other drugs. Of 71 patients with a history of non-cocaine-related seizures, 12 (16.9%) presented with cocaine-induced seizures; most of these were multiple, of the same type as those in their history, and induced by even nasal cocaine. In the 44 cocaine-induced seizure patients, a pattern of habitual cocaine abuse was associated with diffuse brain atrophy on CT and diffuse slowing on EEG.