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Biomedical subjects
Publications and source records attributed to H H Morris.
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The effects of sleep on median nerve short latency somatosensory evoked potentials were studied in 7 subjects made up of 6 patients being evaluated for seizure disorders by all-night electroencephalograms and 1 normal healthy volunteer. The median nerve was stimulated at the wrist, and the peripheral (N9), subcortical (P13) and early cortical (N1, P2) evoked potentials were recorded during full wakefulness and natural night-time sleep. Sleep-wake state was monitored by the simultaneously obtained polysomnogram. The latencies of the cortical responses were prolonged during non-rapid eye movement (NREM) sleep. In 3 of the subjects P2 was consistently bifid during NREM sleep only. The second component of the bifid potential, 3-4 msec longer in latency than the first, appeared to be selectively enhanced during NREM sleep whereas the first component tended to become less prominent or even disappear. This suggests that the 2 peaks have different generators that are affected differently by NREM sleep. These are clinically relevant findings for interpretation of routine clinical studies.
Thromboembolic vascular disease is a frequent precipitant of seizures, and is the most common etiology in older patients. The occurrence of seizures shortly after a stroke, however, does not necessarily indicate that the patient will continue to have seizures following initial recovery. This is true even when patients present in epileptic status. This may be because early and late seizures are produced by different pathophysiologic mechanisms.
We report transient changes in computed tomography (CT) and magnetic resonance imaging (MRI) scans in a patient with focal status epilepticus, referred to us with a tentative diagnosis of neoplasm based on CT and angiographic findings. EEG seizures originated independently from each temporal-occipital area, predominantly from the right. Previous EEGs had shown almost exclusively right temporo-occipital epileptogenic activity. MRI showed increased signal intensity, and CT showed decreased right hemisphere attenuation without enhancement. One month later, there was resolution of the radiological and clinical abnormalities. The transient CT and MRI changes probably represented focal cerebral edema, developing during focal status epilepticus. Lack of change in the left hemisphere probably reflected the quantitative difference in epileptic activity. Clues to the diagnosis of focal edema due to status include: (1) changes on electrical and imaging studies that correlate anatomically with the clinical status, and (2) resolution of abnormalities with appropriate seizure control. In patients with suspected seizure disorders, electrical and clinical data should be correlated before interpretation is made of focal lesions seen by neuroimaging techniques.
In evaluation of patients with complex partial seizures who are candidates for surgical treatment, exact definition of the epileptogenic focus is essential for a good surgical outcome. We report a new technique which permits detailed mapping of the epileptogenic activity in the basal temporal lobe and the convexity of the temporal lobe. The technique consists of placement of at least 16 basal temporal electrodes and an additional 64 electrodes covering the temporal convexity. This extensive coverage permits accurate definition of the limits of the epileptogenic focus and also of adjacent functional areas and therefore allows more significant determination than have previous techniques of the ideal extent of the surgical resection. This accuracy cannot be achieved with depth electrodes or the limited coverage provided by previously reported epidural or subdural electrode techniques.
In our patient population that had undergone antero-temporal lobectomy, we found 20 patients with a unilateral sphenoidal/antero-temporal interictal focus. All patients had normal computed tomography (CT) scans. Invasive recordings with subdural electrode arrays placed over and under the temporal lobe were used in every patient. We found that the scalp interictal focus predicted for all patients that both the interictal sharp waves and ictal onset would be mesiobasal/anterotemporal in location on the subdural arrays. Seventy-five percent of these patients had an excellent outcome with temporal lobectomy.
We retrospectively analyzed the presence of sharp waves in 2-h EEGs performed 6 months after epilepsy surgery in 59 patients. To study the significance of the postoperative interictal epileptiform activity in the tissue remaining after resection, we included only patients with a single epileptic focus (as defined preoperatively by prolonged video/EEG recordings and subdural electrode arrays studies) and no progressive structural lesions. Temporal lobectomy was performed in 51 patients (86%); extratemporal resections were performed in the remainder. The epileptogenic focus was completely resected in 26 patients (44%). The immediate postoperative electrocorticograms (EcoG) showed spikes in 13 patients (22%). At 6-month follow-up, 43 patients (73%) were seizure-free or had auras only and 12 patients (20%) had epileptiform activity on EEG. A significant correlation was noted between presence of sharp waves in the 6-month postoperative EEG and recurrence of seizures (Fisher's exact test p = 0.011) and also with the extent of the resection (complete vs. incomplete p = 0.042). We noted no correlation between postoperative epileptiform activity and location of the resection (temporal vs. extratemporal), presence of spikes in immediate postoperative EcoG, or occurrence of auras only at 6-month follow-up.
The relationship between interictal focal hypometabolism determined by 18-fluorodeoxyglucose positron emission tomography (FDG-PET) scans and memory function with the intracarotid amobarbital procedure (IAP) was evaluated in 23 patients with temporal lobe epilepsy. All patients underwent prolonged EEG/video monitoring. The epileptogenic focus was defined by interictal epileptiform discharges and ictal onsets. All 23 patients had recorded seizures arising exclusively from one temporal lobe. PET showed temporal lobe hypometabolism ipsilateral to the epileptogenic focus in 86% (20 of 23) of patients; IAP showed impaired memory of the hemisphere of seizure onset in 65% (15 of 23). Sixty-five percent (13 of 20) of patients with focal hypometabolism had ipsilateral memory impairment. Memory impairment contralateral to the hypometabolic zone was not observed. Ninety-five percent (22 of 23) of patients demonstrated functional impairment by either PET or IAP (or both) on the epileptogenic side.
Tumors and cortical dysplasia are associated with epilepsy, but few studies have examined the coexistence of neoplasia and dysplasia in these patients. We studied 13 patients (age 4-29 years) with recurrent seizures of 1 month to 21-year' duration (median 72 months). Ten patients were aged < 21 years. Imaging studies localized the lesion to the temporal lobe (10 patients), parietal lobe (2 patients), and frontal lobe (1 patient). Tumors included ganglioglioma (8 patients), dysembryoplastic neuroepithelial tumor (DNT) (3 patients), and low-grade astrocytoma (2 patients). Cortical dysplasia, including atypical aggregates of neurons (6 patients), multifocal loss of the cortical laminar architecture (7 patients), and neurons in the molecular layer of the cortex (3 patients) were observed near but separate from the tumor. Coexistence of certain tumors with cortical dysplasia, most frequently observed in the pediatric population, suggests a hamartomatous/dysplastic nature of the neoplasms.
The value of EEG interictal epileptiform activity in predicting location of the seizure focus remains controversial. In 64 patients, scalp video-EEG monitoring studies showed one or two ipsilateral interictal foci in the temporal lobe. The site of these interictal foci correlated with location of the seizure focus recorded during prolonged video-electrocorticography (ECoG) with use of subdural grids placed under the mesiobasal temporal region and over the lateral temporal convexity. Our findings suggest that unilateral anterotemporal interictal foci can accurately predict location of seizure onset. This is also true in patients with two ipsilateral temporal interictal foci, provided that the dominant focus is localized in anterotemporal regions. We believe that in such patients invasive recordings are not warranted, but we caution against sole use of interictal epileptiform criteria for localization of the seizure focus. Correlation with clinical information, ictal EEG, neuropsychometric, and neuroimaging studies is required before performance of epilepsy surgery.
We identified 39 patients with chronic epilepsy (seizures > or = 2 years) proven to have primary brain tumors. These cases represent approximately 12% of the surgery cases for epilepsy in the same period. Mean age of seizure onset was 13.2 years: mean duration before operation was 10.5 years. Thirty-eight of 39 had normal neurologic examination. Twenty-six tumors were temporal, 7 were frontal, 4 were parietal, and 2 were occipital. Nine of 26 (34.6%) of the temporal group had contralateral interictal EEG spikes. Pathology was 15 ganglioglioma, 13 low-grade astroctoma, 4 oligodendroglioma, 2 low-grade mixed glioma, 1 pleomorphic xanthoastrocytoma, 2 dysembryoplastic neuroepithelial tumor, and 1 ependymoma. Postoperative seizure frequency (minimum follow-up 6 months) ranged from 15 to 16 seizure-free auras only in patients with temporal tumors and total gross tumor removal (mean follow-up 28 months) to 0 of 6 seizure-free in patients with extratemporal tumors who underwent subtotal resection or biopsy.
We made quantitative analysis of seizure frequency 1 week and 6, 12, and 24 months after seizure surgery. Seizure recurrence was significantly higher when seizures occurred in the first postoperative week. Seizure recurrence increased progressively with longer follow-ups, but the 6 month postoperative follow-up period was an excellent index of long-term outcome. In operative follow-up studies, seizure frequency should be reported at fixed follow-up periods, e.g., at 6 months and 1, 2, 5, and 10 years. Meaningful comparison of outcomes between different studies is possible only when reports include outcome at fixed postoperative follow-up periods (as opposed to ranges of follow-up periods).
In evaluation for surgical treatment of intractable psychomotor seizures originating in the language-dominant left mesiotemporal region, subdural grid electrodes were placed in 29 patients over the temporoparietal cortex and over the basotemporal region. In 13 patients, cortical stimulation of the basotemporal region showed interference with language processing. The most anterior border of the basotemporal language area began 1.1 cm posterior to the anterotemporal tip, and the most posterior margin of the language region was located 6.1 cm posterior to the temporal tip. The most lateral and the most mesial border were located 1.4 and 5.9 cm, respectively, from the lateral edge of the temporal lobe. The region in which language disturbance could be elicited included the inferior temporal gyrus, the fusiform (lateral and medial occipitotemporal) gyrus, and the parahippocampal gyrus. The basotemporal area most consistently involved with language function was the fusiform gyrus (60% of affected electrodes), followed by the inferotemporal (30%), and the parahippocampal (10%) gyri.
OBJECTIVE: To report a case of carbamazepine toxicity resulting from a drug interaction with fluconazole, and to review the possible mechanisms of this interaction. DATA SOURCES: Medical record review. DATA SYNTHESIS: A 33-year-old white man with a history of mental retardation and seizures experienced stupor due to carbamazepine toxicity after fluconazole was initiated. The patient had been taking carbamazepine for several years and maintained stable therapeutic concentrations. He started fluconazole therapy after developing a rash presumably due to candidiasis. After admission to the hospital for carbamazepine toxicity, both fluconazole and carbamazepine were withheld and the patient returned to his normal baseline mental status once the carbamazepine concentration declined to a therapeutic range. Carbamazepine was restarted and the patient experienced no further adverse events. Carbamazepine is metabolized by the cytochrome P450 3A4 isoenzyme. Fluconazole is renally excreted but has been noted to inhibit CYP3A4. Fluconazole has also been noted to increase phenytoin concentrations. CONCLUSIONS: Fluconazole may cause carbamazepine toxicity presumably by inhibiting the cytochrome P450 3A4 isoenzyme.
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Explore the source record for details and available documents.