Evidence for epilepsy is rare in patients with psychogenic seizures.
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Biomedical subjects
Publications and source records attributed to D S Dinner.
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A patient had episodes of bilateral paresthesias with retained consciousness. The attacks were clinically considered to be psychogenic seizures. Electroencephalography indicated that the attacks were epileptic, perhaps originating from the second sensory area. Electroencephalographic recording of a seizure is essential in differentiating epileptic from psychogenic episodes.
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Somatosensory evoked potentials were recorded from chronically implanted subdural electrodes in six patients with intractable seizures. The following conclusions were reached: 1) The initial cortical negativity-positivity (N1 with a latency of about 20 msec and P2 with a latency of about 24 msec) recorded in the postcentral area was an expression of the classical primary surface positivity, but N1 was generated by the posterior pole of an early horizontal dipole in area 3b, and P2 was generated by the positive pole of a slightly delayed vertical dipole in area 1 and 2.2) P2 permitted the most accurate localization of the primary somatosensory area. 3) No potentials were elicited in the primary somatosensory area by stimulation of the ipsilateral hand. 4) No cortical potentials were seen at stimulation intensities below the sensory threshold. The cortical distribution of evoked potentials evoked by weak and strong intensities had significantly different distribution. 5) The recovery function of cortical evoked potentials showed a U-curve with an early period of facilitation (10 to 30 msec) followed by a prolonged period of subnormality which peaked at about 50 msec. The recovery curve at different cortical loci differed.
We present a patient with epilepsia partialis continua involving the right leg who demonstrated sharp waves paradoxically distributed over the vertex and right hemisphere. Posterior tibial nerve evoked potentials also showed a similar paradoxical lateralization. We postulate that generators situated on the mesial surface of the left hemisphere projected their activity obliquely, leading to paradoxical lateralization of the recorded electrical activity.
Complex partial status epilepticus with aphasia as the sole manifestation has been reported only twice before. We studied a 60-year-old diabetic who was aphasic for 12 days. The diagnosis of aphasic status was supported by electroencephalographic seizure patterns in the left hemisphere.
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BACKGROUND: There is a controversy regarding the association of obstructive sleep apnea (OSA) and morning headaches. This study investigates whether this relationship exists. METHODS: This is a retrospective study of 80 consecutive patients with OSA who underwent sleep polysomnography from December 1996 to March 1997. Patients were interviewed about their headache history. Headaches were classified according to International Headache Society criteria and the severity graded by the Chronic Pain Index. Headache characteristics were compared with those of 22 control patients with periodic limb movement disorder. Headache response to continuous positive airway pressure or uvulopalatopharyngoplasty in the patients with OSA was also assessed. RESULTS: Forty-eight (60%) patients had headaches in the year prior to study. Twenty-five of the 48 patients had headaches that did not fit any category. Of these 25 patients, 23 (48% of total group) reported awakening headaches. These awakening headaches were significantly more common in the OSA group compared with the periodic limb movement disorder group, 9 (41%) of whom had headaches, none of which occurred on awakening. The proportion of common types of headaches in both groups was similar. The awakening headaches were brief (shorter than 30 minutes), and their occurrence and severity correlated with OSA severity. Of the 29 patients with OSA who were treated with continuous positive airway pressure or uvulopalatopharyngoplasty, awakening headaches improved by a mean of 80% compared with minimal improvement of migraine, tension, and cervicogenic headaches. CONCLUSIONS: Awakening headaches are associated with OSA. These headaches are of brief duration, and their occurrence and severity increase with increasing OSA severity. Treatment of OSA with continuous positive airway pressure or uvulopalatopharyngoplasty can reduce these headaches.
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.
Despite advances in medical and surgical therapy, heart failure (HF) remains a common and serious problem. An association between HF and sleep-related breathing disorders has been recognized since Cheyne's observations in 1818, but only recently have treatment options targeting sleep-related breathing disorders become available. This overview will consider the clinical features, pathophysiology, and treatment options of sleep-related breathing disorders in patients with HF.
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.
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 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).