Cases reported "Epilepsy, Complex Partial"

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1/9. Long-term results of vagus nerve stimulation in refractory epilepsy.

    vagus nerve stimulation (VNS) is an adjunctive antiepileptic treatment for patients with refractory epilepsy. Limited information on long-term treatment with VNS is available. The purpose of this paper is to present our experience with VNS with a follow-up of up to 4 years. Twenty-five patients (13 females and 12 males) with refractory partial epilepsy were treated with VNS. The first 15 patients with a mean age of 30 years and a mean duration of epilepsy of 17.5 years have sufficient follow-up for analysis. Mean post-implantation follow-up was 29 months and mean stimulation output 2.25 mA. There was a mean seizure frequency reduction from 14 complex partial seizures (CPS) per month before implantation to 8 CPS per month after implantation (P = 0.0016; Wilcoxon signed-rank rest (WSRT)). The mean maximum CPS-free interval changed from 9 to 312 days (P = 0.0007; WSRT). Six patients were free of CPS for at least one year. In one patient, one antiepileptic drug (AED) was tapered; in 10 patients, AEDs remained unchanged; in four, one adjunctive AED was administered. Side effects occurred in six patients, three of whom required a temporary reduction of output current. Nine patients reported no side effects at all. Treatment with VNS remains effective in the long-term. In this series 4 / 15 (27%) patients with highly refractory epilepsy experienced entirely seizure-free intervals of 12 months or more.
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2/9. bradycardia and asystole with the use of vagus nerve stimulation for the treatment of epilepsy: a rare complication of intraoperative device testing.

    PURPOSES: A 56-year-old man with mild mental retardation, right congenital hemiparesis, and refractory partial seizures was referred for vagus nerve stimulation (VNS). methods: Routine lead diagnostic testing during the surgical procedure (1.0 mA, 20 Hz, and 500 micros, for approximately 17 s) resulted, during the initial two stimulations, in a bradycardia of approximately 30 beats/min. A third attempt led to transient asystole that required atropine and brief cardiopulmonary resuscitation. RESULTS: The procedure was immediately terminated, the device removed, and the patient recovered completely. A postoperative cardiologic evaluation, including an ECG, 24-h Holter monitor, echocardiogram, and a tilt-table test, was normal. CONCLUSIONS: Possible mechanisms for the bradycardia/asystole include stimulation of cervical cardiac branches of the vagus nerve either by collateral current spread or directly by inadvertent placement of the electrodes on one of these branches; improper plugging of the electrodes into the pulse generator, resulting in erratic varying intensity of stimulation; reverse polarity; and idiosyncratic-type reaction in a hypersusceptible individual. The manufacturer reports the occurrence rate in approximately 3,500 implants for this intraoperative event to be approximately one in 875 cases or 0.1%.
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3/9. Remote effects of cortical dysgenesis on the primary motor cortex: evidence from the silent period following transcranial magnetic stimulation.

    OBJECTIVE: In cortical dysgenesis (CD), animal studies suggested abnormal cortico-cortical connections. Cerebral areas projecting to the primary motor cortex (M1) modulate the cortical silent period (CSP) following transcranial magnetic stimulation (TMS). Therefore, we used the CSP to investigate remote effects of CD on the M1. methods: A detailed investigation, including single-pulse TMS and electrical nerve stimulation, was performed in 3 consecutive adults with focal CD located outside the M1 and in 18 controls. Two patients with unilateral CD were epileptic and treated with anti-epileptic drugs. One patient with focal CD on both sides had no history of seizures. Neurological examination was normal in all patients. Recordings were made from both first dorsal interosseous muscles. RESULTS: In CD patients, the CSP was significantly lengthened contralaterally to the affected hemispheres. In treated patients with unilateral CD, the interside difference of the CSP duration was also significantly increased. In contrast, excitability threshold, peripheral and corticospinal motor conduction studies, and peripheral as well as ipsilateral silent periods were not significantly modified. CONCLUSIONS: Our findings indicate that focal CD outside the M1 may produce CSP modifications, which are likely due to changes of afferent control.
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4/9. Transient hemifacial sensory loss with xerophthalmia following temporal lobectomy.

    OBJECTIVE AND IMPORTANCE: The occurrence of a unilateral sensory loss in the second trigeminal distribution and the inability to tear following an ipsilateral temporal lobectomy has not been noted despite a number of reports of cranial nerve compromise under similar situations. CLINICAL PRESENTATION: A 48-year-old woman experienced complex partial seizures over three years attributable to the presence of cavernous malformations of the right temporal lobe. INTERVENTION: An anterior temporal extrahippocampal resection was performed. The surgery was marked by the need for electrocoagulation of the dural base of the temporal lobe where numerous bleeding points were encountered. Postoperatively, the patient experienced an ipsilateral maxillary division sensory loss, absence of tearing, and diminished nasal congestion for an eight-month period until resolution. CONCLUSION: Injury of the fibers of the maxillary division of the trigeminal nerve and the adjacent greater superficial petrosal nerve appears to be the cause. No prior account of such an occurrence has been published.
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5/9. Pharyngeal dysesthesia in refractory complex partial epilepsy: new seizure or adverse effect of vagal nerve stimulation?

    Sensory symptoms are commonly seen in association with focal epilepsy, but viscerosensory auras, such as pharyngeal dysesthesias, are rarely the main clinical manifestation. With the introduction of vagal nerve stimulation (VNS) for medically refractory epilepsy, viscerosensory symptoms commonly occur as an adverse effect of VNS. voice alterations (hoarseness or tremulousness), local neck or throat pain, and cough are the most common adverse effects seen during active stimulation (on-time). Numbness of the throat, neck, or chin, as well as a tingling sensation of the neck and throat is directly related to stimulation intensity. We present a case in which recurrent pharyngeal sensations caused a diagnostic dilemma and in which monitoring the VNS artifact during video/EEG and correlating this with clinical symptoms helped determine the etiology of the recurrent sensory symptoms.
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6/9. Thalamic hypometabolism in a patient undergoing vagal nerve stimulation seen on F-18 FDG PET imaging.

    A 31-year-old man with a vagal nerve stimulator for seizure control was noted to have decreased metabolism within the thalamus as visualized by F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET). Some investigators think the thalamus plays an important role in the regulation of seizure activity. Vagal nerve stimulation (VNS) may reduce thalamic activity, which in turn may reduce seizure activity. However, because the thalamus has diffuse connections throughout the brain, its role in seizure activity is likely complex. Observing decreased thalamic activity during VNS is just 1 small step toward understanding this role.
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7/9. Effect of vagal nerve electrostimulation on the power spectrum of heart rate variability in man.

    The power spectrum of heart rate variability contains low frequency (LF = 0.08-0.12 Hz) and high frequency (HF = 0.18-0.30 Hz) components said to represent neurocardiac rhythms. To verify whether such a relationship exists we report a unique study where the heart rate autospectrum was determined in a 28-year-old epileptic male patient with an implanted vagal electrical stimulator. The stimulator was activated at 20 Hz, 300 microseconds pulse, and 1.25 V. Continuous ECG and respiratory waveform records were obtained over 45 minutes every 8 hours (7-8 AM; 3-4 PM; 11-12 PM) with the stimulator ON, then 24 hours OFF and then 24 hours ON again. The overall LF:HF peak ratio increased from 0.64 to 1.99 (P less than 0.001) after the stimulator was turned OFF. There was a dramatic increase in the LF peak power (greater than 60%) and a corresponding decrease in the HF peak power (greater than 65%) when the stimulator was turned OFF. These values were reversed when the stimulator was turned ON again. In the early morning and late evening hours, there was a significant rightward shift in the LF peak power frequency (average 0.057 to 0.075 Hz) whenever the stimulator was ON. Otherwise, there were no significant circadian variations in any of the autospectral components. The results demonstrate an unequivocal relationship between selective vagal nerve electrostimulation and alterations in the heart rate autospectrum.
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8/9. Acute effects of high frequency vagal nerve stimulation on balance and cognitive motor performance in epilepsy: three case study reports.

    Quantitative measures of area of sway, total sway, and cognitive function failed to show significant differences in acute (50 minute) "ON-OFF-ON-OFF" studies of high frequency left vagal stimulation in three epileptic patients undergoing treatment for chronic complex partial seizures. Fluctuation in blood levels of anticonvulsants may have been associated with some clinical effects. There were no significant adverse effects of acute left vagal stimulation in these three subjects.
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9/9. Effect of vagal nerve stimulation in a case of Tourette's syndrome and complex partial epilepsy.

    We report on a 30-year-old man with Tourette's syndrome (TS) and medication-refractory epilepsy whose tics improved after implantation of a vagal nerve stimulator (VNS). To verify the patient's observation, we performed a blinded video assessment using the modified Rush video-based tic rating scale. The patient underwent two separate video recordings (VNS on and VNS off). A rater, blinded to patient's VNS status, evaluated the videos with the modified Rush video-based tic rating scale. There were improvements in total tic score and motor and phonic tic frequency. If verified by controlled clinical trials, this observation may provide insights into the pathophysiology of tics and may lead to a novel therapy for patients with severe TS.
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