Cases reported "Epilepsy"

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1/14. Ventricular asystole during vagus nerve stimulation for epilepsy in humans.

    Electrical stimulation of the vagus nerve, a recently available option for patients with refractory epilepsy, has demonstrated safety and efficacy. We report four patients with refractory epilepsy who experienced ventricular asystole intraoperatively during initial testing for implantation of the vagus nerve stimulator. Acute intraoperative vagus nerve stimulation may create ventricular asystole in humans. Extracorporeal cervical vagus nerve stimulation testing with continuous EKG monitoring intraoperatively before generator implantation is warranted.
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2/14. Transient epileptic foci associated with intracranial hemorrhage in patients with subdural and epidural electrode placement.

    We report two cases of transient epileptic foci in humans associated with placement of intracranial electrodes. The abnormalities consisted of restricted areas of active, almost continuous, rhythmic spiking, intermittently evolving into electrographic seizure activity, which resolved spontaneously within 3-4 days. The first occurred after placement of a subdural electrode grid and the second following insertion of epidural peg electrodes. neuroimaging demonstrated a small subdural hematoma overlying the grid and a focal intraparenchymal hemorrhage underlying the affected epidural electrodes. The insertion of intracranial electrodes may be complicated by the induction of transient epileptic foci unrelated to a patient's typical epileptic generator.
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3/14. 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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4/14. sleep in right hemispherectomized patients: evidence of electrophysiological compensation.

    OBJECTIVES: The goal of this study is to provide a better understanding of the role of the cortex in sleep's macro- and microstructure modulation. methods: sleep architecture and phasic events were investigated in 4 patients having undergone right functional or anatomical hemispherectomy and 8 control subjects. Between-groups differences were assessed using the Wilcoxon-Mann-Whitney test. RESULTS: Findings provide evidence for overall similarity between patients' and control subjects' left hemispheric sleep architecture. In addition, results clearly indicate that it is possible to detect electrical activity over the operated side of a hemispherectomized patient's brain, even when resection of the hemi-cortex has been complete. Finally, findings provide evidence for similar left and right hemispheric relative spectral activities and for an increase in fast activity bands over the intact hemisphere in anatomical hemispherectomized patients. CONCLUSIONS: This study provides evidence that right hemispherectomy does not produce significant sleep architecture alterations as recorded over the intact hemisphere. In addition, residual activity detected over the operated side in anatomical hemispherectomized patients is interpreted as resulting from volume conduction originating from generators located in the intact hemisphere. Finally, there is strong evidence for electrophysiological compensation in the intact hemisphere following complete resection of the contralateral hemi-cortex.
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5/14. False localization of seizure activity in the EEG.

    Traditional theories of EEG localization are discussed, along with their limitations and contemporary attempts to minimize false localization. Sources of error include: erratic epileptiform activity, local destruction of generators, evoked responses, and autonomous secondary foci. Several cases are presented which are thought to represent false localization by virtue of incompetent generators. It is emphasized that "epileptiform activity" and "epileptogenicity" are not synonomous.
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6/14. Self-inflicted vocal cord paralysis in patients with vagus nerve stimulators. Report of two cases.

    vagus nerve stimulation for treatment of epilepsy is considered safe; reports of severe complications are rare. The authors report on two developmentally disabled patients who experienced vocal cord paralysis weeks after placement of a vagus nerve stimulator. In both cases, traction injury to the vagus nerve resulting in vocal cord paralysis was caused by rotation of the pulse generator at the subclavicular pocket by the patient. Traumatic vagus nerve injury caused by patients tampering with their device has never been reported and may be analogous to a similar phenomenon reported for cardiac pacemakers in the literature. As the use of vagus nerve stimulation becomes widespread it is important to consider the potential for this adverse event.
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7/14. Combining MEG and MRI with neuronavigation for treatment of an epileptiform spike focus in the precentral region: a technical case report.

    BACKGROUND: Epileptic foci are often located in the vicinity but not necessarily within the boundaries of intra-axial brain tumors. Resection of these tumors is based on two major goals: first, maximizing tumor removal without provoking new neurologic deficits, and second, minimizing epileptic seizure activity. Magnetic source imaging (MSI) depicts the generators of magnetic fields overlaid on individual magnetic resonance (MR) images. Established application areas are lesions located adjacent to or partly within the sensory and motor cortex, or in the depth of the brain, necessitating a surgical approach through functionally highly relevant cortical regions. magnetoencephalography (MEG) is also applicable for epileptiform spike foci recording during interictal activity. CASE DESCRIPTION: A patient with a recurrent glioma close to the Rolandic cortex scheduled for epilepsy and tumor surgery was investigated with MSI. The MSI data showed an epileptiform spike focus outside the tumor boundaries. The resulting MSI images were integrated into our neuronavigation system. This procedure allowed for the preoperative identification of the sensory and motor cortex, the precise localization of the epileptiform spike focus, and careful planning of the surgical procedure. In this case, we were able to safely resect the recurrent tumor and the epileptiform spike focus under general anesthesia using MSI-based neuronavigational guidance but no conventional intraoperative mapping techniques. CONCLUSION: Magnetic source imaging can be a valuable, noninvasive method for planning and performing tumor resections in high-risk brain regions, especially if an epileptiform spike focus has to be localized and included into the resection strategy.
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8/14. Delayed onset of vocal cord paralysis after explantation of a vagus nerve stimulator in a child.

    INTRODUCTION: vagus nerve stimulation for the management of intractable seizure disorders is increasingly being used, especially in younger children. Although complications such as infection or vocal cord paralysis are uncommon, some may be unreported. CLINICAL PRESENTATION: A 3.5-year-old boy with intractable complex partial and generalized seizures had a left vagus nerve stimulator (VNS) successfully implanted. Two weeks later, the cervical incision showed signs of infection, antibiotics were started, and the VNS generator and leads were explanted. Three weeks later the child's mother noted a change in the voice of her son, as well as increased coughing and gagging. Flexible laryngoscopy identified a left vocal cord paralysis, which eventually resolved after 6 months. CONCLUSION: infection requiring explantation of a VNS is uncommon. The risk is higher in younger children, especially in those who are developmentally delayed. These children may continuously drool, with saliva or food soiling the fresh incision, or even pick at the incision to the point of twisting or even pulling out the electrodes. Less common is a vocal cord paralysis, especially occurring in a delayed fashion.
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9/14. EMG vagus nerve stimulator artifact.

    EMG artifact produced by a VNS stimulator is described. A patient with a VNS stimulator underwent an EMG study for suspected ALS. artifacts that appeared similar to positive sharp waves or fibrillations were noted that could produce a false clinical diagnosis. These VNS-EMG artifacts matched well with the VNS generator's set parameters. We conclude that EMG findings must be interpreted with caution in patients with VNS implants and also that EMG may have a possible monitoring value for VNS activity.
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10/14. memory dysfunction in epilepsy patients as a derangement of normal physiology.

    patients with CPS often display recent memory deficits. Typically, general intelligence, perceptual skills, language, remote memory, and primary memory are all normal. However, the ability to learn new combinations of cognitively complex material is deficient. This deficit may be specific for verbal material (e.g., as a difficulty with learning to recall a response word given an unrelated cue word), for nonverbal material (e.g., as a difficulty in drawing a complex figure from memory), or for both verbal and nonverbal material. Because these characteristics are typical of memory deficits after MTL damage, it is reasonable to suspect that these deficits in patients with epilepsy also reflect MTL damage. In many cases, MTL damage is apparent from neuroimaging studies, whereas seizure semiology suggests MTL onset. In these patients, the same pathology might be the cause of both the ictus and memory deficits. In other cases, memory impairment appears to be secondary to seizures. This suggestion is supported by cases where prolonged complex partial status resulted in a permanent global amnesia. Cases with shorter-lasting memory deficits were also presented. Neuropsychological testing revealed specific recent-memory deficits that cleared 2 weeks after a flurry of CPS and 24 hr after a single seizure. Depth recordings have demonstrated that MTL electrographic seizures can occur without subjective manifestations. When these are evoked by local electrical stimulation, a profound inability to learn new material may be observed during the afterdischarge. Similarly, artificially induced MTL spike-and-wave complexes interfere with the memory for simultaneously presented complex visual scenes. Recent evidence suggests that all of the above phenomena may reflect the engagement by epileptiform processes of the association-cortex (AC)-MTL circuits used in normal human memory. In recent memory tasks, cognitive evoked-potential components N4 and P3 are generated in the MTL and to a lesser degree in related AC regions. The N4/P3 are strongly modulated by familiarity in recent memory. This modulation is eliminated by anterior temporal lobectomy. The typical slow wave following spontaneous MTL interictal spikes has the same MTL voltage topography, and thus probably similar synaptic generators, as the cognitive P3 potential. Furthermore, MTL spike-and-wave complexes can be evoked in recent memory tasks at a fixed latency equal to that of the N4.(ABSTRACT TRUNCATED AT 400 WORDS)
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