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Biomedical subjects

Bradley V Vaughn

Publications and source records attributed to Bradley V Vaughn.

7 recordsLinked to original sources

Epilepsy and medication effects on the pattern visual evoked potential.

Visual disruption in patients diagnosed with epilepsy may be attributable to either the disease itself or to the anti-epileptic drugs prescribed to control the seizures. Effects on visual function may be due to perturbations of the GABAergic neurotransmitter system, since deficits in GABAergic cortical interneurons have been hypothesized to underlie some forms of epilepsy, some anti-epileptic medications increase cortical GABA levels, and GABAergic neural circuitry plays an important role in mediating the responses of cells in the visual cortex and retina. This paper characterizes the effects of epilepsy and epilepsy medications on the visual evoked response to patterned stimuli. Steady-state visual evoked potentials (VEP) evoked by onset-offset modulation of high-contrast sine-wave stimuli were measured in 24 control and 54 epileptic patients. Comparisons of VEP spectral amplitude as a function of spatial frequency were made between controls, complex partial, and generalized epilepsy groups. The effects of the GABA-active medication valproate were compared to those of carbamezepine. The amplitude of the fundamental (F1) component of the VEP was found to be sensitive to epilepsy type. Test subjects with generalized epilepsy had F1 spatial frequency-amplitude functions with peaks shifted to lower spatial frequencies relative to controls and test subjects with complex partial epilepsy. This shift may be due to reduced intracortical inhibition in the subjects with generalized epilepsy. The second harmonic component (F2) response was sensitive to medication effects. Complex partial epilepsy patients on VPA therapies showed reduced F2 response amplitude across spatial frequencies, consistent with previous findings that showed the F2 response is sensitive to GABA-ergic effects on transient components of the VEP.

Adult↗

Complete heart block with ventricular asystole during left vagus nerve stimulation for epilepsy.

Vagus nerve stimulation (VNS) is an important therapeutic option for individuals with refractory epilepsy who have failed multiple antiepileptic drugs (AEDs). The intricate relationship of the vagus nerve to cardiac function raises concern that vagal stimulation may affect cardiac rhythm and function. Previous pre- and postmarketing studies have not shown this to be a significant problem, with the incidence of bradyarrhythmias reported to be about 0.1%. We review three cases of ventricular asystole with complete heart block that occurred during intraoperative lead tests. The purpose of these case reports is to identify the specific type of cardiac abnormality associated with vagus nerve stimulation and to identify individuals at risk.

Adult↗

Sleep and epilepsy.

The relationship of sleep and epilepsy demonstrates the delicate association of brain physiology and dysfunction. Sleep affects the distribution and frequency of epileptiform discharges in humans and influences the rate of kindling in animals. Epileptic discharges, on the other hand, alter sleep regulation and provoke sleep disruption. This effect on sleep appears to carry over to sleep complaints in patients with epilepsy. Individuals with epilepsy frequently complain of symptoms suggestive of disturbed sleep, such as excessive daytime sleepiness, insomnia, or with more subtle complaints such as an increase in seizure frequency. More commonly, these symptoms indicate an underlying sleep disorder rather than the effect of epilepsy or medication on sleep. Clinicians must be able to identify and differentiate between potential sleep disorders and sleep dysfunction related to epilepsy and direct therapy to improve the patient's symptoms. The reciprocal relationship of sleep and epilepsy and the management of sleep complaints in the patient with epilepsy will be reviewed.

Epilepsy↗

Driver risk factors for sleep-related crashes.

A population-based case-control study was carried out to examine driver risk factors for sleep-related motor vehicle crashes. Cases included 312 drivers involved in recent North Carolina crashes and identified on police reports as asleep at the time of the crash and 155 drivers identified as fatigued. Controls were 529 drivers also involved in recent crashes but not identified as asleep or fatigued, and 407 drivers not involved in recent crashes. All drivers were contacted for brief telephone interviews. Results showed that drivers in sleep-related crashes were more likely to work multiple jobs, night shifts, or other unusual work schedules. They averaged fewer hours sleep per night, reported poorer quality sleep, were less likely to feel they got enough sleep, were sleepier during the day, drove more often late at night, and had more prior instances of drowsy driving. Compared to drivers in non-sleep-related crashes, they had been driving for longer times, been awake more hours, slept fewer hours the night before, and were more likely to have used soporific medications. Knowledge of specific risk factors for sleep-related crashes is an important first step in reducing the thousands of deaths and injuries each year in the US attributed to drowsy driving.

Accidents, Traffic↗

Obstructive sleep apnea in epilepsy.

Obstructive sleep apnea can affect an individual with epilepsy profoundly. These relatively common disorders can coexist and potentially exacerbate each other. The identification and appropriate treatment of OSA may have far-reaching consequences in improving a patient's quality of life and recurrence of seizures. Clinicians must be aware of the relationship of these disorders and keenly question epilepsy patients, regardless of their body habitus, regarding potential symptoms of sleep apnea. Although the underlying pathogenic mechanisms are unclear, we can model the information gained from the observations to further the understanding of the relationship between sleep and epilepsy.

Clinical Trials as Topic↗

Insertion of vagal nerve stimulator using local and regional anesthesia.

BACKGROUND: Vagal nerve stimulation (VNS) is a valuable therapy for patients with intractable epilepsy. Placement of a vagal nerve stimulator typically requires general anesthesia, which frequently interrupts anticonvulsant therapy. Insertion of the stimulator using regional/local anesthesia may offer the advantages of continuity of anticonvulsant therapy and implantation in the outpatient setting. METHODS: We retrospectively compared the first 10 consecutive patients undergoing VNS implantation under general anesthesia with the first 12 consecutive patients undergoing VNS implantation under regional/local anesthesia. Patients for the regional/local anesthesia were selected on the basis of their ability to cooperate and follow commands. Regional anesthesia for implantation of the VNS leads was achieved by performing superficial and deep cervical plexus blocks. A local anesthetic field block of a small area of the posterior chest provided anesthesia for insertion of the generator. RESULTS: All of the patients undergoing regional/local anesthesia completed the procedure without difficulty and on an outpatient basis. None complained of discomfort, sedation, nausea, or vomiting and none had seizures in the perioperative period. These results contrasted with the group that underwent general anesthesia (n = 10), who had an 80% incidence of nausea and vomiting and a 30% incidence of postoperative seizures. CONCLUSION: VNS implantation under regional/local anesthesia is proficiently performed as an outpatient procedure with minimal postoperative side effects.

Adolescent↗

Non-convulsive status epilepticus induced by tiagabine in a patient with pseudoseizure.

Tiagabine, a novel GABA reuptake inhibitor, has been reported to induce non-convulsive status epilepticus (NCSE) in patients with epilepsy. We report a 27 year old female with history of pseudoseizure documented by video-EEG monitoring who presented confusion while on 56 mg per day of tiagabine. Electroencephalography showed generalized sharp and slow wave discharges, consistent with NCSE. The NCSE was terminated by lorazepam and did not recur after tiagabine was discontinued. This case report suggests that tiagabine may induce NCSE in patients without epilepsy.

Adult↗