Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

4-Aminopyridine (4-AP) is an investigational drug for the treatment of neurologic disorders including multiple sclerosis (MS). Until recently, relatively little was known about 4-AP toxicity in overdose; the only recorded cases involved neurologic symptoms ranging from mild parasthesias to tonic-clonic seizures. We report a case of accidental 4-AP overdose that resulted in continuous, dystonic, choreoathetoid-type movements that responded to treatment with standard anticonvulsant dosages of benzodiazepines.
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PMID:Atypical presentation of 4-aminopyridine overdose. 859 5

Drowsiness is a common complaint among patients with epilepsy taking antiepileptic drugs (AEDs) and may be of particular importance because of the potential effects on cognitive abilities. We used a novel EEG-based measure (the Awake Maintenance Task, AMT) to determine objectively whether patients on chronic, stable AED therapy had impaired ability to maintain wakefulness. Thirty patients receiving AEDs [carbamazepine (CBZ), phenytoin (PHT), phenobarbital (PB), valproate (VPA)] were compared to 35 healthy controls, 12 seizure patients not taking AEDs, and 16 patients with multiple sclerosis. A structured EEG recording was conducted under controlled conditions, and subjects were tested to determine their ability to maintain wakefulness during a 6-min unstimulated trial. Testing also included Digit Symbol, auditory reaction time, and subjective measures of fatigue or sleepiness [Profile of Mood States (POMS), Stanford Sleepiness Scale (SSS)]. Patients receiving AEDs had a mean total drowsiness score of 101 s compared with < or = 12 s for each of the three control groups (P < 0.001). One third of the AED-treated patients had > 120 s of drowsiness, in contrast to only 1 of 63 controls (p < 0.001). Among patients receiving AEDs, objective EEG drowsiness did not correlate with AED levels or performance measures. Untreated seizure patients had significantly greater complaints of lack of vigor despite a near absence of objective drowsiness on the AMT. These results suggest that epilepsy patients receiving chronic AED therapy have impaired ability to maintain wakefulness. Patient self-reports of AED-related sleepiness may not accurately represent this problem.
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PMID:Assessment of drowsiness in epilepsy patients receiving chronic antiepileptic drug therapy. 863 29

We report an unusual cause of periodic lateralized epileptiform discharges (PLEDs) in a young man with a long history of multiple sclerosis. Two exacerbations of multiple sclerosis, 3 years apart, were complicated by complex partial status epilepticus. After each episode, serial electroencephalograms revealed PLEDs (right frontal PLEDs in the first episode and right frontotemporal and bifrontal PLEDs in the second one), which resolved within 2 weeks. With the first episode, magnetic resonance imaging revealed an enhancing white matter lesion in the right frontal area, which improved after 3 weeks. We concluded that in each instance an exacerbation of multiple sclerosis caused the seizures.
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PMID:Periodic lateralized epileptiform discharges in multiple sclerosis. 868 94

A female patient with clinically defined multiple sclerosis presented episodes of audiovisual hallucinations in the form of projections of her own body image speaking to her. EEG and EEG-Holter studies were normal. MRI revealed multiple areas of hypersignals in white matter, particularly in both temporal lobes. The episodes remitted with carbamazepine therapy. We postulate that this phenomenon of autoscopy, which is unusual in multiple sclerosis, may be related to a mechanism of ephaptic transmission in the temporal lobe that is inhibited by carbamazepine, or it may be related to seizure.
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PMID:[Autoscopy and multiple sclerosis]. 876 80

1. Aminopyridines have been used as beneficial symptomatic treatments in a variety of neurological conditions including multiple sclerosis but have been associated with considerable toxicity in the form of abdominal pain, paraesthesias and (rarely) convulsions. 2. Extracellular and intracellular recording was used to characterize action potentials in rat sciatic nerves and dorsal roots and the effects of 4-aminopyridine (4-AP). 3. In sciatic nerve trunks, 1 mM 4-AP produced pronounced after potentials at room temperature secondary to regenerative firing in affected axons (5-10 spikes per stimulus). At physiological temperatures, after potentials (2-3 spikes) were greatly attenuated in peripheral axons. 4. 4-AP evoked more pronounced and prolonged after discharges in isolated dorsal roots at 37 degrees C (3-5.5 mV and 80-100 ms succeeded by a smaller inhibitory/depolarizing voltage shift) which were used to assess the effects of anticonvulsants. 5. Phenytoin, carbamazepine and lamotrigine dose-dependently reduced the area of 4-AP-induced after potentials at 100 and 320 microM but the amplitude of compound action potentials (evoked at 0.5 Hz) was depressed in parallel. 6. The tonic block of sensory action potentials by all three drugs (at 320 microM) was enhanced by high frequency stimulation (5-500 Hz). 7. The lack of selectivity of these frequency-dependent Na+ channel blockers for burst firing compared to low-frequency spikes, is discussed in contrast to their effects on 4-AP-induced seizures and paroxysmal activity in CNS tissue (which is associated with large and sustained depolarizing plateau potentials). 8. In conclusion, these in vitro results confirm the marked sensitivity of sensory axons to 4-AP (the presumptive basis for paraesthesias). Burst firing was not preferentially impaired at relatively high concentrations suggesting that anticonvulsants will not overcome the toxic peripheral actions of 4-AP in neurological patients.
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PMID:The effects of anticonvulsants on 4-aminopyridine-induced bursting: in vitro studies on rat peripheral nerve and dorsal roots. 882 51

Migraine is conventionally regarded as a specific type of headache with a small set of associated neurologic symptoms. Yet, the true scope and frequency of migrainous phenomena are much greater than is generally acknowledged. Six cases are presented to illustrate some of the diverse manifestations of migraine: (1) transient global amnesia, (2) persistent visual phenomena, (3) migraine and seizures, (4) vestibular dysfunction, (5) hearing loss, and (6) migraine masquerading as multiple sclerosis. These and other migraine-associated neurologic symptoms are discussed in relation to previous reports in the literature. Pitfalls in recognizing the diverse manifestations of migraine, which are often underdiagnosed or misdiagnosed, are reviewed. Whether or not the established diagnostic criteria for migraine are too strict, other factors contributing to failure to identify migraine when it causes nonclassic neurologic symptoms include: (1) the belief that these are rare, (2) lack of an objective measure for migraine, (3) inadequate attention to the positive diagnostic features of migraine in the absence of headache, (4) confusion regarding prior migraine history, and (5) dismissing the diagnosis because of reported failure of prior migraine treatment. Recognition of the diversity of migraine helps avoid unnecessary testing and opens the door to effective treatment.
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PMID:The menagerie of migraine. 887 61

We report a case of multiphasic disseminated encephalomyelitis (MDEM) following viral illness presenting as multiple sclerosis (MS) in a 7-year-old boy. The patients had two episodes of alternating hemiparesis and other neurologic symptoms following viral infection, which were separated by 3 years. Neuroimaging studies demonstrated multiple, discrete, small nodules and large globular lesions in the cerebral white matter, basal ganglia, brainstem and cerebellar areas. Based on typical appearance of magnetic resonance imaging (MRI) and clinical manifestations including systemic symptoms such as fever, nausea, vomiting, headache and seizures followed by consciousness disturbance and other multifocal neurologic signs, the diagnosis of MDEM rather than that of MS was made. Because it is difficult to differentiate between MDEM and MS on the basis of the clinical history, the cerebrospinal fluid examination and evoked potential studies, this report emphasizes that the MRI study of the brain may provide an important clue for the diagnosis.
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PMID:Multiphasic disseminated encephalomyelitis mimicking multiple sclerosis. 889 Dec 39

Aphasia due to simple partial status epilepticus is rare. We report a case of prolonged mixed aphasia without clouding of consciousness in a patient with an old history (10 years) of multiple sclerosis (MS). We found a clear clinical-EEG correlation with a continuous epileptic pattern in the shape of periodic lateralized epileptiform discharges (PLEDs). Clinical, laboratory and neuroradiological data ruled out possible etiological conditions other than MS and suggested that the development of new subcortical demyelinating lesions might play a critical role in seizure production. These findings, besides the role of PLEDs as an intrinsic feature of the status epilepticus condition, are discussed in relation to the literature.
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PMID:Aphasic status epilepticus in multiple sclerosis. 895 6

To examine the efficacy and toxicity of oral 3,4 diaminopyridine (DAP) in dosages up to 100 mg/day, 36 patients with multiple sclerosis (MS) enrolled in a randomized, double-blind, placebo-controlled, crossover trial. The primary outcome measure was improvement of a prospectively defined neurologic deficit, which was leg weakness in 34 patients. Secondary outcome measures included the patient's subjective response, scored manual motor testing (MMT) of leg strength, scored leg strength from videotaped motor testing (VMT), quadriceps and hamstrings strength (QMT) measured by isometric dynamometry, neuropsychological testing (NPT), ambulation index (AI), and Expanded Disability Status Scale (EDSS) score. Paresthesias and abdominal pain were common and were dose limiting in eight patients. Three patients had episodes of confusion, and one patient had a seizure while on DAP. Eight patients withdrew from the study, leaving 28 evaluable patients for the efficacy analysis. The prospectively defined neurologic deficit improved in 24 patients-22 on DAP and 2 on placebo (p = 0.0005). All improvements were in leg weakness. Subjective response and measures of leg strength and function (MMT, VMT, QMT, and AI) improved on DAP compared with placebo. Neither NPT nor EDSS scores improved. DAP treatment can induce improvements in leg strength in MS patients, but toxicity is limiting in many patients.
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PMID:Treatment with oral 3,4 diaminopyridine improves leg strength in multiple sclerosis patients: results of a randomized, double-blind, placebo-controlled, crossover trial. 896 Jul 27

We studied the admission rate, risk factors, neurological complications and sequelae of heat stroke (HS) during the 1995 heat wave in Madison, Wisconsin. HS was epidemic in 1995 (2.3 cases/1000 admissions), compared to the ten-fold lower endemic rate in 1994 (0.2/ 1000). There were 11 cases of HS, 9 males and 2 females. Contributing factors were athletic events (2), working outdoors (3) and indoor activity with malfunctioning air-conditioning (6). Medical conditions contributing to poor temperature regulation included schizophrenia with neuroleptic treatment (2), amyotrophic lateral sclerosis receiving nortriptiline (1), multiple sclerosis (1), attention deficit disorder (1), cystic fibrosis (1) and alcoholism (1). Acute neurological complications occurred in all patients on presentation including coma (8/11.73%), stupor (2/ 11.18%) and seizures (1/11.9%). Two patients (1856) had persistent neurological sequelae in the form of a pan-cerebellar syndrome while the remaining 9 recovered fully. Importantly, avoidable factors contributed to all of the patients with underlying diseases. These patients are particularly at risk and should take adequate precautions during summer months.
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PMID:Epidemic heat stroke in a midwest community: risk factors, neurological complications and sequelae. 916 37


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