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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute encephalitis with refractory, repetitive partial seizures (AERRPS) represents a peculiar form of encephalitis mainly affecting children. They usually present abruptly with seizure or impaired consciousness as well as high-grade fever following antecedent infection. Seizures in AERRPS are almost exclusively of localized origin, whose semiology includes eye deviation, hemifacial twitching, hemiclonic convulsion, and autonomic manifestations. Partial seizures are brief, but repeat with increasing frequency and develop status epilepticus at nadir. They are extremely pharmaco-resistant and are only suppressed by intravenous administration of high-dose barbiturates. Although acute seizures are hardly controlled, patients gradually recover with decreasing seizure frequency and continuously evolve into post-encephalitic epilepsy without latent period. Residual cognitive impairment is common. Electroencephalograms in active stage demonstrate electrical seizure activities and interictal periodic discharges. Magnetic resonance imaging reveals late cerebral atrophy with limited signal abnormality. Persistent fever during active stage, cerebrospinal fluid (CSF) pleocytosis, and up-regulation of neopterin raise the hypothesis that inflammatory process is involved in this condition. Furthermore, early production of autoantibody against NMDA receptor 2B in serum and CSF, although its disease specificity is still in controversy, is suggestive of autoimmune etiology. Exploration for definite clinical marker is currently in progress.
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PMID:Acute encephalitis with refractory, repetitive partial seizures. 1932 24

Drug-induced QT prolongation is a potentially dangerous adverse effect of some medication combinations. When QT prolongation progresses to torsade de pointes, life-threatening or fatal outcomes may result. A 57-year-old man with a history of human immunodeficiency syndrome on abacavir, nevirapine, tenofovir, voriconazole, and methadone presented to the emergency department with a chief complaint of new-onset seizures. The physical exam was unremarkable. The electrocardiogram demonstrated sinus bradycardia and a prolonged QT(c) interval of 690 ms. In the emergency department, he had several episodes of torsade de pointes (TdP) and ventricular tachycardia that resolved spontaneously. These episodes were accompanied by an alteration in mentation and generalized twitching. Magnesium and amiodarone were effective in terminating the dysrhythmia. The patient had multiple risk factors for prolonged QT syndrome including human immunodeficiency virus infection, methadone therapy, and polypharmacy leading to potential drug interactions. Physicians must be aware of multidrug interactions potentiating QT prolongation and leading to torsade de pointes.
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PMID:Torsade de pointes caused by polypharmacy and substance abuse in a patient with human immunodeficiency virus. 1938 21

The aim of this study was to investigate the dynamics of lipid peroxidation and the possible correlation between lipid peroxidation in different brain regions and behavioral manifestations in lindane-induced seizures in rats. Male Wistar rats were divided into the following groups: 1. control, saline-treated group; 2. dimethylsulfoxide (DMSO)-treated group; 3. lindane-treated group (8 mg/kg), intraperitoneally. Animals were sacrificed 0.5 or 4 h after treatment and the malondialdehyde level and superoxide dismutase (SOD) activity were determined in various brain regions spectrophotometrically. Behavioral changes were classified according to the descriptive scale (0--no response, 1--head nodding, lower jaw twitching; 2--myoclonic body jerks, bilateral forelimb clonus with full rearing; 3--progression to generalized clonic convulsions followed by tonic extension of fore- and hind limbs and tail; 4--status epilepticus). A significant rise in the malondialdehyde level was detected in the cerebral cortex, hippocampus, and thalamus of lindane-treated animals 0.5 and 4 h after administration (P < 0.05). SOD activity (total and mitochondrial) was significantly decreased in the hippocampus and the cortex of lindane-treated animals at both time points (P < 0.05). An initial fall in SOD activity was detected in the thalamus 4 h after lindane administration (P < 0.05). A positive correlation between seizure severity and the malondialdehyde level was found in the hippocampus at both time points (P < 0.01). These results suggest that lipid peroxidation may contribute to the neurotoxic effects of lindane in early acute lindane intoxication and that behavioral manifestations correlate with lipid peroxidation in the hippocampus of lindane-treated rats.
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PMID:The correlation between lipid peroxidation in different brain regions and the severity of lindane-induced seizures in rats. 1969 53

We report on a case of epilepsia partialis continua with rapid response to intravenous bolus administration of levetiracetam. A 60-year-old woman presented with continuous jerking of the right foot and hallux persisting for more than two days. She had a 9-year history of epilepsy due to a left temporoparietal oligodendroglioma with occasional focal seizures clinically presenting as speech arrest, which was treated with levetiracetam and oxcarbazepine administered orally. After hospital admission, the twitching of the foot and toe was refractory to add-on treatment with lorazepam and diazepam but stopped within 15 min after intravenous bolus administration of 2000 mg levetiracetam. This observation suggests that intravenous bolus administration of levetiracetam may be an effective therapeutic option in epilepsia partialis continua.
Seizure 2009 Dec
PMID:Epilepsia partialis continua responsive to intravenous levetiracetam. 1983 63

Periodic lateralized epileptiform discharges (PLEDs), an EEG pattern that is highly correlated with seizures, may represent an ictal pattern in some patients, but in other patients PLEDs persist despite the absence of seizures or after seizures have been controlled by anti-epileptic drugs. The tenacity of PLEDs was illustrated by continuous EEG recording in a 95-year-old woman with multiple old cerebral infarctions who had been admitted to the hospital because of seizures. The EEG showed PLEDs that were maximal in the left central region. These sometimes evolved into EEG seizure patterns, which were correlated with facial twitching. The seizures were controlled by anti-epileptic drugs (AEDs), but the PLEDs continued. The patient subsequently expired, with EEG monitoring still in progress. The PLEDs persisted as the patient developed agonal respirations. The interval between the epileptiform complexes gradually increased, and they stopped 40 seconds before disappearance of the other EEG background rhythms; cardiac arrest ensued less than 1 minute later. The resistance of the PLEDs to hypoxia reflects the robustness of the mechanisms that produced them, which may also account for their persistence in the face of AED treatment that stopped the seizures.
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PMID:PLEDs following control of seizures and at the end of life. 2030 10

Epilepsy-like convulsive seizures have been induced by cholera toxin administration into the rat amygdaloid complex and lateral ventricle. Between the 8th and 48th h following the administration, rhythmic spike discharges (1-3 spikes/s) were electroencephalographically observed bilaterally in the amygdaloid complexes, and rats exhibited abnormal behaviors such as running, jumping, tail lifting, rearing, vocalization, aggressive behavior, facial twitching and increased salivation. During these stages, high voltage spikes were intermittently observed with generalized convulsive seizures. Duration of the seizure was 1-2 min and the incidence was 0-6 times/h. At 48 h after the administration or thereafter, convulsive seizures disappeared and electroencephalographic abnormalities were gradually normalized. Occasional rhythmic spike discharges, however, were observed more than 168 h after the administration. Intraventricularly administered cholera toxin also induced the same type of convulsive seizures. Cyclic AMP content in the rat cerebrum from toxin-treated animals was significantly higher than that found in controls. The present results clearly indicate that cholera toxin administered intraventricularly as well as into the amygdaloid complexes of the rats induces epileptic attack-like convulsive seizures 8-48 h after the administration and this effect of the toxin is most likely to be related to the increase of cerebral cyclic AMP content.
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PMID:Epilepsy-like convulsive seizures induced by cholera toxin administration into amygdaloid complex and lateral ventricle. 2048 42

To delineate the evolution of non-epileptic and epileptic paroxysmal events in alternating hemiplegia of childhood (AHC), we reviewed clinical information of nine patients (4-40 years) with AHC. Paroxysmal abnormal ocular movements, head turning, and tonic, clonic, or myoclonic limb movements were the initial symptoms (birth-8m) in each patient. Ictal electroencephalography (EEG) of these episodes, as well as hemiplegic periods that accompanied these symptoms later in infancy showed unremarkable findings or generalized slow background activity. Presumptive epileptic seizures appeared at 2-16y in seven patients: generalized tonic, clonic, myoclonic, tonic-clonic, or complex partial seizures often accompanied by cyanosis or prolonged respiratory arrest. Ictal EEGs recorded in four patients revealed focal slow or fast activities during facial or limb twitching, and widespread sharp waves or polyspike-wave activities during clonic/myoclonic seizures. Four patients with neonatal disease onset showed lower psychomotor developmental achievements compared with other patients, and experienced repeated status epilepticus followed by progressive deterioration. Cerebellar atrophy and hippocampal high signal changes on magnetic resonance imaging were common to this group with severe phenotypes. Apart from the paroxysmal motor symptoms accompanying the hemiplegic episodes, many AHC patients suffer from true epilepsies during childhood. Status epilepticus in AHC is linked to severe outcome with psychomotor deterioration. The variations in clinical phenotypes may imply multiple causative genes for AHC. This variation should be considered while managing patients with this disorder.
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PMID:Evolution of hemiplegic attacks and epileptic seizures in alternating hemiplegia of childhood. 2058 May 29

We report a case of late-onset systemic toxicity due to ropivacaine over dose, and its successful reversal with 20% lipid emulsion (20% Intralipos). A 40-year-old woman, 40 kg, ASA-I, was scheduled for laparoscopy-assisted myomectomy of the uterus in which 40 ml of 0.375% ropivacaine was injected for bilateral US guided transversus abdominis plane block (TAPblock) under general anesthesia. Anesthesia proceeded uneventfully and she could go back to the ward 15 min later, but 3 hours after TAPblock, her blood pressure dropped to seventies and she became unresponsive. She also displayed clonic seizure/twitching of limbs. Immediately after diazepam 2 mg injection, clonic seizure disappeared and she could obey verbal commands. Within a few minutes clonic seizure was noted again, and she was hypotensive despite administration of vasopressors. A presumptive diagnosis of local anesthetic toxicity was made, and she received 100 ml bolus of 20% Intralipos. She regained consciousness with spontaneous return of blood pressure. She received a total of 230 ml 20% Intralipos, which was discontinued due to her rapid emergence with no further seizure episodes. This case suggests that early and sufficient use of lipid emulsion may lead to a good outcome. We recommend the immediate availability of lipid emulsion along with other emergency therapeutics at the ward after TAPblock.
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PMID:[Ropivacaine-induced late-onset systemic toxicity after transversus abdominis plane block under general anesthesia: successful reversal with 20% lipid emulsion]. 2122 91

Eight years old girl presented with mucocutaneous candidiasis, nail dystrophy, twitching left half of face, progressively increasing generalized skin hyperpigmentation and hypopigmented patches over both shins. Her investigations revealed low intact PTH level, low serum cortisol, high ACTH, impaired glucose tolerance test and candidal onycomycosis. She was diagnosed as Polyglandular Autoimmune Syndrome (PGA) type I. She also developed idiopathic generalized epileptiform seizures and Alcaligenes faecalis septicemia not previously reported with PGA type I. The patient responded well to alphacalcidol, hydrocortisone, valproate sodium, topical antifungal and systemic antibiotics.
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PMID:A case of polyglandular autoimmune syndrome type I with unusual presentation. 2141 32

Subacute encephalopathy with seizures in chronic alcoholism (SESA) was first described in 1981 by Niedermeyer who reported alcoholic patients presenting with confusion, seizures and focal neurological deficits and is quite distinct from patients presenting with typical alcohol withdrawal seizures. EEG often reveals periodic discharges and spikes, but SESA presenting with non-convulsive status epilepticus has rarely been described. We report a case of SESA with non-convulsive status epilepticus in a patient who was initially suspected of having a typical alcohol withdrawal seizure. A 61 year old woman with a history of chronic alcoholism was admitted at an outside hospital for confusion thought to be secondary to an alcohol withdrawal seizure. She had right hemiparesis and later developed right facial twitching that did not respond to intravenous fosphenytoin and levetiracetam. She was transferred for further management. Upon arrival, lorazepam and fosphenytoin were given and right face clonic movements resolved. However, continuous EEG monitoring revealed ongoing non-convulsive status epilepticus (NCSE). Following treatment with IV valproate and lacosamide, there was resolution of NCSE. SESA is likely an under recognized clinical syndrome that is quite distinct from typical alcohol withdrawal seizures and requires a different diagnostic and management approach. NCSE is likely to account for the encephalopathy and focal neurological deficits seen in patients presenting with the clinical syndrome of SESA. Therefore, a high degree of suspicion is warranted and continuous EEG monitoring is recommended for alcoholic patients with encephalopathy and focal neurological deficits.
Seizure 2011 Jul
PMID:Subacute encephalopathy and seizures in alcoholics (SESA) presenting with non-convulsive status epilepticus. 2145 25


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