Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The excitatory amino acid glutamate plays an important role in the mammalian CNS. Studies conducted from 1940 to 1950 suggested that oral administration of glutamate could have a beneficial effect on normal and retardate intelligence. The neurotoxic nature of glutamate resulting in excitotoxic lesions (neuronal death) is thought possibly to underlie several neurological diseases including Huntington's disease, status epilepticus. Alzheimer's dementia and olivopontocerebellar atrophy. This neurodegenerative effect of glutamate also appears to regulate the formation, modulation and degeneration of brain cytoarchitecture during normal development and adult plasticity, by altering neuronal outgrowth and synaptogenesis. In addition to its function as a neurotransmitter in several regions of the CNS, glutamate seems to be specifically implicated in the memory process. Long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity associated with learning and memory, both involve glutamate receptors. Studies with antagonists of glutamate receptors reveal a highly selective dependency of LTP and LTD on the N-methyl-D-aspartate and quisqualate receptors respectively. The therapeutic value of glutamate receptor antagonists is being actively investigated. The most promising results have been obtained in epilepsy and to some extent in ischaemia and stroke. The major drawback remains the inability of antagonists to permeate the blood-brain barrier when administered systemically. Efforts should be directed towards finding antagonists that are lipid soluble and able to cross the blood-brain barrier and to find precursors that would yield the antagonist intracerebrally.
 ...
PMID:Glutamate in the mammalian CNS. 198 Nov 50

The authors studied specific and sensitive indicators of neuronal adenosine triphosphate (ATP) depletion--hypoxanthine, xanthine and uridine levels--in the cerebrospinal fluid (CSF) of nine children during non-convulsive status epilepticus. No evidence of ATP depletion was found and CSF pH and creatine kinase levels were similar to those of controls. Hypoxanthine, xanthine and uridine had a tendency to be low, but this was significant only for xanthine. The authors speculatively link this reduction to a reduction in neuronal protein synthesis. This might be a mechanism whereby non-convulsive status epilepticus could lead to intellectual deterioration and dementia.
 ...
PMID:Cerebrospinal fluid nucleotide metabolites following non-convulsive status epilepticus. 273 69

We report our experience using barbiturate anesthesia for the treatment of refractory status epilepticus. Following a retrospective review of eight patients treated with a variety of barbiturates and dosing regimens, we established a specific protocol employing pentobarbital and evaluated it prospectively in six patients. Among the 14 patients, intravenous barbiturates, when administered with a loading dose followed by continuous infusion, were uniformly effective in aborting seizures and producing a burst-suppression EEG pattern. Other than the pupillary light reflex, most patients lost all brainstem reflexes and motor responses during therapy. Barbiturate-induced hypotension was observed in 9 of the 14 patients, and required treatment with pressors in seven cases. Three patients died early as a consequence of their underlying illness, while three others died late for reasons unrelated to the status itself or to anticonvulsant therapy. The time to recovery of function following anesthesia varied highly, spanning hours to days for return of motor function and days to weeks for cognition. Of the eight survivors, four were left with mild cognitive deficits, one returned to his baseline dementia, and three had residual encephalopathies (severe in two). We conclude that barbiturate anesthesia is an extremely effective therapy for refractory seizures. However, its use necessitates recognition of untoward cardiovascular responses and prolonged intensive care.
 ...
PMID:Barbiturate anesthesia in the treatment of status epilepticus: clinical experience with 14 patients. 327 38

The presented material comprised 17 cases observed in four Warsaw hospitals in a period of 20 years. Nine patients with the pseudotumour syndrome were diagnosed correctly and referred to neurosurgical services. The remaining eight cases died in neurological hospital departments with the following clinical diagnoses: cerebral stroke 3, subarachnoid haemorrhage 1, comatose state preceded by dementia 1, chronic meningoencephalitis 1, status epilepticus 2 cases postmortem investigations demonstrated cerebral cysticercosis in all cases. In four patients with predominant symptoms of cerebrovascular disease lesions were found of the type of residual vasculitis cysticercosa, the sequelae of which might have caused secondary complications independent of concomitant arteriosclerosis. Dementia appeared in a patient with huge hydrocephalus consequent to numerous cysticerci. The patient with the diagnosis of meningoencephalitis had an inflammatory reaction of the ependyma and meninges caused by a cysticercus floating in the IV ventricle. Of the patients dying in status epilepticus attention is called to a 6-year-old girl with a solitary cysticercus localised subcortically in the motor area. The authors suggest that the possibility of cysticercosis should be kept in mind, despite its rarity, in cases with a not completely clear clinical manifestations of cerebrovascular disease, chronic meningoencephalitis and epilepsy or dementia.
 ...
PMID:[Neuropathologic analysis of 8 undiagnosed cases of cerebral cysticercosis]. 344 11

Rasmussen's encephalitis (RE) is a progressive childhood disorder characterized by intractable focal seizures, hemiplegia, dementia, and inflammatory histopathology. The process is typically limited to one cerebral hemisphere. We report four patients with pathologically confirmed RE who were treated with repeated plasmapheresis. Three patients exhibited repeated, dramatic, transient responses to plasmapheresis, manifested by reduced seizure frequency and improved neurologic function. One patient exhibited marginal improvement after treatment with plasmapheresis. These observations indicate that circulating factors, likely autoantibodies, are pathogenic in at least some patients with RE and suggest that RE is an autoimmune disease. Plasmapheresis may be a useful adjunctive therapy in status epilepticus, and can also aid in assessment of residual function in the diseased hemisphere before surgical resection.
 ...
PMID:Plasmapheresis in Rasmussen's encephalitis. 855 27

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
 ...
PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
 ...
PMID:Electroencephalography as a diagnostic tool in dementia. 906 24

Progressive myoclonic epilepsy (PME) syndromes are intractable to most antiepileptic drugs (AED). The course of these diseases, results in almost total dependency due to continuous myoclonias, repeated episodes of status epilepticus, ataxia and dementia. The need for new treatment strategies is therefore imperative. Zonisamide has previously been reported to be effective in two patients with PME. Case reports of seven patients (ages 19-42) with Unverricht-Lundborgs disease (ULD) and one Lafora Body Disease are presented. Zonisamide was given at doses of 100-600 mg/day for a period of 2 to 3 years. Concomitant AEDs were usually valproate and a benzodiazepine. Zonisamide dramatically reduced the amount of myoclonias and generalized seizures. In three of the cases, the initial dramatic effect on myoclonias wore off after 2-4 years of treatment but patients still experienced moderate efficacy for generalized tonic-clonic seizures. The dramatic reduction of stimulus sensitivity for light, touch and startle by zonisamide was sustained in all patients with ULD. Zonisamide may be a useful agent in the treatment of PME. Controlled clinical trials are warranted to further investigate the antiepileptic effects of this drug, in difficult to treat epileptic syndromes.
 ...
PMID:Zonisamide for progressive myoclonus epilepsy: long-term observations in seven patients. 947 42

Non-convulsive status epilepticus (NCSE) is a common complication of the childhood epileptic encephalopathies. An essential feature for the diagnosis of non-convulsive status epilepticus is a continuous epileptiform activity on the electroencephalogram (EEG). Dementia is thought to be a possible long-term sequel of non-convulsive status epilepticus, the mechanism of which has remained elusive. Neuron specific enolase is a marker of neuronal damage. The serum concentration of neuron specific enolase (sNSE) has been measured in 17 children with continuous epileptiform activity on the EEG and in 16 children with epilepsy but without a continuous dysrhythmia. There was a significant difference in the concentration of sNSE between the two groups.
 ...
PMID:Serum neuron specific enolase: a marker for neuronal dysfunction in children with continuous EEG epileptiform activity. 1072 91

A 62-year-old right-handed woman had presented progressive speech impediment over 4 months. She was alert without any convulsions or involuntary movements. Neurological examination showed Wernicke's aphasia, constructional apraxia. Her magnetic resonance imaging (MRI) showed an old cerebral infarction in the left parieto-occipital area, in addition to ischemic changes in the bilateral deep white matter. Electroencephalography (EEG) revealed periodic lateralized epileptiform discharges (PLEDs) predominant in the posterior left hemisphere. The PLEDs as well as the cortical symptoms improved after an administration of anti-convulsive agents, thus establishing the diagnosis of non-convulsive status epilepticus (NSE). It should be emphasized that NSE manifesting as Wernicke's aphasia should be distinguished from dementia syndrome because it is a treatable disorder.
 ...
PMID:[A case of non-convulsive status epilepticus worsened Wernicke's aphasia reversely]. 1096 50


1 2 3 4 5 Next >>