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)

In patients after craniocerebral trauma 24-hour EEG and routine EEG records were obtained. 44 cases were studied between 6 and 38 days after trauma and 45 cases were examined between 6 and 12 months after trauma. The diagnosis of brain commotion in early phase based on neurological examination and computed tomography was made in 22 cases, while in 22 cases late posttraumatic phase was diagnosed. Brain contusion in early and late phase was diagnosed in 22 and 23 cases, respectively. Early after craniocerebral trauma the study demonstrated changes in routine EEG in 8 cases (18.1%), while 24-hour EEG demonstrated them in 26 cases (59.0%), that is three times more as frequently. Changes in 24-hour EEG were found nearly twice as frequently than in routine EEG 6-12 months after trauma (51.0% and 28.9% respectively). In patients with brain commotion in the first week after trauma only 24-hours EEG revealed changes. Late after trauma 24-hour EEG could demonstrate seizure activity more frequently than routine EEG.
Neurol Neurochir Pol
PMID:[24-hour monitoring of bioelectric activity of the brain in patients after cranial injuries]. 152 75

Authors evaluated the activity of c-AMP in the CSF as the biochemical marker for evaluation of epileptic seizure activity in patients with epilepsy. The impact of monitored phenytoin treatment on c-AMP activity in CSF was investigated. It was shown that the general tonic-clonic seizures cause a significant concentration increase of c-AMP in CSF. Monitored phenytoin treatment had a stabilizing effect on c-AMP activity in CSF.
Neurol Neurochir Pol
PMID:[Changes in the cerebrospinal fluid levels of adenosine cyclic- 3',5'-monophosphate (c-AMP) in patients with generalized tonic-clonic epileptic seizures]. 166 Jan 10

Acute poisoning with ethylene glycol manifests itself often with symptoms of central nervous system involvement. The predominating manifestations include consciousness disturbances, seizures, while focal brain damage signs are less frequent. The reported case was hospitalized after trauma to the head and spine, and had signs suggesting expanding intracranial haematoma. CT excluded haematoma and toxicological investigations demonstrated acute poisoning with ethylene glycol.
Neurol Neurochir Pol
PMID:[Acute ethylene glycol poisoning with the course resembling the development of intracranial hematoma]. 180 62

From 1954 to 1971, 69 operations in patients with crs, resulting in relieving the intracranial hypertension symptoms, were performed. The patients were aged 1-34 years. In 1989, i.e. 20-29 years after the operation (mean 22.8 years), 14 patients were submitted again for a neurological, neuropsychological, EEG and brain CT check-up. The patients were divided into 3 groups: I gr. (3 patients)--with negligible disorders of attention and memory, without neurological changes in the EEG and CT--in a good social and occupational status. II gr. (4 patients)--with slight headaches, with discrete neurological and neuropsychological symptoms, slight generalized changes with the moderate burst activity in EEG, signs of hydrocephalus in CT scan. III. gr (7 patients)--with seizures, deficit symptoms, some with symptoms of mental impairment, generalized epileptic changes in EEG, signs of cortical and subcortical atrophy in CT scan. In this group some patients did not work and had no families. We have found that the frequency of epileptic seizures in the crs patients is higher, and their social and occupational status is worse.
Neurol Neurochir Pol
PMID:[Fate of patients after surgical treatment of premature closure of cranial sutures]. 180 24

The effect of chronic electroconvulsive seizure on the blood brain barrier permeability to albumin was investigated in the male rats. Evans blue was used as a blood brain barrier tracer. The following situations were studied: Acute electroshock: a. one electroshock stimulus, b. ten electroshock stimuli. Chronic electroshock: a) group of animals were pretreated with electroshock given as one electroshock (ES) every other day (ES x 7); b) chronic electroshock + one electroshock, c) chronic electroshock + ten repeated electroshocks. As a result, chronic electroshock per se does not effect the blood-brain barrier permeability.
Pol J Pharmacol Pharm
PMID:Blood-brain barrier permeability during acute and chronic electroconvulsive seizures. 181 Dec 18

Out of 184 patients with posttraumatic intracerebral haematomas 52 were treated conservatively. For this treatment patients were qualified with good consciousness level, in the range of 13-15 GCS score. Presence of massive neurological deficit was not an indication to treatment. Patients with haematomas in the central zone, with multiple haematomas or with contraindications to operation were treated conservatively. Eight patients died (15%), in 2 of them severe brain trauma with multiple haematomas were the cause of death, in 1 case primary brainstem trauma was present, one patient had deeply situated haematoma of the thalamus and ventricular system, and in 4 cases death was due to non-cerebral causes. The size of the haematoma in CT scan was not decisive for the choice of the treatment. Nearly in all cases compression of the ventricular system was present, but in only some cases the ventricles were shifted. In repeated CT scans resorption of the haematomas was observed. Twenty patients were discharged home in good general condition without serious neurological deficit. Twenty-four patients were treated later on in other hospital departments. Later outpatient control examinations showed that even serious neurological deficits regressed in most cases. The main symptoms were those of the post-trauma syndrome. About 25% of patients had epileptic seizures after the treatment. The author believes that if the patient is conscious and his consciousness is not worsening conservative treatment of intracerebral haematomas may be undertaken with good effects, on condition, however, of the availability of immediate surgical intervention if the condition of the patient is deteriorating.
Neurol Neurochir Pol
PMID:[Conservative treatment of post-traumatic intracerebral hematoma]. 192 68

Nifedipine (2.5-10 mg/kg) and verapamil (2.5 and 10 mg/kg) offered some protection against pentylenetetrazol (100 and 130 mg/kg)-induced seizure activity in mice. No protection was provided by diltiazem (1.25-10 mg/kg) in this model of experimental epilepsy. Repeated administration of calcium channel blockers (CCBs) in doses of 5 and 10 mg/kg twice daily for three days resulted in no protective effect against pentylenetetrazol. Regarding electroconvulsions, nifedipine (2.5-10 mg/kg) showed the best anticonvulsive action--for instance, in the dose of 10 mg/kg (60 min--treatment time) it elevated the threshold for electroconvulsions from 7.1 to 10.5 mA. Diltiazem (up to 10 mg/kg) and verapamil (up to 20 mg/kg) were considerably less potent in this respect. After repeated administration, only nifedipine (5-10 mg/kg) retained its protective action against electroconvulsions.
Pol J Pharmacol Pharm
PMID:Influence of calcium channel blockers on pentylenetetrazol and electroshock-induced convulsions in mice. 194 38

In the studies material of 119 children with myasthenia epileptic seizures occurred in 8 cases (7%). They always preceded the appearance of myasthenic symptoms. The seizures were primarily generalized. The EEG tracings varied greatly in morphology and intensity. The authors discuss the relationship between myasthenia and epilepsy and the effects of the used drugs on both these diseases.
Neurol Neurochir Pol
PMID:[Epileptic seizures in children with myasthenia gravis]. 196 79

Investigations were made of the action of ACTH and LH-RH on a number of behavioural paradigms and the possible involvement of neurotransmitters or opiates by pretreatment of receptor blockers in rats and mice. ACTH delayed the extinction of active avoidance behaviour. Atropine and haloperidol blocked this action, whereas phenoxybenzamine and propranolol were ineffective. LH-RH or a highly potent analogue of LH-RH (D-Trp6-LH-RH) decreased the rate of disappearance of dopamine in the hypothalamus following alpha-methyl- paratyrosine inhibition of catecholamine synthesis, and blocked the accumulation of serotonin following MAO inhibition. LH-RH or the analogue attenuated the consolidation of passive avoidance learning. Apomorphine-induced cage-climbing was also inhibited by the LH-RH analogue, but this action was not influenced by naloxone. Open-field activity (ambulation, rearing and grooming) was decreased by the analogue peptide. Naloxone blocked the action on ambulation and rearing, but was ineffective on grooming. The LH-RH analogue caused a dose-dependent increase in cataleptogenic activity. This action could not be blocked with naloxone. The LH-RH analogue suppressed picrotoxin-induced seizures. Naloxone restored the situation to the control level. The data suggested that the effects of some neurohormones are mediated by transmitters or endogenous opiates, and that both peptide-transmitter and peptide-peptide interactions have to be considered in the action of neurohormones.
Pol J Pharmacol Pharm
PMID:Involvement of neurotransmitter and neuropeptides in behavioural action of some neurohormones. 198 90

The behavioural effects of angiotensin II (AT II) were studied using the following paradigms: seizures (threshold and intensity) in mice; active avoidance (shuttle-box) in rats; passive avoidance (step through) in rats; exploratory activity (open field) in rats; apomorphine stereotypy in rats. The involvement of DA- and GABA-ergic transmitter mechanisms in the effects of AT II was also studied. It was found that AT II increased the seizure threshold and decreased the seizure intensity, the effects being potentiated by DA- and GABA-ergic agonists and prevented by DA- and GABA-ergic antagonists. AT II effect on seizure threshold was stronger when AT II was applied after withdrawal of repeatedly injected DA-ergic antagonist pimozide. AT II improved retention in active and passive avoidance tasks. This effect was potentiated by DA- and GABA-ergic agonists. Postrial saralasin and haloperidol abolished the retention-facilitating effect of AT II. Bicuculline and picrotoxin abolished the influence of GABAA-ergic agonists on the memory effect of AT II. AT II changed exploratory behaviour in a nonlinear dose-effect manner. The stimulant effects of AT II were antagonized by saralasin, increased by apomorphine and nomifensine and decreased by haloperidol and alpha-methyl-para-tyrosine (alpha MpT). AT II enhanced apomorphine stereotypy; the effect was decreased by saralasin and alpha MpT, and abolished by haloperidol. These results suggest that the behavioural effects of AT II are mediated by interactions with brain AT II receptors. DA and GABA receptors modulate in some way the AT II activity.
Pol J Pharmacol Pharm
PMID:Involvement of transmitter mechanisms in the behavioural effects of angiotensin II. 198 91


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