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)

The first case of cerebral paragonimiasis was reported by Otani in Japan in 1887. This was nine years after Kerbert's discovery of the fluke in the lungs of Bengal tigers and seven years after a human pulmonary infection by the fluke was demonstrated by Baelz and Manson. The first case was a 26-year-old man who had been suffering from cough and hemosputum for one year. The patient developed convulsive seizures with subsequent coma and died. The postmortem examination showed cystic lesions in the right frontal and occipital lobes. An adult fluke was found in the occipital lesion and another was seen in a gross specimen of normal brain tissue around the affected occipital lobe. Two years after Otani's discovery, at autopsy a 29-year-old man with a history of Jacksonian seizure was reported as having cerebral paragonimiasis. Some time later, however, it was confirmed that the case was actually cerebral schistosomiasis japonica. Subsequently, cases of cerebral paragonimiasis were reported. However, the majority of these cases were not confirmed histologically. It was pointed out that some of these early cases were probably not Paragonimus infection. After World War II, reviews as well as case reports were published. Recently, investigations have been reported from Korea, with a clinicla study on 62 cases of cerebral paragonimiasis seen at the Neurology Department of the National Medical Center, Seoul, between 1958 and 1964. In 1971 Higashi described a statistical study on 105 cases of cerebral paragonimiasis that had been treated surgically in Japan.
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PMID:Cerebral Paragonimiasis. 109 92

A 41-year-old chemist developed methyl iodide intoxication. His case is presented with a review of pertinent literature. Characteristics of the poisoning include a delay between exposure and onset of symptoms; early systemic toxicity with congestive changes in the lungs and oliguric renal failure; prominent cerebellar and Parkinsonian neurologic symptoms as well as seizures and coma in severe cases; and psychiatric disturbances that can last from months to years. Although methyl iodide is a rare form of intoxicant, its manifestations are similar to that of poisoning with the other monohalomethanes that are not uncommon.
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PMID:Methyl iodide intoxication. A case report. 111 68

A case is presented of neurilemmoma of the left oculomotor nerve occurring in a 64-year-old hypertensive woman. The incipient tumour produced ptosis, limited inwards rotation of the eyeball, and persistent pupillary dilatation on the left side. The mechanism of this process is discussed, having regard to the interruption of the fibres innervating these structures by the tumour, and considering the mode of occurrence of the ocular and pupillary impairments. The patient also had generalized athero-sclerosis and fusiform aneurysm of the terminal part of the left internal carotid artery. The symptoms of headache, seizure, coma, and temporary right hemiparesis were considered as manifestations of hypertensive encephalopathy unrelated to the tumour.
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PMID:Neurilemmoma of the oculomotor nerve. 112 61

Two patients with herpes simplex encephalitis had clinical courses consisting of an acute febrile illness with early onset of seizures and rapidly progressive neurologic signs evolving to coma and death within 3 weeks. The electroencephalograms of both patients were similar and showed widespread, periodic, stereotyped sharp-and-slow-wave complexes occurring bilaterally over both hemispheres, as well as transient episodes of electrographic seizure activity occurring unilaterally, with suppression of the periodic activity on that side. Although the electroencephalographic findings are not pathognomonic, when associated with an acute encephalitic process, they would suggest the diagnosis of herpes simplex encephalitis.
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PMID:A distinctive clinical EEG profile in herpes simplex encephalitis. 115 42

Duration of postictal coma following maximal electroshock seizure and monoamine levels in the whole brain were measured in mice. Pretreatment with intraperitoneal alpha-methyl-p-tyrosine (alpha-MT), 5-hydroxytryptophane (5-HTP), or intraventricular 6-hydroxydopamine (6-OHDA) prolonged the coma duration, whereas p-chlorophenylalanine (PCPA) did not affect the coma, and L-DOPA tended to shorten the coma and counteracted the effect of alpha-MT. When the shock was repeated five times with one hour intervals, the duration of coma was progressively increased being accompanied by elevated serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) levels in the brain. In alpha-MT treated group, a striking parallelism was remarked between coma prolongation and norepinephrine (NE) or dopamine (DA) reduction. These data suggest that prolongation of postictal coma is correlated with reduced NE and DA levels and/or with elevated 5-HT and 5-HIAA levels in the brain.
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PMID:Correlation between brain monoamine levels and postictal coma following electroshock. 115 19

Among 1,459 autopsied patients with cancer, 12 had multifocal infarcts of the brain that appeared to be caused by intravascular coagulation. Most of these patients were women with leukemia or lymphoma, and all had a clinical course in which neurologic signs and symptoms were prominent. All had evidence of generalized brain disease (delirium and stupor or coma), and several also had focal brain disease (focal seizures, hemiparesis). All patients had laboratory evidence of coagulation abnormalities, although these were often not severe when neurologic symptoms began. Pathologically, there were multifocal hemorrhagic or ischemic infarcts in the distribution of several cerebral vessels, without a systemic source for cerebral emboli. Fibrin thrombi were identified in cerebral vessels and in vessels of several other organs. The clinical findings fit the pathologic picture, and in most instances the correct diagnosis might have been made earlier had it been considered.
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PMID:Neurologic manifestations of intravascular coagulation in patients with cancer. A clinicopathologic analysis of 12 cases. 117 2

Coma on admission, multiple, deep, or ruptured abscess, inaccurate diagnosis, and inability to prove the diagnosis were factors contributing to mortality. In survivors, abscess generally followed cranial injury, surgery, or contiguous infection; in most fatal cases, brain abscess was secondary to a more remote primary infection. Ruptured or multiple abscesses or positive spinal fluid cultures were not found in survivors, and coma was present in only one. Fatal cases in patients admitted in coma usually did not exhibit focal signs, seizures, or symptoms of meningitis early in the illness; none of these patients had prior cranial injury or surgery. Absence of these delayed their seeking care and accurate diagnosis. Ruptured abscess was frequent in these patients. Most patients not in coma on admission had focal signs, seizures, symptoms or meningitis, or had prior cranial injury or surgery.
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PMID:Factors associated with mortality in brain abscess. 117 17

Phencyclidine is now one of the most frequently used main ingredients of "street drug" preparations. Its effects are highly dose dependent and three varieties of acute intoxication have been seen clinically associated with different dosages and routes of administration. Most persons using phencyclidine smoke it sprinkled on parsley in low doses. The presence of horizontal and vertical nystagmus associated with hypertension in a patient who is agitated or comatose are diagnostic of a phencyclidine intoxicated state. Sensory isolation and intravenous administration of diazepam in the event of seizure activity have proved effective in the treatment of acute intoxicated states. Phencyclidine has pronounced behavioral toxicity and several deaths due to this agent have now been documented. It is unknown whether seizure activity or respiratory depression is the primary cause of death in pharmacological overdoses.
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PMID:Phencyclidine--states of acute intoxication and fatalities. 121 Mar 29

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

A 26-year-old woman developed seizures and psychiatric disorders after having been in coma with encephalitis for a protracted period at age 11. Seizures were psychomotor, minor motor, and major motor with auras of fear, panic, and olfaction. The patient hallucinated, had paranoid ideas, was depressed, and attempted suicide. Medical and psychiatric treatment with anticonvulsants and tranquilizers was ineffective. Depth and surface EEG recordings revealed bilateral discharge abnormality in temporal, frontal, and thalamic areas. Lesions were placed in the temporal and orbitofrontal area bilaterally for the psycho-motor-psychic seizures and in the left thalamus for the minor motor seizure. The seizures were relieved without the incapacitating complications that occur with standard lobotomy and temporal lobe resection. Improvement of the psychic component of the seizures is believed due to interrupting seizure discharging circuitry in the temporal and frontal areas. The term temporofrontal seizures is proposed for the anatomic designation of psychomotor-psychic seizures.
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PMID:Psychomotor-psychic seizures treated with bilateral amygdalotomy and orbitotomy. 124 59


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