Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0494475 (tonic-clonic seizure)
1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four, 57 days old, African hunting dog puppies (Lycaon pictus) from one litter died within three weeks following vaccination with modified-live canine distemper virus (CDV) and killed canine adenovirus type 1, canine parvovirus and Leptospira icterohemorrhagiae and canicola. 18 days post vaccination, the animals developed neurologic disease characterized by episodes of grand mal seizures and circling. Macroscopic, histological and immunohistochemical studies revealed acute systemic CDV infection with acute encephalopathy. Virus isolation attempts using primary dog kidney cells, lung macrophages and Vero cells were negative. Therefore, the question whether the infection was the result of vaccination or natural infection remains open. The benefits and risks regarding the use of modified-live CDV vaccines and killed canine distemper vaccines in exotic carnivores are briefly discussed.
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PMID:Vaccine-associated canine distemper infection in a litter of African hunting dogs (Lycaon pictus). 238 81

A 22-year-old man developed severe encephalopathy, grand mal seizures and visual disturbance after combination chemotherapy with cisplatin, vinblastine and bleomycin for metastatic testicular carcinoma. After excluding treatable causes, only supportive management was given, and the symptoms and signs resolved over several months. We suggest a clinical syndrome of encephalopathy, seizures and visual disturbance represents a rare toxicity of cisplatin-based therapy. Given the wide spread usage of cisplatin, this should be drawn once again to the attention of medical oncologists.
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PMID:Encephalopathy following cisplatin, bleomycin and vinblastine therapy for non-seminomatous germ cell tumour of testis. 245 56

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

The authors studied 286 patients with epilepsy with disease onset past the age of 20 years (176 males, 110 females) from the urban and rural populations. In 57% of cases the aetiology of epilepsy was undetermined. Among the known aetiological factors head trauma accounted for 15.5% of cases, inflammatory processes in the central nervous system for 4.5%, alcoholism for 7%, vascular lesions for 6%, tumours for 5.2%, degenerative and atrophic changes for 1.5%. Over 40% of patients had had attacks for up to 15 years and over 18% for over 20 years. In 80% of cases grand mal seizures occurred, and in 33% of these cases more than 12 attacks occurred annually. Six cases of status epilepticus were observed with 2 deaths. The attacks were precipitated by menstruation, alcohol abuse, infection, stressed, television watching. Among the signs accompanying or following the seizures tongue biting and urination prevailed. Neurological signs were demonstrated in 21% of cases, encephalopathy in 65%, other psychic disturbances in 9.5%. Systematic treatment was received by 75% of the patients (over 80% in urban population), and therapy with multiple drugs was most frequent. Drug-resistant epilepsy was found in 34% of cases. The patients from the rural population had a lower educational level and had more children. About 70% of the patients were in employment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Analysis of clinico-social features of epilepsy]. 404 96

We evaluated central nervous system and psychiatric involvement in a clinical sample of 32 patients with systemic sclerosis (SSc) (scleroderma). All patients underwent clinical neurological examination. Electroencephalography (EEG) and visual evoked potentials (VEPs) were also recorded. Prominent central nervous system (CNS) or psychiatric symptoms were present in 5 patients (16%), including encephalopathy, psychosis, anxiety disorder, grand mal seizures and transient ischemic attack. In addition, abnormal VEPs were recorded from 5/32 patients (16%), suggesting optic neuropathy. EEGs were mainly normal or showed only slight, nonspecific changes. Primary CNS involvement in scleroderma, however, could not be shown in any of the 5 cases with neuropsychiatric symptoms. Our results suggest that neuropsychiatric symptoms in SSc are, if not coincidental, indirectly caused by internal organ involvement of SSc or by possible overlapping connective tissue diseases. On the other hand, optic neuropathy might be a primary complication of SSc.
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PMID:Central nervous system involvement and psychiatric manifestations in systemic sclerosis (scleroderma): clinical and neurophysiological evaluation. 833 43

Previous studies found that seizures in orthotopic liver transplantation (OLT) herald a catastrophic neurologic event, but the studies were done of patients who later died and came to autopsy. We studied 630 OLT patients. Laboratory values, electroencephalography, neuroimaging, and levels of cyclosporine or FK506 were reviewed. Neurotoxicity from immunosuppression was considered a trigger for seizures when toxic blood level or increases > or = to 100% were documented, or when white matter lesions or confusional state or tremors were present. Generalized tonic-clonic seizures occurred in 28 of 630 patients (4%). In 7 patients seizures were part of an agonal event (central nervous system infection [n = 3], anoxic encephalopathy [n = 1], cerebral edema with fulminant hepatic failure [n = 1], intracranial hemorrhage [n = 1], and sepsis [n = 1]. In 17 patients cyclosporine (n = 11) or FK506 (n = 6) could be implicated. Remaining causes were acute uremia (n = 1), meningioma (n = 1), and unknown (n = 2). All patients were initially treated with anticonvulsants. Median follow-up of 2 years did not reveal seizure recurrence after discontinuation of anticonvulsants. We conclude that the majority of new-onset seizures after OLT are not indicative of a poor prognosis. Immunosuppression neurotoxicity is the most frequent cause. Anticonvulsant therapy is not necessary for favorable long-term outcome.
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PMID:Causes and outcome of seizures in liver transplant recipients. 896 Jul 38

We report a surgically treated case of early infantile epileptic encephalopathy (EIEE) with suppression-bursts associated with focal cortical dysplasia. Tonic-clonic seizures followed by a series of spasms occurred about a hundred times a day at a few days of age. Interictal electroencephalogram (EEG) revealed a suppression-burst pattern that was predominant in the left hemisphere. Magnetic resonance imaging (MRI) suggested focal cortical dysplasia in the left prefrontal area. Combination therapies with antiepileptic treatments showed only partial efficacy. The patient underwent lesionectomy at age 4 months, after which he gradually showed psychomotor development and a decrease of spasms to 0-2 series daily. In cases of EIEE with focal cortical dysplasia, surgical treatment may have beneficial effects on both psychomotor development and seizure control.
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PMID:Surgical treatment of a case of early infantile epileptic encephalopathy with suppression-bursts associated with focal cortical dysplasia. 1008 May 20

The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnosed with chronic pancreatitis with pancreatic calcifications and pancreatic duct dilation, although she was completely asymptomatic and with no signs of steatorrhoea. She did not have gallstones and the common bile duct was normal. A possible etiopathogenic pathway for pancreatitis could be a suppressive effect of the mt 3243 mutation on the oxidative phosphorylation in affected mitochondria. Although pancreatitis and pancreatic dysfunction in association with the mt 3243 mutation, especially in patients with comorbidity of MELAS and diabetes, has previously been described as a rare manifestation, this case is specific because of the discrepancy of advanced morphological pancreatic alterations and complete lack of pancreatogenic symptoms.
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PMID:Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family. 1082 13

A 21-year old man with marked developmental delay was referred for the diagnosis of myoclonic jerks (MJ), which were sometimes responsible for sudden falls without loss of consciousness, that had begun 2 years before, and for a recent generalized tonic-clonic seizure preceded by a cluster of MJ. Physical examination revealed a small stature, bilateral pyramidal signs, severe mental retardation, and retinis pigmentosa. Etiological factors for this encephalopathy were not found (muscle and skin biopsies, karyotype and extensive blood chemistry). Waking interictal EEG showed a normal background activity and generalized poly-spike-and wave (PSW) discharges. Photic stimulation disclosed a marked photoparoxysmal response, sometimes associated with myoclonic jerks. Three spontaneous jerks accompanied by a burst of generalized PSW were recorded on awakening from a nap. The MRI disclosed wide ventricles, a thin corpus callosum, brainstem atrophy and a so-called "redundant gyration"; these changes were evocative of acquired perinatal damage. Juvenile myoclonic epilepsy (JME) was diagnosed and valproate was started resulting in complete control of seizures. During a 5-year follow-up, the patient has remained seizure-free and the EEG consistently normal. In our opinion, JME can be diagnosed in very uncommon settings, including patients with significant brain damage, as long as all the other criteria for the diagnosis are present.
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PMID:Is it juvenile myoclonic epilepsy? 1093 68

We report a 52-year-old woman who underwent otoneurosurgery to resect acoustic neurinoma. Bone reconstruction was performed with an aluminium (Al)-containing cement. Six weeks later the patient suffered from loss of consciousness, myoclonic jerks, and persistent grand mal seizures, clinical symptoms that resembled those of lethal dialysis encephalopathy of the 1960s and 1970s. She died 6 months later because of septic complications. Light- and electron-microscopic investigation of the central nervous system (CNS) showed pathognomonic Al-containing intracytoplasmic argyrophilic inclusions in choroid plexus epithelia, neurons, and cortical glia. These changes are characteristics of dialysis-associated encephalopathy (DAE), induced nowadays by long-term ingestion of Al-containing drugs (and with benign clinical courses). Atomic absorption spectrometry showed an increase of mean bulk Al concentration of the cortex and subcortex up to 9.3 microg/g (normal range <2 microg/g); laser microprobe showed the increase of Al in subcellular structures. This unique case again shows the extraordinary neurotoxicity of Al, which was, in our patient, initiated by an amount of about 30 mg Al and apparently caused by direct Al access to the brain parenchyma via a cerebrospinal fluid leakage.
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PMID:Subacute fatal aluminum encephalopathy after reconstructive otoneurosurgery: a case report. 1167 49


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