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Query: UMLS:C0149958 (complex partial seizures)
 2,563 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Machado de Assis (1839-1908) is considered the most important Brazilian writer and a great universal literary figure. Little is know about his medical, personal and family history. He hid his "disease" as much as possible. Machado referred to "strange things" having happened to him in his childhood. He described seizures as "nervous phenomena", "absenses", "my illness". Laet observed a seizure and described it as: "... when Machado approached us and spoke to me in disconnected words. I looked at him in surprise and found his features altered. Knowing that from time to time he had nervous problems, ... and only permitted Machado take the Laranjeiras Street car, when I saw that he was completely well". A photographically documented seizure is shown. Alencar wrote, "The preoccupation with health was frequent: either he was having the consequences of a fit or was foreboding one". It is clear that Machado presented localized symptomatic epilepsy with complex partial seizures secondarily generalized of unknown etiology. The seizures which began in infancy or childhood had remission in adolescence and then recurred in his thirties and became more frequent in his later years. His depression got markedly worse with age. In our opinion, the greatest consequence of Machado's epilepsy, was his psychological suffering due to the prejudice of the times. Despite this Machado showed all his genius, which is still actual and universal.
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PMID:Machado de Assis's epilepsy. 130 19

A 16-year-old patient presenting with complex partial seizures occurring in the transition from a REM period to wakefulness is described. His baseline EEG showed generalized and symmetrical slow spike and wave complexes, on a normal background activity, activated by NREM sleep. Polygraphic and videotape recordings, carried out for several nights, showed that after nearly each REM period, he would wake up briefly, presenting eye blinking followed by a burst of generalized hypersynchronous theta to start his seizures. These were characterized by moaning and autoaggressive behaviour, the ictal EEG showing generalized slow spike and wave complexes in the midst of several movement artifacts. At the end of each fit he fell back to REM sleep. Carbamazepine treatment completely resolved his symptoms, with full normalization of EEG activity.
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PMID:Nocturnal complex partial seizures precipitated by REM sleep. A case report. 278 40

A 28-year-old man with regularly occurring clusters of complex partial seizures was studied over a total of 224 days. His seizure periods lasted 2-4 days and occurred at intervals of 5-6 weeks. Several parameters were studied. The most striking finding was an increase in the serum concentration of thyroxine prior to and during the seizure periods. The concentrations of urine catecholamines and serum cortisol also varied with the seizure periods, but these hormones increased after the seizure periods had begun. To determine if there is a general 4-6-week rhythm in thyroid hormone concentrations, 12 weekly blood samples from 10 healthy male students were analyzed. No rhythmicity was found.
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PMID:Association between regularly occurring complex partial seizures and thyroid function parameters. 372 Jul

MB suffered an episode of status epilepticus of febrile origin at the age of 20 months. This was followed at two years by complex partial seizures of temporal lobe origin and at eight years he had learning difficulties arising from the dominant hemisphere. Subsequent symptoms included auditory, visual and olfactory hallucinations which were not controlled by antipsychotics or antiepileptics. EEG and MRI were unhelpful and alternating diagnoses of schizophrenia and temporal lobe epilepsy were made. Now aged 17 years, he has a diagnosis of schizophreniform psychosis with temporal lobe abnormality from status epilepticus in childhood, and is managed by an adult psychiatrist. His symptoms persist.
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PMID:Psychosis or epilepsy--a diagnostic and management quandary. 789 50

A patient showing seizures presenting ictal automatisms with preserved consciousness is reported. A 30-year-old, right-handed man with normal development and without family history of epilepsy was referred for surgical treatment of epilepsy. At 15 he began to have seizures, starting with an epigastric aura, occasionally developing automatisms (lip-smacking, chewing), sometimes followed by tonic-clonic convulsions. At the time of referral, he averaged six convulsive seizures per year and one nonconvulsive per week. His sleep EEG showed sharpened slow activity over the right anterior quadrant magnetic resonance imaging (MRI) showed a benign lesion in the mesial aspect of the right occipital lobe. Simultaneous video monitoring and intracranial EEG with subdural strips recording from the right temporal and occipital lobes was undertaken. During one seizure, he had pronounced oroalimentary automatisms while holding a conversation with a technician, answering her questions, and explaining details of his seizures. Memory of this event was preserved. At seizure onset, spike activity was seen at the mesial occipital strips. At midseizure, high-voltage sharpened delta was seen throughout the right hemisphere. Left-sided scalp electrodes remained relatively uninvolved. The lesion, a dysembryoplastic neuroepithelial tumour was removed. Surgery was followed by abolition of seizures described. Because it is agreed that complex partial seizures require impaired consciousness, a history of automatisms with retained consciousness usually suggests nonepileptic attacks. This case suggests that automatisms in epileptic seizures can take place with minimal loss of consciousness, particularly if there is widespread but unilateral involvement. The need for a revision of the International Classification is suggested.
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PMID:Ictal oroalimentary automatisms with preserved consciousness: implications for the pathophysiology of automatisms and relevance to the international classification of seizures. 977 35

A Japanese male with mosaicism of ring chromosome 14 and chromosome 14 monosomy is described. He demonstrated the characteristic morphologic features of ring chromosome 14, in addition to mental retardation and epileptic seizures. Clusters of complex partial seizures, one of which originated in the left frontocentral region on electroencephalographic monitoring, were evident. His seizures responded to phenobarbital, and his mental and motor development was only mildly retarded. Magnetic resonance imaging revealed a hypoplastic corpus callosum, previously unknown in association with this syndrome.
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PMID:Ring chromosome 14 complicated with complex partial seizures and hypoplastic corpus callosum. 1002 66

We report an 8-year-old boy with complex partial seizures due to congenital stroke, treated with valproate for more than 3 years (the last 2 years were on monotherapy) with no complications during that period except for transient thrombocytopenia. His sister had uncomplicated hepatitis A. One month later, the patient became jaundiced, went into fulminant hepatic failure, and quickly became encephalopathic despite discontinuation of valproate, aggressive supportive therapy, and treatment with carmitine. He then died. He had positive hepatitis A IgM; other causes for acute hepatitis were ruled out. Liver pathology revealed distended hepatocytes with cholestasis and microvesicular changes. We could find in the literature two other articles on four cases who developed liver failure with hepatitis A while on valproate. All those cases, however, recovered. In our patient a usually benign disease became deadly, probably because of the concomitant use of a hepatotoxic medication. Immunizing, with hepatitis A vaccine, all children on valproate therapy who are living in, or traveling to, endemic areas should be considered and is probably advisable.
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PMID:Fatality from hepatitis A in a child taking valproate. 1069 1

We describe the case of a man with a history of complex partial seizures and severe language, cognitive and behavioural regression during early childhood (3.5 years), who underwent epilepsy surgery at the age of 25 years. His early epilepsy had clinical and electroencephalogram features of the syndromes of epilepsy with continuous spike waves during sleep and acquired epileptic aphasia (Landau-Kleffner syndrome), which we considered initially to be of idiopathic origin. Seizures recurred at 19 years and presurgical investigations at 25 years showed a lateral frontal epileptic focus with spread to Broca's area and the frontal orbital regions. Histopathology revealed a focal cortical dysplasia, not visible on magnetic resonance imaging. The prolonged but reversible early regression and the residual neuropsychological disorders during adulthood were probably the result of an active left frontal epilepsy, which interfered with language and behaviour during development. Our findings raise the question of the role of focal cortical dysplasia as an aetiology in the syndromes of epilepsy with continuous spike waves during sleep and acquired epileptic aphasia.
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PMID:Childhood epilepsy with neuropsychological regression and continuous spike waves during sleep: epilepsy surgery in a young adult. 1072 97

Mesial temporal lobe epilepsy (MTLE) developed in a boy receiving FK506 (tacrolimus) after liver transplantation. He had no history of convulsions. At the age of 7, he underwent liver transplantation 13 days after he developed the abdominal form (fulminant hepatitis) of Wilson's disease. On postoperative day 18, he had a generalized tonic seizure (duration 20 min.) with loss of consciousness. FK506 was discontinued under the suspicion of FK506-induced encephalopathy. His symptoms resolved within a few days. FK506 was readministered at 3 months after transplantation. Ten months later, he developed complex partial seizures characterized by right tonic posturing with oral automatism. EEG revealed sporadic spikes in the anterior temporal region. MRI and SPECT showed bilateral (left side dominant) hippocampal lesion, which suggested the diagnosis of MTLE. Since seizures became refractory to medical treatment with progressive worsening of memory functions, FK506 was discontinued again at 36 months after readministration. Six months later, his memory improved remarkably, but there were no changes in seizure frequency and in MRI and SPECT findings. Our findings indicate that FK506 might damage the hippocampus, thereby causing MTLE. Additional case reports, however, will be required to elucidate this new FK506-related neurological complication.
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PMID:[Mesial temporal lobe epilepsy in a patient with Wilson's disease receiving FK506 (tacrolimus) after liver transplantation]. 1149 78

Temporal lobe epilepsy is a partial epileptic disorder in which mesial structures are responsible for the principal ictal symptoms. Its characteristic feature is the recurrence of simple and complex partial seizures, associated with postictal confusion and amnesia of the event. The facilitating effect of NREM sleep on the propagation of the seizure, as well as the sleep abnormalities provoked by epilepsy were evident in our two patients. Yawning is a physiological reflex induced by arousal and drowsiness and may appear in different neurological conditions. Its relation with epilepsy of limbic origin has been rarely reported. We describe in a 95 year old male patient, the occurrence of yawning followed by complex partial seizure during a state of drowsiness. His EEG showed independent bilateral interictal foci of temporal sharp waves and after being medicated with carbamazepine 400 mg/day, the episode did not recur. Another patient, a 17 year old female, displayed complex partial seizures and secondarily generalized seizures with yawning during the posictal period, after naps. The EEG was normal and her polysomnography showed bilateral synchronous temporal spikes and slow waves with secondarily generalization during stage 2 of NREM sleep that produce paroxysmal microarousals and increased stages 1 and 2 of NREM sleep and REM sleep diminished. After being medicated with divalproex sodium 750 mg/day, she suffered no further seizures. Temporal lobe epilepsy, sleep-wake cycles and yawning seem not only to share the same anatomic structures but also the same neurochemical mechanisms. The fact that endogenous opiods are considered as part of a protective system that stop and prevent seizures may allow us to postulate that yawning would be the expression of the endogenous opiods induced mechanisms that stop and prevent the recurrence of the temporal lobe epilepsy. Another hypothesis may be that this is only a particular form of temporal lobe epilepsy.
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PMID:[Yawning and temporal lobe epilepsy]. 1279 82


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