Cases reported "Epilepsy, Complex Partial"

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11/41. Lack of neuronal damage in atypical absence status epilepticus.

    PURPOSE: Whether status epilepticus of nonconvulsive epileptic seizures is harmful still remains controversial. To investigate this, the presence and/or extent of neuronal damage in patients with absence status epilepticus (ASE) and patients with complex partial status epilepticus (CPSE) was examined and compared. methods: Neuron-specific enolase (NSE) in CSF was examined in the patients with ASE and compared with that of the patients having CPSE. Clinical aspects of these patients also were investigated. RESULTS: CSF NSE levels in ASE patients were lower than those of CPSE patients and were considered as the normal values. No clinical symptoms indicated neuronal damage in the ASE patients. CONCLUSIONS: This study suggests that ASE does not induce neuronal damage. serum NSE is not always correlated to CSF NSE, and determination of serum NSE levels may be an inappropriate method of estimating neuronal damage in some cases of ASE.
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12/41. Transient kluver-bucy syndrome following complex partial status epilepticus.

    The characteristic features of kluver-bucy syndrome include hypersexuality, hyperorality, placidity, hypermetamorphosis, visual agnosia, changes in dietary habits, and memory impairment. Human cases have been reported with herpes simplex encephalitis, head injury, Pick's disease, transtentorial herniation, adrenoleukodystrophy, and Reye's syndrome, all involving bilateral temporal lobe pathology. We present the case of a patient with no evidence of a structural lesion in the temporal lobes and behavioral changes consistent with kluver-bucy syndrome following complex partial status epilepticus.
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13/41. Nonconvulsive status epilepticus due to a de novo contralateral focus during tiagabine adjunctive therapy.

    We describe a 30-year-old woman with an infantile-onset epilepsy due to a left temporal gliotic area who developed a nonconvulsive status epilepticus (NCSE) during tiagabine (TGB) adjunctive therapy. The ictal EEG recording showed a de novo right temporal focus not previously evident. After the i.v. administration of 4 mg lorazepam, the NCSE episode rapidly resolved and her usual left temporal EEG abnormalities reappeared. To our knowledge this is the first case of paradoxical seizure exacerbation associated with TGB therapy in which the clinical and EEG features are congruous with a new contralateral focus.
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14/41. Prolonged absence status epilepticus associated with carbamazepine therapy, increased intracranial pressure, and transient MRI abnormalities.

    We describe an adolescent epileptic patient who presented in nonconvulsive status epilepticus that appeared to be related to treatment with carbamazepine. The absence status, which was resistant to multiple anticonvulsants, produced increased intracranial pressure and transient abnormalities observed on MRI.
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15/41. Prolonged ictal amnesia with transient focal abnormalities on magnetic resonance imaging.

    A previously healthy woman had a prolonged amnestic state caused by complex partial status epilepticus with bilateral mesiotemporal lobe involvement confirmed by EEG with nasopharyngeal electrodes. A magnetic resonance imaging (MRI) scan obtained shortly after recovery from the amnesia showed reversible focal abnormalities consisting of increased signal intensity on T2-weighted scan in the mesiotemporal lobe.
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16/41. MRI evidence for the involvement of basal ganglia in epileptic seizures: an hypothesis.

    Recent clinical and experimental studies have suggested that the basal ganglia are involved in epileptic seizures as a propagation pathway or as a remote inhibitory control circuit. The present case report may provide additional evidence from post-ictal magnetic resonance imaging (MRI) supporting this hypothesis. A healthy 13 year-old boy was admitted for a complex partial status epilepticus. MRI, performed one week later, revealed bilateral T2 hyperintense signals in the striata and a left temporal arachnoid cyst. Left temporal slow waves were noted on EEG recording. No obvious metabolic alterations were identified. During the next six years of follow-up, no seizure occurred and striatal alterations progressively disappeared. The clinical characteristics of the seizures, EEG slow waves, and probably the presence of an arachnoid cyst suggest that seizures originated from the left temporal lobe. The long-lasting MRI changes suggest that bilateral striatal alterations may have been secondary to an inflammatory process, which in turn could have disrupted a striatal inhibitory control over seizures. On the basis of these arguments, we speculate involvement of basal ganglia in epileptic seizures, as a part of a modulatory control system over seizures rather than a propagation pathway. Future reports will support or invalidate our hypothesis.
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17/41. Longitudinal study of MRS metabolites in Rasmussen encephalitis.

    This study analyses the evolution of metabolite changes in an 8-year-old boy with focal Rasmussen encephalitis. Five MRI examinations, including magnetic resonance spectroscopy (MRS) were performed over 9 months. Following complex partial status, T2-weighted imaging showed transient dramatic signal increase in the left superior temporal gyrus and mesial temporal structures. Subsequent scans showed resolution of the swelling and signal normalization, with development of slight focal atrophy. MRS after status showed a reduction in N-acetylaspartate, total creatine and trimethylamines. Subsequent scans showed complete resolution of these metabolite abnormalities, followed later by development of further abnormal metabolite values. Lactate and glutamine/glutamate were elevated after status. After surgery, ex vivo high-field (1)H and (31)P MRS confirmed metabolite abnormalities (elevated choline and decreased aspartate, N-acetylaspartate, [(1)H]glutamate together with altered [(31)P]phospholipid ratios. These findings suggested active disease process in the anterior region of the excised superior temporal gyrus. We conclude that Rasmussen encephalitis is a combination of progressive encephalitic damage and fluctuating seizure effects, in which neuronal injury and recovery can occur. MRS measurements at a single time point should consider the fluctuating metabolite profile related to seizure activity.
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18/41. Palatal myoclonus occurring during complex partial status epilepticus.

    Palatal myoclonus is thought to occur after damage to certain brain-stem structures, and with a delay following the causative lesion. A case of palatal myoclonus, probably of epileptic nature, is described.
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19/41. Status gelasticus after temporal lobectomy: ictal FDG-PET findings and the question of dual pathology involving hypothalamic hamartomas.

    PURPOSE: To present the first ictal fluorodeoxyglucose-positron emission tomography (FDG-PET) evidence of the hypothalamic origin of gelastic seizures in a patient with a hypothalamic hamartoma (HH) and to raise the issue of true dual pathology related to this entity. methods: Ictal FDG-PET was acquired during an episode of status gelasticus with preserved consciousness, in a patient previously operated on for complex partial seizures (CPSs) due to a temporal lobe epileptogenic cyst. RESULTS: Ictal hypermetabolism was localized to the region of the HH during the status gelasticus. CPSs had been completely eliminated after temporal lobe surgery. CONCLUSIONS: Ictal FDG-PET independently confirmed that gelastic seizures in patients with HH do originate in the diencephalic lesion. An HH may coexist with another epileptogenic lesion, in a context of dual pathology.
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20/41. A case of systemic lupus erythematosus with complex partial status epilepticus.

    We describe a woman with systemic lupus erythematosus who had complex partial status epilepticus as the sole epileptic manifestation. The patient presented with a confusional state, initially considered to be psychotic in nature, due to SLE. However, the EEG demonstrated the epileptic etiology of her symptoms. In patients with lupus presenting with prolonged episodes of confusion and behavioural disturbance, an EEG should be performed, whenever possible during the episode, even in the absence of a previous history of epilepsy.
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