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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Complex partial seizures (CPSs) of extratemporal origin are frequently misdiagnosed. Common reasons for diagnostic errors are failure to recognize the epileptic cause of the attacks or to appreciate localizing clinical seizure characteristics and nonspecific or misleading scalp EEG findings. This report describes clinical characteristics of two types of extratemporal CPSs, frontal and occipital. Frontal lobe CPSs are brief, frequent attacks that begin and end suddenly. They are dominated by complex, semi-purposeful motor automatisms, and vocalization and sexual automatisms are common. Their often bizarre appearance frequently leads to a misdiagnosis of hysteria. Occipital lobe CPSs are characterized primarily by their spread pattern, which can follow various paths. They may mimic temporal lobe CPSs, sensorimotor partial seizures, or supplementary motor partial seizures. Scalp EEGs are frequently misleading. The initial clinical symptoms are the most important clue to correct diagnosis and include elemental visual symptoms, visual loss, eye pulling or movement sensations in the absence of detectable movement, rapid forced blinking or eye flutter, and contralateral eye deviation.
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PMID:Clinical and EEG features of complex partial seizures of extratemporal origin. 372 Jul 13

Of 87 patients with complex partial epilepsy who were evaluated with depth electrodes, 8 developed complex partial status epilepticus (CPSE). Seizures originated extratemporally in all 8 patients. Frontal lobe onset was established in 4 patients and was probable in 1 more. Medial parietal onset was documented in 1 patient. Medial occipitoparietal onset occurred in another, and 1 patient had multifocal onsets. Even when seizures did not begin frontrally, the frontal lobes were prominently involved during CPSE. CPSE did not occur in 60 patients with seizures originating in the temporal lobe. Both recurrent clinical seizures and continuous altered behavior were observed. Some patients exhibited both clinical patterns at different times during the same episode. Depth recording consistently demonstrated recurrent isolated seizure discharges throughout episodes. The clinical patterns were related, in part, to electroencephalographic seizure frequency, duration, and intensity. Episodes of CPSE were not associated with intellectual deterioration.
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PMID:Complex partial status epilepticus: a depth-electrode study. 408 48

Ictal sexual automatisms such as masturbatory activity, pelvic thrusting, or similar automatisms for which the patient is amnesic have been attributed to temporal lobe disease. Of 61 patients with medically refractory complex partial seizures, 14 had frontal lobe seizure foci. Four of these patients manifested sexual automatisms in some or all of their seizures. Frontal lobe seizure origin was documented by depth EEG in three patients. In the fourth, a calcified lesion was demonstrated radiologically. In three patients, frontal lobectomy revealed abnormal frontal lobe pathology and was followed by 75 to 100% reduction in seizure frequency. Sexual automatisms did not occur in patients with seizures originating in any area other than the frontal lobe.
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PMID:Sexual automatisms in complex partial seizures. 668 92

We add two cases of neoplastic angioendotheliosis to the previous 13 with central nervous system manifestations. This unusual neoplastic phenomenon is thought to represent a diffuse malignant proliferation of endothelial cells. A man aged 58 first had transient ischemic attacks followed by a subacute profound dementia with psychomotor retardation. Remission followed steroid therapy. Abulia recurred along with a gradually progressive paraplegia leading to death 16 months after onset of symptoms. Pathologic examination showed tumor masses in the basal ganglia and widespread patchy cerebral infarction. The spinal cord below the midthoracic level was destroyed. Microscopically small mononuclear tumor cells were widespread within and largely confined to the lumens of small cerebral blood vessels which showed varying degrees of occlusion and recanalization. Factor 8 antigen, a specific endothelial cell marker, was not present on the surface of the malignant cells. Another man aged 61 developed subacute dementia with frontal lobe signs, dysphasia and impairment of memory. Computerized tomography showed multiple infarcts. A brief respite followed steroid therapy but progressive deterioration led to death in 15 weeks. Frontal lobe biopsy revealed the same neoplastic vascular process. The hallmark of the illness is a progressive subacute lobar dementia. Transient spells may occur. Hemiparesis is unusual and seizures do not occur except terminally. Angiography is normal.
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PMID:Neoplastic angioendotheliosis. 703 26

Patients with epileptic seizures frequently complain of long-lasting cognitive impairment after a seizure. We evaluated this issue in 31 patients with epileptic seizures of a frontal (n = 8) or temporal lobe origin [right temporal lobe (RTL) n = 8/left temporal lobe (LTL) n = 15]. Seizures were secondarily generalized in 18 patients. Computerized testing of verbal and nonverbal recognition memory was performed before the seizure, directly after postictal reorientation, and 30 min and 1 h later. Repeated testing of 14 healthy persons served as control. The following results were obtained: Depending on seizure generalization, postictal reorientation times were 1-45 min. Frontal lobe seizures showed no effect on postictal memory performances, but verbal and visual recognition memory was significantly decreased after temporal lobe seizures. Decrease in either verbal or visual memory and time of recovery were related to lateralization of seizure onset. Functional recovery after reorientation lasted 30 min to 1 h. The decrease in performance was more severe after generalized seizures. Decision times during memory performance were not significantly affected by the seizures. Temporal lobe seizures lead to circumscribed and long-lasting memory deficits, which can be assumed to affect patients' capabilities seriously. Pre- and postictal testing is a useful tool for determining postictal cognitive impairment and in determining the site of seizure onset.
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PMID:Postictal courses of cognitive deficits in focal epilepsies. 792 54

Video-telemetry, with EEG recordings from intracranial electrodes, has been used for the past 15 years at the National Center for Epilepsy to identify candidates for epilepsy surgery. The recordings have been a useful tool for correlating neuroanatomy and ictal, epileptic symptoms. The authors describe the most characteristic clinical symptoms and electroencephalographic findings in seizures deriving from the frontal lobe. An attempt is made to subclassify seizures deriving from different parts of the frontal lobe. Frontal lobe seizures are illustrated by three case histories.
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PMID:[Frontal epileptic seizures]. 799 30

Frontal lobe epilepsies may present difficulties in focus localization in the pre-operative work-up for epilepsy surgery. This is specially true in patients with normal MRIs. We report on a 16 years-old girl that started with seizures by the age of 8 years. They were brief nocturnal episodes with automatisms such as bicycling and boxing. Seizure frequency ranged from 4-10 per night. Scalp EEG showed few right frontal convexity spiking and intense secondary bilateral synchrony (SBS). High resolution MRI directed to the frontal lobes was normal. Ictal SPECT suggested a right fronto-lateral focus. Ictal video-EEG showed no focal onset. She was submitted to invasive recordings after subdural plates implantation. Electrodes covered all the frontal convexity and mesial surface bilaterally. Ictal recordings disclosed stereotyped seizures starting from the right mesial frontal. Using a high-resolution tool to measure intra and interhemispheric latencies, the timing and direction of seizure spread from the right fronto-mesial region were studied. Motor strip mapping was performed by means of electrical stimulation. She was submitted to a right frontal lobe resection, 1.5 cm ahead of the motor strip and has been seizure free since surgery (8 months). Pathological examination found a 4 mm area of cortical dysplasia. Invasive studies are needed to allow adequate localization in patients with non-localizatory non-invasive work-up and may lead to excellent results in relation to seizures after surgery.
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PMID:Secondary bilateral synchrony due to fronto-mesial lesions. An invasive recording study. 1066 89

Bilateral perisylvian polymicrogyria (BPP) is a malformation of cortical development, frequently associated with severe dysarthria or anarthria. BPP patients are therefore often labeled as severely retarded, but a detailed neuropsychological profile has not been reported to date. In a series of 14 patients, we demonstrated that only a minority had extremely low intelligence, and that some aspects of cognitive function correlated with the extent of the cortical disorganization. Early age at seizure onset correlated positively with Performance IQ scores (P<0.05) and negatively with the extent of the lesion (P<0.01), reflecting that patients with more severe BPP are more likely to have early seizure onset, resulting in greater interference with ongoing cognitive development. Receptive and expressive language skills were found to be equally poor. Frontal lobe function and memory abilities were relatively well preserved, suggesting that the observed cognitive profiles were related, at least in part, to specific areas of cortical dysfunction and not only to global dysfunction.
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PMID:Cognitive functioning in bilateral perisylvian polymicrogyria (BPP): clinical and radiological correlations. 1582 Mar 49

A 1-year-old girl with influenza-associated encephalopathy initially exhibited prolonged febrile convulsions and subsequent drowsiness. She became unconsciousness and experienced a cluster of seizures 4 days later. Diffusion-weighted magnetic resonance imaging (DWI) showed high signal intensity in the bilateral frontal white matter. This signal change migrated to the bifrontal cortical areas and the caudate nuclei within 10 days, when T2 elongation appeared over the gray and white matter of frontal lobes. Choreoathetosis and oculogyric crisis were transiently noted at this period. Frontal lobe signs, including the forded mouth opening response, after diminution of these movement disorders. The DWI signal change subsequently resolved and frontal cortical atrophy appeared thereafter. Levels of inflammatory cytokines in the cerebrospinal fluid were normal during the acute phase of clinical course. The biphasic clinical course with initial prolonged seizure, involvement of the frontal lobes, and the progression of signal change on DWI from white to gray matter, meets the characteristics of "status epilepticus-type acute encephalopathy" suggested by Shiomi et al. Although pentobarbital infusion, steroid pulse therapy and mild hypothermia did not show any apparent effects on the clinical course of this patient, further trial of these therapies may be warranted for the treatment of this type of encephalopathy.
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PMID:[Influenza-associated encephalopathy with onset of prolonged convulsion: a case report]. 1709 68

The neurobiological basis of attention-deficit hyperactivity disorder (ADHD) in tuberous sclerosis complex is still largely unknown. Cortical tubers may disrupt several brain networks that control different types of attention. Frontal lobe dysfunction due to seizures or epileptiform electroencephalographic discharges may perturb the development of brain systems that underpin attentional and hyperactive functions during a critical early stage of brain maturation. Comorbidity of attention-deficit hyperactivity disorder (ADHD) with mental retardation and autism spectrum disorders is frequent in children with tuberous sclerosis. Attention-deficit hyperactivity disorder (ADHD) may also reflect a direct effect of the abnormal genetic program. Treatment of children with tuberous sclerosis complex with combined symptoms of attention-deficit hyperactivity disorder (ADHD) and epilepsy may represent a challenge for clinicians, because antiepileptic therapy and drugs used to treat attention-deficit hyperactivity disorder (ADHD) may aggravate the clinical picture of each other.
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PMID:Attention-deficit hyperactivity disorder (ADHD) and tuberous sclerosis complex. 1980 24


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