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

Developmental dyscalculia (DC) is a primary cognitive disorder of childhood manifested by disturbance of arithmetic ability. As an isolated learning disability (LD), it is usually treated by remedial education and not referred for further medical evaluation. We examined a group of 7 third-grade children with DC attending a mainstream school who had not progressed academically in spite of specific special education intervention. We were able to identify in all 7 children neurological conditions that had direct bearing on the children's cognitive disabilities and remedial programs. One child had petit mal seizures, another developmental Gerstmann syndrome, a third had dyslexia for numbers, and 4 children had attention deficit disorders without hyperactivity. Based on this experience, we suggest that the indications for medical or neurological assessment be broadened to include children who are not improving academically in spite of appropriate professional intervention.
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PMID:Developmental dyscalculia and medical assessment. 768 63

We report on a normal 6-year-old boy in whom a trivial head injury triggered a severe seizure, behavioural and cognitive disorder. Complete recovery occurred within 6 months. An aetiology such as trivial head injury is significant for prognosis as the outcome is invariably excellent.
Seizure 1997 Dec
PMID:An aggressive seizure and behavioural disorder following trivial head injury. 953 Sep 49

The use of complementary and alternative veterinary medicine in treating neurologic disorders has increased in popularity in response to advances in human alternative and integrative therapies. Neurolocalization of lesions to the brain, spinal cord, and neuromuscular systems is discussed, as well as the diagnostics and therapeutics used to treat such disorders. Emphasis is placed on integrative and alternative treatments for such neurologic diseases as seizures, cerebrovascular accidents, canine cognitive disorder, meningitis, intervertebral disc disease, fibrocartilagenous embolism, degenerative myelopathy, and myopathies. Thorough physical and neurologic examinations, establishment of a correct diagnosis, and integrative therapeutics are aimed at improving the overall quality of life of the veterinary patient.
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PMID:Complementary and alternative medicine for neurologic disorders. 1189 Jan 24

Aicardi syndrome is a congenital disorder characterized by severe psychomotor retardation, corpus callosum agenesis, chorioretinal lacunae, and early-onset infantile spasms. The prognosis is generally poor for children with the classical form. We report a peculiar case of Aicardi syndrome characterized by corpus callosum hypoplasia, brain malformations with subependymal heterotopias, extensive chorioretinal lacunae, seizures, and normal cognitive functions. Therefore, the clinical picture of the syndrome is broader than originally described. Cognitive disorders should not be considered inevitable and the prognosis not ineludibly poor.
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PMID:Aicardi syndrome with favorable outcome: case report and review. 1720 97

It is evident that in chronic epilepsy--both symptomatic and nonsymptomatic--cognitive dysfunction precedes the onset of seizures. Cognitive disorders emerge with the underlying lesion or the concomitant physiological process. The presumed additive effect of seizures has not been decisively clarified. The degree of damage may consecutively accumulate with a disease duration of more than three decades and an unfavorable course with frequent secondary generalized seizures. Long-term follow-up investigation of cognition in different epileptic syndromes is needed to address the question of their specific role in cognitive decline. Treatments successful in seizure control may however also hold cognitive risks. Additional memory impairment due to the surgical treatment of left-sided temporal lobe epilepsy ranks first among them. Cognitive side effects of antiepileptic medication may have considerable adverse effects on patients. The need of individual assessment of cognitive side effects draws increasing attention as a precondition for treatment optimized to each patient.
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PMID:[Cognition and epilepsies]. 1868 23

Infantile spasms syndrome (ISS) is a catastrophic pediatric epilepsy with motor spasms, persistent seizures, mental retardation, and in some cases, autism. One of its monogenic causes is an insertion mutation [c.304ins (GCG)(7)] on the X chromosome, expanding the first polyalanine tract of the interneuron-specific transcription factor Aristaless-related homeobox (ARX) from 16 to 23 alanine codons. Null mutation of the Arx gene impairs GABA and cholinergic interneuronal migration but results in a neonatal lethal phenotype. We developed the first viable genetic mouse model of ISS that spontaneously recapitulates salient phenotypic features of the human triplet repeat expansion mutation. Arx((GCG)10+7) ("Arx plus 7") pups display abnormal spasm-like myoclonus and other key EEG features, including multifocal spikes, electrodecremental episodes, and spontaneous seizures persisting into maturity. The neurobehavioral profile of Arx mutants was remarkable for lowered anxiety, impaired associative learning, and abnormal social interaction. Laminar decreases of Arx+ cortical interneurons and a selective reduction of calbindin-, but not parvalbumin- or calretinin-expressing interneurons in neocortical layers and hippocampus indicate that specific classes of synaptic inhibition are missing from the adult forebrain, providing a basis for the seizures and cognitive disorder. A significant reduction of calbindin-, NPY (neuropeptide Y)-expressing, and cholinergic interneurons in the mutant striatum suggest that dysinhibition within this network may contribute to the dyskinetic motor spasms. This mouse model narrows the range of critical pathogenic elements within brain inhibitory networks essential to recreate this complex neurodevelopmental syndrome.
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PMID:A triplet repeat expansion genetic mouse model of infantile spasms syndrome, Arx(GCG)10+7, with interneuronopathy, spasms in infancy, persistent seizures, and adult cognitive and behavioral impairment. 2012 36

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

A total of 25 patients with gliomatosis cerebri (19 males and 6 females; median age 51 years, range 10-73 years) were diagnosed and treated at the Sheba Medical Center between 1995 and 2009. Of these, 3 patients were 10 years old at the time of diagnosis. Seizures were the initial clinical presentation in 19 patients, focal signs in 16 patients, headaches in 7 patients, cognitive disorder in 4 patients and rapidly progressive hemiparesis in 1 patient. Magnetic resonance imaging (MRI) was performed in the patients and demonstrated a diffuse infiltrative process with a hyperintensity signal on T2-weighted images and a minimal mass effect. Some level of enhancement on MRI was observed in 6 patients. The infiltrative process involved at least two lobes in each patient. Biopsy was performed for diagnosis in the majority of patients. In 1 patient with a markedly rapid deterioration, the diagnosis was established at autopsy. The pathology was compatible with gliomatosis with a diffuse infiltrative low-grade astrocytoma in 21 patients and anaplastic astrocytoma in 5 patients. The patients were treated with whole-brain radiation therapy and 7 patients were treated with combined whole-brain radiation therapy and chemotherapy. Treatment appeared to stabilize 6 patients or improve the clinical condition in 7 patients. Due to the small number of patients in the present study, however, further studies are required to determine the effect of treatment on the natural history of the disease.
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PMID:Presentation patterns and outcome of gliomatosis cerebri. 2274 Aug 82

Cognitive disorders in patients with epilepsy were studied before and after the 6-week treatment with encephabol. The data on the examination of 24 patients were summarized. Before the treatment, patients with epilepsy demonstrated a larger number of errors, lower speed of reading and worse learning of the content compared to the controls (18 healthy people). Encephabol was prescribed in dosage 600 mg/day to people over 12 years of age and in dosage 300-400 mg/day to people younger than 12 years. The statistically significant improvement of the global self-rating of cognitive functions, speed of reading, decrease of errors as well as learning of the content were seen after the end of treatment. The improvement of cognitive traits was correlated with the improvement of computed EEG parameters (the decrease of delta power in the right temporal and frontal regions). Encephabol did not lead to the increase of epileptiform activity in the EEG. No increase in the number and severity of seizures was noted. In conclusion, encephabol may be used in treatment of cognitive disorders in epilepsy.
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PMID:[Encephabol in the treatment of cognitive disorders in epilepsy]. 2312 Jul 94

Episodic memory deficit is a common cognitive disorder in human temporal lobe epilepsy (TLE). However, no animal model of TLE has been shown to specifically replicate this cognitive dysfunction, which has limited its translational appeal. Here, using a task that tests for nonverbal correlates of episodic-like memory in rats, we show that kainate-treated TLE rats exhibit a selective impairment of the "what-where-when" memory while preserving other forms of hippocampal-dependent memories. Assisted by multisite silicon probes, we recorded from the dorsal hippocampus of behaving animals to control for seizure-related factors and to look for electrophysiological signatures of cognitive impairment. Analyses of hippocampal local field potentials showed that both the power of theta rhythm and its coordination across CA1 and the DG-measured as theta coherence and phase locking-were selectively disrupted. This disruption represented a basal condition of the chronic epileptic hippocampus that was linked to different features of memory impairment. Theta power was more correlated with the spatial than with the temporal component of the task, while measures of theta coordination correlated with the temporal component. We conclude that episodic-like memory, as tested in the what-where-when task, is specifically affected in experimental TLE and that the impairment of hippocampal theta activity might be central to this dysfunction.
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PMID:Specific impairment of "what-where-when" episodic-like memory in experimental models of temporal lobe epilepsy. 2419 66


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