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

Multiple subpial transection (MST) is a new surgical technique for treating seizures that arise from functionally critical cortical areas. It has a reported efficacy comparable to that of standard temporal lobe resections. Although the mechanism through which MST works is unknown, the carefully controlled lesions, placed 5 mm apart at the midlevel of the cortical gyri, could produce fiber damage that would prevent horizontal synchronization and spread of epileptic discharges while allowing normal cortical functions such as those related to movement or speech to be preserved. We studied the acute neuropathological features associated with MST in 8 patients with intractable temporal lobe epilepsy. Transections were made along major temporal gyri just before standard lobectomy was performed. After resection, tissue was processed by conventional histological and immunocytochemical techniques. Macroscopically, subpial transections (STs) were perpendicular to the main gyral axis and had an appropriate spacing. Microscopically, most of the lesions were perpendicular and at midlevel. However, many transections involved the lateral aspects of the small gyri, resulting in oblique or deep STs, some of which reached the gray-white matter junction due to the complex microscopic neocortical architecture, in which small gyri are superimposed on major lobar gyri, and to the variable cortical thickness. Extensive acute pyknosis and tissue edema were also evident adjacent to the transections. These changes were variable and extenDed 1-3 mm laterally as irregular columnar blocks. In the deep lesions, myelin pallor and decreased neurofilament immunoreactivity were observed in the white matter. Based on the distribution of STs and their adjacent parenchymal injury, we conclude that this technique produces block-type lesions that probably disrupt propagation of epileptogenic activity. In most instances, midlevel horizontal fibers are damaged; one third of the cases showed additional deep injury that would sever afferent and efferent axons. Therefore, in addition to horizontal desynchronization, a deafferentation mechanism involving different fiber systems may contribute to the anti-seizure effects of MST. We hypothesize that preservation of cortical function is mediated by cortex remaining in the sulcus and gyral crown and possibly by reorganization of tissue adjacent to transections.
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PMID:Treatment of epilepsy with multiple subpial transections: an acute histologic analysis in human subjects. 904 82

We performed a pathologic examination of the brains of three dogs in an epileptic beagle colony. Histologically, all the cases had diffuse astrocytosis in the cerebral cortex and basal ganglia as well as the hippocampus, whereas they showed acute nerve cell change in the hippocampus and some other areas of the cerebrum. One of these animals showed laminar myelin pallor associated with the presence of many vacuoles in the IV to VI layers of the bilateral motor cortices. Most of the vacuoles contained fine granules stained with luxol-fast-blue stain. Ultrastructural examination revealed that some oligodendrocytes and perineuronal satellite oligodendrocytes in the bilateral cerebral motor cortices of the two affected dogs had many vacuoles surrounded by myelin-like lamellar structures. These findings suggest a possibility that astrocytosis in the cerebrum and vacuolar degeneration of oligodendrocytes in the cerebral motor cortex may be, at least in part, related to the occurrence or development of seizures.
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PMID:Oligodendroglial vacuolar degeneration in the bilateral motor cortices and astrocytosis in epileptic beagle dogs. 1008 46

Early-onset benign childhood occipital seizures (EBOS) described by Panayiotopoulos constitute the commoner after the rolandic phenotype of a childhood seizure susceptibility syndrome. EBOS are the clinical representative of occipital spikes. Their cardinal features are infrequent (often single) partial seizures manifested with deviation of the eyes and vomiting, frequently evolving to hemi- or generalized convulsions. Ictal behavioral changes, irritability, pallor, and rarely cyanosis, and eyes wide open are frequent. Retching, coughing, aphemia, oropharyngolaryngeal movements, and incontinence may occur. Consciousness is usually impaired or lost, either from the onset or the course of the fits, but in a few children, it may be preserved. Duration varies from a few minutes to hours (partial status epilepticus). Seizures are usually nocturnal, but semiology is similar in nocturnal or diurnal fits. Onset is between 1 and 12 years with a peak at 5 years. One third of children have a single seizure, the median total number of fits is two to three, and the prognosis is invariably excellent, with remission usually occurring within 1 year from onset. A few children may later develop rolandic or other benign partial seizures. The likelihood to have seizures after age 12 years is exceptional and rarer than that of febrile convulsions. EEG shows occipital paroxysms demonstrating fixation-off sensitivity, but random occipital spikes, occipital spikes in sleep EEG alone, or normal EEG may occur. Centrotemporal and other spike foci may appear in the same or more frequently in subsequent EEGs. The EEG does not reflect clinical course and severity.
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PMID:Early-onset benign childhood occipital seizure susceptibility syndrome: a syndrome to recognize. 1038 32

A retrospective study is presented of the clinical features and outcome of late onset haemorrhagic disease due to vitamin K deficiency in 11 babies who were admitted to the emergency or child neurology unit during a 4-year period (January 1994-December 1997). The disease occurred in infants between 30 and 119 days of age (mean: 56+/-24 days). None of them received vitamin K after birth and all were breastfed. The presenting complaints were seizures (91%), drowsiness (82%), poor sucking (64%), vomiting (46%), fever (46%), pallor (46%), acute diarrhoea (27%), irritability and high-pitched cry (18%). On examination, tense or bulging fontanelle (73%), anisocoria (36%), weak neonatal reflexes (18%), cyanoses (18%) were the most frequent findings. The localizations of the intracranial haemorrhage were as follows: intracerebral (91%), subarachnoid (46%), subdural (27%), and intraventricular (27%). No fatality was observed. However, after a follow-up period ranging from 6 to 48 months (mean: 21+/-13 months), only three (27%) infants remained neurologically normal. Seizure disorders (73%), severe psychomotor retardation (46%), cerebral palsy (46%) and microcephaly (46%) were observed in the remainder. Hydrocephalus developed in three (27%) babies but none of them required shunt replacement. The value is emphasized of vitamin K prophylaxis in the newborn to reduce the incidence of late onset intracranial haemorrhage and handicap in children.
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PMID:Vitamin K deficiency--late onset intracranial haemorrhage. 1072 92

We report the case of a 4-year-old boy with pure red-cell aplasia associated with sodium valproate monotherapy. Treatment with valproate was initiated because of idiopathic tonic-clonic seizures; he became free of seizures. During the introduction of and ongoing antiepileptic drug treatment, clinical and laboratory controls using electroencephalographic (EEG) spectral analysis were performed at regular intervals and disclosed normal values. Ten months after the introduction of valproate, clinical examination was normal except for marked pallor. Peripheral blood showed macrocytic anemia and the bone marrow finding was isolated absolute erythroblastopenia. At the same time, significant changes in EEG background activity were present as well-defined slowing. There was an increase in the relative power of theta activity and a decrease in alpha 2 activity in the occipital regions. Valproate was discontinued and phenobarbital therapy introduced. A complete resolution of the hematologic damage was observed after valproate withdrawal. Recovery of the hematologic parameters started 14 days after discontinuation of valproate therapy, while normalization of EEG background activity was observed earlier. The patient maintained stable hematologic values and seizure control without disturbances of the spectral EEG. After 6 months of phenobarbital therapy, re-administration of sodium valproate was not followed by recurrence of any clinical or electrophysiologic symptoms or abnormalities.
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PMID:Temporary pure red-cell aplasia during valproate monotherapy: clinical observations and spectral electroencephalographic aspects. 1092 23

Specific recommendations on how to deal with drug overdoses and how to identify an individual who has overdosed are provided. Some signs of overdose are pallor, limpness, difficulty breathing, foaming at the mouth, vomiting and seizures. An overdose may be fatal. If a person is overdosing, check the person's pulse and respiration and try to revive him by using cold water on the face. If possible, get them up and walking and try to keep them talking. It may be necessary to call an ambulance. Steps not to take are listed. Finally, information about needle exchange programs is provided.
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PMID:[Drug overdoses: how to identify them and what to do about them]. 1136 31

The differential diagnosis of acute loss of vision in children includes acute loss of vision due to retinal or optic nerve disease, and cortical blindness. The retinal disorders which may be mis diagnosed as optic neuritis include Leber neuroretinitis, Leber hereditary optic neuropathy, and Stargardt macular dystrophy. Retinal changes which evolve in neuroretinitis, and the pseudopapilledema in Leber heredity optic neuropathy are helpful in differentiating these disorders from optic neuritis. Stargardt macular dystrophy, a disorder associated with a variety of mutations, may be mis diagnosed as psychogenic visual loss due to the early normal appearance of the retina, and the loss of vision over a period of weeks. The differentiation of optic neuritis from anterior ischemic optic neuropathy (AION), depends upon the initial appearance of the optic disc (in AION either hyperemia due to reperfusion, or swelling and pallor if total infarction has occurred). The authors have described children with abrupt loss of vision during renal dialysis, whose risk factors for AION included systemic hypotension and intra ocular hypertension. Children with vigorous treatment of accelerated hypertension, and children with migraine and pro thrombotic disorders have also incurred AION. Thus, AION should be suspected when acute loss of vision occurs in association with certain ocular and systemic risk factors. In children capable of cooperating for visual field examination, the typical change in AION is an altitudinal defect, while optic neuritis it is a central scotoma. The association of optic neuritis with multiple sclerosis, DeVic disease, and with acute demyelinating1 encephalomyelitis require special consideration in regard to treatment and prognosis. Acute loss of vision due to cerebral cortical insults involves a large differential diagnosis which includes vascular, metabolic and infective disease; as well as disorders causing transitory blindness such as seizures and migraine
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PMID:[Acute loss of vision in children]. 1259 57

The clinical features of 14 infants diagnosed with late hemorrhagic disease of newborn (LHDN), of which 10 did not receive vitamin K prophylaxis, are presented. All infants were exclusively breast-fed and 12 did not have any underlying illness to explain the abnormal coagulation profile. The common presenting symptoms were seizures (71%), vomiting (57%), poor feeding (50%) and altered sensorium (36%). Physical examination shared pallor in all infants and a bulging anterior fontanel in 64%. Intracranial bleed was the predominant manifestation (93%), with CT scan showing intracranial bleed in 78%. Eight infants (57%) succumbed to their illness, while 36%had neurological sequelae. Since LHDN leads to significant morbidity and mortality, it should be prevented by providing vitamin K prophylaxis to all newborns.
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PMID:Late hemorrhagic disease of newborn. 1295 87

OBJECTIVE: To describe an unusual case with clinical features of the antiphospholipid syndrome. DESCRIPTION: White child, two years and six months old, with renal failure, renal arterial thrombosis, and diagnosis of antiphospholipid syndrome was hospitalized with a history of abdominal pain, pallor, lethargy, and anuria for 36 hours. On physical examination, the patient showed malnutrition, high blood pressure, moderate edema, and hypochondrial pain. Laboratory findings included: urea=112mg/dl, serum creatinine= 4.5 mg/dl, blood pH= 7.47, blood bicarbonate= 12.8 mmol/L, K=7.2 mEq/L. Peritoneal dialysis was started and maintained for 11 days. After 7 weeks, the patient still needed anti-hypertensive drugs and the renal function was still abnormal. Renal biopsy was performed and revealed renal infarction. The result of Doppler ultrasonography revealed absent renal blood flow on the right side. Renal arteriography showed total occlusion of the right renal artery. Results for collagen diseases were negative. A right nephrectomy was performed and the blood pressure was controlled. The child was hospitalized again at 5 years and 8 months old with episodes of absence seizures and abdominal and precordial pain. Anticardiolipin antibody test was positive. The child is now 7 years old, asymptomatic, with negative anticardiolipin antibody, and has been under regular follow-up. COMMENTS: Children with arterial thrombosis should be investigated for a possible association with the antiphospholipid antibody syndrome even in the absence of collagen disease.
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PMID:[Renal arterial thrombosis and the antiphospholipid antibody syndrome: a case report] 1464 33

We have observed an increasing number of autopsies on patients with chemotherapy-related complications. One complication is toxic leukoencephalopathy, which is due to a direct toxic effect of chemotherapeutic agents on the central nervous system white matter. Autopsies of four cases of toxic leukoencephalopathy were performed following standard protocols. The brain and spinal cord were examined routinely, and histological sections were taken for evaluation. We report here three patients with hematologic malignancies and one patient with metastatic carcinoma with chemotherapy-induced leukoencephalopathy. The first was a 56-year-old male treated with multiple chemotherapeutics for multiple myeloma. He presented with confusion and focal seizures with a rapid progression to coma and decerebrate posturing. The second was a 36-year-old male who developed mental status changes, ataxia and dysarthria following treatment for lymphoma. The third was a 16-year-old male who developed a profound peripheral and central neuropathy after chemotherapy treatment for T-cell acute lymphoblastic leukemia. The fourth was a 49-year-old female patient who was treated with multiple chemotherapeutics for Stage II breast carcinoma and subsequently developed visual acuity and field defects. The neuropathologic findings in these cases, although similar, varied in severity and distribution. The white matter was affected by severe myelin pallor, edema, and a prominent macrophage infiltrate in each of the cases. The location and extent of the central nervous system pathology correlated with the type and severity of clinical symptoms. These four cases, with their varied presenting symptoms, clinical courses, and degree of pathology, emphasize the importance of considering toxic leukoencephalopathy as an etiology of acute neurologic deterioration following high-dose chemotherapy.
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PMID:Chemotherapy-induced toxic leukoencephalopathy causes a wide range of symptoms: a series of four autopsies. 1470 18


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