Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presented material comprised 17 cases observed in four Warsaw hospitals in a period of 20 years. Nine patients with the pseudotumour syndrome were diagnosed correctly and referred to neurosurgical services. The remaining eight cases died in neurological hospital departments with the following clinical diagnoses: cerebral stroke 3, subarachnoid haemorrhage 1, comatose state preceded by dementia 1, chronic meningoencephalitis 1, status epilepticus 2 cases postmortem investigations demonstrated cerebral cysticercosis in all cases. In four patients with predominant symptoms of cerebrovascular disease lesions were found of the type of residual vasculitis cysticercosa, the sequelae of which might have caused secondary complications independent of concomitant arteriosclerosis. Dementia appeared in a patient with huge hydrocephalus consequent to numerous cysticerci. The patient with the diagnosis of meningoencephalitis had an inflammatory reaction of the ependyma and meninges caused by a cysticercus floating in the IV ventricle. Of the patients dying in status epilepticus attention is called to a 6-year-old girl with a solitary cysticercus localised subcortically in the motor area. The authors suggest that the possibility of cysticercosis should be kept in mind, despite its rarity, in cases with a not completely clear clinical manifestations of cerebrovascular disease, chronic meningoencephalitis and epilepsy or dementia.
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PMID:[Neuropathologic analysis of 8 undiagnosed cases of cerebral cysticercosis]. 344 11

Seizures are a frequent neurologic complication of cancer. Seizures may develop as a consequence of direct extension of cancer into the brain or surrounding meninges, an underlying metabolic imbalance from treatment or the tumor, or the neurotoxic effects of cancer therapy. Emergency treatment is essential for status epilepticus and seizures that occur frequently to prevent permanent neurologic sequelae. In all cases, a diagnostic evaluation is required to discover the underlying cause of the seizures. Often, an easily reversible process will be uncovered, and the complete resolution of the seizure disorder can occur. In other circumstances, determining the cause of the seizure may allow early diagnosis and treatment of brain lesions or may disclose neurotoxicity, thereby modifying future treatment. This article reviews the causes, diagnostic evaluation, and treatment of seizures in adult patients with cancer, providing an overview of the medical and nursing aspects of patient management.
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PMID:Management of seizures in the adult patient with cancer. 759 70

We have previously shown that IL-6 protein levels are increased in cerebrospinal fluid in humans after recent tonic-clonic seizures with unchanged levels of IL-1beta and TNFalpha. Here we studied the expression of cytokines IL-6, LIF, IL-1beta and TNFalpha and cytokine receptors IL-6R, LIFR and Gp130 in the rat brain after kainic acid-induced status epilepticus using Northern blot analysis and in situ hybridization histochemistry. After seizures, IL-6 mRNA was induced in the hippocampus, cortex, amygdala and meninges, and IL-6R was up-regulated in the hippocampus. LIF was up-regulated in the hippocampus, cortex and meninges after seizures, and LIFR mRNA was induced in the hippocampus and cortex. Gp130 was constitutively expressed in the brain. After seizures, Gp130 transcription was rapidly induced in the meninges. In thalamus, cortex, amygdala and hippocampus Gp130 mRNA was induced in a delayed fashion. IL-1beta transcription was induced in the temporal lobe cortex and thalamus, and TNFalpha in the hippocampus. In general, the cytokine and their receptor mRNA levels were low in intact rat brain, but were induced by seizures. Since IL-6 and LIF transcripts were induced in the meninges after seizures, the protein products of these transcripts may be more readily released in cerebrospinal fluid after seizures. In addition, the activity of IL-6 and LIF signaling pathways may be influenced by increased expression of their receptors after seizures.
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PMID:Expression of cytokines and cytokine receptors in the rat brain after kainic acid-induced seizures. 1259 Nov 61

Eosinophilic meningoencephalitis (EME) has been described in various species of animals and in humans. In dogs it has been associated with protozoal infections, cuterebral myiasis and various other aetiologies. Ten cases of idiopathic eosinophilic meningoencephalitis have been reported in dogs and one in a cat where the origin was uncertain or unknown. The dogs were all males, of various breeds but with a predominance of Golden Retrievers and Rottweilers; they generally had a young age of onset. Two cases with no apparent underlying aetiology were diagnosed on post mortem examination. The 18-month-old, male Boerboel presented with sudden onset of cerebellar ataxia, as well as various asymmetrical cranial nerve deficits of 2 weeks' duration and without progression. Haematology revealed a peripheral eosinophilia. Necropsy showed extreme generalised congestion especially of the meninges and blood smear and histological sections of various tissues showed intravascular erythrocyte fragmentation with the formation of microcytes. Histopathology revealed severe diffuse cerebrocortical subarachnoidal meningitis and submeningeal encephalitis, the exudate containing variable numbers of eosinophils together with neutrophils and mononuclear cells. There was also deeper white matter and hippocampal multifocal perivascular mononuclear encephalitis and multifocal periventricular malacia, gliosis and phagocytosis of white matter. The cerebellum, brain stem and spinal c showed only mild multifocal oedema or scattered occasional axon and myelin degeneration respectively, with no inflammation. Immunohistochemical staining of central nervous tissue for Toxoplasma gondii failed to show any antigen in the central nervous tissue. Ultrastructure of a single submeningeal suspected parasitic cyst showed it to be chromatin clumping within a neuron nucleus indicating karyorrhexis. Gram stain provided no evidence of an aetiological agent. The 3-year-old Beagle bitch had a Caesarian section after developing a non-responsive inertia 8 days prior to presentation. This animal's clinical signs included status epilepticus seizures unrelated to hypocalcaemia and warranted induction of a barbiturate coma. She died 4 hours later. Post mortem and histopathological findings in the brain were almost identical to those of the Boerboel and she also showed histological evidence of recent active intravascular haemolysis with microcyte formation. Rabies, distemper and Neospora caninum immunohistochemical stains were negative in the brains of both dogs. Immunohistochemical staining of the cerebral and meningeal exudates of the Beagle for T- and B-lymphocyte (CD3 and CD79a) markers showed a predominance of T-lymphocytes with fewer scattered B lymphocytes. A possible allergic response to amoxicillin/clavulanate is considered, as this appeared to be the only feature common to the recent history of both animals. An overview of EME in humans, dogs and cats is given and the previously published cases of idiopathic EME in dogs and the single published cat case are briefly reviewed.
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PMID:Review of idiopathic eosinophilic meningitis in dogs and cats, with a detailed description of two recent cases in dogs. 1949 20

Central nervous system (CNS) vasculitis is a rare group of disorders that affect vessels of the brain parenchyma and meninges. It presents with headache, cognitive changes, or seizures, yet without aggressive management, it carries a high degree of morbidity and mortality. Refractory status epilepticus (SE) has been reported with CNS vasculitis. Patients are treated with immunosuppression, antiepileptic drugs (AED), and anesthetic agents. Outcomes are usually poor. Epilepsy surgery for refractory partial SE has succeeded in patients. We present a comparison of two patients with refractory partial SE due to CNS vasculitis. One patient was treated medically and died, while the other underwent epilepsy surgery to remove the epileptic focus along with medical therapy and the patient had substantial recovery. We describe clinical, electrophysiological, pathological, and treatment features of both patients and discuss rationale for surgical intervention. This is the first case report of the use of epilepsy surgery for the treatment of refractory SE associated with CNS vasculitis.
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PMID:Refractory status epilepticus secondary to CNS vasculitis, a role for epilepsy surgery. 2217 80