Gene/Protein Disease Symptom Drug Enzyme Compound
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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myelinolysis is a neurologic disorder that can occur after rapid correction of hyponatremia. Initially named "central pontine myelinolysis," this disease is now known to also affect extrapontine brain areas. Manifestations of myelinolysis usually evolve several days after correction of hyponatremia. Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobulbar palsy, and mental disorders ranging from mild confusion to coma. Death may occur. The motor and localizing signs of myelinolysis differ from the generalized encephalopathy that is caused by untreated hyponatremia. Experiments have duplicated the clinical and pathologic features of myelinolysis by rapidly reversing hyponatremia in animals. Myelinolysis is more likely to occur after the treatment of chronic rather than acute hyponatremia and is more likely to occur with a rapid rate of correction. The exact pathogenesis of myelinolysis has not been determined. Optimal management of hyponatremic patients involves weighing the risk for illness and death from untreated hyponatremia against the risk for myelinolysis due to correction of hyponatremia. Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a rate less than 10 mmol/L in any 24-hour period.
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PMID:Myelinolysis after correction of hyponatremia. 923 10

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
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PMID:Electroencephalography as a diagnostic tool in dementia. 906 24

A 72-year-old male treated with flutamide for metastatic prostate cancer developed lethargy and confusion. He was noted to be icteric and his liver enzymes were elevated. Within a week of discontinuing the medication, the patient's mental status and liver function returned to normal. Although flutamide-induced near fatal liver dysfunction has been described, progression to encephalopathy is a rare occurrence. Based on a review of the literature, management guidelines for the use of flutamide are suggested.
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PMID:[Hepatic encephalopathy induced by flutamide administered for the treatment of prostatic cancer]. 909 57

Two patients underwent acoustic schwannoma surgery by transmastoid approach. Petrous bone defect was filled in with aluminium-containing bone cement (Ionocem). A pseudomeningocele by CSF accumulation in subcutaneous temporoparietal area appeared after the procedure and, in subsequent weeks, encephalopathy with confusion and seizures. MRI showed cerebral involvement with herpes-like disposition. Temporal stereotactic biopsy in a case did not confirm viral encephalitis but disclosed cellular accumulation of lipofucsin and particles highly suggestive of aluminum-inclusions. Aluminium's levels in blood and CSF of both patients were very high and confirm the brain's toxic involvement. Aluminium's toxicity would be advocated in patients with neurologic disorders who have undergone maxillofacial or skull bone-cementoplasty by an aluminum-containing biomaterial, if this cement is in contact with CSF.
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PMID:[Toxic aluminum encephalopathy. Predominant involvement of the limbic system on MRI]. 909 10

Metabolic encephalopathies are common among patients in the critical care unit. Septic, hypoxic-ischaemic, hepatic and uraemic encephalopathies are most frequently seen. They produce global neurological dysfunctions ranging from lethargy or mild confusion to coma. Metabolic encephalopathies must be distinguished from other conditions such as structural brain lesions, infections of the central nervous system or drug reactions. Neurological manifestations are often present in the early stages of systemic illness and may be the first symptom. The severity of encephalopathy generally correlates with that of the systemic illness. Appropriate investigations often include drug and metabolic screens, cultures of blood and cerebrospinal fluids and neuro-imaging studies. Electroencephalogram is useful to grade the severity of encephalopathy. With some exceptions such as hypoxic-ischaemic encephalopathy, most metabolic encephalopathies are reversible unless secondary complications such as brain herniation occurred. Treatment is generally that of the underlying systemic illness and supportive measures.
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PMID:Metabolic encephalopathies. 911 77

We describe a patient with a clinical picture characterized by subacute onset of confusion, myoclonus, tremor and generalized convulsive seizures with a relapsing course, which was attributed to Hashimoto's encephalopathy. EEG and MRI were diffusely abnormal. High titers of antithyroid antibodies were detected in her serum. She responded well to corticosteroids and her condition remained good during a one-year follow-up.
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PMID:Hashimoto's encephalopathy: clinical and laboratory findings. 911 67

Children appear particularly susceptible to severe but reversible neurological symptoms and/or signs after minor head injury; these include headache, confusion, drowsiness, vomiting, hemiparesis, cortical blindness, or seizures. Significantly, these neurological episodes are not associated with any identifiable structural brain abnormality on neuro-imaging. We propose that the cause of this condition is a reactive hyperaemia, a 'benign hyperaemic encephalopathy' mediated via activation of the trigeminovascular system.
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PMID:Neurological episodes after minor head injury and trigeminovascular activation. 918 32

Cisplatin is a widely used chemotherapeutic agent implicated in a range of adverse effects affecting the nervous system. Among the others, convulsive encephalopathy is rare and its pathogenesis is unknown. We report an 84-year-old woman with adenocarcinoma of the ovary who developed two fully reversible episodes of non-convulsive encephalopathy, each following a course of cisplatin-based chemotherapy and thus confirming a causal relationship to the agent. The patient presented 7 and 10 days after treatment with acute confusional state, a partial left homonymous hemianopia and a left extinction hemihypesthesia. Brain MRI showed old-standing cerebral microvascular changes and EEG revealed right parieto-occipital periodic lateralized epileptiform discharges over a generalized background activity slowing. This case adds further to the clinical diversity of cisplatin toxicity and, in view of the similarity to a recently defined disorder of posterior leukoencephalopathy, suggests regional endovascular injury rather than a direct cerebral toxicity as the initial event in the evolution of encephalopathy.
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PMID:Cisplatin-induced non-convulsive encephalopathy. 949 99

We describe a novel, biotin-responsive basal ganglia disease in 10 patients. At onset, it appears as a subacute encephalopathy, with confusion, dysarthria and dysphagia with occasional supranuclear facial nerve palsy or external ophthalmoplegia, and progresses to severe cogwheel rigidity, dystonia and quadriparesis. These symptoms disappear within a few days if biotin (5-10 mg/kg/day) is administered, and there are no neurological sequelae. They reappear within 1 month if biotin is discontinued. Patients diagnosed late, or who have had repeated episodes, suffer from residual symptoms such as paraparesis, mild mental retardation or dystonia. The numerous biochemical studies of intermediary metabolism, like the autoimmune and toxicological studies, enzyme assays including biotinidase, carboxylase and lysosomal activities, and bacterial and viral studies were all normal. The aetiology may be related to a defect in the transporter of biotin across the blood-brain barrier. The only consistent radiological abnormality was central necrosis of the head of the caudate bilaterally and complete, or partial, involvement of the putamen on brain MRI. This was present during the initial acute encephalopathy and remained unchanged during follow-up of 3-10 years. Although its aetiology is unknown, it is important to recognize this disease, since its symptoms may be reversed and the progression of its clinical course prevented simply by providing biotin.
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PMID:Biotin-responsive basal ganglia disease: a novel entity. 967 79

Seizures are commonly encountered in patients who do not have epilepsy. Factors that may provoke such seizures include organ failure, electrolyte imbalance, medication and medication withdrawal, and hypersensitive encephalopathy. There is usually one underlying cause, which may be reversible in some patients. A full assessment should be done to rule out primary neurological disease. Treatment of seizures in medically ill patients is aimed at correction of the underlying cause with appropriate short-term anticonvulsant medication. Phenytoin is ineffective in the management of seizures secondary to alcohol withdrawal, and in those due to theophylline or isoniazid toxicity. Control of blood pressure is important in patients with renal failure and seizures. Non-convulsive status epilepticus should be considered in any patient with confusion or coma of unclear cause, and electroencephalography should be done at the earliest opportunity. Most ill patients with secondary seizures do not have epilepsy, and this should be explained to patients and their families. Only those patients with recurrent seizures and uncorrectable predisposing factors need long-term treatment with anticonvulsant medication.
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PMID:Medical causes of seizures. 980 2


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