Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A distinct neurological syndrome in twelve chronic haemodialysis patients is described. This syndrome is currently the leading cause of death in one Denver dialysis unit. The hallmarks of this syndrome are progressive speech difficulties, mental changes, and a markedly abnormal electroencephalogram which may be present months before the clinical signs appear. Additional clinical features including seizures, myoclonus, asterixis, apraxia, focal neurological signs, and psychiatric symptoms may also be observed. Neuropathological changes are slight and non-specific. The aetiology of this syndrome is unknown but the clinical and pathological features suggest a toxic/metabolic disorder. To date, this disorder has been refractory to several therapeutic measures.
 ...
PMID:A fatal encephalopathy in chronic haemodialysis patients. 5 86

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
 ...
PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

Cerebral dyspraxia associated with hemodialysis is a progressive, fatal syndrome. Patients suffer from a combination of psychiatric and neurological signs and symptoms. Psychiatric manifestations include anxiety, depression, paranoid ideation, and a progressive dementia with impaired concentration, decreased memory, personality changes, and hallucinations. Neurological findings include deliberate speech, stuttering, dysarthria, dyspraxia of speech and movement, tremulousness, myoclonic activity, asterixis, and seizures. These symptoms are aggravated during and immediately following dialysis. Patients usually die within 6 months of its onset. The etiology is unknown. Treatment efforts have failed to reverse its course. Recognition of this syndrome is highlighted so that informed, critical decisions can be made as to whether to continue dialysis therapy.
 ...
PMID:Clinical and psychological test findings in cerebral dyspraxia associated with hemodialysis. 125 51

Three children had both nocturnal unilateral motor seizures and daytime ipsilateral "negative myoclonus" which occurred so frequently that it resembled asterixis. Neurophysiologic studies demonstrated lateralized spike discharges that were time-locked to postural lapse in the contralateral outstretched arm. The clinical course was characterized by good seizure control with benzodiazepines.
 ...
PMID:Partial motor epilepsy with "negative myoclonus". 189 21

Movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.
 ...
PMID:Movement disorders as a manifestation of nonketotic hyperglycemia. 260 Mar 93

Asterixis is a disorder of motor control characterized by irregular myoclonic lapses of posture affecting various parts of the body independently. These lapses are caused by involuntary 50- to 200-msec silent periods appearing in muscles (even antagonistic groups of muscles) which are tonically active. That is, the silent periods and postural lapses occur in muscles that have been contracting for a time whether or not there has been slow shortening or lengthening but probably do not occur during or immediately after a sudden movement at a joint. What constitutes a sudden as opposed to a slow movement remains to be defined. When bilateral asterixis is present, one cannot rule out the possibility of a focal lesion (see Table 2), but it is almost always due to a metabolic encephalopathy (with a wide variety of possible causes). Unilateral asterixis is due to a localized lesion, perhaps otherwise not clinically evident, in the contralateral cerebral hemisphere. This episodic dysfunction within neural circuits which are normally concerned with maintenance of sustained or tonic muscle contraction may be released by focal lesions only in specific CNS areas (such as ventrolateral thalamus) or by a more generalized neurochemical imbalance (metabolic encephalopathies of various kinds). The system, a lesion or metabolic dysfunction which produces asterixis, is presumably an anatomically and/or pharmacologically distinct one; asterixis is not the result of a nonspecific disorder any more than are seizures. Presumably, those aspects of each of the different factors (e.g., subdural hematomas, drugs, electrolyte imbalance, cerebrovascular accidents, intracerebral tumors) that may produce asterixis or a seizure are mediated through some fundamental neuronal or neural systems process. To label asterixis or seizures nonspecific results of CNS disorders or results of nonspecific CNS disorders may be simply to avoid confronting our ignorance of the specific pathophysiologic mechanisms involved. Although the anatomy, neurochemistry, and physiologic function of this asterixogenic system remain to be elucidated, observations that asterixis may be caused by discrete anatomic or pharmacologic (e.g., phenytoin) lesions should tell us something important about mechanisms underlying sustained muscle contraction in humans. Unfortunately clinicoanatomic correlations alone cannot provide precise answers because even those reasonably focal vascular lesions that cause asterixis are too gross to permit localization or identification of the neural systems involved.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Asterixis: one type of negative myoclonus. 394 9

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
 ...
PMID:Pathogenesis of dialysis encephalopathy. 636 3

Sodium valproate was administered to 38 patients, admitted to our unit in the last 18 months, and chosen because they had: (1) poor control of their seizures; (2) therapeutic concentrations in their plasma of at least two major antiepileptic drugs. In 8 of them, a therapeutic dosage of VPA caused modifications of the state of consciousness ranging from coma to drowsiness and stupor. These patients also showed gastrointestinal disturbances, asterixis, ataxia, tremor and a worsening of EEG abnormalities. The side effects of the drug were constantly associated with increased concentration of blood ammonia. Better penetration of ammonia into the CNS of patients undergoing frequent seizures and possibly having imperfectly functioning biological barriers, could explain our observations. In view of the unusually high percentage of patients suffering from serious VPA side effects, it is probably advisable to carefully monitor ammonemia in the first few days of VPA therapy in every patient treated with multiple anticonvulsants.
 ...
PMID:Hyperammonemia and valproate-induced alterations of the state of consciousness. A report of 8 cases. 642 61

Metrizamide, a nonionic, water-soluble contrast medium, has been increasingly used for myelography. We saw a patient with cortical blindness, seizure, organic psychosis, and asterixis after undergoing attempted metrizamide myelography via C1-2 puncture. Computed tomography demonstrated early penetrance of metrizamide into the brain parenchyma, most prominently in the occipital lobes. A mechanism of direct metrizamide neurotoxicity was proposed.
 ...
PMID:Cortical blindness after metrizamide myelography. Report of a case and proposed pathophysiologic mechanism. 669 31

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
 ...
PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30


1 2 Next >>