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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although acute lead encephalopathy is rare in adults, the authors had the opportunity to observe a case in a patient who had been exposed to lead occupationally for 25 years. This patient was also seen to be suffering from anemia and polyneuropathy. The blood lead level was 591 micrograms/100 ml (28,52 mumol/l). A review of the literature concerning the principal sources of lead poisoning, routes of absorption, metabolism and consequences of poisoning is conducted. Treatment by chelating agents is discussed. CaNa2-EDTA was administered by i.v. infusion over 24 hours and a favorable evolution was rapidly observable in the encephalopathy and anemia. On the other hand, the polyneuropathy was intensified, a fact which may have been caused by redistribution of lead in the soft tissues.
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PMID:[Lead poisoning. Apropos of a case of acute encephalopathy in an adult]. 21 72

In a series of examinations of more than 1000 psychiatricneurological patients we tried to state the effects of diabetes mellitus on the nervous system. We attempted to diagnose the diabetic metabolic error by means of using the oral glucose tolerance test (100 g glucose), the plasma insulin levels and many other laboratory-technical examinations (altogether about 23 000 individual tests). It was found that 21,6% of the patients had a pathological glucose tolerance, 29.6% of them had a pathological insulin response and 5,5% of them showed a known and manifest diabetes mellitus. The comparison between the number of patients with a metabolic disturbance and the frequency of sick persons to be expected epidemiologically shows that an influence exercised by the diabetic metabolism may be stated in neurological and psychic disturbances of cerebral sclerosis and polyneuropathy. The central syndromes are more frequent than the peripheric ones. Mainly low plasma insulin is present. As a rule, pathological results may be seen more often during pathological glucose tolerance in electroencephalography, pneumencephalography, CSF-examinations, personality and intelligence states. This suggests that a diffuse disturbance upon the nervous system comes from the diabetic metabolism, without any acute metabolic disturbance which we did not find among our patients. This disturbance is evident clinically as so-called diabetic polyneuropathy and also encephalopathy. In opposition to that very often pathological changes can be seen by technical research methods in other neurological and psychiatric diagnoses without influencing essentially the autonomous progress of the psychiatricneurological illness.
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PMID:[Diseases of the central nervous system in diabetes mellitus]. 61 60

An investigation has been conducted into clinical signs and concomitant ultrastructural alterations in the peripheral nerves of 4 patients who developed polyneuropathy and, in part, encephalopathy following gentamicin therapy. The ultrastructural analysis of the nerve biopsy afforded evidence of an induced lysosomal abnormality comparable to the changes observed in gentamicin nephrotoxicity. As in nephrotoxicity, the neurotoxic effect seems to be reversible.
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PMID:[Gentamicin neurotoxicity (polyneuropathy--encephalopathy)]. 83 Dec 49

Disturbances of the central and peripheral nervous system in Crohn's disease can be directly or indirectly caused by the disease itself or by the treatment. The first mentioned disturbances are very seldom. Cerebral arterial and venous thromboses can be attributed to hypercoagulation. Malabsorption of vitamin B 12 or folic acid can lead to a subacute combined degeneration of the spinal cord, sometimes in combination with a polyneuropathy and an encephalopathy. Spinal abscesses very seldom occur. An opticusneuropathy can be caused either by vasculitis or by a lack of vitamin A and/or vitamin B. Polyneuropathies in Crohn's disease which are not induced by drugs are manifested as mononeuritis multiplex or as symmetrical sensory neuropathy. An autoimmune process is being discussed as the probable cause of there diseases. In some cases large doses and prolonged administration of metronidazole can lead to cerebral dysfunctions with state of confusion, alterations of consciousness, cerebral convulsions and cerebellar syndrome. Most of these symptoms disappear rapidly after this drug is not longer administered. In long-term administration of metronidazole 10-50% of the patients develop a sensory polyneuropathy with a total dosis of at least 22.5 g, but mostly above 60 g. After the use of metronidazole is stopped, it takes a substantial period of time until there is a full recovery from the symptoms.
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PMID:[Neurologic concomitant diseases in Crohn disease]. 128 45

A review of the neurological complications presenting in uremia and an account of their presumed pathophysiology is given. With the introduction of different dialytic procedures during the last twenty years, the incidence and severity of neurological complications have declined. Nevertheless, some disturbances related to the uremic syndrome fail to respond to dialytic therapy and these therapeutic measures may even be responsible for the appearance of some new abnormalities. The clinical manifestations of uremic encephalopathy and polyneuropathy are presented. The review of the presumed pathophysiology of these syndromes illustrates the still existing controversies. Nevertheless, some promising new lines of research are reviewed. In addition, some complications of uremic treatment, including dialysis disequilibrium syndrome and dialysis encephalopathy are presented.
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PMID:Clinical and pathophysiological aspects of neurological complications in renal failure. 133 59

The nervous system involvement of 8 patients with end-stage liver disease was evaluated by means of clinical neurological, neuropsychological, neurophysiological and neuroradiological investigation before and 6-12 months after a successful liver transplantation. Preoperatively, all subjects (7 women, 1 man; mean age 40 years, range 30-54 years) exhibited decreased muscle strength and 2 patients manifested clinical signs of polyneuropathy. In neuropsychological tests, slight visuoconstructive apraxia, and disturbances of verbal memory and cognitive function were observed. Magnetic resonance imaging (MRI) revealed cerebral lesions in two patients. After transplantation, muscle strength reverted to normal in all patients, polyneuropathy improved and in all but 2 patients recovery of neuropsychological functioning was observed. Clinical signs of encephalopathy had disappeared. All patients were emotionally better adjusted after transplantation. Four subjects showed new, albeit mild changes in neurophysiological and neuropsychological tests postoperatively. We conclude that the majority of neurological impairment disappeared after liver transplantation. We want to stress that evaluation of neurological sequelae of liver transplantation needs to be based on assessments both before and after liver transplantation.
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PMID:Encephalopathy and neuropathy in end-stage liver disease before and after liver transplantation. 133 12

In the group of 37 patients with chronic carbon disulphide (CS2) intoxication manifested by encephalopathy, polyneuropathy or psycho-organic syndrome and complaining for vertigo, a statokinesiometric test was performed with open and closed eyes, and with visual stimulation. Basic test parameters of stabilograms and statokinesiograms were compared with standard values of the control group. Results of the test were additionally verified by electronystagmography with the recording of spontaneous, positional, optokinetic and post-rotatory nystagmus as well as the eye-tracking test. The statokinesiometry revealed postural stability disorder in 72.9% of patients. Balance disorders detected by means of this test showed high compatibility with results of electronystagmography which confirmed damage of the central part of vestibular system due to CS2 intoxication.
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PMID:The statokinesiometry in evaluation of the balance system in persons with chronic carbon disulphide intoxication. 149 Jan 26

Lyme neuroborreliosis is one of the chronic manifestations of Lyme disease and is caused by the neurotropic spirochete, Borrelia burgdorferi. Two of the three stages of Lyme disease potentially involve the central nervous system: a second stage that may manifest as meningitis, cranial neuritis, or radiculoneuritis; and a third stage, or chronic neuroborreliosis, with parenchymal involvement. The tertiary stage may mimic many conditions, including multiple sclerosis, polyneuropathy, viral encephalitis, brain tumor, vasculitis, encephalopathy, psychiatric illness, and myelopathy. We report a 10-year-old child with signs, symptoms, and radiological manifestations of intracranial mass lesions, without previously recognized manifestations of Lyme disease. This proved to be Lyme neuroborreliosis, documented by histological and serological examination, which responded well to antibiotic therapy. The need to establish a tissue diagnosis of intracranial mass lesions is emphasized, and the utility of a computed tomographic-guided stereotactic system for this purpose is discussed.
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PMID:Lyme neuroborreliosis manifesting as an intracranial mass lesion. 158 93

The sedative thalidomide was withdrawn from the market 30 years ago because of its teratogenic and neurotoxic adverse effects. The compound was later discovered to be extremely effective in the treatment of erythema nodosum leprosum, a complication of lepromatous leprosy. This effect is probably due to a direct influence on the immune system, because thalidomide possesses no antibacterial activity. The compound is presently used as an experimental drug in the treatment of a variety of diseases with an autoimmune character, including recurrent aphthosis of nonviral and nonfungal origin in human immunodeficiency virus (HIV) patients. This article reviews the most important chemical and pharmacokinetic properties of thalidomide. The possible mechanisms of the nonsedative effects of thalidomide with respect to the safety of its use in HIV patients are discussed. Because the mechanism of the immunomodulatory effect of thalidomide is unknown, the possibility that the administration of this compound will accelerate the deterioration of the immunological status of HIV patients cannot be excluded. Clinical evidence suggests that thalidomide may aggravate the condition of patients with preexisting peripheral neuropathy. Hypersensitivity reactions to thalidomide may occur more frequently in HIV patients than in other patient groups. Because of the teratogenic activity of thalidomide, reliable contraception must be provided to female patients of childbearing age. Before the introduction of thalidomide therapy to an HIV patient presenting with oral ulcers, a fungal or viral origin of the lesions should be excluded. Thalidomide should not be used in patients with preexisting HIV-related peripheral polyneuropathy, polyradiculopathy or encephalopathy. In patients experiencing a complete remission, the discontinuation of thalidomide treatment and its reintroduction in the case of a relapse are preferable to maintenance therapy.
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PMID:Thalidomide in human immunodeficiency virus (HIV) patients. A review of safety considerations. 160 98

According to the authors' observations, the symptoms of nervous system derangement associated with legionnaires' disease rather often enter the disease structure and can virtually be characterized as a manifestation of infectious and toxic encephalopathy and polyneuropathy (encephalopolyneuropathy). In the majority of cases, the neurological disorders develop acutely or subacutely after or simultaneously with respiratory lesions. The clinical picture of encephalopathy is marked by permanent headache, mental abnormalities, memory disturbances, insomnia, pronounced astheno-vegetative and vascular manifestations. In patients with legionellosis, polyneuropathy is manifested by paresthesias, less frequently by pains in the distal parts of the limbs and myasthenia without visible atrophies. Vegetative disorders such as vegetative polyneuropathy of the hands and legs, visceral polyneuropathies are typical symptoms of the disease whatever its gravity. Vegetovascular dystonia together with long-term AP instability is an obligate sign of the disease. Electrophysiological examinations (EEG, REG, EMG) support the clinical findings and may serve the basis for an objective evaluation of the gravity of the neurological disorders. The degree of pulmonary lesions and the intensity of vegetative disorders eventually determine the torpidity and characteristics of the disease course.
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PMID:[Nervous system involvement in legionellosis (legionnaires' disease)]. 164 36


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