Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of nine patients with neurologic complications of hepatitis C virus infection is reported. Seven patients presented a combination of chronic sensory polyneuropathy, multineuropathy, and encephalopathy related to cryoglobulinemia. The noncryoglobulinemic symptoms consisted of an anterior optic neuropathy and a restless legs syndrome with small-fiber neuropathy. Corticosteroids and cyclophosphamide were useful in controlling vasculitic episodes. Interferon-alpha caused remission in half of the treated patients.
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PMID:Neurologic complications associated with hepatitis C virus infection. 1093 99

During the period from May 1997 to October 1998, eight patients with coeliac disease or dermatitis herpetiformis and neurological disorders were admitted to the Department of Neurology, University Hospital of Bergen. The most frequent conditions were polyneuropathy (seven patients) and spinocerebellar ataxia (three patients). Other conditions were lower motor neuron disease, myelopathy, epilepsy and encephalopathy. The patients used various degrees of gluten-free diet at the time of admission. It remains unclear whether there is a shared common pathogenetic mechanism or the neurological disorder is a complication to the coeliac disease. Both vitamin depletion and immunological mechanisms may cause neurological disorder. Neurological manifestations may occur before the gastrointestinal symptoms. With reference to our patients and available literature we discuss prevalence, clinical picture, pathogenesis, treatment and prognosis. Neurologists, gastroenterologists and general practitioners should be aware that coeliac disease can cause neurological diseases, especially polyneuropathy, cerebellar ataxia and encephalopathy.
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PMID:[Neurological diseases associated with celiac disease]. 1086 1

Carbon disulfide is a poison of particularly neotropic properties. In order to diagnose chronic occupational intoxication with carbon disulfide, a very careful examination of the central and peripheral nervous systems in required. The presence of subjective disorders only does not as yet provide grounds for diagnosing chronic intoxication. Organic changes like chronic encephalopathy or polyneuropathy after excluding the so called 'idiopathic' neurological diseases, may serve as a basis for certifying occupational disease.
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PMID:[Diagnostic neurologic procedures and certification in persons chronically exposed to carbon disulfide in light of personal cases]. 1105 7

We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.
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PMID:Carbon disulfide vasculopathy: a small vessel disease. 1130 75

We describe three patients with acute encephalitis and motor-dominant polyneuropathy. All three patients were in their middle age and presented with features of encephalopathy with flu like illness. Cerebrospinal fluid (CSF) studies showed lymphocytic pleocytosis with increased protein. Brain magnetic resonance imagings (MRIs) showed symmetric high signal intensities in bilateral mesial temporal lobes and bilateral thalami in all patients. All three patients became quadriplegic and areflexic within two hospital days (HDs) and electrophysiologic studies revealed motor polyneuropathy. Viral or atypical bacterial infection was suspected, but no causative agent could be found. One patient expired on the twentieth hospital day, and the other two patients showed no or little improvement. To our knowledge, this combination of acute encephalitis with motor polyneuropathy has not been reported.
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PMID:Encephalitis associated with motor polyneuropathy. 1178 52

The nervous system is the major target of the toxic effect of manganese (Mn) and its compounds. Nowadays, neurological diagnostics is directed towards early detection of symptoms and abortive forms, and the cases of serious damage of the nervous system are no longer reported. The aim of the present study was to assess the effects of manganese on the functions of the nervous system in workers exposed to this metal in the ship and electrical industries. The study covered a selected group of 75 male workers (mean age 39.17 yr +/- 9.79; range 20-56 yr), including 62 welders and fitters, as well as 13 workers involved in the battery production. Their employment duration ranged between 1 and 41 yr (mean 17.5 yr +/- 10.81). During the welding process the air Mn concentrations varied from 0.004 to 2.67 mg/m3 (arithmetic mean, 0.399 mg/m3; geometric mean, 0.154 mg/m3; standard deviation, 0.586). Of the 62 workers, 30 worked in the area with exceeding MAC value of 0.3 mg/m3. At the battery production workposts, Mn concentrations fell within 0.086-1.164 mg/m3 (arithmetic mean, 0.338 mg/m3, geometric mean, 0.261 mg/m3; standard deviation, 0.292). The values of current Mn exposure in the study group fell within the range below 0.01 and 2.67 mg/m3 (arithmetic mean, 0.4 mg/m; geometric mean, 0.15 mg/m3). Of the 13 subjects, 6 worked at the Mn air concentration exceeding MAC values. In the exposed group, the values of cumulated exposure index ranged from 0.008 to 35.52 (arithmetic mean, 8.045; geometric mean, 4.615; standard deviation, 6.562). The control group consisted of 62 men non-occupationally exposed to Mn, matched by sex, age and work shift distribution. Clinically, the increased emotional irritability, dysmnesia, concentration difficulties, sleepiness and limb paresthesia predominated among the disorders of the nervous system functions in workers chronically exposed to manganese. Neither in the central nor in the peripheral nervous system, the objective examinations revealed organic lesions that could provide grounds for diagnosing toxic encephalopathy or polyneuropathy. Generalized and paroxysmal changes were the most common recordings in the abnormal electroencephalography. Visual evoked potentials examinations showed abnormalities in the response evoked, which could be a signal of the optic neuron disorders and their significant relationship with cumulated exposure. The results of the study demonstrate that Mn exposure within the range of <0.01-2.67 mg/m3 (arithmetic mean, 0.4 mg/m3; geometric mean, 0.15 mg/m3) induces subclinical effects on the nervous system.
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PMID:Neurological and neurophysiological examinations of workers occupationally exposed to manganese. 1188 16

The role of free radicals (FR) in the pathogenesis and in the progression of many diseases has been often discussed, but not widely investigated. However, the total antioxidant capacity in the serum seems to be of great evidence. Total antioxidant capacity was determined using oxygen absorbance capacity assay (ORAC) in serum of patients suffering from depression, schizophrenia, Alzheimer's disease (AD), anorexia nervosa, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Aids-encephalopathy, diabetic polyneuropathy (PNP), cardiomyopathy (CM), renal disease, and healthy individuals as controls (C). The results showed that the total antioxidant capacity in serum decreased significantly (p < 0.01) by 24, 20, 13, and 17% for anorexia nervosa, Aids-encephalopathy, PNP and CM respectively. In serum of patients with renal disease significantly elevated antioxidant capacity was found. The data indicated that increased oxidative stress can be involved in the pathogenesis or in the progression of PNP and CM. Decrease of serum antioxidant capacity in patients with anorexia nervosa and Aids-encephalopathy are probably due primarily to malnutrition and secondly to insufficient antioxidant and immune system. In renal disease, the accumulation of urea in serum seems to be responsible for high antioxidant capacity. In contrast, there were no changes in PD, AD, depression syndrome and schizophrenia.
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PMID:Serum antioxidant capacity in neurological, psychiatric, renal diseases and cardiomyopathy. 1211 62

We presented atypical manifestations in tuberculous meningitis (TbM) and herpes simplex encephalitis (HSE), lymphocytic dominant cerebrospinal fluid pleocytosis in bacterial meningitis, and a hitherto easily overlooked critical illness polyneuropathy (CIP) associated with sepsis. 1) We presented 2 TbM patients with atypical manifestations. One patient was a 25-year-old man who exhibited polymorphonuclear (PMN) dominant pleocytosis in CSF throughout his clinical course. He died the next day after a CSF culture yielded the growth of tuberculous bacilli, before receiving appropriate anti-TBM therapy. This was a rare TbM example of persistent PMN dominant CSF pleocytosis. The other patient was a 39-year-old woman whose CSF pleocytosis changed from lymphocytic dominant to PMN dominant about 1 month after the initiation of antituberculous chemotherapy. This CSF change was followed by multiple cerebral infarcts due to vauculitis caused by TbM. Administration of prednisolone caused marked improvement of the patient's symptomatology. Tuberculomas appeared transiently during anti-TbM therapy, consistent with paradoxical progression of tuberculoma. 2) A few patients with HSE may show atypical CSF findings such as PMN dominant pleocytosis, absence of pleocytosis, and low sugar value. Our national survey of HSE patients showed following percentages of these atypical findings: PMN dominant pleocytosis observed in 10% of the patients in the early stage and at the time of exacerbation, no pleocytosis in 0.9% (1 patient), and low sugar value in 4%. 3) Bacterial meningitis typically causes PMN dominant CSF pleocytosis. However, Listeria meningitis (LM) may cause lymphocytic dominant pleocytosis in 30% of the patients, particularly in elderly ones. We showed one such 69-year-old patient with persistent lymphocytic dominant CSF pleocytosis throughout the clinical course. 4) CIP, septic encephalopathy and critical illness myopathy are 3 major complications associated with sepsis. CIP is a frequent cause of neuromuscular weakness due to axonal dysfunction, which occurs to critically ill patients with sepsis, particularly when multiple organ dysfunctions are present. We showed our CIP patient associated with acute bacterial endocarditis and multiple organ failure. We should bear in mind these atypical manifestations, and frequent and important complications associated with sepsis such as CIP, to provide appropriate management to patients with neuro-infection and sepsis.
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PMID:[Neuro-infections to be borne in mind]. 1223 30

Peripheral neuropathy is one of the clinical manifestations of the MELAS (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) syndrome, but its frequency and phenotypic variability have not been properly characterised. We therefore studied the clinical and electrophysiological features of peripheral neuropathy in 32 patients with the 3243A > G mutation in mitochondrial DNA by using clinical examination, assessment of Neuropathy Symptom Score, Neuropathy Disability Score, and electrophysiological examinations. Seven patients (22 %; 95 % confidence interval, 9-40 %) fulfilled the electrodiagnostic criteria for polyneuropathy. Mixed axon loss and demyelinating sensorimotor neuropathy was the most common type of polyneuropathy, while one patient presented with uniform demyelinating sensorimotor polyneuropathy. Sensory more than motor neuropathy was diagnosed in four patients. Clinically and electrophysiologically confirmed carpal tunnel syndrome (CTS) occurred in three patients (9.4 %), suggesting a higher prevalence than in the general population. Patients with neuropathy were in general more severely affected than those without neuropathy, although no correlation was found between the presence of neuropathy and the degree of mutant heteroplasmy in muscle. Higher age and male gender were associated with an increased risk of neuropathy. Our results show that peripheral neuropathy is not uncommon in patients with the 3243A > G mutation, and they also may have an increased risk of CTS.
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PMID:Peripheral neuropathy in patients with the 3243A>G mutation in mitochondrial DNA. 1257 54

The authors, on performing a critical analysis of reported data on clinical manifestations of lead intoxication, suggest that the initial manifestations thereof presenting as changes in no other indices but laboratory ones, be regarded as a preclinical stage. Aside from generally recognized concepts of "mild" and "prominent" stages in lead intoxication the authors consider it logical and expediant to introduce a moderately severe stage manifested by vegetosensory polyneuropathy, astheno-vegetative syndrome, dyskinesia of the biliary and intestinal tracts, spastic colitis. It is in this very stage of lead intoxication that the patient, to the author's thinking, is to be assigned to some other job where he/she will not be exposed to lead or other adverse occupational factors. This will, we believe, permit preventing development of a clinically significant stage of lead intoxication manifested by encephalopathy, motor form of polyneuropathy, lead colic, anemia and hepatitis.
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PMID:[Clinical stages of lead intoxication]. 1258 28


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