Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclosporine has been associated with various neurological side-effects including postural tremor, seizures, headaches, encephalopathy, cortical blindness, and visual hallucinations. We describe here two patients who developed parkinsonism, with rest tremor and bradykinesia, after receiving cyclosporin A following allogeneic bone marrow transplantation. The patients did not have pre-existing neurological disorders, and had not received significant amounts of dopamine-blocking drugs. One patient improved markedly with Sinemet (carbidopa-levodopa), while the other (who did not tolerate Sinemet) improved with decrease in cyclosporine dosage. The relation of the parkinsonian symptoms to cyclosporine therapy and lack of other evident causes for the symptoms, suggests that parkinsonism may be an occasional consequence of cyclosporine.
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PMID:Parkinsonism during cyclosporine treatment. 887 34

A 59-year-old woman presented with consciousness disturbance with flapping tremor. Laboratory examinations revealed normal liver functions, and imaging studies, ultrasonography, magnetic resonance imaging, and angiography, showed portal vein aneurysm communicating from the portal vein to the hepatic vein, splenomegaly, and splenic artery aneurysm. These examinations confirmed porto-systemic shunt leading to hepatic encephalopathy. Porto-hepatic venous shunt via portal vein aneurysm is extremely rare, and there are few reports that it causes encephalopathy; therefore, little is known about the entity and this association. The literature in English is reviewed and the etiology, clinical features, and prognosis discussed.
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PMID:Porto-hepatic venous shunt via portal vein aneurysm with splenomegaly. 896

Type II citrullinemia is an adult-onset hepatocerebral disease caused by a deficiency of argininosuccinate synthetase in liver. A 25-year-old Japanese man suddenly developed encephalopathy, showing disorientation and flapping tremor. Plasma concentrations of ammonia and citrulline were extremely high, and hepatic argininosuccinate synthetase activity was deficient. The patient's condition deteriorated rapidly in spite of intensive medications. Therefore, we performed a partial liver transplantation using a graft obtained from his healthy 61-year-old father. After surgery, his neurological symptoms soon disappeared and plasma levels of ammonia and citrulline were normalized within 3 months after operation. Type II citrullinemia is one fulminant form of various liver-based metabolic diseases, and immediate liver transplantation is necessary to rescue patients with this disease. As liver transplantation from cadaveric donor is still not possible in Japan, it seems justifiable to use living related partial liver transplantation for our patient.
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PMID:Complete neurological recovery of an adult patient with type II citrullinemia after living related partial liver transplantation. 897 Jun 29

A 30 months-old boy developed bilateral nistagmus, tremor, gait disturbance, hypotonia and disartria. The diagnose of Leigh encephalopathy was suggested on the basis of clinical, neuroimaging and laboratory findings. Computed tomography and magnetic resonance imaging (MRI) at an early stage revealed bilateral and symmetric lesions in the putamen, appearing as hyperintense signal on T2-weighted images. Twelve months later a relatively large hypertense area in the posterior brainstem was observed. At this stage, the patient exhibited marked deterioration, dystonic manifestations, rigidity and respiratory disturbances. He died 6 months later for respiratory arrest during bronconeumonic infection. We believe MRI is a valuable means to allow assessment of the evolution of the disease.
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PMID:[Leigh's encephalopathy (subacute necrotizing encephalopathy). Documentation of its evolution through neuroimaging]. 898 56

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

Sudden and brief involuntary movements of central nervous system (CNS) origin called myoclonus may be cortical (motor strip), thalamocortical (thalamocortical loop) or reticular (caudal reticular formation). Epileptic, cortical and thalamocortical myoclonus are combined with a spike which, when it is focal, needs back-averaging to be demonstrated. Negative myoclonus due to lapse of tone can only be demonstrated during antigravidic posture and may be combined with either a slow wave or the second, positive component of a polyspike-wave. Epileptic myoclonus must be distinguished from epileptic spasms and tonic seizures, and from non-epileptic myoclonus, tics, tremor and chorea. Myoclonus may occur in partial symptomatic (mainly Rasmussen and dysplasia), cryptogenic (frontal) or idiopathic (negative myoclonus in CSWS) epilepsy. Generalized myoclonus is part of inborn errors of metabolism, non-progressive encephalopathy (mainly Angelman) and idiopathic epilepsy (juvenile and infantile benign and severe forms, and myoclonic-astatic epilepsy). Carbamazepine, vigabatrin and eventually lamotrigine may worsen myoclonus whereas it may be improved by benzodiazepines, valproate, lamotrigine, zonisamide and piracetam according to etiology. Pathophysiology must take in account maturation processes, lesions and genetic predisposition. However, precise mechanisms remain unknown and only hypotheses can be proposed, that could clarify the age-related EEG and clinical expression of the various syndromes.
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PMID:Myoclonus and epilepsy in childhood: 1996 Royaumont meeting. 960 May 41

Carbon disulfide toxicity is well characterized. The principal target organ is the nervous system, although cardiovascular, reproductive, ophthalmologic, and other effects are also recognized. The neurotoxicity manifests in three ways: encephalopathy, peripheral and cranial nerve dysfunction, and movement abnormalities. This report describes a case of olivopontocerebellar atrophy, a form of multiple system atrophy, developing in an adult after over 30 years of occupational exposure to carbon disulfide. The patient presented with the insidious onset of balance problems, impotence, and irritability, without tremor, cogwheel rigidity, bradykinesia, or changes in facial expression. Over the next few years severe ataxia developed, and the clinical diagnosis was confirmed with computed tomography and magnetic resonance imaging scans. The patient experienced multiple medical complications and died approximately 9 years after diagnosis. This case is consistent with a large body of clinical and experimental literature, much of it 50 years old, showing that carbon disulfide can cause movement disorders. It also serves as a reminder that movement disorders, ranging from parkinsonism to dystonia, are associated with a variety of toxic exposures such as manganese, carbon monoxide, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and medications.
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PMID:Multiple system atrophy following chronic carbon disulfide exposure. 1070 37

Substance abuse through the deliberate inhalation of petrol (petrol sniffing or gasoline sniffing) is prevalent in inner-urban and remote rural communities. Although acute toxic encephalopathy is a well-documented consequence of petrol sniffing, the neurological and cognitive effects of chronic petrol sniffing are unknown. A structured neurological examination and the Cambridge Neuropsychological Test Automated Battery (CANTAB) were used to assess neurological and cognitive function in 33 current-sniffers (individuals who had sniffed petrol for >6 months), 30 ex-sniffers (individuals who had sniffed petrol in the past but had abstained for 6 months) and 34 matched non-sniffers (individuals who had never sniffed petrol). No subject was, or had been, encephalopathic from petrol sniffing and all were residing in their community. Blood lead and hydrocarbon levels and information about petrol sniffing behaviour were obtained from each subject. When compared with non-sniffers, current-sniffers showed higher rates of abnormal tandem gait, rapid alternating hand movements, finger to nose movements, postural tremor, bilateral palmomental reflexes and brisk deep reflexes. Cognitive deficits occurred in the areas of visual attention, visual recognition memory and visual paired associate learning. Ex-petrol sniffers showed higher rates of abnormal tandem gait and bilateral palmomental reflexes and cognitive deficits in the areas of visual recognition memory and pattern-location paired associate learning. Blood lead levels and length of time of petrol sniffing correlated significantly with the magnitude of neurological and cognitive deficits. Blood hydrocarbon levels were not related to neurocognitive deficits, although this may have been due to methodological difficulties in obtaining hydrocarbon levels. These results suggest that subtle neurological and cognitive abnormalities do occur in individuals who abuse petrol but who do not have acute toxic encephalopathy and that the severity of these abnormalities is reduced with abstinence.
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PMID:Neurological and cognitive abnormalities associated with chronic petrol sniffing. 979 46

HIV-associated neurological manifestations: dementia, myelopathy, and neuropathy, have become one of the commonest causes of neurological disorders in young people. Cognitive impairment develops in about 30 p. 100 of patients with AIDS and frank dementia in 15 to 20 p. 100 with an annual incidence after AIDS of approximatively 7 p. 100. Typically, the onset of dementia is relatively abrupt over a few weeks or months. The clinical manifestations of the encephalopathy now termed "HIV-dementia", suggest predominant subcortical or frontal involvement. Typical presentation includes apathy and inertia, memory loss and cognitive slowing, minor depressive symptoms and withdrawal from usual activities. Neurological examination may show hypertonia of lower limbs, tremor, clonus, frontal release signs and hyperactive reflexes. Terminally, the patient is bedbound, incontinent, abulic or mute with decorticate posturing leading to death over 3 to 6 months. However, a stabilisation and even a regression of the cognitive disorders have been observed following antiretroviral treatment. Radiological features of HIV dementia include both central and cortical atrophy and white matter rarefaction. However they are neither invariable nor specific. Together with CSF examination, they are more important to exclude opportunistic infections. Indeed, although a completely normal CSF profile may reasonably exclude the diagnosis; at present, no single test or combination of tests can reliably diagnose HIV dementia. Although the clinical characteristics of HIV-dementia are now clearly established, its pathogenesis is unclear and its pathological counterpart remains a matter of debate. A number of "HIV-induced" lesions may be found in the brain of AIDS patients and their causative role in HIV-dementia has been considered. They include HIV encephalitis due to productive CNS infection by the virus, diffuse white matter pallor "HIV-leukoencephalopathy" reflecting an abnormality of the blood brain barrier, involvement of the grey matter, "diffuse poliodystrophy", with neuronal loss that results, at least partly, from a process of programmed cell death and axonal damage. These changes are variably associated in patients with HIV dementia, however none of them can be closely related to the cognitive disorders. This suggests that the neuronal dysfunction underlying HIV-dementia results from different mechanisms that are variably associated and may interact mutually. These include production of viral proteins, microglial activation with consequent production of neurotoxic factors such as proinflammatory cytokines, free radicals, derivates of arachidonic acid, or quinoleic acid, and blood borne neurotoxic factors in particular cytokines.
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PMID:[Dementia and human inmmunodeficiency virus infection]. 983 49

Cocaine abuse is a well known cause of cerebrovascular complications. An inflammatory vasculopathy hypothesis has been proposed, but the medical literature has only reported a few pathological confirmations. We report a case with a biopsy demonstrating cerebral inflammatory vascular changes that are associated with cocaine abuse. A 21-year-old male, a twice weekly cocaine abuser, developed encephalopathy, apraxia and left hemiparesis with hemisensory loss during the first week after his last cocaine intake; postural tremor and dystonia appeared later. Laboratory data were unrevealing. Cerebral angiography showed a lack of vascularization in the left precentral and central arterial groups. A corticomeningeal cerebral biopsy demonstrated perivascular cell collection and transmural lymphomonocytic infiltration of the small cortical vessels. All symptoms improved with corticosteroid treatment, but 4 years later, the patient returned with a worsening of his encephalopathy and a severe memory impairment, emotional lability and apraxia. A cerebral magnetic resonance image (MRI) showed subcortical and periventricular lesions suggesting ischemic damage in small-size vessel areas as well as cortical atrophy. This new case supports the existence of an encephalopathy associated with vascular inflammatory changes in a cocaine abuser, although more clinical and experimental data are necessary to define its physiopathology.
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PMID:Encephalopathy and biopsy-proven cerebrovascular inflammatory changes in a cocaine abuser. 1021 Aug 20


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