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)

Tremor is frequently described in patients with multiple sclerosis (MS) but remains poorly characterized using neurophysiological techniques. Accelerometric (ACC) and electromyographic (EMG) recordings were performed in 26 MS patients complaining of clumsiness, associated (n = 16) or not associated (n = 10) with visible tremor. Seventeen healthy subjects with physiological tremor (PT) and eight patients with essential tremor (ET) served as controls. Signals were analyzed using non-linear Empirical Mode Decomposition (EMD) and related Hilbert-Huang Transform (HHT), compared to the standard linear spectral analysis using Fast Fourier Transform (FFT). The presence of cerebellar signs and motor deficit was assessed on clinical examination. Using FFT, tremor was found in all patients with ET and 12% of subjects with PT, but in none of the MS patients, even in the presence of visible tremor. In contrast, EMD-HHT analysis of ACC-EMG coupling showed common frequency peaks characterizing tremor related to a central generator in 62.5% of MS patients with visible tremor, 40% of MS patients without visible tremor, 29% of subjects with PT, and all patients with ET. In EMD-HHT analysis, tremor characteristics were similar in subjects with PT and MS patients, regardless of the presence of a visible tremor, but these characteristics clearly differed in patients with ET. A visible tremor in MS patients was associated with more frequent cerebellar signs and less motor deficit at the upper limb. The low-frequency tremor observed in MS patients could therefore originate in lesions of the brainstem (midbrain) or cerebellothalamic circuits, or may correspond to an enhanced PT, partly favored by cerebellar dysfunction and being more visible during movement execution in the absence of concomitant motor deficit.
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PMID:Analysis of tremor in multiple sclerosis using Hilbert-Huang Transform. 2677 79

Corticobasal degeneration is a rare, progressive neurodegenerative disease and a member of the 'parkinsonian' group of disorders, which also includes Parkinson's disease, progressive supranuclear palsy, dementia with Lewy bodies and multiple system atrophy. The most common initial symptom is limb clumsiness, usually affecting one side of the body, with or without accompanying rigidity or tremor. Subsequently, the disease affects gait and there is a slow progression to influence ipsilateral arms and legs. Apraxia and dementia are the most common cortical signs. Corticobasal degeneration can be difficult to distinguish from other parkinsonian syndromes but if ocular signs and symptoms are present, they may aid clinical diagnosis. Typical ocular features include increased latency of saccadic eye movements ipsilateral to the side exhibiting apraxia, impaired smooth pursuit movements and visuo-spatial dysfunction, especially involving spatial rather than object-based tasks. Less typical features include reduction in saccadic velocity, vertical gaze palsy, visual hallucinations, sleep disturbance and an impaired electroretinogram. Aspects of primary vision such as visual acuity and colour vision are usually unaffected. Management of the condition to deal with problems of walking, movement, daily tasks and speech problems is an important aspect of the disease.
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PMID:Visual signs and symptoms of corticobasal degeneration. 2755 83

Wilson's disease is characterised by deposition of copper in various tissues of the body, most markedly in the liver and the brain. Cerebral involvement, evident as neuropsychiatric symptoms, may be the presenting form of the illness in up to 50% of the adults. When patients present initially with psychiatric manifestations, the correct diagnosis is frequently missed. This case report describes an adult in his late 20's who presented with symptoms of major depressive disorder, but failed to respond to standard antidepressant treatment. He instead developed neurologic symptoms like tremor, gait disturbance, weakness of grip and clumsiness. Diagnosed as a case of conversion disorder, brain MRI showed abnormalities in the basal ganglia. Further investigations revealed that he had adult-onset Wilson's disease. Because of rarity, adult Wilson's disease patients with initial psychiatric presentations are frequently misdiagnosed and definitive treatment with chelating agents is not offered with continual organ damage from copper accumulation.
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PMID:A Rare Neuropsychiatric Presentation of Adult-Onset Wilson's Disease. 2866 14


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