Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We elicited motor evoked potentials (MEPs) using transcortical magnetic stimulation in 150 control subjects aged 14 to 85 years and 275 patients with a variety of diseases. There were no significant side effects. Cortex-to-target muscle latencies measured 20.2 +/- 1.6 ms (thenar), 14.2 +/- 1.7 ms (extensor digitorum communis), 9.4 +/- 1.7 ms (biceps), and 27.2 +/- 2.9 ms (tibialis anterior). Central motor delay between the cortex and the C-7 and L-5 measured 6.7 +/- 1.2 ms and 13.1 +/- 3.8 ms, respectively. Mean spinal cord motor conduction velocity measured 65.4 m/s. MEP amplitude expressed as a percentage of the maximum M wave was never less than 20% of the M wave. A value of less than 10% is considered abnormal. MEP latency increases linearly with age and central motor delay is longer in older subjects. Compound muscle action potentials and absolute MEP amplitudes decreased linearly with age. In multiple sclerosis (MS), MEP latency and central delay were often very prolonged. The MEP was more sensitive than the SEP in MS. In amyotrophic lateral sclerosis, MEP latencies were only modestly prolonged; the characteristic abnormality was reduced amplitude. When pseudobulbar features predominated MEPs were often absent. The MEP was of normal latency in Parkinson's disease, but age-related amplitude was often increased. MEP latency and amplitude were normal in Huntington's disease. Abnormal MEPs persisted several months after stroke despite good functional recovery. The MEP could be used to advantage to demonstrate proximal conduction slowing and block in demyelinating neuropathies. In plexopathy, ability to elicit an MEP several days after onset of paresis was good evidence of neuronal continuity in motor fibers.
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PMID:AAEM minimonograph #35: Clinical experience with transcranial magnetic stimulation. 793 34

A number of cortical and subcortical areas are involved in the control of saccades and smooth pursuit, and lesions affecting these areas result in various ocular motor syndromes. Most of these syndromes are relatively subtle and have to be ascertained using recordings, because other brain areas may largely take over the function of a damaged area. Anterior cortical, posterior cortical, large and bilateral cortical, subcortical and degenerative cerebral lesions are successively reviewed. In the anterior part of the cerebral hemisphere, the frontal eye field (FEF), supplementary eye field (SEF) and prefrontal cortex (PFC), i.e. area 46 of Brodmann, control eye movements. The FEF appears to be principally involved in the control of intentional saccades, in particular those made with a retinotopic reference system, and in smooth pursuit. The SEF could control saccades made with a spatiotopic reference system, and sequences of saccades (requiring a temporal working memory). The PFC could control the inhibition of unwanted reflexive saccades, and be involved in spatial memory used for programming all types of memory-guided saccades. In the posterior part of the cerebral hemisphere, the parietal eye field (PEF) is involved in the triggering of reflexive visually guided saccades, and the middle temporal (MT) and medial superior temporal (MST) areas in smooth pursuit. Acute and large unilateral lesions usually result in transitory ipsilateral conjugate eye deviation. Bilateral lesions affecting both the FEF and the PEF result in severe saccade and smooth-pursuit paresis, whereas bilateral posterior temporoparietal lesions result in Balint's syndrome, consisting of both eye movement and visual-attention abnormalities. Subcortical lesions also result in various eye movement abnormalities, which have been little documented to date. Lastly, degenerative cerebral diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, progressive supranuclear palsy and corticobasal degeneration result in more or less severe eye movement disturbances. Eye movement recordings may contribute to early differential diagnosis of some of these degenerative diseases.
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PMID:Saccade and smooth-pursuit impairment after cerebral hemispheric lesions. 803 37

Cholesterol is an essential component of both the peripheral and central nervous systems of mammals. Over the last decade, evidence has accumulated that disturbances in cholesterol metabolism are associated with the development of various neurological conditions. In addition to genetically defined defects in cholesterol synthesis, which will be covered in another review in this Thematic Series, defects in cholesterol metabolism (cerebrotendinous xanthomatosis) and intracellular transport (Niemann Pick Syndrome) lead to neurological disease. A subform of hereditary spastic paresis (type SPG5) and Huntington's disease are neurological diseases with mutations in genes that are of importance for cholesterol metabolism. Neurodegeneration is generally associated with disturbances in cholesterol metabolism, and presence of the E4 isoform of the cholesterol transporter apolipoprotein E as well as hypercholesterolemia are important risk factors for development of Alzheimer's disease. In the present review, we discuss the links between genetic disturbances in cholesterol metabolism and the above neurological disorders.
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PMID:Genetic connections between neurological disorders and cholesterol metabolism. 2046 96

A variety of neurodegenerative diseases can underlie dementia syndromes. In addition to Alzheimer's disease (AD) and its prodromal stages, these include in particular frontotemporal degeneration, Lewy body dementia and Parkinson's dementia, progressive supranuclear paresis, corticobasal degeneration and chorea Huntington. Although not classified as a neurodegenerative brain disease, for all clinical diagnoses there must be a differential diagnostic separation from vascular forms of dementia. Furthermore an exclusion of affective disorders, such as minor depression is necessary from a clinical psychiatric perspective. Moreover the preclinical stages of AD often present with uncharacteristic symptoms. Especially affective symptoms can occur in addition to initial cognitive deficits such as memory decline. In summary, clinical and neuropsychological procedures together with functional imaging techniques allow a detailed diagnostic assessment of neurodegenerative dementia syndromes which can be additionally supported by neurochemical biomarkers and innovative imaging procedures, such as diffusion imaging or magnetic resonance spectroscopy.
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PMID:[Symptoms and imaging diagnostics of neurodegenerative dementia]. 2146 5