Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal unoperated rats were tested for rotation (i.e., circling behavior) in a spherical "rotometer" and dose-response relationships were generated using d-amphetamine, apomorphine, L-Dopa, haloperidol, and scopolamine. The rotation induced by amphetamine was significantly antagonized by alpha-methyl-p-tyrosine and haloperidol, but not by diethyldithiocarbamate. The rotation elicited by apomorphine was unaffected by alpha-methyl-p-tyrosine. Rotation was not necessarily in the same direction with high and low doses of amphetamine, or amphetamine and apomorphine administered a week apart from each other. Dopaminergic-cholinergic interactions were evident, since pilocarpine antagonized amphetamine-induced rotation whereas scopolamine did not; scopolamine elicited rotation in the same direction as that induced by amphetamine. Left and right striatal dopamine and tel-diencephalic norepinephrine levels were determined in rats injected with various doses of amphetamine and tested for rotation. There were significant bilateral differences in striatal dopamine which were related to the direction of rotation. Since amphetamine was found to be equally distributed to the two sides of the brain, the difference in striatal dopamine appeared to be the neurochemical substrate for rotation in normal rats. These results suggest that normal rats have asymmetrical levels of striatal dopamine as well as an asymmetrical complement of striatal dopamine receptors.
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PMID:Drug-induced rotation in rats without lesions: behavioral and neurochemical indices of a normal asymmetry in nigro-striatal function. 82 60

We report a case of a woman with L-Dopa resistant asymmetrical parkinsonism with a posterior fossa cyst compressing the lower brainstem on MR. She did not show improvement in any of her symptoms after cysto-cardiac derivation. It was not possible to delineate if this was a case of a new malformative syndrome or the coincidence of two different disorders.
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PMID:L-dopa resistant parkinsonism in an adult woman with a cyst in the posterior fossa. 750 37

Humans with Parkinson's disease (PD) often have problems in righting themselves, in that they have difficulty in recruiting their axial musculature to rotate the body to prone. Since this "axial apraxia' is not ameliorated by L-DOPA therapy, it has been concluded that dopamine (DA) does not play a role in recruiting axial rotation of the body [14]. This hypothesis was tested by comparing the righting of rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra (SN) with that of intact rats. Body-on-body righting, where asymmetrical tactile stimulation of the body initiates hindquarter righting, was used to specifically test tactile righting independently of righting triggered or influenced by other sensory systems. In this behavioral test, rats are placed on their sides, their forequarters are held down and their hindquarters released. The DA-depleted rats took longer to begin righting, to complete righting, and used more limb action to right themselves than did control rats. These findings suggest that for this tactile based form of righting, DA-depletion produces axial apraxia. However, frame-by-frame analysis of righting sequences of DA-depleted rats showed that pelvis-led axial rotation could occur, but the spatio-temporal relationship between body and limb movements was disorganized. Therefore, following DA-depletion axial apraxia-like deficits appear to arise from sensorimotor disruption. This raises the issue of whether the axial apraxia in PD patients arises from damage to systems beyond the nigrostriatal DA system, or from interference with sensorimotor integration that is not ameliorated by replacement therapy.
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PMID:Spatio-temporal impairments in limb and body movements during righting in an hemiparkinsonian rat analogue: relevance to axial apraxia in humans. 889 8

We described the clinical and neuroradiological findings together with a transcranial magnetic stimulation study in two patient with hemiparkinson-hemiatrophy syndrome (HP-HA). In both patients the neuroradiological findings (MRI) and the central motor conduction were normal whereas the functional imaging studies (SPECT) showed asymmetrical perfusion in the basal ganglia; the intracortical inhibition at short interstimulus intervals and the silent period duration in the motor cortex contralateral to hemiparkinsonism were significantly increased only in one of the patient which has a poor response to L-Dopa therapy. These studies suggest that intracortical or thalamo-cortical neuronal inhibition may be increased in HP-HA. The etiopathogenetic considerations, the diagnostic criteria and the prognostic value of our finding to evaluate the clinical evolution of parkinsonism are discussed in the context of current models of basal ganglia-thalamo-cortical connectivity. Transcranial magnetic stimulation will provide valuable information for the differential diagnosis of the parkinsonian disorders and may predict the efficacy of L-Dopa therapy.
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PMID:Hemiparkinson-hemiatrophy syndrome: a transcranial magnetic stimulation study. 1283 89

Cortico-basal degeneration is a rare degenerative disease connected with Tau protein pathology. Epidemiology of cortico-basal degeneration is unknown. The authors present a case of 59 years old woman with suspicion of cortico-basal degeneration. The extrapyramidal symptoms mainly on the right side with "alien limb phenomenon" and dystonia of lower limb is observed in our patient. Cortico-subcortical brain atrophy was present in MRI scans. EEG was asymmetrical. No improvement was noticed after L-Dopa. Treatment of amantidine caused the transient improvement.
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PMID:[Cortico-basal degeneration: the rare form of tau protein disease]. 1509 33

We describe features of a patient that broadens the clinical and pathological spectrum of neurofilament inclusion disease (NFID). The patient was a 52-year-old man with a 5--6 year history of progressive, asymmetrical spastic weakness of the upper and lower extremities; L-DOPA-unresponsive parkinsonism; and SPECT evidence of asymmetrical frontoparietal and basal ganglia hypoperfusion. The brain had marked frontoparietal parasagittal cortical atrophy, including the motor cortex, with histopathological evidence of neurofilament- and alpha-internexin-immunoreactive neuronal inclusions. The corticospinal tract had degeneration, but there was minimal lower motor neuron pathology. There was also severe neuronal loss and gliosis in the posterolateral putamen and the substantia nigra, mimicking multiple system atrophy; however, glial cytoplasmic inclusions were not detected with alpha-synuclein immunohistochemistry. This case extends the clinical and pathological spectrum of NFID to include cases with predominant parkinsonian and pyramidal features.
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PMID:Extending the clinicopathological spectrum of neurofilament inclusion disease. 1575 70

Atypical Parkinsonism associated with white matter pathology has been described in cerebrovascular diseases, mitochondrial cytopathies, osmotic demyelinating disorders, leukoencephalopathies leukodystrophies, and others. Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is an autosomal dominant disorder with symptomatic onset in midlife and death within a few years after symptom onset. Neuroimaging reveals cerebral white matter lesions that are pathologically characterized by non-inflammatory myelin loss, reactive astrocytosis, and axonal spheroids. Most cases are caused by mutations in the colony-stimulating factor 1 receptor (CSF1R) gene. We studied neuropathologically verified HDLS patients with CSF1R mutations to assess parkinsonian features. Ten families were evaluated with 16 affected individuals. During the course of the illness, all patients had at least some degree of bradykinesia. Fifteen patients had postural instability, and seven had rigidity. Two patients initially presented with parkinsonian gait and asymmetrical bradykinesia. These two patients and two others exhibited bradykinesia, rigidity, postural instability, and tremor (two with resting) early in the course of the illness. Levodopa/carbidopa therapy in these four patients provided no benefit, and the remaining 12 patients were not treated. The mean age of onset for all patients was about 45 years (range, 18-71) and the mean disease duration was approximately six years (range, 3-11). We also reviewed HDLS patients published prior to the CSF1R discovery for the presence of parkinsonian features. Out of 50 patients, 37 had gait impairments, 8 rigidity, 7 bradykinesia, and 5 resting tremor. Our report emphasizes the presence of atypical Parkinsonism in HDLS due to CSF1R mutations.
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PMID:Parkinsonian features in hereditary diffuse leukoencephalopathy with spheroids (HDLS) and CSF1R mutations. 2378 35

18F-FDOPA PET has been historically used for the evaluation of parkinsonian syndromes in research settings. With the wider availability of PET cameras and 18F-DOPA this method can be used as a clinical diagnostic tool. Current acquisition protocols are simple with a 10 minute static acquisition performed 90 minutes post injection. Criteria for precise visual analysis of the images are defined. The performances of the method are reviewed throughout the literature. The method is very sensitive for detection of IPD versus normal patients. Few studies comparing 18F-FDOPA PET and DAT SPECT did not show any difference in diagnostic accuracy. 18F-FDOPA PET is reliable for evaluation of IPD progression. In general, atypical Parkinson's syndromes cannot be reliably differentiated from IPD since they share a similar nigro-striatal degeneration process. However, some patterns such as the asymmetrical faint homogeneous striatal uptake reduction pattern of CBD can be recognized. The short acquisition protocol, the various indications in oncology of 18F-FDOPA and the high quality of PET images are in favor of this technique in daily clinical practice for the improvement of diagnosis of parkinsonian syndromes.
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PMID:18F-FDOPA PET for the diagnosis of parkinsonian syndromes. 2536 11

Corticobasal syndrome is a rare neurodegenerative disorder, which presents with a progressive, asymmetrical, akinetic rigid syndrome and early cortical signs. However, clinical, pathological, and electrophysiological heterogeneity makes the understanding of this syndrome challenging. Corticobasal syndrome can have various pathological substrates including corticobasal degeneration, Alzheimer's disease, Fronto-temporal degeneration with TDP inclusions, Creutzfeldt-Jakob disease, and progressive supranuclear palsy (PSP). Furthermore, tools such as transcranial magnetic stimulation (TMS) and functional neuroimaging techniques like PET and SPECT have not been adequately used to supplement the clinico-pathological heterogeneity. TMS studies in CBS have revealed changes in cortical excitability and transcortical inhibition. Despite the availability of more than 2 decades, its potential in CBS has not been fully utilized in studying the cortical plasticity and effect of Levodopa on central neurophysiology. PET and SPECT studies in CBS have shown abnormalities in regional glucose metabolism, asymmetrical involvement of presynaptic dopaminergic system, and ascending cholinergic connections to the cortex. While most studies have shown normal D2 receptor-binding activity in striatum of CBS cases, the results have not been unanimous. Functional neuroimaging and TMS studies in CBS have shown the involvement of GABAergic, muscarinic, and dopaminergic systems. In this review, we aim to provide the current state of understanding of central neurophysiology and neurochemistry of CBS using TMS and functional neuroimaging techniques. We also highlight the heterogeneous nature of this disorder and the existing knowledge gaps.
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PMID:Neurophysiology and neurochemistry of corticobasal syndrome. 2930 7

Dementia with Lewy body is a neurodegenerative disorder affecting both cognitive and motor domains. Motor impairment manifests predominantly as a symmetrical/mild asymmetrical parkinsonian syndrome that is only mildly responsive to Levodopa. To characterize motor dysfunction in dementia with Lewy body, we quantitatively assessed upper limb movements using a motion-capture system. Ten patients and ten healthy controls were tested while performing the hand-to-mouth movement of which speed, smoothness and accuracy features were measured. The results showed that individuals with dementia with Lewy body required a longer time to complete the task, particularly due to a prolonged duration of the adjusting phase (i.e., when approaching the target/mouth). The overall motor performance of dementia with Lewy body patients closely resembled what previously observed in patients affected by both Parkinson's disease and ataxia while performing the same task. Moreover, the severity of parkinsonian symptoms as assessed by the UPDRS-III scale impacted on the velocity of movement alone whereas impairment of executive functions correlated with variables related to the phase of targeting the mouth. This study provides new information about upper limb motor dysfunction in dementia with Lewy body.
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PMID:Upper limb movements in dementia with Lewy body: a quantitative analysis. 3117 96


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