Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0426980 (motor symptom)
 471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Caudal regression sequence (CRS) is a rare congenital defect of the lower spinal segments and the neural tube. Motor symptoms as well as neurological deficits and loss of bladder and bowel function are usually present. CRS is also associated with anomalies in other systems such as the gastrointestinal and genitourinary tract. Etiology and pathogenesis are poorly understood.A newborn presented with anomalies of the spinal column (lumbosacral) with absence/hypoplasia of the 12th thoracic and first lumbar vertebral anomaly body. Bladder and bowel initially were functional. MR-angiography exhibited an anomaly of the unpaired vessels originating from the aorta, a likely relict of a persisting vitelline artery. These findings indicate a potential vascular genesis of CRS, much as in sirenomelia.
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PMID:Caudal regression sequence: vascular origin? 1680 60

Levodopa (LD) application improves motor symptoms in patients with Parkinson's disease (PD) patients. Little is known on further effects of LD, which induced lower plasma levels of cortisol and lower serotonergic activity in certain brain areas of fish. Objectives of this trial were to analyse levels of cortisol, LD and 3-O-methyldopa (3-OMD) after administration of LD/benserazide in long term treated PD patients. 12 PD patients, taken off their regular treatment for at least 12 hours, received soluble 200 mg LD/50 mg benserazide under stress free conditions. Motor symptoms improved, LD and 3-OMD levels increased, whereas cortisol concentrations started to decrease significantly 30 minutes after LD intake. This reduced cortisol release may result from an overflow of exogenous LD in the brainstem. This hypothetically causes an reduced 5-HT content in neurons projecting to the hypothalamic structures, which are involved in the partial 5-HT dependent central regulation of peripheral cortisol release.
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PMID:Acute levodopa administration reduces cortisol release in patients with Parkinson's disease. 1693 91

The relation of body side of motor symptom onset in Parkinson's disease (PD) to memory measures associated with hemispheric dominance was examined. Fourteen patients with right body side motor symptom onset (RPD, inferred left hemisphere dysfunction) and 16 patients with left side onset (LPD, right hemisphere dysfunction) were administered measures of verbal (Hopkins Verbal Learning Test-Revised) and visual memory (Brief Visual Memory Test-Revised), that require similar task demands and are associated with left or right hemisphere dominance, respectively. The LPD group demonstrated poorer visual than verbal memory, both within group and in comparison to the RPD group. By contrast, the RPD group showed poorer verbal than visual memory within group. These findings suggest that side of motor symptom onset is associated with asymmetrical memory dysfunction.
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PMID:Body side of motor symptom onset in Parkinson's disease is associated with memory performance. 1696 53

It is well known that many patients with Parkinson's disease experience neuropsychological decline. However, the nature and extent of mental status change varies widely, with some patients showing mild or no cognitive impairments and others exhibiting frank dementia. Research has shown that several clinical disease parameters may differentially correlate with patterns of neuropsychological dysfunction. The present study examined side and type of motor symptom at disease onset and their relationship to cognition in idiopathic Parkinson's disease (PD). We identified 58 patients who initially presented with one of the following symptom profiles: right-side tremor onset (RSO-T; n = 15), right-side bradykinesia/rigidity onset (n = 12), left-side tremor onset (n = 19), and left-side bradykinesia/rigidity onset (n = 12). There were no differences between groups in disease duration, overall mental status, education, or depression severity. We administered a battery of neuropsychological measures to the four PD subgroups and a group of matched control subjects (n = 40). MANCOVAs controlling for age revealed patients with RSO-T performed significantly better than the other three PD subgroups across the entire neuropsychological battery. Further, the RSO-T subgroup performed comparably to controls. In contrast, the other three PD subgroups showed widespread cognitive deficits. These findings suggest an intricate relationship between motor symptom and side of disease onset and it is the combination of these factors that may influence the disease course and extent of cognitive deterioration. Furthermore, patients who develop tremor on the right side of their body represent a distinct subgroup of PD patients who exhibit relative sparing of cognitive function.
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PMID:Side and type of motor symptom influence cognition in Parkinson's disease. 1699 Nov 55

Wilson's disease (WD) is an inherited disorder of copper metabolism yielding marked motor deficits, including a severely disabling tremor. As a structural correlate of the disease, a variety of cerebral abnormalities has been revealed. However, the relationship between motor deficits and cerebral lesions has remained largely unknown. Here, we investigated correlation between WD tremor and cerebral magnetic resonance imaging (MRI) findings. Cerebral MRI abnormalities in 6 symptomatic WD patients were compared to findings in 6 asymptomatic WD patients and 10 healthy controls. All patients were treated with long-term copper chelating therapy. Motor symptoms including tremor were determined by Unified Parkinson's Disease Rating Scale Part III (UPDRS-III). MRI findings in symptomatic WD patients revealed significant symmetric T2*-weighted hypointense signal alterations of globus pallidus, head of the caudate nucleus, and substantia nigra. In contrast, MRI of asymptomatic WD patients did not differ from healthy controls. Correlation analysis revealed a significant positive correlation between MRI basal ganglia lesions and UPDRS action tremor score. Our results demonstrate for the first time that Wilson's disease tremor is associated with lesions of the globus pallidus, the head of the caudate nucleus, and the substantia nigra.
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PMID:Wilson's disease tremor is associated with magnetic resonance imaging lesions in basal ganglia structures. 1704 91

Parkinson's disease is classically characterised as a motor neurodegenerative disorder. Motor symptoms in the disorder are secondary to an altered dopamine-acetylcholine balance due to reduced striatal dopaminergic tone and subsequent cholinergic overactivity. In the past, anticholinergic drugs were given to improve motor aspects of the disease. There is now an increasing interest in the cognitive and non-motor symptoms of Parkinson's disease and in cholinesterase-inhibitor therapy for dementia associated with Parkinson's disease. In this Personal View, we reconsider the dopamine-acetylcholine balance theory and look at recent clinical findings and the possible cooperative role of dopamine and acetylcholine in the induction and maintenance of the long-lasting changes of striatal and cortical synaptic plasticity. We also discuss a convergent versus parallel model to explain cognitive dysfunctions in Parkinson's disease according to dopamine-acetylcholine dependent alterations in synaptic plasticity.
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PMID:A convergent model for cognitive dysfunctions in Parkinson's disease: the critical dopamine-acetylcholine synaptic balance. 1705 64

Depression is a common comorbid condition in Parkinson's disease (PD) and a major contributor to poor quality of life and disability. However, depression can be difficult to assess in patients with PD due to overlapping symptoms and difficulties in the assessment of depression in cognitively impaired patients. As several rating scales have been used to assess depression in PD (dPD), the Movement Disorder Society commissioned a task force to assess their clinimetric properties and make clinical recommendations regarding their use. A systematic literature review was conducted to explore the use of depression scales in PD and determine which scales should be selected for this review. The scales reviewed were the Beck Depression Inventory (BDI), Hamilton Depression Scale (Ham-D), Hospital Anxiety and Depression Scale (HADS), Zung Self-Rating Depression Scale (SDS), Geriatric Depression Scale (GDS), Montgomery-Asberg Depression Rating Scale (MADRS), Unified Parkinson's Disease Rating Scale (UPDRS) Part I, Cornell Scale for the Assessment of Depression in Dementia (CSDD), and the Center for Epidemiologic Studies Depression Scale (CES-D). Seven clinical researchers with clinical and research experience in the assessment of dPD were assigned to review the scales using a structured format. The most appropriate scale is dependent on the clinical or research goal. However, observer-rated scales are preferred if the study or clinical situation permits. For screening purposes, the HAM-D, BDI, HADS, MADRS, and GDS are valid in dPD. The CES-D and CSDD are alternative instruments that need validation in dPD. For measurement of severity of depressive symptoms, the Ham-D, MADRS, BDI, and SDS scales are recommended. Further studies are needed to validate the CSDD, which could be particularly useful for the assessment of severity of dPD in patients with comorbid dementia. To account for overlapping motor and nonmotor symptoms of depression, adjusted instrument cutoff scores may be needed for dPD, and scales to assess severity of motor symptoms (e.g., UPDRS) should also be included to help adjust for confounding factors. The HADS and the GDS include limited motor symptom assessment and may, therefore, be most useful in rating depression severity across a range of PD severity; however, these scales appear insensitive in severe depression. The complex and time-consuming task of developing a new scale to measure depression specifically for patients with PD is currently not warranted.
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PMID:Depression rating scales in Parkinson's disease: critique and recommendations. 1739 34

Autism spectrum disorders (ASD) are manifest as impairments in social interaction, language and speech development, and the appearance of repetitive behaviors with restricted interests. Motor impairments in individuals with ASD have been categorized as "associated symptoms". The objective of this study was to describe the prevalence of motor deficits in ASD. Specifically, using retrospective clinical record review, we report the prevalence of hypotonia, motor apraxia, reduced ankle mobility, history of gross motor delay, and toe-walking, as well as the improvement of these symptoms with age, in a cohort of 154 children with ASD. The possible association of motor deficits with epilepsy or developmental regression was also assessed. To address whether the motor deficits in children with ASD were properly identified and treated, we evaluated whether the children with the motor deficits were more likely to receive physical and/or occupational therapies as compared to the children with ASD who did not show motor deficits. Hypotonia was the most common motor symptom in our ASD cohort (51%) and this appeared to improve over time, as suggested by the significant reduction in prevalence in older children (p=0.002). Likewise, motor apraxia (34%) showed a tendency to be more prevalent among younger children as compared with older children (p=0.06). Historical intermittent toe-walking was found in 19% of children while reduced ankle mobility was a rare occurrence. Gross motor delay was reported in 9% of children, all of whom gained motor independence by the time of examination. Except for gross motor delay, ASD children with fine motor deficits were not more likely to receive interventional services, as compared with ASD children without the motor deficits. The results suggest that fine motor control and programming deficits are common co-occurrence of children with ASD in this cohort. The reduced prevalence of these motor deficits in older children suggests improvement over time, whether through natural progression, results of interventional therapy, or the combination of the two. However, ASD children with the motor deficits were not more likely to receive service than those without the motor deficits.
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PMID:Prevalence of motor impairment in autism spectrum disorders. 1746 40

Motor symptoms form the hallmark of Parkinson's disease (PD), although other features such as depression are often present. Currently-used depression rating scales measure affective and somatic symptoms. These somatic symptoms of depression can also be core PD symptoms, suggesting an overlap of symptoms between depression and PD. Using in vivo radiotracer methods, striatal dopaminergic dysfunction is found in both PD and depression. This study investigates to what extent the overlapping symptoms of depression and PD are associated with the striatal dopaminergic dysfunction typical of PD. Symptoms of depression were assessed in 23 PD patients who did not have major depression according to the Montgomery-Asberg depression rating scale (MADRS; cut-off < 18) and according to a trained psychologist who interviewed all patients. The striatal dopaminergic activity of patients was assessed with FDOPA-PET. Dopaminergic activity of the putamen and caudate nucleus was associated with MADRS total score and specifically with the symptom 'Concentration difficulties'. These results suggest that the typical striatal dopaminergic dysfunction of PD can cause symptoms that can also be categorized as symptoms of depression. In particular, cognitive symptoms measured with a depression rating scale may be based on the dopaminergic dysfunction of the striatum in PD patients.
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PMID:Striatal dopaminergic activity (FDOPA-PET) associated with cognitive items of a depression scale (MADRS) in Parkinson's disease. 1756 26

Gastrointestinal (GI) dysfunction is the most common non-motor symptom of Parkinson's disease (PD). Symptoms of GI dysmotility include early satiety and nausea from delayed gastric emptying, bloating from poor small bowel coordination, and constipation and defecatory dysfunction from impaired colonic transit. Understanding the pathophysiology and treatment of these symptoms in PD patients has been hampered by the lack of investigation into GI symptoms and pathology in PD animal models. We report that the prototypical parkinsonian neurotoxin, MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine), is a selective dopamine neuron toxin in the enteric nervous system (ENS). When examined 10 days after treatment, there was a 40% reduction of dopamine neurons in the ENS of C57Bl/6 mice administered MPTP (60 mg/kg). There were no differences in the density of cholinergic or nitric oxide neurons. Electrophysiological recording of neural-mediated muscle contraction in isolated colon from MPTP-treated animals confirmed a relaxation defect associated with dopaminergic degeneration. Behaviorally, MPTP induced a transient increase in colon motility, but no changes in gastric emptying or small intestine transit. These results provide the first comprehensive assessment of gastrointestinal pathophysiology in an animal model of PD. They provide insight into the impact of dopaminergic dysfunction on gastrointestinal motility and a benchmark for assessment of other PD model systems.
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PMID:Loss of enteric dopaminergic neurons and associated changes in colon motility in an MPTP mouse model of Parkinson's disease. 1827 53


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