Bradykinesia akinesia inco-ordination test (BRAIN TEST): an objective computerised assessment of upper limb motor function. (1/306)

OBJECTIVES: A simple and rapid computerised keyboard test, based on the alternating finger tapping test, has been developed to quantify upper limb motor function. The test generates several variables: (1) kinesia score: the number of keystrokes in 60 seconds; (2) akinesia time: cumulative time that keys are depressed; (3) dysmetria score: a weighted index calculated using the number of incorrectly hit keys corrected for speed; (4) incoordination score: a measure of rhythmicity which corresponds to the variance of the time interval between keystrokes. METHODS: The BRAIN TEST(Copyright ) was assessed on 35 patients with idiopathic Parkinson's disease, 12 patients with cerebellar dysfunction, and 27 normal control subjects. RESULTS: The mean kinesia scores of patients with Parkinson's disease or cerebellar dysfunction were significantly slower than normal controls (Parkinson's disease=107 (SD 28) keys/min v cerebellar dysfunction=86+/- (SD 28) v normal controls=182 (SD 26), p<0.001) and correlated with the UPDRS (r =-0.69, p<0.001). The akinesia time is very insensitive and was only abnormal in patients with severe parkinsonism. The median dysmetria (cerebellar dysfunction=13.8 v Parkinson's disease=6.1 v normal controls=4.2, p=0.002) and inco-ordination scores (cerebellar dysfunction=5.12 v Parkinson's disease=0.84 v normal controls=0.15, p=0.002) were significantly higher in patients with cerebellar dysfunction, in whom the dysmetria score correlated with a cerebellar disease rating scale (r=0.64, p=0.02). CONCLUSION: The BRAIN TEST(Copyright ) provides a simple, rapid, and objective assessment of upper limb motor function. It assesses speed, accuracy, and rhythmicity of upper limb movements regardless of their physiological basis. The results of the test correlate well with clinical rating scales in Parkinson's disease and cerebellar dysfunction. The BRAIN test will be useful in clinical studies. It can be downloaded from the Internet ().  (+info)

The coordination of bimanual prehension movements in a centrally deafferented patient. (2/306)

Many everyday tasks require that we use our hands co-operatively, for example, when unscrewing a jar. For tasks where both hands are required to perform the same action, a common motor programme can be used. However, where each hand needs to perform a different action, some degree of independent control of each hand is required. We examined the coordination of bimanual movement kinematics in a female patient recovering from a cerebrovascular accident involving anterior regions of the parietal lobe of the right hemisphere, which resulted in a dense hemianaesthesia of her left arm. Our results indicate that unimanual movements executed by our patient using her non-sensate hand are relatively unimpaired. In contrast, during bimanual movements, reaches executed by our patient using her non-sensate hand show gross directional errors and spatiotemporal irregularities, including the inappropriate coupling of movement velocities. These data are discussed with reference to the role played by limb proprioception in the planning and control of prehension movements.  (+info)

Cortical motor reorganization in akinetic patients with Parkinson's disease: a functional MRI study. (3/306)

Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies. Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex. These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex. These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.  (+info)

Effects of attentional focus, self-control, and dyad training on motor learning: implications for physical rehabilitation. (4/306)

In this article, the authors review recent studies on 3 factors that have been shown to affect the learning of motor skills-the performer's attentional focus, self-control, and practice in dyads-and discuss their implications for rehabilitation. Research has shown that directing learners' attention to the effects of their movements can be more beneficial for learning than directing their attention to the details of their own actions. Furthermore, giving learners some control over the training regimen has been found to enhance learning, unlike prescriptive training protocols that dictate when feedback will be delivered, how often, and the order that tasks will be practiced. Finally, not only can practice in dyads (or larger groups) reduce the costs of training, but it can also result in more effective learning than individual practice sessions. The incorporation of these factors into rehabilitation practice can potentially enhance the effectiveness and efficiency of rehabilitation.  (+info)

Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease. (5/306)

Neurodegenerative disorders like Huntington's disease (HD) are characterized by progressive and putative irreversible clinical and neuropathological symptoms, including neuronal protein aggregates. Conditional transgenic models of neurodegenerative diseases therefore could be a powerful means to explore the relationship between mutant protein expression and progression of the disease. We have created a conditional model of HD by using the tet-regulatable system. Mice expressing a mutated huntingtin fragment demonstrate neuronal inclusions, characteristic neuropathology, and progressive motor dysfunction. Blockade of expression in symptomatic mice leads to a disappearance of inclusions and an amelioration of the behavioral phenotype. We thus demonstrate that a continuous influx of the mutant protein is required to maintain inclusions and symptoms, raising the possibility that HD may be reversible.  (+info)

Childhood neuromotor dysfunction in schizophrenia patients and their unaffected siblings: a prospective cohort study. (6/306)

Neuromotor dysfunction is a consistent finding in high-risk and archival studies of schizophrenia, but the sources of this dysfunction and its role in the developmental course of the disorder remain poorly understood. This study examined childhood motor predictors of adult psychiatric outcome in a birth cohort sample (72 patients with schizophrenia or schizoaffective disorder, 63 unaffected siblings, and 7,941 nonpsychiatric controls), evaluated prospectively with neurologic examinations at 8 months, 4 years, and 7 years of age. Deviance on motor coordination measures at 7 years was associated with both adult schizophrenia and unaffected sibling status, suggesting that a cofamilial (and perhaps genetic) factor underlies motor coordination deficits in schizophrenia. Unusual movements at ages 4 and 7 predicted adult schizophrenia but not unaffected sibling status, indicating that these deficits may be specific to those who will develop the clinical phenotype. None of the motor precursors were confined to patients with an early age at first treatment contact. Fetal hypoxia predicted unusual movements at 4 but not 7 years among the preschizophrenia subjects, suggesting neurodevelopmental dependence of its functional effects. Neither prenatal complications nor birth weight were associated with motor dysfunction in preschizophrenia subjects or their unaffected siblings at any age. Finally, preschizophrenia children did not show the expected developmental decline in unusual movements, perhaps reflecting aberrant functional maturation of cortical-subcortical pathways.  (+info)

Upper limb motor function at 5000 metres: determinants of performance and residual sequelae. (7/306)

Little is known about the effects of age and symptoms of acute mountain sickness and the potential benefit of short term acclimatisation on fine motor performance at altitude. There is uncertainty about whether time spent at altitude results in permanent neurological sequelae. Nine hole pegboard tests were performed on a group of trekkers at sea level (n=61), after ascending to Kanchenjunga base camp (5100 m; n=46), and 20 weeks after return to sea level (n=43). Comparison of baseline and altitude times showed a mean slowing from 36.2 to 39.0 seconds, a 7. 8% deterioration in performance (p<0.0001), which was greatest in subjects aged 50 years or older (5.04 v 1.93 seconds, p=0.017), those tested within 24 hours of arrival at 5100 m (4.75 seconds, 13. 3% v 0.48 seconds, 1.3% p<0.001), and persons experiencing symptoms of acute mountain sickness (p=0.012), each of which were independent determinants of deterioration. Repeat pegboard testing at sea level after 20 weeks showed no significant change compared with baseline (p=0.68). This confirms the deleterious effects of altitude on fine motor function, emphasises the benefit of acclimatisation, and suggests that older persons and those with symptoms of acute mountain sickness are particularly susceptible. The risk of long term motor dysfunction after exposure to these relatively moderate altitudes seems to be small.  (+info)

Repetitive speech phenomena in Parkinson's disease. (8/306)

OBJECTIVES: Repetitive speech phenomena are morphologically heterogeneous iterations of speech which have been described in several neurological disorders such as vascular dementia, progressive supranuclear palsy, Wilson's disease, and Parkinson's disease, and which are presently only poorly understood. The present, prospective study investigated repetitive speech phenomena in Parkinson's disease to describe their morphology, assess their prevalence, and to establish their relation with neuropsychological and clinical background data. METHODS: Twenty four patients with advanced Parkinson's disease and 29 subjects with mid-stage, stable idiopathic disease were screened for appearance, forms, and frequency of repetitive speech phenomena, and underwent a neuropsychological screening procedure comprising tests of general mental functioning, divergent thinking and memory. Patients with advanced Parkinson's disease had a significantly higher disease impairment, longer disease duration, and an unstable motor response to levodopa with frequent on-off fluctuations. Both groups were well matched as to their demographical, clinical, and cognitive background. Perceptual speech evaluation was used to count and differentiate forms of repetitive speech phenomena in different speech tasks. To compare the effect of the motor state, the appearance of repetitive speech phenomena was also assessed in a subgroup of patients with advanced Parkinson's disease during the on versus the off state. RESULTS: Speech repetitions emerged mainly in two variants, one hyperfluent, formally resembling palilalia, and one dysfluent, stuttering-like. Both forms were present in each patient producing repetitive speech phenomena. The repetitive speech phenomena appeared in 15 patients (28.3 %), 13 of whom belonged to the advanced disease group, indicating a significant preponderance of repetitive speech phenomena in patients with a long term, fluctuating disease course. Repetitive speech phenomena appeared with almost equal frequency during the on and the off state of patients with advanced Parkinson's disease. Their distribution among different variants of speech was disproportional, with effort demanding speech tasks producing a significantly higher number of repetitive speech phenomena over semiautomatic forms of speech. CONCLUSIONS: In idiopathic Parkinson's disease repetitive speech phenomena seem to emerge predominantly in a subgroup of patients with advanced disease impairment; manifest dementia is not a necessary prerequisite. They seem to represent a deficit of motor speech control; however, linguistic factors may also contribute to their generation. It is suggested that repetitions of speech in Parkinson's disease represent a distinctive speech disorder, which is caused by changes related to the progression of Parkinson's disease.  (+info)