Changes in the organization of the brain after recovery from aphasia were investigated by measuring increases in regional cerebral blood flow (rCBF) during repetition of pseudowords and during verb generation. Six right-handed patients who had recovered from Wernicke's aphasia caused by an infarction destroying the left posterior perisylvian language zone were compared with 6 healthy, right-handed volunteers. In the control subjects, strong rCBF increases were found in the left hemisphere in the posterior part of the superior and middle temporal gyrus (Wernicke's area), and during the generation task in lateral prefrontal cortex (LPFC) and in inferior frontal gyrus (Broca's area). There were some weak right hemisphere increases in superior temporal gyrus and inferior premotor cortex. In the patients, rCBF increases were preserved in the frontal areas. There was clear right hemisphere activation in superior temporal gyrus and inferior premotor and lateral prefrontal cortices, homotopic to the left hemisphere language zones. Increased left frontal and right perisylvian activity in patients with persisting destruction of Wernicke's area emphasizes redistribution of activity within the framework of a preexisting, parallel processing and bilateral network as the central mechanism in functional reorganization of the language system after stroke.
In order to investigate sensorimotor processing and force development in Parkinson's disease, 16 patients, four patients with hemiparkinsonism and 12 age-matched normal subjects were assessed during lifting and holding of an object in a precision grip between thumb and forefinger, or holding the object in this grip at a fixed height above a table. In the former case, object loading could be changed between lifts without warning. In the latter case, unexpected step load changes to the object were applied to the object with a torque motor. All procedures could be applied with or without visual control of the hand and the object. Normal subjects lifted an unpredictable load employing the grip force parameters used in the preceding lift. If a load change was encountered, the parameters became adapted to the new conditions during the lift, modulating grip forces to match the loading. Parkinsonian patients retained this strategy and the ability to regulate grip forces according to load. Under all conditions, however, parkinsonian subjects developed abnormally high grip forces in both the lift and the hold phase, although the ratio of these forces remained normal. Lifting height was normal in parkinsonian subjects, but the duration of the lifting task was significantly prolonged, due to a marked slowing in the rate of grip force development in the lead-up to object lift-off and to prolongation of the movement phase. Forewarning of object loading, with or without visual control, did not reduce timing deficits or improve the rate of grip force development. However, it did allow parkinsonian subjects to reduce the safety margin significantly. Responses to step load changes imposed during holding without visual control showed minor abnormalities in the parkinsonian patients: onset latencies and EMG activity in the first dorsal interosseus and thenar muscles were normal up to 140 ms after displacement. Subsequent EMG activity in the first dorsal interosseus remained largely normal, but activity later in the slip response (140-210 ms), subject to voluntary influence, was reduced in the thenar muscle. Differences were less marked under visual conditions, but remained significant. We concluded that the internal parameter set for lifting an object in a precision grip and the automatic processes adapting precision grip to actual conditions are intact in Parkinson's disease. However, parkinsonian subjects generate abnormally high grip forces and require longer than normal subjects to complete a lift, particularly with lighter loads. This deterioration in performance reflects both reduced effectiveness of sensorimotor processing and impairment in the rate of force development in Parkinson's disease.
1. The surface electromyogram (EMG) of human leg muscles was recorded during running at different speeds; The EMG was compared with the simultaneously recorded vertical force exerted by the foot and with the angle of the ankle joint. 2. During running, the electrical activity of the gastrocnemius muscle increased sharply 35--45 ms after ground contact and reached its maximum at the end of muscle stretch; This activity was superimposed on a slowly increasing level of activation, which began 120--180 ms before ground contact. At the end of the stance phase, gastrocnemius became inactive and, simultaneously, there was a sudden increase in tibialis anterior activity. The assumption that the steep increase in the gastrocnemius EMG reflects the spinal stretch reflex of alpha-motoneurons is supported by the following findings. 3. The peak level of gastrocnemius EMG in the stance phase of fast running was 2--3 times higher than the activity during maximum voluntary contraction. 4. With stimulation of the tibial nerve at different rates, the maximum isometric force was about 30--40% higher than the maximum voluntary isometric contraction. 5. The increase in EMG at 35--45 ms after ground contact was markedly diminished during running, after partial blockage of Ia afferents by ischemia, at a time when the strength of voluntary contraction was shown to be uninfluenced by the ischemia. 6. The gastrocnemius activity during running was simulated by electrical stimulation of the tibial nerve. The rate of stimulation was varied so as to approximate to the EMG profile during running. This indicated that a spinal stretch reflex could become mechanically effective within the shortest stance phase measured in a fast sprint (ca. 120 ms).
Mutations in DJ-1 are less frequent than mutations in Parkin in EOPD patients but should be considered as a possible cause of EOPD. The effect of single heterozygous mutations in DJ-1 on the nigrostriatal system, as described for heterozygous changes in Parkin and PARK6, remains to be elucidated.
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