[Analytical study of visual-motor function in children with cerebral palsy--recognition and reconstruction].
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1. Behavioral studies of rats with ibotenic acid-induced lesions of distinctive regions of the rostral striatum demonstrated clearcut motoric impairments after lesions of the lateral striatum, but not after lesions of the medial striatum. 2. Differential effects of dorsolateral and ventrolateral lesions on segmental bodily movements indicated a somatomotor map in the lateral region. 3. Neurotoxic lesions of the lateral striatum produced deficits of motor energizing analogous to those of human parkinsonism. 4. These results support the hypothesis that neurodegenerative processes affecting the lateral striatum (putamen) in humans may specifically account for parkinsonian symptoms. 5. The implications of this hypothesis for the treatment of parkinsonism using the grafting technique are discussed.
In experimental spinal cord injury studies, animal models are widely used to examine anatomical and functional changes after different treatments and lesion types. A variety of behavioral paradigms exists in the literature, but definitions and criteria for motor performance vary considerably. In this study, we examined the outcome and relation of tests such as the BBB open field locomotion score, footprint analysis, kinematic analysis, placing response, grid walk and narrow beam crossing following two different lesion types. The information obtained was used to design an efficient and reliable testing strategy, which includes a broad spectrum of parameters to enhance sensitivity. This approach should help to standardize modular testing procedures across different laboratories working on spinal cord injury.
Orphanin FQ/nociceptin (OFQ/N) is a preferred endogenous ligand for the orphan opioid receptor-like-1 receptor. This peptide has been reported to increase intestinal, but not gastric, motor activity. In the present study, OFQ/N (0.6-60 nmol kg(-1) i.v.) increased intragastric pressure and antral contractility and, as expected, decreased blood pressure in anaesthetized rats. The gastric motor effects of OFQ/N (6 nmol kg(-1)) were not affected by inhibition of nitric oxide synthase or opioid receptor blockade. OFQ/N (6 nmol kg(-1)) evoked gastric motor increases and hypotension were not affected by prior administration of its derivative [Phe(1)Psi(CH(2)-NH)Gly(2)]nociceptin-(1-13)-NH(2) unless the pseudopepotide was administered shortly (5 min) prior to OFQ/N. This putative antagonist (6-300 nmol kg(-1)) alone increased antral motility with approximately 100 fold lower potency than OFQ/N. Neither bilateral vagotomy nor spinal cord transection altered OFQ/N-evoked increases in intragastric pressure and antral contractility. In conclusion, OFQ/N induces gastric motor excitation in addition to its known effects to increase intestinal motility. The gastric responses to OFQ/N are not dependent on 'classical' opioid receptor activation or nitric oxide, similar to the case for the intestines. The primary site of action of OFQ/N on the stomach is probably via enteric nerves, since central descending vagal or sympathetic pathways are not necessary for OFQ/N to increase gastric motility. The gastric motor effects of the derivative [Phe(1)Psi(CH(2)-NH)Gly(2)]nociceptin-(1-13)-NH(2) are similar to OFQ/N, although with lower potency. The effects of the derivative as a partial agonist or antagonist in different experimental paradigms may reflect tissue OFQ/N receptor reserve.
Calculous cholecystitis in patients is associated with considerable disturbances of the duodenal peristalsis, a hyper- and akinetic type of disorders in the motoricity being observed. Due to the results obtained in all patients with calculous cholecystitis an examination of the duodenal peristalsis should be recommended during the period of diagnostic studies.
Esophageal carcinoma is one of the most common malignant diseases in China. In order to clarify the pathophysiology of the esophageal motor dysfunction in the disease, a comparative study was done with esophageal manometry and 24 hour pH monitoring in 90 patients with esophageal carcinoma (EC) including 17 cardiac carcinoma (CC) and 56 healthy adult volunteers. The results showed that the resting pressure of the esophagus in patients was lower, particularly during swallowing and Valsalva test, than that of the normal subjects. It indicated that the patients with EC and CC had a hypodynamic esophagus so that a series of abnormal esophageal peristalsis and contractive waves were found. Besides the effect of mechanical obstruction of the tumor itself, it was believed to be a causative factor, at least in part, for the production of the clinical symptoms such as dysphagia and spastic odynophagia occurred during swallowing. Being the lower LESP, the patients with EC and CC presented pathological gastroesophageal reflux which was proved by 24 hour pH monitoring findings.
It has been shown that the neural channels from the otolith organs and the vertical semicircular canals connect to the cyclo-rotatory oculomotor system. However, only a few studies have been conducted to examine the relationship between the cyclo-rotatory optokinetic (COK) and the vestibular inputs. Accordingly, we have analyzed the cyclo-rotatory oculomotor output evoked by a COK stimulus, in 30 subjects; 21 normal adults, 4 elderly persons, and 5 persons with unilateral vestibular dysfunction. In addition, the spinal motor output was simultaneously recorded and comparatively analyzed. The increase in COK nystagmus (COKN) was less than that in horizontal and vertical OKN. There was a significant decline in the maximum slow phase eye velocity in the elderly subjects as well as in the subjects with unilateral vestibular dysfunction, compared to that in the normal adult subjects. Regarding the spinal motor output, in the subjects with unilateral vestibular dysfunction, a pronouned increase in the sway distance from the center of gravity was found with COK stimulus forward the lesioned side. However, with the COK stimulus, there was no significant correlation between the output functions of the cyclorotatory oculomotor system and those of the spinal motor system.
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This study describes the long-term deficits of a patient who, after a toxic encephalopathy, sustained extensive bilateral damage to both segments of the globus pallidus (GP) and the right substantia nigra (SN). There were no signs of lesions of the pyramidal tracts or of other motor structures. The most obvious deficits were an abnormal gait with an exaggerated knee extension and a tendency to fall slowly, especially when pushed backward. In contrast, Romberg's test on an unstable platform was normal, as were long-latency leg reflexes induced by perturbations. Inadequate anticipatory and compensatory postural responses, in particular across the hip and knee joints, and slow movements seemed responsible for the falls. Muscle tone was normal but reflex studies showed signs of abnormal facilitation and inhibition at various levels of the neuraxis. We conclude that the GP and SN lesions caused defective input to premotor cortical and brain stem target zones. Dysfunctioning of these zones leads to improper control of the descending ventromedial motor system responsible for locomotion, postural control, and reflex status. The deficits in upper extremity motor performance included delayed and slow movements, inaccurate amplitudes of ballistic responses, a lack of predictive control, and deficits in bimanual coordination. Sensory feedback, proprioceptive more than visual, played a powerful compensating role in rapid aiming movements. Regional blood flow (studied using 15(O)2) was reduced in multiple frontal cortical regions, among which are the hand areas of the supplementary and premotor cortex. We hypothesize that this reflected impaired functioning of these areas, caused by defective bilateral output from GP and SN, and resulting in the motor deficits of the arm and hand.
Freezing of gait (FOG) is a disabling phenomenon common in patients with advanced Parkinson's disease (PD). The cause of FOG is unclear. The objective of this study was to explore a novel hypothesis stating that FOG is related to asymmetric motor performance. We compared PD patients that experience FOG episodes (PD+FOG) with PD patients that do not (PD-FOG) and studied the relationship of FOG to asymmetry in gait and in rhythmic hand movement performance to determine whether potential FOG-related gait asymmetry is unique to walking or whether it is systemic. Subjects were tested in an "off" (unmedicated) and again in an "on" (medicated) state. Gait was more asymmetric in PD+FOG than in PD-FOG during "off" state (p = 0.005) and during "on" (p = 0.016). Rhythmicity of foot swing in one leg was correlated with the other leg in PD-FOG but not in PD+FOG. There was no difference in asymmetry in performance of rhythmic hand movements between the two groups. No correlation was found between asymmetry of clinical symptoms and gait asymmetry. Taken together, the results of this study suggest that bilateral uncoordinated gait and marked gait asymmetry, but not asymmetry in motor performance in general, are associated with FOG.
After partial (spared-root) or complete hindlimb deafferentation, locomotion and accurate limb placement during locomotion recover considerably. In the present study movement was studied during and after recovery to determine whether altered motor patterns could substitute for normal ones in the recovery of motor behavior. In acute L6 spared-root preparations somatosensory postural reflexes are impaired, accurate limb placement deficient and joint angle measurements show altered kinematic motor patterns during locomotion. As somatosensory postural reflexes and accurate limb placement recover, so do the motor patterns. After complete deafferentation motor patterns are more disturbed. Somatosensory postural reflexes remain absent but as descending reflexes recover, so does accurate limb placement during locomotion. In deafferented hindlimbs, in contrast to spared-root preparations motor patterns observed chronically (after recovery of accurate placement) are persistently abnormal indicating that novel motor patterns can replace normal ones in the recovery of goal-directed behavior. The results suggest that behavioral substitution can contribute to recovery of useful movement.