Deficits in sensorimotor control during precise hand movements in Huntington's disease.

OBJECTIVES: To investigate the performance of patients with Huntington's disease (HD) while manipulating objects using a precision grip. METHODS: The grip forces developed by the fingers were studied while subjects lifted an object of unpredictable weight in the hand. The ability to stabilize grip force after externally imposed weight change was also studied. RESULTS: Patients used higher grip forces than the normal subjects in both the lifting and holding phases, particularly with a lighter weight. Lift timing was slowed in the patients, most markedly with a lighter weight. Increased levels of inter-trial variation were observed only with a light weight. This indicates that the slowing in HD differs from that in Parkinson's disease, which remains constant regardless of object load, and that the slowing in HD is not due to involuntary antagonist muscle activity resulting from an underlying chorea. The grip force response to sudden weight change was normal, but appeared after a delay which increased at lower rates of weight change. CONCLUSIONS: Disturbances in precision grip timing and magnitude in HD may result from a reduced ability to process relevant tactile afferent input. The delay in the adaptive response suggests an increased threshold for detection of weight change in HD. Alternatively, this delay may arise from mediation of the response over an additional cerebellar pathway to compensate for damage to the basal ganglia.     

Glucagon stimulation of plasma renin activity in humans.

Administration of 0.2 mg of glucagon by intravenous bolus resulted in an increase in plasma renin activity (PRA) in 2 of 5 normal volunteers on their usual diet. Two of the nonresponders subsequently showed a PRA response to glucagon after sodium depletion. A lower dose of glucagon (0.01 mg) had no effect on PRA despite a 31 mg/100 ml rise in blood glucose and peak plasma glucagon of over 2000 pg/ml. In conclusion, glucagon can stimulate PRA but it is not a potent stimulator; its effect may be potentiated by sodium depletion.     

Idiopathic Pulmonary Fibrosis and Gastroesophageal Reflux. Implications for Treatment

Background

Even though the pathogenesis of idiopathic pulmonary fibrosis (IPF) is unknown, there is mounting evidence that abnormal reflux (GERD) and aspiration of gastric contents may play a role in the pathogenesis of this disease.

Aims

The aims of this study were to determine in patients with GERD and IPF: (a) the clinical presentation, (b) the esophageal function, and (c) the reflux profile.

Methods

We compared the clinical presentation, the esophageal function (as defined by high-resolution manometry), and the reflux profile (by dual sensor pH monitoring) in 80 patients with GERD (group A) and in 22 patients with GERD and IPF (group B).

Results

Heartburn was present in less than 60 % of patients with GERD and IPF. Lower esophageal sphincter pressure and peristalsis were normal in both groups, while the upper esophageal sphincter (UES) was more frequently hypotensive in IPF patients (p?=?0.008). In patients with GERD and IPF, the proximal esophageal acid exposure was higher (p?=?0.047) and the supine acid clearance was slower as compared with patients with GERD only (p?<?0.001).

Conclusions

The results of this study show that in patients with GERD and IPF: (a) reflux is frequently silent, (b) with the exception of a weaker UES, the esophageal function is preserved, and (c) proximal reflux is more common, and in the supine position, it is coupled with a slower acid clearance. Because these factors predisposing IPF patients to the risk of aspiration, antireflux surgery should be considered early after the diagnosis of IPF and GERD is established.     

Dynamics of microglial activation in the spinal cord after cerebral infarction are revealed by expression of MHC class II antigen

Microglial reactivity associated with induction of MHC class II (HLA-DR) antigen is a sensitive indicator for pathological events in the CNS. To assess the response of glial cells after lesions of supraspinal descending tracts, HLA-DR, CD68 and GFAP were studied immunohistochemically on spinal cord tissue of 5 patients who died after unilateral infarction of the middle cerebral artery territory, and 5 control cases. In patients who died shortly after a stroke (4–14 days) increased HLA-DR-immunoreactivity (HLA-DR-IR) could be observed in the intermediate grey matter and in the ventral horn. The CD68-IR was much less intense. After longer survival times (5 weeks to 4 months), HLA-DR-IR in the grey matter was clearly lower than that observed in the spinal cord of short survival times, but very abundant in the dorsolateral funiculus, specifically within the corticospinal tract. In white matter areas, CD68-IR was almost identical to the HLA-DR-IR. Within the grey matter, CD68-IR was similar to the control tissue. A moderate increase of GFAP-positive astrocytes could be seen only in the grey matter after longer survival times. It seems probable, that the dynamics of HLA-DR-positive microglia reflect the early phagocytosis of presynaptic terminals by microglia in target regions of descending fibre tracts. In the white matter, the removal of degenerating axons by phagocytosing microglia expressing HLA-DR and CD68 antigens is a slower process which occurs over a period of months.     

Recovery from wernicke's aphasia: A positron emission tomographic study

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.     

Transient decrease of acetylcholinesterase in ventral horn neurons caudal to a low thoracic spinal cord hemisection in the adult rat

Light microscopic enzyme: histochemistry was employed to study the alterations of acetylcholinesterase (AChE) within lumbosacral ventral horn neurons at survival times of 1, 4, 7, 14, 28, 60, and 90 days after low thoracic spinal cord hemisection in adult rats. The intensity of histochemical staining was quantified using densitometric techniques. Virtually all ventral horn neurons of sham-operated and unoperated animals, which served as controls, displayed intense AChE staining. Hemisection of the spinal cord induced a transient, ipsilateral decrease of AChE staining in most neuronal cell bodies and in the neuropil of lamina IX at all segmental levels caudal to the lesion. Quantitative analysis of representative segments revealed a reduction of AChE in the ventral horn during a postoperative (p.o.) period of 1 to 28 days followed by a phase of recovery over the next two months. AChE activity still remained slightly reduced, even at 90 days p.o. The transient decrease in ACNE is a well-known metabolic response of axotomized motoneurons. However, the observed changes of AChE reactivity in intact motoneurons ipsilateral and caudal to the hemisection are presumably induced by the interruption of supraspinal descending pathways. These metabolic changes may functionally affect the whole motor unit and be involved in the disturbances of motor function following spinal cord injury.