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C Tsering

Publications and source records attributed to C Tsering.

9 recordsLinked to original sources
PubMed2002

The clock drawing test is a poor screen for very mild dementia.

OBJECTIVE: To determine whether performance on the clock drawing test varies as a function of dementia severity and particularly whether it differentiates cognitively normal older adults from those with very mild dementia. METHODS: Clock drawings were obtained during the initial clinical assessments of 75 participants in a longitudinal study of healthy aging and dementia of the Alzheimer type (15 cognitively normal, 25 with very mild dementia, 21 with mild dementia, and 14 with moderate to severe dementia, as staged by the Clinical Dementia Rating). Each clock drawing later was judged blindly and independently by two raters according to six commonly used sets of scoring criteria. RESULTS: The same pattern of results was obtained for all six scoring methods. Inter-rater reliability was consistently high. Spearman correlations indicated that as dementia severity increased, clock drawing performance decreased. Analyses of variance revealed that although those with mild or moderate/severe dementia performed significantly worse on the clock drawing test than did individuals who had very mild dementia or who were cognitively normal, the latter two groups did not differ significantly. Sensitivity and specificity analyses revealed that all methods could distinguish between normal aging and dementia of at least mild severity. However, sensitivity for detecting very mild dementia was poor. CONCLUSION: Although the clock drawing test can be scored reliably and can differentiate cognitively normal older adults from those with at least mild dementia of the Alzheimer type, it does not appear to be a useful screening instrument for detecting very mild dementia.

Aged↗
PubMed1992

Further studies on platelet-mediated neurotoxicity.

The mechanism of ischemic neuronal injury is not fully resolved. The present view is that vascular occlusion per se does not fully account for the extent of neurological dysfunction. We hypothesized that platelet secretory products might contribute to ischemic neuronal injury in the central nervous system (CNS) (Joseph et al., Stroke, 20 (1989) 38-44 and 1316-1319). Our preliminary studies using organotypic rat spinal cord cultures exposed to human platelet and its secretory products, revealed that platelet product(s) had neurotoxicity. Further studies, using the same methods, were conducted here, with the addition of several refinements such as use of gel-filtered platelets (as opposed to washed platelets), adding additional relevant controls including platelet membranes, red blood cells and washed rat platelets. The results confirmed our initial finding that an agent(s) in platelet secretion is neurotoxic. Subsequently, we identified serotonin (5HT), a major platelet product, as having toxic effects on neurons. This toxicity of 5HT appeared to be blocked by ketanserin, a 5HT2 receptor antagonist. Judging by the concentrations of 5HT that demonstrated neurotoxicity in these in vitro studies, it appears that products secreted from activated platelets could have pathological significance in vivo.

Animals↗
PubMed1992

Serotonin may have neurotoxic properties.

Serotonin (5HT), a major platelet secretory product, has been shown to suppress CNS function in vivo. As part of an ongoing project to study interactions between neuron and platelet, we used organotypic explant cultures of rat spinal cord to study if 5HT had a morphologically demonstrable neurotoxic effect. The results suggest that serotonin may be neurotoxic, and that this effect may be prevented by ketanserin, a specific 5HT2 antagonist. Related experiments, using acetylcholinesterase (AChE) enzyme activity as a biochemical parameter, indicate that 5HT hastens the decline of enzyme activity. The concentrations of 5HT at which neurotoxicity was demonstrated were comparable to the calculated 5HT concentration potentially present in the vicinity of an acute cerebral thrombus. These findings could provide new insight into the mechanism of ischemic neuronal injury.

Acetylcholinesterase↗
PubMed1992

Platelet activity and stroke severity.

Although platelets constitute the major component of a thrombus, its role in determining the clinical severity of thrombotic stroke is unknown. Therefore, we investigated the relationship between platelet ionized calcium ([Ca2+i]), a measure of platelet activity and presumably proneness to thrombosis, and clinical stroke severity in 45 consecutively studied acute ischemic stroke patients. Even though there was no correlation between the clinical neurological scores and the levels of baseline and activated platelet [Ca2+i], stroke was less severe in patients who had been taking aspirin at the time of stroke onset. These results raise several important questions: (a) is the extent of platelet activation a reflection of thrombus volume, (b) does the clinical severity of neurological deficit reflect the causative thrombus volume, and (c) whether the beneficial effect of aspirin in stroke prophylaxis is through its inhibition of platelets alone.

Aged↗
PubMed1992

Demonstration of segmental arrangement of thoracic spinal motor neurons using lipophilic dyes.

Unlike the afferent input into the spinal cord, it is generally believed that the motor efferent system in the mammalian spinal cord is more segmental in arrangement. Isolated comments in recent reports suggest that motor neurons in the mammalian spinal cord may be strictly segmental, contrary to many earlier reports using less sophisticated methods. We have attempted to address the question of the segmental arrangement of motor neurons in a mammalian spinal cord using single and double labelling with the fluorescent lipophilic dyes, Di I and Di A. These dyes have the ability to diffuse along and stain the plasma membrane of the neural elements in aldehyde-fixed specimens. Sprague-Dawley rat fetuses and early postnatal pups were used. The study was conducted on the thoracic spinal cord. The results confirm that thoracic spinal motor neurons are restricted to the segments from which their axons exit via the ventral roots in the intrauterine stages of development. The segmental arrangement of motor neurons in the thoracic spinal cord corresponded well with that of the sympathetic preganglionic neurons which were stained simultaneously.

Animals↗
PubMed1992

Study of platelet-mediated neurotoxicity in rat brain.

BACKGROUND AND PURPOSE: The mechanism of ischemic neuronal injury is not fully resolved. The present view is that vascular occlusion per se does not fully account for the extent of neurological dysfunction. We previously hypothesized that platelet secretory products might contribute to neuronal injury in the central nervous system. Our preliminary studies using organotypic rat spinal cord cultures exposed to human platelet and its secretory products revealed that platelet products had neurotoxic properties. METHODS: Further studies, using the same methods, were conducted, with the addition of several refinements such as use of gel-filtered platelets (as opposed to washed platelets) and adding additional relevant controls including platelet membranes, red blood cells, and washed rat platelets. RESULTS: Exposure of spinal cord explant cultures to platelet secretory products resulted in reduced number of neurons per ventral horn compared with control. CONCLUSIONS: Our findings suggest that platelet secretory products have neurotoxic properties. This effect was seen with platelet secretion obtained from physiological platelet concentrations. It appears possible that more abundant release of platelet products at the site of thrombus formation could have pathological significance in vivo.

Animals↗
PubMed1992

Interactions between dorsal root axons and their target motor neurons in developing mammalian spinal cord.

We have utilized the lipid-soluble tracers Dil and DiA to investigate interactions between group la dorsal root afferent axons and their target motor neurons in developing rat spinal cord. We show here that la axons project toward motor pools in fascicles that exhibit a considerable degree of spatial order. A rough topography is present in that axons that innervate medially located axial motor neurons cross over others in the intermediate zone and follow a separate path along the midline toward their appropriate targets. Surprisingly, we have also found that motor neuron dendritic projections are well established in the transverse plane prior to the arrival of la afferents. Although dendrites from motor pools innervating limb muscles project directly in the path of incoming la afferents, they do not guide afferents to appropriate motor pools. The la afferents pass over the distal dendrites and grow all the way to the border between gray and developing white matter. A significant amount of terminal branching and bouton formation is in the vicinity of motor neuron somata and proximal regions of the dendritic arbors. Few boutons are found near dendrites that project dorsal to the motor pools, and virtually no boutons are found on dendrites in white matter. Our results show that la afferent axons are not guided to appropriate motor pools by random encounters with motor dendrites, and raise the possibility that mechanisms exist that promote an orderly projection of la afferents to particular regions of the ventral horn. The striking lack of innervation of white matter and dorsally directed dendrites by la afferents raises the question of whether descending and intersegmental systems have their initial interactions with these regions of the motor neuron dendritic arbor.

Animals↗
PubMed1991

Platelet secretory products may contribute to neuronal injury.

BACKGROUND: We do not fully understand the mechanisms for neuronal damage following cerebral arterial occlusion by a thrombus that consists mainly of platelets. The view that certain endogenous substances, such as glutamate, may also contribute to neuronal injury is now reasonably well established. Blood platelets are known to contain and secrete a number of substances that have been associated with neuronal dysfunction. Therefore, we hypothesize that a high concentration (approximately several thousand-fold higher than in plasma, in our estimation) of locally released platelet secretory products derived from the causative thrombus may contribute to neuronal injury and promote reactive gliosis. SUMMARY OF COMMENT: We have recently been able to report some direct support for this concept. When organotypic spinal cord cultures were exposed to platelet and platelet products, a significant reduction in the number and the size of the surviving neurons occurred in comparison with those in controls. We further observed that serotonin, a major platelet product, has neurotoxic properties. There may be other platelet components with similar effect. CONCLUSIONS: The hypothesis of platelet-mediated neurotoxicity gains some support from these recent in vitro findings. The concept could provide a new area of research in stroke, both at the clinical and basic levels.

Animals↗