Table 4 - uploaded by Natasha A. Lannin
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OBJECTIVE. The Western Neuro Sensory Stimulation Profile (WNSSP) presents a hierarchy of items sug-gestive of a sequence of recovery. The aim of this study was to understand the sequence of recovery of neurobehavioral function in patients with brain injury and determine whether this sequence was consistent with the WNSSP test item order. METHOD. We...
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Context 1
... the exception of Arousal/Attention, observed subscale item order also was not consistent with the in- strument item order (Table 4). Arousal/Attention ob- served recovery did follow the test item sequence proposed (i.e., Item 1 recovered first, followed by Items 2, 3, and then 4). ...
Context 2
... found that the observed sequence of recovery matched test item order for the Arousal/Attention sub- scale but not for the other subscales. A revised item order may be required to reflect the observed order presented in Table 4. Visual Response, for example, with the exception Cognitive score 5.3 (1.3) 5, 5-12 (5) 13.1 (9.7) 10, 5-32 (5) ...
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Background/aimThe Western Neuro Sensory Stimulation Profile (WNSSP) is designed to measure disorders of consciousness in people with severe traumatic brain injury who are slow-to-recover. This study explores internal consistency reliability and concurrent validity of the WNSSP with function and two other consciousness measures.Method
Retrospective chart audit of all severe traumatic brain injury patients admitted to a specialist neurological rehabilitation centre from January 2001 to December 2006 in a vegetative or minimally conscious state. Medical record of demographical, clinical and Glasgow Coma Scale (GCS) data were recorded. To be included in the study, patients needed admission and discharge WNSSP results; plus Functional Independence Measure™ (FIM™) and Rancho Los Amigos Scale (RLAS) scores.ResultsOf 37 potential participants, 33 had required WNSSP results (mean age 28 years; 27 male participants). Internal consistency reliability was very high (α = 0.933). Concurrent validity in relation to function was significant but weak at admission for FIM™ Total-scale but not subscales (rs = −0.146, P = 0.0424). At discharge, there was a modest relationship with FIM™ Motor-subscale (rs = 0.374; P = 0.045), and FIM™ Cognition-subscale (rs = 0.412; P = 0.026) scores, but not the FIM™ Total-scale. Concurrent validity in relation to the RLAS was strong at admission (rs = 0.693, P = 0.01) and discharge (rs = 0.788, P = 0.01). The WNSSP and GCS scores were not associated.Conclusion
The WNSSP is sensitive to behavioural change in slow-to-recover patients with severe traumatic brain injury. It demonstrates very high internal consistency reliability, and positive evidence of concurrent validity with FIM™ and the RLAS providing detailed description of cognitive-sensory behaviour within RLAS-levels.
Traumatic brain injury (TBI) is a major cause of disability or death worldwide, especially in the young. Thus, effective medication with few side effects needs to be developed. This work aimed to explore the potential benefits of formononetin (FN) on TBI rodent model and to discuss the regarding mechanism. These findings showed that FN effectively increased the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in brain tissue of TBI rats (P<0.01), while it reduced intracephalic malonaldehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) concentrations (P<0.01). Meanwhile, the hydrocephalus in theTBI rat was alleviated, and the injured nerve cell of the lesioned brain was reduced as showed in hematoxylin-eosin (HE) staining assay. In addition, the endogenous mRNA level of cyclooxygenase-2 (COX-2) in the brain of the TBI rat was significantly down-regulated (P<0.01). Furthermore, the protein expression of nuclear factor E2-related factor 2 (Nrf2) was effectively up-regulated (P<0.01). Taken together, we conclude that formononetin mediates the promising anti-TBI effects against neurocyte damage, which the underlying mechanisms are associated with inhibiting intracephalic inflammatory response and oxidative stress for neuroprotection.
