William H Shull | PubMed Health

PubMed2006

Formation and validation of a telephone battery to assess cognitive function in acute respiratory distress syndrome survivors.

PURPOSE: Describe initial development and validation of a test battery composed of established instruments designed to detect, via telephone interview, cognitive abnormalities in survivors of acute respiratory distress syndrome. METHODS: Two cross-sectional studies were performed, including the following phases: (1) initial battery construction, (2) feasibility, (3) item reduction, (4) convergent and divergent validity, and (5) telephone administration compared with in-face interviews in a separate population. RESULTS: There was a broad range of cognitive function detected in the derivation population, and all subjects completed the interview. There was convergence of cognitive impairment with moderate/severe anxiety (P = .008), the Sickness Impact Profile Psychosocial Summary Score (mean difference, 15.3; 95% CI, 7.74-22.9; P = .0001), and the mental health domains of the Short Form 36. Subjects with cognitive impairment had no detectable difference in the physical function domains of the Short Form 36. When administered to the validation population, telephone tests of memory, attention, reasoning, and executive functions had good intraclass correlation with the in-face interviews (P < .01). CONCLUSIONS: Detection of cognitive abnormalities in acute respiratory distress syndrome survivors using a telephone-administered test battery derived from standard cognitive tests is feasible and has evidence of construct validity. This battery may be useful as a research tool when in-face interviews are not feasible.

Adult↗

PubMedDate not supplied

Diffuse axonal injury in head trauma.

BACKGROUND: Diffuse axonal injury (DAI) is one of the most common and important pathologic features of traumatic brain injury (TBI). The susceptibility of axons to mechanical injury appears to be due to both their viscoelastic properties and their high organization in white matter tracts. Although axons are supple under normal conditions, they become brittle when exposed to rapid deformations associated with brain trauma. Accordingly, rapid stretch of axons can damage the axonal cytoskeleton resulting in a loss of elasticity and impairment of axoplasmic transport. Subsequent swelling of the axon occurs in discrete bulb formations or in elongated varicosities that accumulate transported proteins. Calcium entry into damaged axons is thought to initiate further damage by the activation of proteases. Ultimately, swollen axons may become disconnected and contribute to additional neuropathologic changes in brain tissue. DAI may largely account for the clinical manifestations of brain trauma. However, DAI is extremely difficult to detect noninvasively and is poorly defined as clinical syndrome. CONCLUSIONS: Future advancements in the diagnosis and treatment of DAI will be dependent on our collective understanding of injury biomechanics, temporal axonal pathophysiology, and its role in patient outcome.

Alzheimer Disease↗