A systematic review of evidence for fitness-to-drive among people with the mental health conditions of schizophrenia, stress/anxiety disorder, depression, personality disorder and obsessive compulsive disorder

BACKGROUND: Limited evidence exists regarding fitness-to-drive for people with the mental health conditions of schizophrenia, stress/anxiety disorder, depression, personality disorder and obsessive compulsive disorder (herein simply referred to as 'mental health conditions'). The aim of this paper was to systematically search and classify all published studies regarding driving for this population, and then critically appraise papers addressing assessment of fitness-to-drive where the focus was not on the impact of medication on driving. METHODS: A systematic search of three databases (CINAHL, PSYCHINFO, EMBASE) was completed from inception to May 2016 to identify all articles on driving and mental health conditions. Papers meeting the eligibility criteria of including data relating to assessment of fitness-to-drive were critically appraised using the American Academy of Neurology and Centre for Evidence-Based Medicine protocols. RESULTS: A total of 58 articles met the inclusion criteria of driving among people with mental health conditions studied, and of these, 16 contained data and an explicit focus on assessment of fitness-to-drive. Assessment of fitness-to-drive was reported in three ways: 1) factors impacting on the ability to drive safely among people with mental health conditions, 2) capability and perception of health professionals assessing fitness-to-drive of people with mental health conditions, and 3) crash rates. The level of evidence of the published studies was low due to the absence of controls, and the inability to pool data from different diagnostic groups. Evidence supporting fitness-to-drive is conflicting. CONCLUSIONS: There is a relatively small literature in the area of driving with mental health conditions, and the overall quality of studies examining fitness-to-drive is low. Large-scale longitudinal studies with age-matched controls are urgently needed in order to determine the effects of different conditions on fitness-to-drive

Left ventricular hypertrophy induced by aortic banding impairs relaxation of isolated coronary arteries

A B S T R A C T LVH (left ventricular hypertrophy) is associated with impaired coronary vascular reserve. In the present study, we examined the effect of pressure-overload hypertrophy on vasorelaxant responses of guinea-pig isolated coronary small arteries and compared them with mesenteric small arteries. Pressure-overload was induced by banding the ascending aorta of guinea-pigs. Haemodynamics, and ventricular, atrial and lung weights were measured 168 days after banding. Isolated coronary and mesenteric small arteries were contracted with a thromboxane mimetic (U46619) and relaxation to ACH (acetylcholine), ISO (isoprenaline), FSK (forskolin) and SNP (sodium nitroprusside) was examined. Arterial wall morphology was examined by light microscopy. Aortic banding reduced cardiac output and increased systemic vascular resistance; atrial, ventricular and lung weights were increased. Coronary artery adventitial and medial thickness were increased, but mesenteric arterial wall morphology was unaffected. Coronary artery relaxation to ACH, ISO, FSK and SNP were reduced in banded animals. In contrast, relaxation of mesenteric arteries to ACH, FSK and SNP were unaffected by banding, although ISO-induced relaxation was reduced. A COX (cyclo-oxygenase) inhibitor, indomethacin, had no effect on coronary artery responses to ACH in banded or sham animals, but the differences in relaxation of coronary arteries between banded and sham animals were no longer significant following preincubation with the NO inhibitors L-NMMA (N G -monomethyl-L-arginine) and oxyhaemoglobin. In conclusion, pressure-overload-induced LVH causes impaired relaxation of small coronary arteries to endothelium-dependent and -independent relaxants. These findings are indicative of alterations in vascular smooth muscle responsiveness to vasodilators. Impairment of coronary arterial vasodilation may contribute to the reduced coronary vascular reserve seen in LVH

Temporal change in gene expression in the rat dentate gyrus following passive avoidance learning

A learning event initiates a cascade of altered gene expression leading to synaptic remodelling within the hippocampal dentate gyrus, a structure vital to memory formation. To illuminate this transcriptional program of synaptic plasticity we used microarrays to quantify mRNA from the rat dentate gyrus at increasing times following passive avoidance learning. Approximately, 500 known genes were transcriptionally regulated across the 24 h post-training period. The 0–2 h period saw up-regulation of genes involved in transcription while genes with a role in synaptic/cytoskeletal structure increased 0–6 h, consistent with structural rearrangements known to occur at these times. The most striking feature was the profound down-regulation, across all functional groups, 12 h post-training. Bioinformatics analysis identified the likely transcription factors controlling gene expression in each post-training period. The role of NFjB, implicated in the early post-training period was subsequently confirmed with activation and nuclear translocation seen in dentate granule neurons following training. mRNA changes for four genes, LRP3 (0 h), alpha actin (3 h), SNAP25 and NSF (6–12 h), were validated at message and/or protein level and shown to be learning specific. Thus, the memoryassociated transcriptional cascade supports the cardinal periods of synaptic loosening, reorganisation and selection thought to underpin the process of long-term memory consolidation in the hippocampus