Serum neurone-specific enolase (NSE) and computerized tomography (CT) stroke volume were compared in patients admitted within 24 h of an acute stroke. Serum samples were obtained on admission and daily for the next 4 days. Of 163 patients, CT scans revealed 25 with intracerebral haemorrhages, one haemorrhagic infarct and 83 measurable acute infarcts. The serum NSE levels of those with infarcts was significantly higher than in those with haemorrhages at 48 (P = 0.0003) and 72 h (P = 0.04). The maximum serum NSE value tended to occur later in those with large infarcts (P = 0.0035). There was a significant correlation between infarct volume and serum NSE at 48 h (r = 0.27, P = 0.015) and 96 h (r = 0.27, P = 0.015) and with the maximum serum NSE over the 4 days (r = 0.36, P = 0.001). There was no significant correlation between haemorrhage volume and NSE. In conclusion, serum NSE may be a useful marker of infarct volume in studies of therapy in acute stroke. Sampling for NSE should continue, at least in those with large infarcts, for longer than 4 days. Serum NSE cannot be used to distinguish between haemorrhage and infarction in patients with an acute stroke.

A patient (B.J.) is reported who developed severe memory impairment following a penetrating brain injury caused by a snooker cue which entered through his left nostril into the basal regions of the brain. Initially, his memory disorder had the clinical features of a dense amnesic syndrome, with both anterograde and retrograde amnesia, but B.J. subsequently showed significant recovery of memory function. Formal memory testing was carried out 21 months after injury. This demonstrated marked verbal memory impairment, as severe as that seen in patients with the amnesic syndrome. On nonverbal memory tests, his impairment was relatively mild and patchy. His retrograde amnesia had regressed mainly to affect a 6 month period before the injury. On other cognitive tasks, he performed at an average or above average level, and there was no neuropsychological evidence of frontal lobe dysfunction. Neuroradiological investigations at various stages after his injury failed to demonstrate a lesion in any of the thalamic nuclei. Magnetic resonance imaging showed a lesion in the hypothalamus in the region of the mamillary bodies. Our study demonstrates that marked, relatively focal, memory disorder after diencephalic injury can occur without direct pathology to the body of the thalamus. It also indicates that structures in or adjacent to the hypothalamus, such as the mamillary bodies, may play a more important role in human memory functioning than has hitherto been considered.

A radioimmunoassay has been developed and used to measure serum neurone specific enolase (NSE) concentrations in 24 patients, following cerebral infarction. A significant correlation between cerebral infarct volume and maximum serum NSE concentration was observed (P = 0.047). Serum NSE was also assayed at times 24, 48, 72 and 96 h post ictus. At 72 h a significant correlation existed between serum NSE levels and infarct volume (P = 0.012), and levels appeared to be approaching statistical significance at 48 h (P = 0.067). No correlation existed at 24 and 96 h. In addition serum concentrations of NSE were compared to clinical outcome as determined by the Glasgow Outcome Score. Using the Mann-Whitney U test, there was no significant difference in maximum NSE level between patients graded 1-3 on the Glasgow Outcome Score and those graded 4 and 5. However, further studies are required on a larger population to more completely assess this. NSE may prove to be a useful marker of neuronal damage in the study of stroke, with particular application in the assessment of treatment.

Background and objective: Hypercapnia is associated with worse clinical outcomes in exacerbations of COPD. The present study aimed to determine the effects of nasal high flow (NHF) therapy on transcutaneous partial pressure of carbon dioxide (PtCO 2 ) in stable COPD patients. Methods: In a single-blind randomized controlled crossover trial, 48 participants with COPD were allocated in random order to all of four 20 min interventions: NHF at 15 L/min, 30 L/min and 45 L/min or breathing room air with each intervention followed by a washout period of 15 min. The primary outcome measure was PtCO 2 at 20 min, adjusted for baseline PtCO 2 . Secondary outcomes included respiratory rate at 20 min, adjusted for baseline. Results: The mean (95% CI) change in PtCO 2 at 20 min was −0.6 mm Hg (−1.1 to 0.0), P = 0.06; −1.3 mm Hg (−1.9 to 0.8), P < 0.001; and −2.4 mm Hg (−2.9 to −1.8), P < 0.001; for NHF at 15 L/min, 30 L/min and 45 L/min compared with room air, respectively. The mean (95% CI) change in respiratory rate at 20 min was −1.5 (−2.7 to −0.3), P = 0.02; −4.1 (−5.3 to −2.9), P < 0.001; and −4.3 (−5.5 to −3.1), P < 0.001; breaths per minute compared with room air, respectively. Conclusion: NHF results in a small flow-dependent reduction in PtCO 2 and respiratory rate in patients with stable COPD.