In a study of internal rotation in methanol, the millimeter wave spectra of CH3OH, CD3OH, and CH3OD have been investigated between 90 and 200 Gc/sec. In the analysis of the spectra, torsion–vibration–rotation interactions were treated as adjustable parameters in semiempirical formulas. Kivelson's formula for a-type ΔK = 0 transitions was tested over a wide range of quantum numbers. It reproduced the CH3OH and CD3OH spectra quite well, but the approximations used in the calculations appear to start breaking down for the larger asymmetry of CH3OD. For assignment of b-type ΔK = ± 1 transitions, a method was developed based on the wide spectral range of the millimeter wave spectrometer. Sufficient b-type data were obtained for CH3OH to permit a test of Kirtman's formula for origins of Q branches. Convergence difficulties in the Q-branch least-squares fit prompted a re-examination of the theory, which revealed an interesting linear relation coupling six of the parameters. This relation shows that for any molecule the torsional barrier terms V3 and V6, the two moments of inertia about the near-symmetry axis, and two of the adjustable interaction parameters cannot be independently determined from the spectrum of a single isotopic species. This casts some doubt on values previously reported for V6 in other molecules and adds further uncertainty to V3 determinations. The effective V3 obtained by ignoring torsion–vibration–rotation interactions was found to decrease slightly on deuteration, values of 375.6, 371.8, and 370.3 cm− 1 being obtained for CH3OH, CD3OH, and CH3OD, respectively. Although it is impossible to determine V6 unambiguously from the spectrum of CH3OH alone, a qualitative argument suggests that V6 lies between 0 and −0.8 cm−1. The geometry of the molecule has been completely determined from the experimental data.

Context:Prolonged symptoms after concussion are called post-concussion syndrome (PCS), which is a controversial disorder with a wide differential diagnosis.Evidence Acquisition:MEDLINE and PubMed searches were conducted for the years 1966 to 2011 using the search terms brain concussion/complications OR brain concussion/diagnosis OR brain concussion/therapy AND sports OR athletic injuries. Secondary search terms included post-concussion syndrome, trauma, symptoms, metabolic, sports medicine, cognitive behavioral therapy, treatment and rehabilitation. Additional articles were identified from the bibliographies of recent reviews.Results:Of 564 studies that fulfilled preliminary search criteria, 119 focused on the diagnosis, pathophysiology, and treatment/rehabilitation of concussion and PCS and formed the basis of this review. Rest is the primary treatment for the acute symptoms of concussion. Ongoing symptoms are either a prolonged version of the concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual dysfunction, or some combination of conditions. The pathophysiology of ongoing symptoms from the original concussion injury may reflect multiple causes: anatomic, neurometabolic, and physiologic.Conclusions:Treatment approaches depend on the clinician’s ability to differentiate among the various conditions associated with PCS. Early education, cognitive behavioral therapy, and aerobic exercise therapy have shown efficacy in certain patients but have limitations of study design. An algorithm is presented to aid clinicians in the evaluation and treatment of concussion and PCS and in the return-to-activity decision.

Systematic evaluation of exercise tolerance using the BCTT within 1 week after SRC did not affect recovery. The degree of early exercise intolerance after SRC was important for prognosis. This has implications for school academic and team preparation.

The Balke exercise treadmill protocol has very good IRR and sufficient RTR for identifying patients with symptom exacerbation from concussion.

SummaryBackgroundResults of small trials indicate that fluoxetine might improve functional outcomes after stroke. The FOCUS trial aimed to provide a precise estimate of these effects.MethodsFOCUS was a pragmatic, multicentre, parallel group, double-blind, randomised, placebo-controlled trial done at 103 hospitals in the UK. Patients were eligible if they were aged 18 years or older, had a clinical stroke diagnosis, were enrolled and randomly assigned between 2 days and 15 days after onset, and had focal neurological deficits. Patients were randomly allocated fluoxetine 20 mg or matching placebo orally once daily for 6 months via a web-based system by use of a minimisation algorithm. The primary outcome was functional status, measured with the modified Rankin Scale (mRS), at 6 months. Patients, carers, health-care staff, and the trial team were masked to treatment allocation. Functional status was assessed at 6 months and 12 months after randomisation. Patients were analysed according to their treatment allocation. This trial is registered with the ISRCTN registry, number ISRCTN83290762.FindingsBetween Sept 10, 2012, and March 31, 2017, 3127 patients were recruited. 1564 patients were allocated fluoxetine and 1563 allocated placebo. mRS data at 6 months were available for 1553 (99·3%) patients in each treatment group. The distribution across mRS categories at 6 months was similar in the fluoxetine and placebo groups (common odds ratio adjusted for minimisation variables 0·951 [95% CI 0·839–1·079]; p=0·439). Patients allocated fluoxetine were less likely than those allocated placebo to develop new depression by 6 months (210 [13·43%] patients vs 269 [17·21%]; difference 3·78% [95% CI 1·26–6·30]; p=0·0033), but they had more bone fractures (45 [2·88%] vs 23 [1·47%]; difference 1·41% [95% CI 0·38–2·43]; p=0·0070). There were no significant differences in any other event at 6 or 12 months.InterpretationFluoxetine 20 mg given daily for 6 months after acute stroke does not seem to improve functional outcomes. Although the treatment reduced the occurrence of depression, it increased the frequency of bone fractures. These results do not support the routine use of fluoxetine either for the prevention of post-stroke depression or to promote recovery of function.FundingUK Stroke Association and NIHR Health Technology Assessment Programme.