Spontaneous intracranial hypotension (SIH) is a well-recognized neurologic disorder that typically presents with orthostatic headaches, low cerebral spinal fluid pressures and distinct abnormalities on magnetic resonance imaging.

We present a case of a rare presentation of SIH.

A 49-year-old man presented with a two week history of orthostatic headaches that rapidly progressed to encephalopathy and coma, requiring intubation. Neuroimaging revealed abnormalities typical of SIH; diffusely enhancing pachymeninges, subdural fluid collections, and descent of the brain. Treatment with an epidural blood patch reversed his coma within minutes. Following a second blood patch, the patient became asymptomatic. No cerebral spinal leak could be identified on magnetic resonance imaging or on a nuclear medicine technetium cerebral spinal fluid flow study. At six month follow-up, he remained symptom free.

The mechanism of coma in SIH is presumed to be compression of the diencephalon from downward displacement of the brain. Although it is very unusual for patients with SIH to present with coma, it is important to recognize since the coma may be reversible with epidural blood patches.

To evaluate the incidence of hypoglycemia, hyperglycemia and blood glucose (BG) variability in brain-injured patients and their association with clinical outcomes.

Retrospective cohort study of brain-injured patients admitted to an 11- bed neurosciences intensive care unit (ICU) from January 1 to December 31, 2003.

We included 606 patients. Mean age was 52.3 years, 60.6% were male, 11.9% had diabetes mellitus, and 64% were post-operative. Seventy-five (12.4%) received intensive insulin therapy (IIT) for a median (IQR) 72 (24-154) hours. Hypoglycemia and hyperglycemia occurred in 4.6% (96.4% receiving IIT) and 9.6% (77.6% receiving IIT). Median number of episodes per patient was 3 (75% with ≥2) and 4 (81% with ≥2) for hypoglycemia and hyperglycemia. Variable glycemic control occurred in 3.8% (100% receiving IIT) with median number of 13 episodes per patient. In-hospital mortality was 16.7%, median (IQR) ICU and hospital lengths of stay were 2 (1-5) and 8 (3-19) days. Hypoglycemia, hyperglycemia and BG variability showed non-significant but consistent associations with hospital mortality and prolonged lengths of ICU and hospital stay. The rate of recurrence of episodes showed stronger and significant associations with outcome, in particular for BG variability and hyperglycemia.

Hypoglycemia, hyperglycemia and BG variability are relatively common in brain-injured patients and are associated with IIT. An increased frequency of episodes, in particular for BG variability and hyperglycemia, was associated with greater risk of both hospital death and prolonged duration of stay.

1. To determine the awareness of the literature concerning therapeutic manoeuvres in severe closed head injury (CHI) among Canadian critical care clinicians and neurosurgeons, 2. To identify factors that affect utilization of these manoeuvres, and 3. To compare reported appropriateness and frequency of use with #1 and #2.

The study design was a systematic scenario-based survey of all neurosurgeons and critical care physicians treating patients with severe CHI in Canada.

Fifty-nine of 99 neurosurgeons and 82 of 148 critical care physicians responded (57%). The majority of respondents were not able to identify the highest level of published evidence for most manoeuvres, except for the avoidance of corticosteroids (51%). The factor identified by most respondents as being most important in motivating use of any given manoeuvres was the level of published evidence (25%). Although reported appropriateness and frequency of use of most manoeuvres correlated well with each other, they did not correlate with awareness of evidence. In the case of corticosteroids, there was a strong correlation between non-use of steroids and awareness of evidence (R = - 0.30, p = 0.0003).

Respondents to this survey of Canadian physicians treating patients with severe head injury reported published evidence as being the most significant factor affecting use of a therapy. However, most respondents did not correctly identify the highest published level of evidence for most therapies. This study has identified difficulty with research translation that may have clinical implications.

To determine: 1. the degrees of consensus and disagreement among Canadian critical care clinicians regarding the appropriateness (benefit exceeding risk) of common therapeutic manoeuvres in patients with severe closed head injury (CHI), and 2. the frequency with which clinicians employed these manoeuvres.

The study design was a systematic scenario-based survey of all neurosurgeons and critical care physicians treating patients with severe CHI in Canada.

In the scenario of acute epidural hematoma with mass effect, respondents agreed very strongly that surgery was appropriate. Clinicians reported mannitol and hypertonic saline as appropriate. Beyond these two interventions, agreement was less strong, and the use of the extraventricular drain (EVD), phenytoin, cooling, hyperventilation, nimodipine, and jugular venous oximetry (JVO) were of uncertain appropriateness. Steroids were considered inappropriate. In a scenario of diffuse axonal injury (DAI), clinicians agreed strongly that fever reduction, early enteral feeding, intensive glucose control, and cerebral perfusion pressure (CPP)-directed management were appropriate. The use of mannitol, hypertonic saline, EVD, JVO, narcotics and propofol were also appropriate. Neuromuscular blockade, surgery, and hyperventilation were of uncertain appropriateness. The appropriateness ratings of the interventions considered in the scenario of an intracranial contusion mirrored the DAI scenario. In general, correlations between the reported appropriateness and frequency of use of each intervention were very high. An exception noted was the use of the JVO. The correlation between CPP-guided therapy and the use of the EVD was weak.

This survey has described current practice with regard to treatment of patients with severe CHI. Areas of variation in perceived appropriateness were identified that may benefit from further evaluation. Suggested priorities for evaluation include the use of osmotic diuretics, anticonvulsants, and intracranial manometry.

Depression and pain are both burdensome ailments that affect a major proportion of the population. It is evident that depression and pain frequently coexist, with treatment and outcome implications.

To review the literature on the nature, prevalence and co-morbidity of depression and pain, the biological and psychological mechanisms involved and treatment options, thus presenting a broad overview of the current information available.

Relevant sources were identified from PubMed and Medline databases using a combination of keywords including depression, pain, prevalence, co-morbidity, biological and psychological mechanisms, serotonin (5-HT), norepinephrine (NE), hypothalamic-pituitary-adrenal (HPA) axis, amygdala, functional magnetic resonance imaging (fMRI), antidepressant and psychological therapy.

It is evident from the research that depression and pain are common co-morbidities. Pain as a physical symptom of depression affects approximately 65% of patients, leading to less favourable outcomes and greater health care utilization. Moreover, depression is a common feature in chronic pain patients and can affect pain threshold and tolerance. Evidence from biological and psychological studies has revealed mechanisms that link chronic pain to depression. Several classes of anti-depressants and psychological interventions have been used successfully in the treatment of somatic symptoms of depression and for a variety of pain syndromes.

Pain and depression are linked by overlapping phenomenology, neurobiology and therapy. They are mutually interacting, and the interaction has significant treatment and outcome implications.

Epidemiological evidence supports a relationship between vitamin D and mental well-being, although evidence from large-scale placebo-controlled intervention trials is lacking.

To examine if vitamin D supplementation has a beneficial effect on mood in community-dwelling older women; if a single annual large dose of vitamin D has a role in the prevention of depressive symptoms; and if there is an association between serum 25-hydroxyvitamin D levels and mental health.

A double-blind, randomised, placebo-controlled trial of women aged 70 or older (the Vital D Study: ISRCTN83409867 and ACTR12605000658617). Participants were randomly assigned to receive 500 000 IU vitamin D3 (cholecalciferol) orally or placebo every autumn/winter for 3–5 consecutive years. The tools utilised at various time points were the General Health Questionnaire, the 12-item Short Form Health Survey, the Patient Global Impression–Improvement scale and the WHO Well-Being Index. Serum 25-hydroxyvitamin D levels were measured in a subset of 102 participants.

In this non-clinical population, no significant differences between the vitamin D and placebo groups were detected in any of the measured outcomes of mental health. Serum 25-hydroxyvitamin D levels in the vitamin D group were 41% higher than the placebo group 12 months following their annual dose. Despite this difference, scores from the questionnaires did not differ. Furthermore, there was no interaction between those on antidepressant/anxiety medication at baseline and the treatment groups.

The lack of improvement in indices of mental well-being in the vitamin D group does not support the hypothesis that an annual high dose of vitamin D3 is a practical intervention to prevent depressive symptoms in older community-dwelling women.

Although there is cross-sectional evidence that changes in the immune system contribute to the pathophysiology of depression, longitudinal data capable of elucidating cause and effect relationships are lacking.

We aimed to determine whether subclinical systemic inflammation, as measured by serum high-sensitivity C-reactive protein (hsCRP) concentration, is associated with an increased risk of de novo major depressive disorder.

Major depressive disorder was diagnosed using a clinical interview (SCID–I/NP). This is a retrospective cohort study; from a population-based sample of 1494 randomly selected women recruited at baseline during the period 1994–7, 822 were followed for a decade and provided measures of both exposure and outcome. Of these women, 644 (aged 20–84 years) had no prior history of depression at baseline and were eligible for analysis.

During 5827 person-years of follow-up, 48 cases of de novo major depressive disorder were identified. The hazard ratio (HR) for depression increased by 44% for each standard deviation increase in log-transformed hsCRP (ln-hsCRP) (HR = 1.44, 95% CI 1.04–1.99), after adjusting for weight, smoking and use of non-steroidal anti-inflammatory drugs. Further adjustment for other lifestyle factors, medications and comorbidity failed to explain the observed increased risk for depression.

Serum hsCRP is an independent risk marker for de novo major depressive disorder in women. This supports an aetiological role for inflammatory activity in the pathophysiology of depression.

Smoking is disproportionately prevalent among people with psychiatric illness.

To investigate smoking as a risk factor for major depressive disorder.

A population-based sample of women was studied using case–control and retrospective cohort study designs. Exposure to smoking was self-reported, and major depressive disorder diagnosed using the Structured Clinical Interview for DSM–IV–TR (SCID–I/NP).

Among 165 people with major depressive disorder and 806 controls, smoking was associated with increased odds for major depressive disorder (age-adjusted odds ratio (OR)=1.46, 95% CI 1.03–2.07). Compared with non-smokers, odds for major depressive disorder more than doubled for heavy smokers (>20 cigarettes/day). Among 671 women with no history of major depressive disorder at baseline, 13 of 87 smokers and 38 of 584 non-smokers developed de novo major depressive disorder during a decade of follow-up. Smoking increased major depressive disorder risk by 93% (hazard ratio (HR)=1.93, 95% CI 1.02–3.69); this was not explained by physical activity or alcohol consumption.

Evidence from cross-sectional and longitudinal data suggests that smoking increases the risk of major depressive disorder in women.