A national Swedish case-control study investigating incidence and factors associated with idiopathic intracranial hypertension.

OBJECTIVE: To study the incidence of idiopathic intracranial hypertension in Sweden and to explore whether previously proposed risk factors are associated with idiopathic intracranial hypertension by investigating the odds of exposure one year prior to diagnosis in patients compared to controls. METHODS: Using Swedish health care registers and validated diagnostic algorithms, idiopathic intracranial hypertension patients diagnosed between 2000-2016 were compared with randomly selected matched controls, five from the general population and five with obesity. RESULTS: We identified 902 idiopathic intracranial hypertension patients and 4510 matched individuals in each control group. Mean incidence among inhabitants ≥18 years of age was 0.71 per 100,000; rising from 0.53 in 2000-2005 to 0.95 in 2012-2016. There were increased odds for idiopathic intracranial hypertension patients compared to general population for exposure to: kidney failure (odds ratio =13.2 (4.1-42.0)), arterial hypertension (odds ratio =17.5 (10.5-29.3)), systemic lupus erythematosus (odds ratio =13.8 (4.3-44.7)), tetracyclines, sulphonamides, lithium, and corticosteroids. In obese controls, odds ratios were also significantly increased for these exposures. Hormonal contraceptive use and exposure to pregnancy did not appear to be associated factors for idiopathic intracranial hypertension development. CONCLUSIONS: The incidence of idiopathic intracranial hypertension in Sweden is lower relative to reports from other countries but is on the rise. This case-control study confirms several previously reported risk factors associated with idiopathic intracranial hypertension.

Infectious and inflammatory disorders might increase the risk of developing idiopathic intracranial hypertension - a national case-control study.

OBJECTIVE: To investigate whether conditions causing inflammatory activation are associated with increased risk of idiopathic intracranial hypertension. METHODS: All newly diagnosed idiopathic intracranial hypertension patients (cases) in Sweden between 2000-2016 were identified using pre-determined algorithms (n = 902) and matched with five controls from the general population and five individuals with an obesity diagnosis (n = 4510) for age, sex, region, and vital status. National health registers provided information on infections, inflammatory disorders and dispensed medications. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals. RESULTS: Compared to general population controls, the cases had fourfold increased odds of having an infection (odds ratio = 4.3, 95% confidence interval 3.3-5.6), and threefold increased odds of an inflammatory disorder the year prior to idiopathic intracranial hypertension diagnosis (odds ratio = 3.2, 95% confidence interval 2.4-4.3). Organ specific analyses showed that odds were increased for the study diseases in the respiratory organ, kidney organ and gastrointestinal tract, but not for female genital infections. Similar results were found when comparing idiopathic intracranial hypertension with obese controls though the odds ratios were of lower magnitude. Sub-analyses on exposure to anti-infectious and anti-inflammatory drugs confirmed the increased odds ratios for idiopathic intracranial hypertension patients. CONCLUSIONS: These findings suggest that major inflammatory activation may be a risk factor in idiopathic intracranial hypertension development.

Role of nitric oxide in cluster headache.

Nitric oxide (NO) is an important molecule in headache pathophysiology. NO regulates vascular tone and acts as a potent vasodilator, and thus participates in regulating blood flow. NO is also considered to play a role in processing sensory information and pain sensitization. In this article, we review the role of NO in one of the primary headache disorders, cluster headache (CH). The pathophysiology of CH is still not completely understood. A multifactorial genesis where NO is likely to be involved is probable. The level of NO production has been shown to correlate with disease activity in several inflammatory disorders, such as cystitis, multiple sclerosis, and cerebral lupus erythematosus. In this article, the issue of whether similar circumstances apply for CH and also the role of NO in the pathophysiology of CH in a wider perspective are discussed.

Re-utilization of Schwann cells during ingrowth of ventral root afferents in perinatal kittens.

Ventral roots in all mammalian species, including humans, contain significant numbers of unmyelinated axons, many of them afferents transmitting nociceptive signals from receptive fields in skin, viscera, muscles and joints. Observations in cats indicate that these afferents do not enter the spinal cord via the ventral root, but rather turn distally and enter the dorsal root. Some unmyelinated axons are postganglionic autonomic efferents that innervate blood vessels of the root and the pia mater. In the feline L7 segment, a substantial proportion of unmyelinated axons are not detectable until late in perinatal development. The mechanisms inducing this late ingrowth, and the recruitment of Schwann cells (indispensable, at this stage, for axonal survival and sustenance), are unknown. We have counted axons and Schwann cells in both ends of the L7 ventral root in young kittens and made the following observations. (1) The total number of axons detectable in the root increased throughout the range of investigated ages. (2) The number of myelinated axons was similar in the root's proximal and distal ends. The increased number of unmyelinated axons with age is thus due to increased numbers of small unmyelinated axons. (3) The number of separated large probably promyelin axons was about the same in the proximal and distal ends of the root. (4) Schwann cells appeared to undergo redistribution, from myelinated to unmyelinated axons. (5) During redistribution of Schwann cells they first appear as aberrant Schwann cells and then become endoneurial X-cells temporarily free of axonal contact. We hypothesize that unmyelinated axons invade the ventral root from its distal end, that this ingrowth is particularly intense during the first postnatal month and that disengaged Schwann cells, eliminated from myelinated motoneuron axons, provide the ingrowing axons with structural and trophic support.