Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Reported prevalence of idiopathic intracranial hypertension without papilledema (IIHWOP) in series of patients with chronic or transformed migraine is significantly higher than expected; yet, IIHWOP is not included among the risk factors for migraine progression. However, several studies provided evidences suggesting that IIHWOP could represent a possible, largely underestimated, risk factor for progression of pain in migraine and, possibly, in other primary headaches. Data from two recent studies, albeit aimed to different end-points, strongly support this hypothesis. ⋯ Moreover, after the diagnostic lumbar puncture, a transient improvement of headache frequency has been observed in the majority of intracranial hypertensive chronic headache subjects. Taken together, the data of these two recent papers rise the following hypothesis: (1) asymptomatic IIHWOP is much more prevalent than expected in general population; (2) IIHWOP is a powerful and largely unrecognized risk factor for progression of pain in primary headache patients; (3) sinus venous stenosis at MRV is a reliable predictor of raised intracranial hypertension also in asymptomatic patients; (4) sinus venous stenosis has a causative role in IIH pathophysiology. These assumptions share a potential high clinical impact and need to be urgently tested in adequately designed controlled studies.
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Undertreatment in patients with primary headaches was evaluated in 600 patients attending 7 headache centres in Lombardy by assessing the rates of acute and prophylactic treatments used before the first visit and the rates of prescription of acute and prophylactic treatments after the visit at the headache centre. Our results clearly showed that most headache patients are likely to receive suboptimal treatments, confirming the utility of headache centres as well as the need for promoting education of GPs and the development of appropriate networks to reduce undertreatment rates, in order to highlight the negative impact caused by primary headache on individuals and on the society.
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The aim of the present study was to investigate the impact of comorbid migraine on quality of life (QoL) of patients with multiple sclerosis (MS). Forty-four MS patients with comorbid migraine and 44 sex/age-matched MS subjects free from primary headache were evaluated. ⋯ Significant correlations between MIDAS score and RL-P (r = -0.43, p = 0.003), BP (r = -0.51; p < 0.001), and HP (r = -0.38; p = 0.01) were also found. In conclusion, we suggest that investigating and treating migraine in MS patients might contribute to improve their QoL.
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Even if sometimes combined oral contraceptives (COCs) can initiate or aggravate headaches, in particular migraine, the headaches generally tend to improve after the first months of COC use. If migraine persists, in many patients the attacks are more likely to occur during the pill-free week, and an oral contraceptive-induced menstrual migraine (OCMM) occurs. ⋯ It is possible to use a continuous COCs regimen, to shorten the HFI to less than the traditional 7 days, to use a low-dose estrogen supplementation after the 21 days of COCs or to prescribe a progestogen-only pill (POP). Interestingly, the use of a POP is a safe option also for women suffering from migraine with aura (in which COCs are absolutely contraindicated) and a recent trial suggests that its use can reduce the frequency of migraine attacks and the duration of aura symptoms too.
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Pain has always been considered as part of a defensive strategy, whose specific role is to signal an immediate, active danger. This definition partially fits acute pain, but certainly not chronic pain, that is maintained also in the absence of an active noxa or danger and that nowadays is considered a disease by itself. ⋯ Pain itself can be considered to share the same genesis as emotions and as a specific emotion in contributing to the maintenance of the homeostasis of each unique subject. Interestingly, this role of pain reaches its maximal development in the human; some even argue that it is specific for the human primate.