Risk factors of migraine-related brain white matter hyperintensities: an investigation of 186 patients

Brain white matter hyperintensities are more prevalent in migraine patients than in the general population, but the pathogenesis and the risk factors of these hyperintensities are not fully elucidated. The authors analyzed the routine clinical data of 186 migraine patients who were referred to the Outpatient Headache Department of the Department of Neurology, Medical School, University of Pécs, Hungary between 2007 and 2009: 58 patients with white matter hyperintensities and 128 patients without white matter hyperintensities on 3 T MRI. Significant associations between the presence of white matter hyperintensities and longer disease duration (14.4 vs. 19.9 years, p = 0.004), higher headache frequency (4.1 vs. 5.5 attacks/month, p = 0.017), hyperhomocysteinemia (incidence of hyperintensity is 9/9 = 100%, p = 0.009) and thyroid gland dysfunction (incidence of hyperintensity is 8/14 = 57.1%, p = 0.038) were found. These data support the theory that both the disease duration and the attack frequency have a key role in the formation of migraine-related brain white matter hyperintensities, but the effects of comorbid diseases may also contribute to the development of the hyperintensities

Migrénhez köthető intracerebralis fehérállományi léziók vizsgálata

Migraine is defined by the International Headache Society (IHS) as a recurrent primary headache disorder, usually unilateral and pulsatile in nature with moderate to severe pain, with attacks lasting for 4-72 hours, and may associate with aura, nausea, vertigo and autonomic symptoms in adulthood. Migraine is more common in adults (11%, lifetime 15%) than in children/adolescents (7%, lifetime 5%), with a decreasing prevalence (6%, lifetime 8%) in adults over the age of 60 years. In all categories, migraine is more prevalent in women than in men, with 14% vs 6% in adults, 9% vs 7% in children/adolescents and 8% vs 3% in the elderly. The trigemino-vascular system provides an important pain-transmission link between the vascular (dural and cortical) and neuronal (brainstem and thalamus) regions. Since the posterior and lateral regions of the hypothalamus is activated in the early premonitory phase of migraine, it is likely that the hypothalamus is a key organ in the initiation of migraine headache by activation of different brainstem structures. Cortical spreading depression (CSD) starts in the occipital cortex, and it is an appearance of depolarization waves of the neurons and neuroglia that propagate across the gray matter at a velocity of 2–5 mm/min. CSD is a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids (e.g., glutamate) from nerve cells, and increased energy metabolism. CSD is present not just in aura patients, but in aura-free migraineurs, as well. CSD may activate the meningeal nociceptors of trigeminal sensory afferents, resulting in a release of vasoactive neuropeptides (CGRP, SP, NKA, PACAP, VIP). This process leads to the activation of the second-order neurons in the trigeminocervical complex, the third order neurons of the thalamus, and the fourth-order neurons in the sensory cortex (central sensitization). Blood flow is increased in the brainstem nuclei, called “migraine generators” (locus coeruleus, periaqueductal grey matter, raphe nuclei). Cranial parasympathetic fibres are activated in the superior salivatory nucleus in the brainstem. Postganglionic parasympathetic fibres project to the lacrimal, nasal mucosa and salivary glands, and the craniofacial vasculature, and induce lacrimation and rhinorrhoea. The descending pain modulatory pathway activity is decreased, and it may cause more intensive pain

A hypertonia drasztikus csökkentésének veszélyei | Unfavorable outcome of aggressive lowering of high blood pressure. Case report

Az agy véráramlásának szabályozásában az autoreguláció alapvető jelentőségű. Az agyi perfúzió – a szisztémás vérnyomás ingadozásai ellenére – az autoregulációnak köszönhetően jelentős tartományban (egészségesekben 50–150 Hgmm között) állandó. Hypertoniásokban az autoregulációs görbe jobbra, azaz nagyobb vérnyomásértékek felé tolódik el (patológiás autoreguláció). A vérnyomás drasztikus csökkentése, ha a vérnyomás az autoregulációs sáv alsó szintje alá esik, az agyi véráramlás redukciójához vezet. A szerzők 73 éves generalizált érbeteg férfi esetét ismertetik. Klinikai felvétele előtt a betegnél magasabb vérnyomást (160/100 Hgmm) és vércukorértéket (14,8 mmol/l) észlelt orvosa, ezek gyors rendezése után rövid időn belül a beteg kontaktusképtelenné vált. A klinika ambulanciájára érkezésekor kontaktusba nem volt vonható, soporocomatosus volt és agytörzsi tüneteket észleltek nála. Akut koponya-komputertomográfiás vizsgálattal vérzés, friss ischaemia nem ábrázolódott. Két nappal később készült kontroll-komputertomográfiás vizsgálat mindkét arteria carotis interna ellátási területét érintő, szekunder agytörzsi kompressziót okozó, friss ischaemiát detektált. Komputertomográfiás angiográfia során kétoldali arteria carotis interna okklúzió igazolódott. Az eset kapcsán megállapítható, hogy a nagyfokú vérnyomáscsökkenés önmagában ischaemiához vezethet, különösen krónikusan fennálló hypertonia, illetve az agyat ellátó erek szűkülete esetén. Orv. Hetil., 2014, 155(42), 1685–1689. | Cerebral autoregulation is essential in the maintenance of cerebral blood flow. Due to this autoregulation, cerebral perfusion is constant in healthy subjects if blood pressure values are between 50–150 mmHg. In hypertensive patients the curve is right-shifted towards higher blood pressure values (pathological autoregulation). Aggressive blood pressure reduction can lead to severe ischaemia. The authors report the history of a 73-year-old man with the background history of widespread atherosclerotic disease. The patient complained about headache and dizziness and was found to have high blood pressure (160/100 mmHg) and increased blood glucose (14.8 mmol/l). Prior to his admission an aggressive blood pressure and blood sugar reduction was carried out and, within a short period of time he became unconscious and was transferred to the department of the authors with the possible diagnosis of brainstem stroke. On admission the patient was unresponsive, comatose with brainstem symptoms. Urgent brain computed tomography failed to show any acute alterations. However, repeat CT scan revealed extensive bilateral space occupying ischemic changes involving in territories of both internal carotid arteries with consequent brainstem compression. Computed tomography angiography confirmed bilateral internal carotid artery occlusion. The authors conclude that intensive blood pressure reduction result in ischemic lesions via hypoperfusion especially in patients with widespread atherosclerotic disease and significant carotid vessel pathology. Orv. Hetil., 2014, 155(42), 1685–1689

Bi-exponential diffusion signal decay in normal appearing white matter of multiple sclerosis

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