Major depression increased the risk for migraine, and migraine increased the risk for major depression. This bidirectional association, with each disorder increasing the risk for first onset of the other, was not observed in relation to other severe headaches. With respect to other severe headaches, there was no increased risk associated with pre-existing major depression, although the possibility of an influence in the reverse direction (i.e., from severe headaches to depression) cannot be securely ruled out.
The contrasting results regarding the relationship of major depression with migraine versus other severe headaches suggest that different causes may underlie the co-occurrence of major depression in persons with migraine compared with persons with other severe headaches.
An MR tissue signature model of ischemic histopathology using ADCw and T2 can now be tested for its potential to predict reversible and identify irreversible cellular damage in human ischemic brain regions.
Background and Purpose: Cerebellar infarction displays diflerent clinical features, depending on the vascular territory involved. We studied patients with infarcts in the territories of the posterior inferior cerebellar artery or the superior cerebellar artery to compare their clinical presentation, course, and prognosis.Methods: We retrospectively analyzed the clinical features, laboratory data, and imaging studies of 66 patients with cerebellar infarction collected consecutively at five institutions. All the cerebellar infarcts were documented on computed tomographic scan or magnetic resonance imaging.Results: Two distinct profiles emerged, depending on the vascular territory involved. In 36 patients with posterior inferior cerebellar artery territory infarcts, a triad of vertigo, headache, and gait imbalance predominated at stroke onset. Computed tomography showed severe cerebellar mass effect in 11 cases (30%1), with associated hydrocephalus in seven. In these seven patients (19%), postinfarct swelling led to brain stem compression that resulted in four deaths. In 30 patients with superior cerebellar artery infarcts, gait disturbance predominated at onset; vertigo and headache were significantly less common.
We investigate and characterize the magnetoencephalographic waveforms from patients during spontaneous and visually induced migraine aura. Direct current neuromagnetic fields were measured during spontaneous onset of migraine auras in 4 migraine patients, and compared with recordings from 8 migraine-with-aura patients and 6 normal controls during visual stimulation of the occipital cortex. Complex direct current magnetoencephalographic shifts, similar in waveform, were observed in spontaneous and visually induced migraine patients, but not in controls. Two-dimensional inverse imaging showed multiple cortical areas activated in spontaneous and visually induced migraine aura patients. In normal subjects, activation was only observed in the primary visual cortex. Results support a spreading, depression-like neuroelectric event occurring during migraine aura that can arise spontaneously or be visually triggered in widespread regions of hyperexcitable occipital cortex.
There is a difference in threshold for excitability of occipital cortex in migraineurs and controls. The hyperexcitable visual cortex in migraine is predisposed to visually triggered headache.
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