Hyperperfusion of Cerebral Cortex, Thalamus and Basal Ganglia During Spontaneously Occurring Migraine Headaches

Abstract

Color-coded, cross-sectional imaging of local cerebral blood flow (LCBF) was made in a prospective manner among 22 patients with well-established common or classic migraine utilizing the stable xenon-enhanced computed tomographic (Xe CT-CBF) method. LCBF in patients during spontaneously occurring headaches (N = 12) were significantly higher compared to patients without headache (N = 10) by 25-35%. The hyperperfusion involved not only cerebral cortex but also subcortical structures including thalamus, basal ganglia, and subcortical white matter. LCBF increases were not bilateral and sometimes asymmetrical, but LCBF increases were not consistently related to the preponderant side of headache. No significant differences were observed in the degree or pattern of cerebral hyperperfusion during headaches compared among common (N = 6) and classic (N = 6) migraineurs. Results suggest a common etiology for both common and classic migraine. Results are not consistent with spreading oligemia or spreading cortical depression as a cause of migraine. The cerebral hyperperfusion appears to be mediated by various neurogenic and chemical changes accompanying migraine. The unilateral nature of migraine head pain is more likely due to dilation of extracranial vessels.

The effect of propranolol on cerebrovascular reactivity to visual stimulation in migraine

“…Shields et al reported that propranolol inhibited thalamocortical activity in response to nociceptive trigeminovascular input via β1 receptor antagonism [14]. There have been various studies that have considered the thalamus or brainstem, as well as the cerebral cortex, as pathophysiologic targets in migraine [30][31][32]. Our results best fit this theory of the action of propranolol on the brainstem or thalamic centers that control vessel tone sensitivity to visual stimulation.…”

The Role of Thalamic Damage in Mild Traumatic Brain Injury

“…24 More commonly, however, patient complaints closely resemble the prodromic symptoms in migraine which, by analogy, despite etiological and pathogenic differences, still suggest the potential involvement of the thalamus and thalamocortical circuits. Kobari and colleagues 25 examined patients during spontaneously-occurring migraine using xenon enhanced CT and reported hemodynamic changes in the thalamus, the basal ganglia, and the cerebral cortex. Coppola and colleagues 26 suggested, after studying high frequency oscillations of sensory evoked potentials in patients with migraine, that activity in thalamocortical projections is interictally decreased in migraine and could possibly explain the reduced pre-activation level of sensory cortices.…”

Altered Structure and Resting-State Functional Connectivity of the Basal Ganglia in Migraine Patients Without Aura

“…20,28 It is worth noting that some new findings are pointing toward a potential role of several new brain areas in migraine neuropathology such as the basal ganglia (BG). 18,23,25 The important role of the BG in migraine neuropathology has been investigated. 18,23,31 The increased activation (local cerebral blood flow) in the BG during spontaneously occurring headaches was observed in migraine patients.…”