A review of diagnostic and functional imaging in headache

The neuroimaging of headache patients has revolutionised our understanding of the pathophysiology of primary headaches and provided unique insights into these syndromes. Modern imaging studies point, together with the clinical picture, towards a central triggering cause. The early functional imaging work using positron emission tomography shed light on the genesis of some syndromes, and has recently been refined, implying that the observed activation in migraine (brainstem) and in several trigeminal-autonomic headaches (hypothalamic grey) is involved in the pain process in either a permissive or triggering manner rather than simply as a response to first-division nociception per se. Using the advanced method of voxel-based morphometry, it has been suggested that there is a correlation between the brain area activated specifically in acute cluster headache — the posterior hypothalamic grey matter — and an increase in grey matter in the same region. No structural changes have been found for migraine and medication overuse headache, whereas patients with chronic tension-type headache demonstrated a significant grey matter decrease in regions known to be involved in pain processing. Modern neuroimaging thus clearly suggests that most primary headache syndromes are predominantly driven from the brain, activating the trigeminovascular reflex and needing therapeutics that act on both sides: centrally and peripherally

Facial flushing after thermocoagulation of the Gasserian ganglion

The development of a facial flush during thermocoagulation of the Gasserian ganglion was monitored in 16 patients with pulse recording techniques and in a further 17 patients with thermography. There was a close association between the development of the facial flush in the distribution of one or more divisions of the trigeminal nerve and the subsequent demonstration of postoperative analgesia. In regions where significant changes took place, vascular pulsations increased 25-233% (mean 96%) and facial temperature rose 0.5-2.0 degrees C. The response persisted for up to an hour postoperatively, and was not diminished in patients with pre-operative analgesia from a previous procedure. Possible mechanisms for the facial flush, including stimulation of an active vasodilator system, the antidromic release of vasoactive substances from trigeminal nerve terminals and the release of tonic vasoconstriction are discussed. A practical application of the pulse recording technique used in the present investigation would be to monitor the distribution of vasodilatation at operation to avoid unwanted first division sensory loss

Mechanisms of normal and abnormal facial flushing and sweating

Abstract not availabl

Extracranial vascular reactivity in migraine and tension headache

The amplitude of temporal artery pulsation was monitored at rest, after standing from the sitting position and after exercise in 23 normal controls, 10 patients subject to chronic tension headache and 107 migrainous patients. The pulses of migrainous patients did not differ from normal at rest or on standing. On exercise, the temporal artery on the habitually affected side of migrainous patients dilated more than the headache-free side, while exercise-induced changes in tension headache patients were less than those in normal controls. The responses were not influenced by previous or current medication

Facial temperature in migraine, tension-vascular and tension headache

The relationship between clinical features and changes in the extracranial circulation was studied during 209 separate attacks of headache affecting the anterior part of the head. Extracranial vascular changes were assessed thermographically and by the change in headache intensity when pressure was applied over the superficial temporal and common carotid arteries. In unilateral headaches, increased heat loss from the affected frontotemporal region was observed most frequently in attacks which were temporarily relieved by compression of the superficial temporal artery: thermographic asymmetry disappeared as the headache abated. Although such headaches were associated more frequently with migrainous features than attacks which did not respond to arterial compression, many headaches with clinical features of migraine had no vascular component detectable by thermography or vascular compression. Furthermore, the response to arterial compression was not consistent from one headache to another in the same patient. It was concluded that extracranial vascular changes recur intermittently in headache-prone patients, depending on the severity of pain and association with other features commonly regarded as migrainous. However, there was no clear demarcation point between entities diagnosed clinically as 'migraine' and 'tension headache'

Extracranial vascular changes and the source of pain in migraine headache

The extracranial circulation of 66 migrainous patients was assessed during unilateral headache by recording the pulse amplitude of the superficial temporal artery and its main frontal branch, by facial thermography, and by changes in the intensity of headache when temporal or carotid arteries were compressed.Amplitude of pulsation of the superficial temporal artery did not differ between headache and headache-free sides but the amplitude of its frontal branch was increased on the headache side, specifically in a subgroup of patients whose headache was relieved by compressing the superficial temporal artery (ldquoextracranial vascularrdquo group). Facial thermograms demonstrated significant differences in heat loss from the temples and orbits between migrainous patients and controls, frontotemporal changes being more conspicuous in the extracranial vascular group. It was concluded that dilatation of the superficial temporal artery and its branches contributes substantially to migraine headache in only a minority of patients

Cranial syndromes of abnormal sweating, flushing and pupillary abnormalities

Abstract not availabl

Neurovascular disturbances in headache patients

The prevalence of icecream headache, icepick-like pains and premonitory symptoms (changes in mood, appetite and alertness one to 24 hours before headache onset) was studied in 530 patients referred for neurological assessment of headache. Pain in the head after icecream or cold drinks was reported by 37% of patients, more often by those whose headaches were associated with focal neurological symptoms and gastrointestinal disturbances. The affected region coincided with that of the customary headache in 33% of patients questioned. Icepick-like pains were reported by 39% of patients and were restricted to the distribution of the customary headache in 40% of these. Premonitory symptoms were noted by 30% of patients, particularly those with focal neurological symptoms before or during the attack. Premonitory symptoms may form part of a diffuse cerebral or hypothalamic disturbance preceding headache, while the prevalence of icecream headache and icepick-like pains suggests that pain pathways and neurovascular reflexes to sensory stimulation are hyperexcitable even between headache episodes. These phenomena favour a neurological origin of migrainous headache