Cerebrovascular function in tension-type headache and migraine with or without aura: Transcranial Doppler study | Scientific Reports

Few studies have examined cerebrovascular function in tension headache type versus control or versus migraine headache. The present results showed that changes in cerebrovascular function are present both in patients with TTH and in patients with migraine without aura. The former had a low flow velocity of the MCA whereas the latter had a high flow velocity in the ACA.

Compared with the control group there was a significantly lower PSV and MFV of the MCA of the chronic TTH group. This is consistent with the theory of cerebrovascular alteration in chronic TTH with predominant involvement of the MCA. Drummond26 reported that exercise-induced changes in the amplitude of temporal artery pulsation were smaller in patients with TTH than in a healthy control group. The authors suggested that this was due to extracranial vasoconstriction.

In contrast there have been reports of a higher time-averaged mean velocity (TAMV) in episodic TTH patients than in controls31. Wallasch also reported increased cerebral blood flow velocities (CBF) velocities in the MCA, ACA, and PCA as well as decreased PI in patients with episodic TTH, although there was no difference between controls and patients with chronic TTH32. Our results also differ from those of Ozkalayci et al.2 They reported a significant increase in CBF in the basilar artery relative to controls (p > 0.001).

The data showed a higher MFVin the ACA of patients with migraine without aura than controls, a finding that may support the arteriolar vasodilatation theory in migraine without aura. Abernathy et al.33, Fiermonte et al.18, and Kastrup et al.8 found migraineurs to have higher MFV in the anterior circulation, while others found migraineurs to have higher MFV in the posterior circulation compared to controls11,34. However, many previous studies failed to find differences in MFV in either the anterior or posterior circulation between migraineurs and controls19,24,31,35,36,37,38,39,40,41,42,43,44,45,46.

It has been hypothesized that repeated episodes of migraine may alter cerebrovascular function through repeated exposure to neurogenic inflammation, plasma protein extravasation and the release of vasoactive neuropeptides during migraine episodes. If so, abnormalities of cerebrovascular function may be expected to be more evident in migraine patients without aura than controls35,41. Another potential explanation is linked to the observation of Lagrèze et al.47 who found major abnormalities in rCBF in the grey matter of migraineurs that was normalized by treatment with a calcium entry blocker that prevents migraine attacks. It is therefore possible that the alteration of rCBF or flow velocity could reflect instability of vascular tone especially in migraine without aura. Nevertheless, it remains to be explained whether the modifications of vascular tone are chronic or are an expression of transient abnormalities not associated with headache attacks.

The chronic TH group had lower PSV in the MCA and PCA than the group of migraine with aura. They also had a significantly lower PSV and MFV of the MCA as well as a lower EDV in the VA than in the group of migraine without aura. These results suggest cerebrovascular function in patients with chronic TH differs from that in migraine with or without an aura. Arjona et al.31 found a higher TAMV in the MCA in patients who had migraine without aura than in episodic TH. Cerebral autoregulation describes the process whereby cerebral blood flow is maintained constant over a wide range of cerebral perfusion pressure, often from 50 to 150 mmHg in healthy adults. Interestingly, Reinhard et al.40 reported that migraineurs with aura have poorer autoregulation in the cerebellar circulation than controls.

In the present study we found no significant difference between migraineurs with or without aura. Asghar et al.48 reported that patients who had migraine with aura had a lower blood flow at an earlier stage of the disease than those who had migraine without aura. They suggested that hypoperfusion, or decreased cerebral blood flow, during the aura phase could account for this finding48. However, Zaletel et al.49 postulated that increased neuronal excitability and neurovascular coupling in migraine could be linked with reduced arteriolar resistance and increased regional blood flow (rCBF)50 which can result in the increased flow velocity in the insonated large arteries51.

The data of De Benedittis et al.52 are consistent with the results of the current study since they found that no significant rCBF difference between migraine with and without aura using single photon emission computed tomography (SPECT) and TCD as measured during headache free-intervals and spontaneous/histamine-induced attacks.

The PI is a non-dimensional parameter that is calculated from the doppler wave form and approximates the value of peripheral resistance to flow (although it can be affected by other hemodynamic factors). Thie et al.9 and Fiermonte et al.18 reported a lower PI in the cerebral arteries of patients with migraine than in controls. In contrast our data showed no significant changes in PI in any of the three patient groups compared with the control group or between tension headache versus migraine with or without aura.

Silvestrini et al.53 suggested that a lower PI was linked to arteriolar vasodilatation. Many studies used TCD ultrasound to compare PI in the anterior circulation of migraineurs and controls19,31,40,45,54. Most of them found no significant difference in PI between migraineurs and controls40,45,54. Only two studies Chernyshev et al.34 and Totaro et al.10 found significantly higher PI in the anterior circulation of migraineurs than controls, whereas one study found that migraine patients had lower PI than controls18. Few studies compared PI in the posterior circulation of migraineurs to controls; no significant difference in PI between migraines and controls was reported2,10,34,40.

Although previous work has shown that cerebral blood flow is altered in migraineurs, it is unknown if these processes are differentially involved in chronic versus episodic forms of the disease. As far as we know there has been no previous study directly comparing episodic versus chronic types of headache. However the present study found no significant differences between episodic and chronic headache in TTH. However, in migraine the PI of the MCA and PCA were significantly higher in patients with chronic versus episodic symptoms. it is possible that a higher frequency of migraine attacks increases PI, which possibly due to arteriolar vasodilatation rather than reduced lumen diameter in the basal arteries.

The present results found abnormal cerebrovascular function in patients with TTH and in migraine without aura. There was a low MFV of the MCA for patients with TTH and a higher MFV of the ACA for patients who had migraine without aura. The increased MFV in migraine without aura may be attributable to arteriolar vasodilatation rather than reduced lumen diameter in the MCA since there was no change in PI.