Transcranial Doppler ultrasonic features in episodic tension-type headache
Thomas-Martin Wallasch
Department of .Neurology, Christian-Albrechts University, Niemannsweg 147 2300 Kiel, Germany Cephalalgia
Wallasch TM. Transcranial Doppler ultrasonic features in episodic tension-type headache, Cephalalgia 1992;12:293-6. Oslo. ISSN 0333-1024 In a pilot study we used transcranial Doppler ultrasound (TCD) to measure cerebral blood flow velocities in 21 headache-free episodic tension-type headache sufferers and in the same number of age- and sex-matched control subjects. We found increased blood flow velocities in the anterior, middle and posterior cerebral arteries and a decreased pulsality index in the middle and posterior cerebral arteries in tension-type headache sufferers compared to controls. Vascular bruits were significantly more frequent in the basal cerebral arteries of the patients compared to controls. There were no significant asymmetries of blood flow velocities in corresponding arteries. The findings suggest a multifactorial pathogenesis in episodic tension type headache including vascular abnormalities. • Blood flow velocity, headache, tension-type headache, transcranial Doppler ultrasound Thomas-Martin Wallasch, Department of Neurology, Christian Albrechts University, Niemannsweg 147 2300 KieI, Germany. Received 2 February 1992, accepted 1 June 1992
The new International Classification of Headache (1) separates tension-type headaches into episodic and chronic subgroups. Muscle contraction on palpation or a raised EMG level of the pericranial musculature at rest or during physiological tests is specified as diagnostic criteria. There is no consideration of cerebrovascular function in this headache type. The relationship between migraine and tension-type headache is controversial (2, 3). Rather than separate entities, these headaches may represent varying symptom intensities of the same condition. In previous studies no cerebral blood flow (CBF) changes were demonstrated in chronic tension-type headache using 133XE methodology (4). In episodic tension-type headache, however, possible cerebrovascular alterations have not been studied by transcranial Doppler (TCD), a non-invasive ultrasound method used to evaluate blood flow velocity in the basal cerebral arteries (5, 6). TCD is a non-invasive method used to evaluate blood flow velocity in the basal cerebral arteries (5, 6). In migraine sufferers, Thie et al. (7) reported an elevated mean flow velocity (MFV) in the basal cerebral vessels compared to healthy young controls. In particular, characteristic vascular bruits were detected in 56%. Recently, we have reported elevated MFV and vascular bruits in two cases of episodic tension-type headache (8). In order to evaluate vascular features in tension-type headache, 21 patients suffering from episodic tension-type headache were examined in a pilot study. The ultrasonic patterns were compared with those of an age-and sex-matched healthy control group. Subjects and methods Subjects
Twenty-one consecutive outpatients suffering from episodic tension-type headache (IHS diagnosis: 2.1) visiting the Department of Neurology of the Kiel University Hospital were studied. Mean age of the total group of tension-type headache ,sufferers was 28 ± 7 with a range of 19-51 years. Twenty-one healthy volunteers matched for age and sex served as the control group. Each group consisted of 11 women and 10 men. A complete medical history was obtained and the diagnosis was made in accordance with the criteria of the IHS classification (1). Patients suffering from mi-graine and tension-type headache (formerly so-called "combination headache") were excluded. Further exclusion criteria were psychiatric diseases, diabetes mellitus, epilepsy, hypertension, cardiovascular disorders (arrhythmia, stenoses), abuse of analgesics, narcotics or ergotamines. None of the patients received a prophylactic medication within eight weeks before testing. The examination was carried out in a semi-darkened and temperature controlled room (20 to 22°C) with the patient in the supine position. The subjects relaxed for at least 10 min before testing. During the TCD examination there was no conversation. TCD recordings were carried out during the headache-free interval (at least five headache-free days). Caffeine was not consumed and patients did not smoke for 3 h before testing. All TCD examinations were carried out by the same experienced examiner, who was blinded to the diagnosis. Methods The EME TC2-64B transcranial Doppler device (EME, Überlingen, Germany) with a hand-held 2 MHz probe was used for all examinations. Systolic peak (SFV) and mean (MFV) flow velocities were quantified bilaterally. In addition, the pulsality index (PI) as
defined by Gosling (9) (systolic minus diastolic flow velocity divided by MFV) was determined. The internal carotid artery (ICA) was insonated in the extra-cranial portion in the neck, at the mandibular angle, at a depth of 45 and 50 mm. The middle (MCA), anterior (ACA) and posterior (PCA) cerebral arteries were recorded using the "temporal window" by means of standard techniques (10). The basilary artery (BA) signal was taken at a depth of 90 to 100 mm using the transnuchal approach. Only measurements with the best signal-to-noise ratio were used and the highest values of SFV, MFV and PI were selected for analysis. Since there were no significant side differences of blood flow velocities and PI, the highest values of each paired arteries were used for statistical procedures. Continuous-wave Doppler ultrasonography of the extracranial arteries of the head was performed in all subjects to exclude stenoses. Blood pressure (Finapres system, Ohmeda, Puchheim, Germany) and end-tidal pCO2 concentrations (CO2 monitor, Dräger, Lübeck, Germany) were obtained from each subject. Ultrasonic recordings were only performed within a pCO2 range of 38 to 42 mmHg. Non-parametric statistical testing was performed using the Mann-Whitney U test; statistical significance was accepted at a p < 0.05 level. Results
Systolic and diastolic blood pressures (median, 25th and 75th percentiles) were 130 (120-140) and 80 (70-90) mmHg in the controls and 130 (120-135) and 80 (70-80) mmHg in the group of tension-type headache patients. There were no significant differences. The extracranial ICA and the MCA were insonated in all subjects. The ACA was recorded on both sides in all control subjects and 20 of 21 tension-type headache sufferers. Ultrasonic Doppler recordings of the PCA were made on both sides in 12 patients and 17 control subjects. BA was detected in 20 of the patients suffering from tension-type headache and in all controls. Mean flow velocities (MFV) in the anterior (ACA), middle (MCA) and posterior cerebral artery (PCA) were significantly increased in episodic tension-type headache sufferers compared to controls (Table 1). The extracranial ICA and the BA showed no significant differences in MFV between the groups. MCA and ACA SFV's were significantly increased in patients compared to controls (Table 2). PI values were significantly decreased in the MCA and PCA in patients compared to controls (Table 3), while there were no significant differences in any of the other arteries. There were no significant side-to-side differences of MFV, SFV or PI in the extracranial ICA and the paired basal cerebral arteries. Bruits are indicated on the Doppler spectrum (Fig. 1) as a symmetrical pattern shown above and below the zero frequency baseline (11). Bruits were heard in 47.6% of the tension-type headache patients and in 19% of the controls (p < 0.017). Bruits were detected in 2 or more basal cerebral arteries in 8 of 21 episodic Table 1. TCD features in tension-type headaches-maximal mean flow velocities in normal controls (n = 21) and episodic tension-type headache (n = 21). Mean flow velocity (cm/s)† Controls Headache ICA 44 (38-48) 46 (38-50) MCA 63 (60-70) 76 (68-86) ACA 46 (36-52) 56 (50-66) PCA 40 (36-44) 44 (40-52) BA 47 (42-52) 49 (41-61) * p < 0.05; ** p < 0.01; *** p < 0.001. † Median value (25th-75th percentile).
p 0.583 0.002 0.001 0.049 0.299
** *** *
Table 2. TCD features in tension-type headaches-systolic peak flow velocities in normal controls (n = 21) and episodic tension-type headache sufferers (n = 21). Peak flow velocity (cm/s)† Controls Patients p ICA 74 (66-84) 76 (68-82) 0.933 MCA 107 (98-118) 120 (110-130) 0.011 * ACA 72 (66-96) 98 (86-100) 0.005 ** PCA 68 (64-74) 74 (67-78) 0.178 BA 70 (66-76) 74 (65-85) 0.273 * p < 0.05; **p < 0.01. † Median value (25-75th percentlie).
Table 3. TCD features in tension-type headaches-pulsality indices in normal controls (n = 21) and episodic tension-type headache (n = 21). Pulsality index† Controls Headache p ICA 1.08 (0.98-1.29) 1.01 (0.95-1.23) 0.455 MCA 1.00 (0.98-1.21) 0.92 (0.79-1.05) 0.030 ACA 0.92 (0.83-1.18) 0.99 (0.79-1.20) 0.922 PCA 0.93 (0.89-1.09) 0.80 (0.70-0.88) 0.006 BA 0.84 (0.79-0.91) 0.80 (0.73-0.85) 0.096 * p < 0.05, ** p < 0.01. † Median value ( ) 25-75th percentile.
* **
tension-type headache sufferers, but only in 1 control subject. Discussion
This is the first report of abnormal transcranial Doppler ultrasonic features in tension-type headaches. Our findings suggest cerebrovascular aberrations in episodic tension-type headache. When headache-free, patients meeting the IHS criteria for episodic tension-type headache have increased blood flow velocities in the MCA, ACA and PCA, and decreased PI. These findings indicate either constriction of the cerebral conductance vessels or dilatation of the resistance vessels. Direct measurements of brain tissue blood flow will be needed to distinguish these flow states. Also our finding of increased vascular bruits support an unstable cerebrovascular tone in episodic tension-type headache sufferers. Vascular aspects of tension-type headache have not been a topic of interest. Using Xenon-SPECT, Anderson et al. (4) found no cerebral blood flow changes in patients with chronic tension headache. However, several investigators (12-15) have implicated cephalic vascular factors in tension-type headache. The implications of vascular mechanisms of tension-type headache are supported by our ultrasonic findings, which in fact are similar to the reported interictal TCD changes in migraine sufferers (7). As suggested by Featherstone (2), primary headache disorders (e.g. migraine and tension headache) could be different only in clinical expression rather than pathophysiology. The vascular changes we described in patients with tension-type headache, together with our recent report of disturbed central motor activity control of pericranial musculature in a group of tension-type headache sufferers (16), suggest multiple factors in the pathogenesis of tension headaches. This theory has been emphasized by Olesen et al. (17, 18), who described a new vascular-supraspinal-moyogenic model of primary headaches. Further more extensive studies are needed to establish the possible vascular pathophysiology of tension-type headache. Ultrasonic findings should be correlated especially to clinical symptoms. Such studies are in preparation in our laboratories. References
1.
Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8(suppl 7):1-96
2.
Featherstone HJ. Migraine and muscle contraction headache: a continuum. Headache 1985;25:194-8
3.
Pikoff H. Is the muscular model of headache still viable? a review of conflicting data. Headache 1984;24:186-98
4.
Andersen AR, Langemark M, Olesen J. Regional cerebral blood flow in chronic tension-type headache. In: Olesen J ed Migraine and other headaches. The vascular mechanisms. Frontiers in Headache Research, vol 1. New York: Raven Press, 1991;319-21
5.
Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial Doppler ultrasound recordings of flow velocities in basal cerebral arteries. J Neurosurg 1982;57:769-74
6.
Aaslid R, Huber P, Nornes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 1984; 60:37-41
7.
Thie A, Fuhlendorf A, Spitzer K, Kunze K. Transcranial
Doppler evaluation of common and classic migraine. Part I. Ultrasonic features during the headache-free period. Headache 1990;30:201-8 8.
Wallasch TM, Soyka D. Vascular bruits detected by transcranical Doppler ultrasound in episodic headache of tension-type: a case report. Headache Quarterly 1991;2:210-13
9.
Gosling RG, King DH. Arterial assessment by Doppler-shift ultrasound. Proc R Soc Med 1974;67:447-9
10.
Hennerici M, Rautenberg W, Sitzer G, Schwartz A. Transcranial Doppler ultrasound for the assessment of intracranial arterial flow velocity. Part I. Examination technique and normal values. Surg Neurol 1987;27:439-48
11.
Spencer MP. Vascular bruits. In: Spencer MP ed Ultrasonic diagnosis of cerebrovascular disease. Dordrecht: Martinus Nijhoff, pp. 147-56
12.
Drummond PD, Lance JW. Extracranial vascular reactivity in migraine and tension headache. Cephalalgia 1981;1:149-55
13.
Cannon LR, Haynes SN, Cuevas J, Chavez R. Psychophysiological correlates of induced headaches. J Behav Med 1987;10: 411-23
14.
Haynes SN, Cuevas J, Gannon LR. The psychophysiological etiology of muscle-contraction headache. Headache 1982;22: 122 -32
15.
Haynes SN, Gannon LR, Bank J, Shelton D, Goodwin J. Cephalic blood flow correlates of induced headaches. J Behav Med 1990;13:467-80
16.
Wallasch TM, Reinecke M, Langohr HD. EMG analysis of the late exteroceptive suppression period of temporal muscle activity in episodic and chronic tension-type headaches. Cephalalgia 1991;11:109-12
17.
Olesen J, Jensen R. Getting away from simple muscle contraction as a mechanism of tension-type headache. Pain 1991;46: 123 -4
18.
Olesen J. Clinical and pathophysiological observations in mi-graine and tension-type headache explained by integration of vascular, supraspinal and myofascial inputs. Pain 1991;46:125-32
Thomas-Martin Wallasch
Department of .Neurology, Christian-Albrechts University, Niemannsweg 147 2300 Kiel, Germany Cephalalgia
Wallasch TM. Transcranial Doppler ultrasonic features in episodic tension-type headache, Cephalalgia 1992;12:293-6. Oslo. ISSN 0333-1024 In a pilot study we used transcranial Doppler ultrasound (TCD) to measure cerebral blood flow velocities in 21 headache-free episodic tension-type headache sufferers and in the same number of age- and sex-matched control subjects. We found increased blood flow velocities in the anterior, middle and posterior cerebral arteries and a decreased pulsality index in the middle and posterior cerebral arteries in tension-type headache sufferers compared to controls. Vascular bruits were significantly more frequent in the basal cerebral arteries of the patients compared to controls. There were no significant asymmetries of blood flow velocities in corresponding arteries. The findings suggest a multifactorial pathogenesis in episodic tension type headache including vascular abnormalities. • Blood flow velocity, headache, tension-type headache, transcranial Doppler ultrasound Thomas-Martin Wallasch, Department of Neurology, Christian Albrechts University, Niemannsweg 147 2300 KieI, Germany. Received 2 February 1992, accepted 1 June 1992
The new International Classification of Headache (1) separates tension-type headaches into episodic and chronic subgroups. Muscle contraction on palpation or a raised EMG level of the pericranial musculature at rest or during physiological tests is specified as diagnostic criteria. There is no consideration of cerebrovascular function in this headache type. The relationship between migraine and tension-type headache is controversial (2, 3). Rather than separate entities, these headaches may represent varying symptom intensities of the same condition. In previous studies no cerebral blood flow (CBF) changes were demonstrated in chronic tension-type headache using 133XE methodology (4). In episodic tension-type headache, however, possible cerebrovascular alterations have not been studied by transcranial Doppler (TCD), a non-invasive ultrasound method used to evaluate blood flow velocity in the basal cerebral arteries (5, 6). TCD is a non-invasive method used to evaluate blood flow velocity in the basal cerebral arteries (5, 6). In migraine sufferers, Thie et al. (7) reported an elevated mean flow velocity (MFV) in the basal cerebral vessels compared to healthy young controls. In particular, characteristic vascular bruits were detected in 56%. Recently, we have reported elevated MFV and vascular bruits in two cases of episodic tension-type headache (8). In order to evaluate vascular features in tension-type headache, 21 patients suffering from episodic tension-type headache were examined in a pilot study. The ultrasonic patterns were compared with those of an age-and sex-matched healthy control group. Subjects and methods Subjects
Twenty-one consecutive outpatients suffering from episodic tension-type headache (IHS diagnosis: 2.1) visiting the Department of Neurology of the Kiel University Hospital were studied. Mean age of the total group of tension-type headache ,sufferers was 28 ± 7 with a range of 19-51 years. Twenty-one healthy volunteers matched for age and sex served as the control group. Each group consisted of 11 women and 10 men. A complete medical history was obtained and the diagnosis was made in accordance with the criteria of the IHS classification (1). Patients suffering from mi-graine and tension-type headache (formerly so-called "combination headache") were excluded. Further exclusion criteria were psychiatric diseases, diabetes mellitus, epilepsy, hypertension, cardiovascular disorders (arrhythmia, stenoses), abuse of analgesics, narcotics or ergotamines. None of the patients received a prophylactic medication within eight weeks before testing. The examination was carried out in a semi-darkened and temperature controlled room (20 to 22°C) with the patient in the supine position. The subjects relaxed for at least 10 min before testing. During the TCD examination there was no conversation. TCD recordings were carried out during the headache-free interval (at least five headache-free days). Caffeine was not consumed and patients did not smoke for 3 h before testing. All TCD examinations were carried out by the same experienced examiner, who was blinded to the diagnosis. Methods The EME TC2-64B transcranial Doppler device (EME, Überlingen, Germany) with a hand-held 2 MHz probe was used for all examinations. Systolic peak (SFV) and mean (MFV) flow velocities were quantified bilaterally. In addition, the pulsality index (PI) as
defined by Gosling (9) (systolic minus diastolic flow velocity divided by MFV) was determined. The internal carotid artery (ICA) was insonated in the extra-cranial portion in the neck, at the mandibular angle, at a depth of 45 and 50 mm. The middle (MCA), anterior (ACA) and posterior (PCA) cerebral arteries were recorded using the "temporal window" by means of standard techniques (10). The basilary artery (BA) signal was taken at a depth of 90 to 100 mm using the transnuchal approach. Only measurements with the best signal-to-noise ratio were used and the highest values of SFV, MFV and PI were selected for analysis. Since there were no significant side differences of blood flow velocities and PI, the highest values of each paired arteries were used for statistical procedures. Continuous-wave Doppler ultrasonography of the extracranial arteries of the head was performed in all subjects to exclude stenoses. Blood pressure (Finapres system, Ohmeda, Puchheim, Germany) and end-tidal pCO2 concentrations (CO2 monitor, Dräger, Lübeck, Germany) were obtained from each subject. Ultrasonic recordings were only performed within a pCO2 range of 38 to 42 mmHg. Non-parametric statistical testing was performed using the Mann-Whitney U test; statistical significance was accepted at a p < 0.05 level. Results
Systolic and diastolic blood pressures (median, 25th and 75th percentiles) were 130 (120-140) and 80 (70-90) mmHg in the controls and 130 (120-135) and 80 (70-80) mmHg in the group of tension-type headache patients. There were no significant differences. The extracranial ICA and the MCA were insonated in all subjects. The ACA was recorded on both sides in all control subjects and 20 of 21 tension-type headache sufferers. Ultrasonic Doppler recordings of the PCA were made on both sides in 12 patients and 17 control subjects. BA was detected in 20 of the patients suffering from tension-type headache and in all controls. Mean flow velocities (MFV) in the anterior (ACA), middle (MCA) and posterior cerebral artery (PCA) were significantly increased in episodic tension-type headache sufferers compared to controls (Table 1). The extracranial ICA and the BA showed no significant differences in MFV between the groups. MCA and ACA SFV's were significantly increased in patients compared to controls (Table 2). PI values were significantly decreased in the MCA and PCA in patients compared to controls (Table 3), while there were no significant differences in any of the other arteries. There were no significant side-to-side differences of MFV, SFV or PI in the extracranial ICA and the paired basal cerebral arteries. Bruits are indicated on the Doppler spectrum (Fig. 1) as a symmetrical pattern shown above and below the zero frequency baseline (11). Bruits were heard in 47.6% of the tension-type headache patients and in 19% of the controls (p < 0.017). Bruits were detected in 2 or more basal cerebral arteries in 8 of 21 episodic Table 1. TCD features in tension-type headaches-maximal mean flow velocities in normal controls (n = 21) and episodic tension-type headache (n = 21). Mean flow velocity (cm/s)† Controls Headache ICA 44 (38-48) 46 (38-50) MCA 63 (60-70) 76 (68-86) ACA 46 (36-52) 56 (50-66) PCA 40 (36-44) 44 (40-52) BA 47 (42-52) 49 (41-61) * p < 0.05; ** p < 0.01; *** p < 0.001. † Median value (25th-75th percentile).
p 0.583 0.002 0.001 0.049 0.299
** *** *
Table 2. TCD features in tension-type headaches-systolic peak flow velocities in normal controls (n = 21) and episodic tension-type headache sufferers (n = 21). Peak flow velocity (cm/s)† Controls Patients p ICA 74 (66-84) 76 (68-82) 0.933 MCA 107 (98-118) 120 (110-130) 0.011 * ACA 72 (66-96) 98 (86-100) 0.005 ** PCA 68 (64-74) 74 (67-78) 0.178 BA 70 (66-76) 74 (65-85) 0.273 * p < 0.05; **p < 0.01. † Median value (25-75th percentlie).
Table 3. TCD features in tension-type headaches-pulsality indices in normal controls (n = 21) and episodic tension-type headache (n = 21). Pulsality index† Controls Headache p ICA 1.08 (0.98-1.29) 1.01 (0.95-1.23) 0.455 MCA 1.00 (0.98-1.21) 0.92 (0.79-1.05) 0.030 ACA 0.92 (0.83-1.18) 0.99 (0.79-1.20) 0.922 PCA 0.93 (0.89-1.09) 0.80 (0.70-0.88) 0.006 BA 0.84 (0.79-0.91) 0.80 (0.73-0.85) 0.096 * p < 0.05, ** p < 0.01. † Median value ( ) 25-75th percentile.
* **
tension-type headache sufferers, but only in 1 control subject. Discussion
This is the first report of abnormal transcranial Doppler ultrasonic features in tension-type headaches. Our findings suggest cerebrovascular aberrations in episodic tension-type headache. When headache-free, patients meeting the IHS criteria for episodic tension-type headache have increased blood flow velocities in the MCA, ACA and PCA, and decreased PI. These findings indicate either constriction of the cerebral conductance vessels or dilatation of the resistance vessels. Direct measurements of brain tissue blood flow will be needed to distinguish these flow states. Also our finding of increased vascular bruits support an unstable cerebrovascular tone in episodic tension-type headache sufferers. Vascular aspects of tension-type headache have not been a topic of interest. Using Xenon-SPECT, Anderson et al. (4) found no cerebral blood flow changes in patients with chronic tension headache. However, several investigators (12-15) have implicated cephalic vascular factors in tension-type headache. The implications of vascular mechanisms of tension-type headache are supported by our ultrasonic findings, which in fact are similar to the reported interictal TCD changes in migraine sufferers (7). As suggested by Featherstone (2), primary headache disorders (e.g. migraine and tension headache) could be different only in clinical expression rather than pathophysiology. The vascular changes we described in patients with tension-type headache, together with our recent report of disturbed central motor activity control of pericranial musculature in a group of tension-type headache sufferers (16), suggest multiple factors in the pathogenesis of tension headaches. This theory has been emphasized by Olesen et al. (17, 18), who described a new vascular-supraspinal-moyogenic model of primary headaches. Further more extensive studies are needed to establish the possible vascular pathophysiology of tension-type headache. Ultrasonic findings should be correlated especially to clinical symptoms. Such studies are in preparation in our laboratories. References
1.
Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8(suppl 7):1-96
2.
Featherstone HJ. Migraine and muscle contraction headache: a continuum. Headache 1985;25:194-8
3.
Pikoff H. Is the muscular model of headache still viable? a review of conflicting data. Headache 1984;24:186-98
4.
Andersen AR, Langemark M, Olesen J. Regional cerebral blood flow in chronic tension-type headache. In: Olesen J ed Migraine and other headaches. The vascular mechanisms. Frontiers in Headache Research, vol 1. New York: Raven Press, 1991;319-21
5.
Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial Doppler ultrasound recordings of flow velocities in basal cerebral arteries. J Neurosurg 1982;57:769-74
6.
Aaslid R, Huber P, Nornes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 1984; 60:37-41
7.
Thie A, Fuhlendorf A, Spitzer K, Kunze K. Transcranial
Doppler evaluation of common and classic migraine. Part I. Ultrasonic features during the headache-free period. Headache 1990;30:201-8 8.
Wallasch TM, Soyka D. Vascular bruits detected by transcranical Doppler ultrasound in episodic headache of tension-type: a case report. Headache Quarterly 1991;2:210-13
9.
Gosling RG, King DH. Arterial assessment by Doppler-shift ultrasound. Proc R Soc Med 1974;67:447-9
10.
Hennerici M, Rautenberg W, Sitzer G, Schwartz A. Transcranial Doppler ultrasound for the assessment of intracranial arterial flow velocity. Part I. Examination technique and normal values. Surg Neurol 1987;27:439-48
11.
Spencer MP. Vascular bruits. In: Spencer MP ed Ultrasonic diagnosis of cerebrovascular disease. Dordrecht: Martinus Nijhoff, pp. 147-56
12.
Drummond PD, Lance JW. Extracranial vascular reactivity in migraine and tension headache. Cephalalgia 1981;1:149-55
13.
Cannon LR, Haynes SN, Cuevas J, Chavez R. Psychophysiological correlates of induced headaches. J Behav Med 1987;10: 411-23
14.
Haynes SN, Cuevas J, Gannon LR. The psychophysiological etiology of muscle-contraction headache. Headache 1982;22: 122 -32
15.
Haynes SN, Gannon LR, Bank J, Shelton D, Goodwin J. Cephalic blood flow correlates of induced headaches. J Behav Med 1990;13:467-80
16.
Wallasch TM, Reinecke M, Langohr HD. EMG analysis of the late exteroceptive suppression period of temporal muscle activity in episodic and chronic tension-type headaches. Cephalalgia 1991;11:109-12
17.
Olesen J, Jensen R. Getting away from simple muscle contraction as a mechanism of tension-type headache. Pain 1991;46: 123 -4
18.
Olesen J. Clinical and pathophysiological observations in mi-graine and tension-type headache explained by integration of vascular, supraspinal and myofascial inputs. Pain 1991;46:125-32
