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Letters to the Editor |
PO Box 12005, Dubai, United Arab Emirates
e-mail: vinodkgupta9{at}gmail.com
Editor:
In their article in the May 2005 issue of Radiology (1), Drs Tsushima and Endo reinforce the limited role of neuroimaging in primary headaches (2). Some patients demand repeated magnetic resonance (MR) examinations (1) because the origin of primary headaches is believed to lie in the brain. Researchers ignore overwhelming pharmacologic evidence to the contrary (2–5). Unexpectedly, atenolol prevents migraine aura and headache as effectively as propranolol even though it does not freely cross the intact blood-brain barrier (BBB) (3,4). Atenolol is a first-line drug for the prevention of migraine; nadolol and verapamil also do not readily cross the BBB (4). Moreover, migraine aura is almost instantaneously aborted by drugs that do not cross the BBB, such as verapamil and isoproterenol (3). Drugs that do not readily cross the intact BBB are very unlikely to substantially influence brain neuronal function, including cortical spreading depression (3,4). Finally, there is a substantial delay in the onset of migraine aura or headache after exposure to diverse headache-provoking stimuli or circumstances (6). Brain neuroimaging during migraine aura or headache records substantially late physiologic events. Neuroimaging studies must also address the issue of lateralization of primary headaches (4,5). While migraine headaches might be unilateral, bilateral, or side-shifting, cluster headaches and other "trigeminal autonomic cephalalgias" are strictly lateralizing (side-locked) and are only rarely side-shifting. Changes in functional neuroimaging during primary headaches do not indicate the nature of the underlying physiologic process.
While patients with persistent lateralizing neurologic defects (eg, homonymous hemianopia) (1) certainly merit MR imaging, particularly in the absence of headache or with a history of recurrent migraine headaches, patients with a known background of recurrent migraine headaches with nonlateralizing and transient scintillating scotomata probably do not. Atypical features of headache or aura should always alert the therapist to obtain MR images. By itself, side-locking in recurrent headaches should not be perceived as an indication for MR imaging. Also, patients with a chronic daily headache that is not responsive to established regimens within 4 weeks should probably undergo MR imaging.
Migraine, hypertensive encephalopathy, transient global amnesia, and lacunar infarctions are associated with the presence of white matter hyperintensities (WMHs); this MR imaging feature appears to be linked to brain hyperperfusion, breakdown of the BBB, and localized cerebral edema, rather than to primary ischemia (7–9). Diffuse nonlateralizing brain hyperperfusion generally prevails during migraine attacks for more than 48 hours in the cerebral cortex, thalamus, and basal ganglia (10). The propensity of WMHs to manifest around the periventricular region and deeper regions of the brain parenchyma might reflect a particular susceptibility of deeper (nonsurface or tissue-embedded) arterioles to leak in the face of pressure diapedesis following brain hyperperfusion (7–9).
References
Department of Diagnostic Radiology and Nuclear Medicine, Gunma University Hospital, 3-39-22 Showa-machi, Maebashi, Gunma 371–8511, Japan
e-mail: yoshito@xa2.so-net.ne.jp
We thank Dr Gupta for expressing his interest in our article on the role of MR imaging in chronic or recurrent headache (1). We acknowledge his contributions to showing some important points when we use neuroimaging to search for the origin of primary headache and conduct any radiologic research concerning headache.
When we confront a patient who complains of headache, the quality, location, duration, and time course of the headache and the conditions that produce, exacerbate, or relieve it should be carefully reviewed with the patient. Information regarding the patient's medical history, such as systemic hypertension, as well as family history, should also be taken into consideration. These clinical data may provide clues to the underlying cause of headache, although it is actually difficult to decide which patients will benefit from neuroimaging.
We reported in our article (1) that the presence of prolonged aura in patients with migraine may be an important clinical sign that aids in the identification of patients who should undergo MR imaging. In addition to this clue, Dr Gupta indicated that the use of medications, the presence of persistent lateralizing neurologic defects such as homonymous hemianopia, and long-standing daily headache lasting over 4 weeks may also aid in the identification of patients who should undergo neuroimaging. As he correctly indicated, since the presence of WMHs may be linked to brain hyperperfusion, this finding might be important in some patients complaining of headache.
We encourage further research concerning the importance of clinical information in deciding on the use of neuroimaging in patients with chronic or recurrent headache.
Reference
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