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Papers: S Artero, H Tiemeier, N D Prins, R Sabatier, M M B Breteler, and K Ritchie Neuroanatomical localisation and clinical correlates of white matter lesions in the elderly J Neurol Neurosurg Psychiatry 2004; 75: 1304-1308 [Abstract] [Full text] [PDF]

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White matter lesions in MRI: searching a concept for a finding

Vinod K Gupta   (31 January 2005)

White matter lesions in MRI: searching a concept for a finding 31 January 2005
Vinod K Gupta, Physician Dubai Police Medical Services, P.O. Box 12005, Dubai, United Arab Emirates Send letter to journal: Re: White matter lesions in MRI: searching a concept for a finding docgupta{at}emirates.net.ae Vinod K Gupta	Dear Editor, Artero and colleagues detected a patterned non-random distribution of white matter lesions (WML) in the aging brain associated with symptoms and suggest progression of lesions from frontal through parietal to temporal and occipital regions. Since blood pressure is an established risk factor for the presence and severity of WML, the rheological state of the brain circulation appears to be the critical factor influencing distribution of such lesions. Alterations in mental state or cognition are commonly accompanied by alterations in blood pressure and thereby cranial blood flow; such alterations in brain neuronal function are unlikely to be causal or primarily responsible for the appearance of WML. WML are neither age- specific nor generally heritable, having been found in both sexes in hypertensive encephalopathy, puerperal eclampsia, migraine, and therapy with cyclosporin, interferon-alpha, and tacrolimus. [1] In migraine patients, the occurrence of predominantly posterior circulation territory infarcts in contrast to anterior circulation infarcts in embolic or atherosclerotic thrombotic strokes is probably related to rheological factors; anatomical vulnerability of the posterior cerebral artery renders it particularly susceptible to vasospastic influences in migraine patients. [2] Conversely, diffuse, non-lateralizing distribution of deep WML in migraine patients unaffected by triptan use indicates that these MRI aberrations do not reflect the outcome of vasospastic ischemia; sustained vasodilatation and vasogenic cerebal oedema probably underlies WML in both migraine as well as hypertensive encephalopathy. [2,3] Mechanistically, there appears to be a fundamental difference in the pathogenesis of brain infarcts and WML. While Artero et al allude to a particular ‘vulnerability’ of frontal areas to WML that transcends disease entities but appears linked to symptoms, disease symptomatology cannot logically be dissociated from the disease process. The general susceptibility of the frontal regions to develop WML earlier than other brain regions probably reflects the outcome of a regional variation in density of autonomic innervation of the cranial circulation. By virtue of the tonic vasoconstrictive influence on posterior cranial circulation, [2,4] the occipital region appear to be least susceptible to surges in cranial blood flow and, therefore, are least likely to develop WML. The proposal to study longitudinally the distribution of WML in the general population, as suggested by these investigators, is complicated by the intrinsic reversibility of such lesions. [1,3] In such a situation, there is little to distinguish whether any location-specific WML detected at MRI at two different points in time, say five years apart, represents the same or a different newer lesion – the previous lesion at the same site having resolved completely. All investigative modalities have their limitations; issues primarily related to natural variations in the index disease have to be addressed through conceptual groundwork rather than the accretion of more ‘hard evidence’. References (1). Gupta VK. White matter hyperintensities: pearls and pitfalls in interpretation of MRI abnormalities. Stroke 2004; 35: 2756-2757. (2). Gupta VK. Regional cerebral blood flow patterns in migraine: what is the contribution to insight into disease mechanisms? Eur J Neurol 1995;2:586-587. (3). Donnan GA. Posterior leucoencephalopathy syndrome. Lancet 1996;347:988. (4). Molliver ME. Serotonergic neuronal systems: what their anatomic organizations tell us about function. J Clin Psychopharmacol 1987; 7 (suppl 6):3S-23S.