Ioannis Mavridis, M.D., Sophia Anagnostopoulou, M.D., Ph.D., Assoc. Professor

Department of Anatomy, University of Athens School of Medicine

Corresponding author: Ioannis N. Mavridis, M.D. Department of Anatomy, Medical School, University of Athens, Mikras Assias str. 75, Goudi, 11527 Athens, Greece Tel.: 0030-210 74 62 404 Fax: 0030-210 74 62 398 e-mail: pap-van@otenet.gr

Dear Sir/Madam,

We read the article by Mok et al (2011) on cortical and frontal atrophy associated with cognitive impairment in age-related confluent white-matter lesion (WML).[1] They interestingly reported that cognitive impairment in patients with confluent WML is mediated by global and frontal cortical atrophy and that the mechanisms whereby WML induces cognitive impairment are uncertain.[1] They also mentioned that factors such as infarct load and location, microbleed, global atrophy, central atrophy, regional brain atrophy and Alzheimer's pathology may also affect cognition.[1] They concluded that cognitive impairment in confluent WML is probably mediated by frontal and global cortical atrophy. We agree with the authors and we would like to comment on the relation between regional brain atrophy and cognitive impairment. We experienced a case of a 94-years-old female who had suffered a stroke (a few years prior to her death) which caused focal brain atrophy and was followed by the clinical expression of a psychotic syndrome. The brain atrophy was found during a cadaveric study in the dissection room of our Department. During our macroscopic pathological investigation we noticed a fossa, surrounded by a few petechiae, on the external surface of the right parietal lobe, at the posterior end of the Sylvian fissure. At this area, the cerebral gyri were excessively atrophic and the fossa so deep that almost reached the external wall of the lateral ventricle. The minimum gyri thickness was approximately 1 mm, after removing the meninges. The tissue of the atrophic gyri was soft like a chewing gum, despite the rest gyri of the same brain. Checking out the arteries of the Willis circle, we found a 25 mm long red fussiform thrombus occluding the right middle cerebral artery (MCA). It was beginning from the bifurcation of the right internal carotid artery and extending within the MCA, occluding it completely. The microscopic pathological investigation of the atrophic gyri revealed degenerative lesions with microcycts, edema and many PAS(+) amyloidal bodies. Oxymoronically, clear microscopic findings of an infarct were absent. Persson et al (1989) supported that focal ischemic changes produced by MCA occlusion constitute a dynamic process in which several pathophysiologic events occur over an extended period.[2] Tamura et al (1991) reported that delayed neuropathologic changes following cerebral ischemia have attracted widespread attention and their results demonstrate the significance of remote changes over a long period of time following focal brain injury. This phenomenon could be important in understanding the pathophysiologic changes during the chronic phase of cerebral infarction.[3] We believe that, in our case, the dynamic pathophysiologic process followed MCA occlusion, combined with delayed neuropathologic changes during the chronic phase of the stroke, resulted to the regional atrophy and the cognitive impairment (regarded as a 'psychotic syndrome'). Finally, we support that major cerebrovascular accidents can rarely cause regional brain atrophy. Perhaps the microvascular condition of an old brain could partially help in understanding not only the pathogenesis of this unusual phenomenon, but also the developed cognitive impairment. Moreover, the pathophysiologic mechanism which resulted to the observed atrophy could be also involved in the clinical expression of cognitive impairment. We hope that future studies will illuminate such paths of the human brain physiology and pathophysiology, which are still remaining dark and mysterious and therefore challenging and admirable.

References

1. Mok V, Wong KK, Xiong Y, et al. Cortical and frontal atrophy are associated with cognitive impairment in age-related confluent white-matter lesion. J Neurol Neurosurg Psychiatry 2011;82:52-7. 2. Persson L, Hardemark HG, Bolander HG, et al. Neurologic and neuropathologic outcome after middle cerebral artery occlusion in rats. Stroke 1989;20:641-5. 3. Tamura A, Tahira Y, Nagashima H, et al. Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery. Stroke 1991;22:615-8.

Conflict of Interest:

None declared