wonderful historical perspective on two of the points that we tried to make: that the common denominator seemed to be white-matter rarefac¬ tion, and that the descriptive term did not imply a specific etiology. We are uncertain whether Durand-Fardel's entity encompasses all of the phenom¬ ena that can lead to leuko-araiosis on CT and MRI images, but it brings to mind Goethe's reflection that "all insightful thoughts have already been thought, we must but try to think them again."2 We have no quarrel with Dr Roman's arguments that Binswang¬ er's disease represents a form of white-matter multi-infarct dementia. However, Binswanger's disease im¬ plies both a clinical course and a pathologic entity. Not all subjects showing leuko-araiosis on brain images will prove to have Binswang¬ er's disease at autopsy, nor will they all have obvious dementia. The term multi-infarct dementia was coined to imply quantal damage and refers to "large and small infarcts of the brain,"3 which clearly can be of gray or white matter. The effects can be through direct cortical damage or through disconnection syndromes, as Dr Román suggested. The suggestion by Drs Roullet, Gray, and Dubas that leuko-araiosis may be caused by cerebral amyloid angiopathy is intriguing. Leukoaraiosis is common in Alzheimer's disease,4·5 as is amyloid angiopathy.6 It is eminently reasonable to theorize that the latter may produce the former, and we concur that further pathologic studies should examine this hypothesis. We agree with Dr Román that "leu¬ ko-araiosis" should not be used to refer to a clinical form of dementia, but rather, that it be related to an appearance on CT and MRI scanning, accompanied by an accurate descrip¬ tion of technique and patients. If all do this, we may find that we can learn to identify several entities giving rise 1. Lee D, Fox A, Vinuela F, et al: Interobserver variation in computed tomography of the brain. Arch Neurol 1987;44:30-31. 2. Von G\l=o"\theJW: Alles Gescheite ist schon gedacht Worden, man muss nur Versuchen, es nochmal zu Denken. Maximen und Reflexionen, No. 441, in Poetische Werke, Vollst\l=a"\ndigeAusgabe. Stuttgart, West Germany, JG Cotta, 1950, vol 2, p 723. 3. Hachinski VC, Illif LD, Zilkha E, et al: Cerebral blood flow in dementia. Arch Neurol 1975;32:632-637. 4. Inzitari D, Diaz F, Fox A, et al: Vascular risk factors and leuko-araiosis. Arch Neurol 1987;44:42-47. 5. Brun A, Englund A: A white-matter disorder in dementia of the Alzheimer type: A patho-$ anatomical study. Ann Neurol 1986;19:253-262. 6. Glenner GG, Henry JH, Fujihara S: Congophilic angiopathy in the pathogenesis of Alzheimer's degeneration. Ann Pathol 1981;2:120\x=req-\ 129. 7. Hachinski VC, Potter P, Merskey H: Leukoaraiosis. Arch Neurol 1987;44:21-23. Global Aphasia Without Other Lateralizing Signs To the Editor.\p=m-\Tworecent articles have addressed the topographic correlates and the specificity of the syndrome of global aphasia without hemiparesis.1,2 Tranel et al1 confirmed the initial article by Van Horn and Hawes,3 because they found that this syndrome was related to two discrete ischemic lesions in the dominant hemisphere (one frontal, one temporoparietal), which were probably of embolic origin. On the other hand, other reports suggested that the syndrome can also be related to a single frontotemporoparietal lesion, which can sometimes be hemorrhagic.2,4 Unfortunately, this debate is confused by the fact that, although hemiparesis said to be absent, ten of the 12 described patients had some degree of right-sided weakness or corticospinal was Computed tomographic scan of left hemisphere infarct. showing single temporoparietal to what now seem similar appear¬ CT and MRI scanning, and the term leuko-araiosis will become obsolete as "labeling is replaced by ances on understanding."7 Vladimir Hachinski, MD Thomas Mirsen, MD Paul Potter, MD, PhD Donald Lee, MD Allan Fox, MD Harold Merskey, DM For the University of Western Ontario Dementia Study Group Department of Clinical Neurological Sciences University Hospital PO Box 5339 Postal Station "A" London, Ontario, Canada N6A 5A5 Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/11/2015 dysfunction (increased tendon reflexes, Babinski's sign), or other lateralizing signs (hemianopia). Global aphasia without other lateralizing signs was reported in only two patients (case 2 of Van Horn and Hawes,3 case 3 of Tranel et al1) who both had discrete ischemie lesions due to probable embolism from the heart or carotid artery. However, I would like to draw attention to the fact that even the syndrome of global aphasia without other localizing signs may not be specific for two remote infarcts. Report of a Case.—A 78-year-old man with atrial fibrillation was admitted after he suddenly developed speech distur¬ bances. On examination, he had global aphasia with severely reduced speech, pho¬ nemic paraphasias, poor comprehension, and repetition. The rest of the neurologic examination was entirely normal. On admission, a computed tomographic (CT) scan was normal, but three days later it showed a single temporoparietal infarct in the left hemisphere (Figure). Single photonemission CT (iodoamphetamine 123) showed an isolated area of decreased per¬ fusion in the same territory Comment—Recent studies have emphasized the occurrence of global aphasia in lesions sparing Broca's or Wernicke's area on CT.S·6 Although an associated small cortical frontal lesion may be missed on CT, a purely posterior lesion sparing Broca's area may account for 8% of the cases of global aphasia.6 Our patient probably represents one such case; he had no other lateralizing sign than the apha¬ sia itself. These findings suggest that two infarcts are not necessary to yield global aphasia without hemiparesis or other lateralizing signs, and that this syndrome does not imply a single topographic correlate and etiology. On the other hand, its recognition remains warranted, as it implies a better outcome of aphasia than classic global aphasia due to a frontotempo¬ ral lesion. Julien Bogousslavsky, MD Department of Neurology CHUV 1011 Lausanne, Switzerland 1. Tranel D, Biller J, Damasio H, et al: Global aphasia without hemiparesis. Arch Neurol 1987;44:304-308. 2. Legatt AD, Rubin MJ, Kaplan LR, et al: Global aphasia without hemiparesis: Multiple etiologies. Neurology 1987;37:201-205. 3. Van Horn G, Hawes A: Global aphasia without hemiparesis: A sign of embolic encephalopathy. Neurology 1982;32:403-406. 4. Ferro JM: Global aphasia without hemiparesis. Neurology 1983;33:1106. 5. Basso A, Roch LeCours A, Maraschini S, et al: Anatomoclinical correlations of the aphasias as defined through CT: Exceptions. Brain Lang 1985;26:201-229. 6. Vignolo LA, Boccardi E, Caverni L: Unexpected CT-scan findings in global aphasia. Cortex 1986;22:55-69.