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BRIEF COMMUNICATIONS: E. Perry, I. Ziabreva, R. Perry, D. Aarsland, and C. Ballard Absence of cholinergic deficits in "pure" vascular dementia Neurology 2005; 64: 132-133 [Abstract] [Full text] [PDF]

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Absence of cholinergic deficits in "pure" vascular dementia

Hidekazu Tomimoto, Ryo Ohtani and Masafumi Ihara   (1 March 2005)

Reply to Tomimoto

E.K. Perry   (1 March 2005)

Absence of cholinergic deficits in "pure" vascular dementia 1 March 2005
Hidekazu Tomimoto, Department of Neurology, Graduate School of Medicine, Kyoto University Shogoin, Kawaharacho 54, Sakyoku, Kyoto 606-8504, Japan, Ryo Ohtani and Masafumi Ihara Send Correspondence to journal: Re: Absence of cholinergic deficits in "pure" vascular dementia tomimoto{at}kuhp.kyoto-u.ac.jp Hidekazu Tomimoto, et al.	We read the manuscript by Perry et al [1] with great interest. They showed that choline acetyl transferase activity was maintained in the temporal cortices of brains with pathologically confirmed "pure" vascular dementia, and suggested that the cholinergic deficits observed in vascular dementia may be attributed to concurrent Alzheimer's pathology. Vascular dementia is a heterogeneous syndrome consisting of small vessel disease and large vessel disease. Since cholinergic deficits have been shown in CADASIL, [2] a genetically-determined small vessel disease, it is possible that cholinergic deficits are limited to small vessel dementia. Recent data have indicated that white matter lesions involve the external capsules in small vessel dementia, [3] and these cholinergic fiber tracts are strategically damaged. [4] We also observed cholinergic fiber damage in the external capsule of brains with Binswanger's disease, in which Alzheimer's pathologies did not coexist. [5] Damage to the cholinergic fibers may depend on the type of vascular dementia. The radiological and pathological details of white matter lesions and lacunes in the patients' brains must be clarified. Mesulam et al demonstrated cholinergic deficits in the parietal, occipital and dorsolateral frontal cortices, but not in the temporal cortex in CADASIL. This suggests that there was a differential pattern from Alzheimer's disease. This is relevant in terms of relative paucity of white matter lesions in the temporal lobe as well as damages to the cholinergic pathway projecting to the temporal cortex. Information on the regional distribution of cholinergic markers is of interest, since this may be another reason for the absence of cholinergic deficits in "pure" vascular dementia. References 1. Perry E, Ziabreva I, Perry R, Aarsland D, Ballard C. Absence of cholinergic deficits in "pure" vascular dementia. Neurology 2005; 64:132-133. 2. Mesulam M, Siddique T, Cohen B. Cholinergic denervation in a pure multi-infarct state: observations on CADASIL. Neurology 2003; 60: 1183-1185. 3. Auer DP, Putz B, Gossl C, Elbel G, Gasser T, Dichgans M. Differential lesion patterns in CADASIL and sporadic subcortical arteriosclerotic encephalopathy: MR imaging study with statistical parametric group comparison. Radiology 2001; 218: 443-451. 4. Swartz RH, Sahlas DJ, Black SE. Strategic involvement of cholinergic pathways and executive dysfunction: Does location of white matter signal hyperintensities matter? J Stroke Cerebrovasc Dis 2003; 12: 29-23. 5. Tomimoto H, Ohtani R, Shibata M, Nakamura N, Ihara M; Loss of cholinergic pathway in vascular dementia of the Binswanger type. Dement Geriatr Cogn Disord, in press.
Reply to Tomimoto 1 March 2005
E.K. Perry, Newcastle General Hospital, MRC Bldg Westgate Rd., Newcastle upon Tyne, NE4 6BE, UK Send Correspondence to journal: Re: Reply to Tomimoto e.k.perry{at}newcastle.ac.uk E.K. Perry	It is intriguing although not unexpected to learn that cortical cholinergic deficits are apparent in Binswanger's disease. This raises the question - as Dr Tomimoto does - of routinely assessing white matter pathology in conjunction with functional activities that depend on cortical innervation from subcortical nuclei, in 'small vessel dementia'. Although it is widely agreed that vascular dementia is heterogeneous, our study indicated that despite any heterogeneity, temporal cortical cholinergic activity was preserved in a group in which there was no concurrent Alzheimer pathology. As we stated in the original paper, the possibility that other cortical areas may have been affected by cholinergic deficits as in CADASIL cannot be excluded.