Neuropsychology Central

[208er]

I recently conducted a neuro eval on a pt being assessed to determine dementia etiology...vascular v. alzheimers. He has a rather extensive hx of vascular d/o's....a left hemisphere stroke (temporoparietal region) in 98 and seizure activity in 01. It wasn't noted but i'm assuming it was a ischemic stroke and not a hemorrhagic one cuz he's currently on blood thinners...if it were hemorrhagic, that'd be just plain cruel. He is currently suffering from dysphasia s/p '98 cva and recently experiencing numbness in his left leg, likely owing to a current right caratoid artery bruit. He's also been suffering from dep. and sig hearing loss since the cva, but his cognitive probs are beyond the scope expected from dep and hearing loss. Anyway, it was difficult to tease out what were his actual cognitive deficits and what sections were beyond his scope of comprehension due to the dysphasia and hearing difficulty. The gestalt of his constructions were impressive and intact, save a complex 3-D cube, which could indicate some FL dysfunction, and lend further support to a VaD instead of AD. Set establishing, shifting and maintaining were poor and there were frequent perseveration errors. So i'm thinking that pretty much all signs are pointing to a VaD instead of AD, but i'm just hung up on the fact that the ver. learning tasks may be suspect due to the dysphasia/comprehension difficulties. Just wanted to get some feedback before making my recommendation...any other background hx i should investigate? It's sounding like a relatively clear cut case of VaD but just wanna be sure...thanks for any input

[Paendrag]

Naming?
Anosmia?
Visual learning intact?
What kind of aphasia?
Phonemic vs semantic fluency performance?
finger agnosia?
Independent living skills?
How severe is the dementia?

[lash]

I have a silly question, but since you're talking about a dementia eval, how's his memory performance? Also, his processing speed and his digit span?
_________________
Lee Ashendorf, Ph.D.
Edith Nourse Rogers Memorial VA
Co-Webmaster, Neuropsychology Central

[208er]

1. His naming was fine
2. No anosmia
3. Visual learning was impaired
4. As he had difficulty with receptive and expressive langauge, i'm thinking it was a transcortical aphasia, i'm not positive though (still learning )
5. speech seemed to be semantically fluent
6. no finger agnosia
7. independent living skills seemed moderately intact as he would still do household chores according to his spouse, and for some reason was still driving...though i question the accuracy of his spouse's historical accounts
8. it's difficult to tell how severe the dementia is as it was tough to tease out what his actual cognitive deficits were as opposed to what he could simply not understand due to the dysphasia



His memory performance was impaired across both verbal and visual tasks. He performed better on the visual tasks, not sure if it's because he didn't have to comprehend language in order to understand them or if it's because his right hem is less compromised than his left due to the left hem cva.......his processing speed was slower than what would appear normal, didn't haev a quantified measure on the battery but a few tasks, although not the main measure, do display processing speed. Also didn't do digit span, even if i did, i'm unsure as to his ability to comprehend the task and repeat what i said due to dysphasia....again, although there was not a specific test for it, his working memory appeared to be less functinoal than normal

[lash]

So, the interpretive dilemma is, I'd have trouble on verbal learning tasks too if I had significant receptive and expressive language impairments. Did you test anosmia or were you just saying there's no report of anosmia? I assume you didn't test it, but if you did then that would also argue against Alzheimer's. In any event, I wouldn't diagnose AD just because all the cool kids do it. If it looks like a duck, and quacks like a duck, why complicate things? Particularly in light of intact naming, without anything that seems wholly consistent with Alzheimer's, I'd probably say most of the deficits appear to be due to ischemic factors (especially the stroke, of course).