I'm not sure what stage of training you're in exactly, but if a medical
student on morning rounds told me he'd ordered a CXR as part of a
dementia workup on a patient admitted the night before, I'd ask him to
justify it with more than a sentence in a book.

I've never been at a place where Kumar and Clark was considered the
bible of clinical medicine, and I have no opinion on it, but getting a
CXR for dementia is not an issue of what people really do versus what
the books say. Major texts (like Harrison's) do not recommend a CXR as
part of a dementia workup.

I'm pushing on this because you seem to have recognized that a CXR made
no sense (which caused your original post) and yet seem to be planning
to regurgitate this recommendation when asked (thus causing your fellow
students and perhaps some interns and residents to learn the wrong
workup for dementia) rather than planning to let people know that you
read the chapter that says this but can find no justification for the
recommendation. Honestly, if you get in trouble with some resident or
attending for questioning this sort of mistaken information in a book
that's a real problem.

If this is in the first two years and you're talking about paper exams
administered by nonclinicians, then I agree that the easier path may be
to answer the question as you've been taught, sadly.

COMMENT:

Oh, bad news. I'm afraid what's actually DONE is usually what you're
reading in your textbook. And most of it is a terrific waste of money.
Not quite as bad as the serial MRIs done by some docs every time some
demented person has a small change in mental status--- but still a lot
of money down the rat-hole. And one reason why medicare and medicaid
are in serious danger of pulling us all under, in the good old US of A.

There are cases in medicine where really high tech stuff saves money.
For example, if you think treating AIDS is expensive with modern HAART
therapy, try treating as we did in the bad old days when all there was,
was AZT or nothing.

PET/CT is a little bit like that. It's a decent quality CT done in the
same machine as a PET (like the CDI REACT scanner), so you get a
"2-fer", plus much better quality on localizing the PET image, since
you can superimpose the images. It can make the diagnosis of
Alzheimer's and rule out mass lesions like large tumors or chronic
subdurals, in one swoop. And it's pretty good at telling you about
multi-infarct processes also, since to the extent that these cause
dementia, they affect frontal lobe metabolism and you see that directly
on 19-FDG PET, just as you do on SPECT.

Remember, the reason you image the head in dementia is to get
information to rule out chronic subdural hematoma, tumor, and
hydrocephalus. These all increase intercranial pressure and so affect
the whole brain. Strokes
don't do that. And strokes don't cause dementia unless there are very
many of them. You can get all the gross info from a CT.

People do MRIs on demented people to look for diffuse white matter
changes and vascular dementia, but this is usually a mistake, because
the truth of the matter is that these aren't very specific. You can see
them in non-demented people too. You're looking for their *metabolic
effect,* in working up dementia and PET tells you that directly. In
theory, the newer MRI techniques (functional or fMRI) can also, but
using fMRI to evaluate dementia is still in the research phase. What's
actually being *done* out there, is to use conventional MRI on
dementia, and conventional MRI is not sensitive OR specific. PET picks
up Alzheimer's LONG before anything shows up on MRI, and PET will also
tell you if vascular changes in MRI are likely to be dementing or not,
by looking at cortical metabolism. So all of that doesn't leave much
place for the standard MRI at all--- yet it's still the most common
modality used on demented patients. In fact, it's often used again and
again and again on them. People have such a terrible urge to look
inside the head to see if there's anything grossly wrong, that they'll
do it over and over, even if they know they'll usually see nothing of
value. So long as they're not paying for it (a similar thing happens in
low back pain).

You will find that head imaging, particular MRI, is used often to
substitute for the careful neurological exam, which takes time that
nobody wants to pay the clinician for (but there's no escaping paying
for the MRI). And this is particularly egregious in dementia, where the
workup is slow and the medicare payments to the clinician are small.
But even here the system could save a lot of money if people would pay
attention to even the gross things. For example, the demented elderly
person with the shuffling gait might have any possible cause for
dementia, but the demented elderly person with a good well-coordinated
gait (and there are many of these) almost certainly does NOT have
vascular dementia (aka multi-infarct dementia). Yet another reason to
save yourself that useless MRI, which will at best will only tell you
the same, and at worst will confuse you by showing you incidental white
matter disease which isn't causing the dementia you see clinically.

Steve

1:Top Magn Reson Imaging. 2004 Dec;15(6):369-89.

Pathological aging of the brain: an overview.

Bastos Leite AJ, Scheltens P, Barkhof F.

Department of Radiology, Vrije Universiteit (VU) Medical Center,
Amsterdam, the Netherlands. A.bastosleite@vumc.nl

The number of elderly people is increasing rapidly and, therefore, an
increase in neurodegenerative and cerebrovascular disorders causing
dementia is expected. Alzheimer disease (AD) is the most common cause
of dementia. Vascular dementia, dementia with Lewy bodies, and
frontotemporal dementia are the most frequent causes after AD, but a
large proportion of patients have a combination of degenerative and
vascular brain pathology. Characteristic magnetic resonance (MR)
imaging findings can contribute to the identification of different
diseases causing dementia. The MR imaging protocol should include axial
T2-weighted images (T2-WI), axial fluid-attenuated inversion recovery
(FLAIR) or proton density-weighted images, and axial gradient-echo
T2*-weighted images, for the detection of cerebrovascular pathology.
Structural neuroimaging in dementia is
focused on detection of brain atrophy, especially in the medial
temporal lobe, for which coronal high resolution T1-weighted images
perpendicular to the long axis of the temporal lobe are extremely
important. Single photon emission computed tomography and positron
emission tomography may have added value in the diagnosis of dementia
and may become more important in the future, due to the development of
radioligands for in vivo detection of AD pathology. New functional MR
techniques and serial volumetric imaging studies to identify subtle
brain abnormalities may also provide surrogate markers for pathologic
processes that occur in diseases causing dementia and, in conjunction
with clinical evaluation, may enable a more rigorous and early
diagnosis, approaching the accuracy of neuropathology.

PMID: 16041289 [PubMed - in process]

2: Dement Geriatr Cogn Disord. 2005 May 20;20(2-3):63-70 [Epub ahead of
print]

Diagnostic Value of FDG-PET and HMPAO-SPET in Patients with Mild
Dementia and Mild Cognitive Impairment: Metabolic Index and Perfusion
Index.

Dobert N, Pantel J, Frolich L, Hamscho N, Menzel C, Grunwald F.

Department of Nuclear Medicine, University of Frankfurt, Frankfurt,
Germany.

Objective: The diagnostic potential of F-18-2-fluoro-2-deoxy-D-glucose
positron emission tomography (PET) and technetium-99m
hexamethylpropylene amine oxime single-photon emission tomography
(SPET) in early detection and differential diagnosis of early dementia
was evaluated including a comparison of metabolic and perfusion indices
(PI). Methods: Twenty-four patients with initial clinical suspicion of
beginning dementia were examined, 12 of them with mild cognitive
impairment. All patients underwent SPET and PET within 2 weeks. Data
were compared with the final clinical diagnosis at follow-up - 9 with
Alzheimer's disease (AD), 1 with frontotemporal dementia, 1 with
vascular dementia (VD), 7 with mixed type of dementia (MIX) and 6
without any type of dementia. Metabolic
indices (MI) and PI were compared with each other. The regional
cerebral blood flow difference (rCBFdiff) calculated as local uptake
difference between the right and left hemisphere was measured for
patients with VD and MIX. Results: PET showed higher sensitivity and
specificity in identifying the different types of early dementia (44-91
and 78-89%, respectively) than SPET (11-64 and 79-89%, respectively),
especially in detecting AD (sensitivity 44%, specificity 83%) and MIX
(sensitivity 71%, specificity 78%). Especially in patients with mild
cognitive impairment, PET was the superior imaging modality for
predicting dementia. Using PET, dementia could be excluded in all
patients who did not develop dementia during the follow-up. In all
patients, a weak correlation between PI and MI was observed (rho =
0.64, p < 0.002). The rCBFdiff in patients
with VD and MIX ranged from 7 to 37%. Conclusion: In this study on
patients with initial suspicion of beginning dementia who underwent
both imaging modalities, PET and SPET, PET was the superior imaging
method, especially in the detection of early AD or MIX. Copyright (c)
2005 S. Karger AG, Basel.

PMID: 15908747 [PubMed - as supplied by publisher]

3: Nucl Med Commun. 2005 Mar;26(3):189-96.

Emission tomography in dementia.

Pakrasi S, O'Brien JT.

Institute for Health and Ageing, Wolfson Research Centre, Newcastle
General
Hospital, Newcastle upon Tyne, NE4 6BE, UK. sanjeet.pakrasi@ncl.ac.uk

Dementia is a chronic brain syndrome with enormous impact on health
care
provision. Emission tomography (single photon emission computed
tomography
(SPECT) and positron emission tomography (PET)) provides a unique tool
to
investigate functional and neurochemical changes, both in those with
established dementia and in those at risk of subsequent cognitive
decline. Alzheimer's disease is characterized by bilateral
temporoparietal hypoperfusion on SPECT and hypometabolism on PET, which
may precede the onset of dementia as similar changes can be
demonstrated in those with mild cognitive impairment and in those
genetically at risk of developing Alzheimer's disease. In dementia with
Lewy bodies medial parietal and occipital perfusion deficits are seen
together with pre-synaptic and post-synaptic dopaminergic changes, most
particularly a reduction in the striatal pre-synaptic dopamine
transporter which can be visualized using appropriate ligands (e.g.,
(123)I-FP-CIT). Vascular dementia is
associated with multiple, asymmetric, perfusion deficits in
multi-infarct
dementia. In contrast, subcortical vascular dementia is associated with
reduced perfusion but preserved oxygen extraction fraction on PET.
Fronto-temporal dementia is characterized by both hypometabolism and
hypoperfusion in fronto-temporal lobes, though hypometabolism appears
more extensive, affecting large areas of the cerebral hemispheres.
Longitudinal studies of treatment response in Alzheimer's disease with
cholinergic drugs have found changes in regional blood flow and
nicotinic and muscarinic receptor function in those patients who
respond to treatment. Currently, emission tomography is widely used for
assisting with clinical differential diagnosis. Future developments
will entail the development and application of more specific
neurochemical ligands and those which bear a closer relationship to the
underlying disease processes,
including markers of tau, amyloid and synuclein pathology.

Publication Types:
   Review
   Review, Tutorial

PMID: 15722899 [PubMed - indexed for MEDLINE]

4: Arch Neurol. 2004 Oct;61(10):1545-50.

Effects of white matter lesions and lacunes on cortical function.

Reed BR, Eberling JL, Mungas D, Weiner M, Kramer JH, Jagust WJ.

University of California Davis Alzheimer's Disease Center, Martinez, CA
94553,USA. brreed@ucdavis.edu

BACKGROUND: Subcortical ischemic vascular dementia has been ascribed to
prominent frontal lobe dysfunction secondary to ischemic lesions in
frontothalamic circuits.Whether small-vessel disease in fact
predominantly
affects the frontal lobes is not well documented. OBJECTIVE: To
ivestigate the effects of subcortical lesions (lacunes and white matter
lesions [WML]) on cortical function, as reflected in glucose metabolism
and cognitive function, in elderly individuals. DESIGN: Cross-sectional
analyses of case series. SETTING: Multicenter, university-based study
of subcortical vascular dementia. PATIENTS: Persons with normal
cognition, mild cognitive impairment, or dementia and with and without
lacunes on magnetic resonance images. MAIN OUTCOME MEASURES: Regional
cerebral glucose metabolism, normalized regional metabolic activity,
and neuropsychological test scores. Major hypotheses were that volume
of lacunes and WML correlate selectively with hypometabolism of
prefrontal cortex and failure of executive cognitive ability. RESULTS:
Lacunes correlated with metabolic rates in dorsolateral frontal cortex
(DLF); WML substantially reduced metabolic rates throughout cortex,
most strongly so in DLF. When regional metabolic activity was
normalized to whole brain activity, lacunes remained correlated with
DLF activity, whereas the WML effect was no longer found, probably
because of its general distribution. Regional cerebral glucose
metabolism and normalized activity in DLF also correlated with cortical
atrophy. Metabolic activity in DLF correlated with executive function,
memory, and global cognitive function, while activity in middle
temporal gyrus correlated with memory and global function but not
executive function. CONCLUSIONS: The  metabolic effects of lacunes and
WML are most apparent in DLF, but the effects of WML are generalized
and frontal hypometabolism correlates with memory and
global impairment, cognitive as well as executive function. The effects
of
subcortical cerebrovascular disease appear to converge on the frontal
lobes but are diffuse, complex, and of modest magnitude.

Publication Types:
   Multicenter Study

PMID: 15477508 [PubMed - indexed for MEDLINE]

5: Neurology. 2004 Jul 27;63(2):246-53.

White matter lesions impair frontal lobe function regardless of their
location.

Tullberg M, Fletcher E, DeCarli C, Mungas D, Reed BR, Harvey DJ, Weiner
MW, Chui HC, Jagust WJ.

Department of Neurology, School of Medicine, University of California,
Davis, USA. mats.tullberg@neuro.gu.se

OBJECTIVE: To analyze the effect of white matter lesions in different
brain
regions on regional cortical glucose metabolism, regional cortical
atrophy, and cognitive function in a sample with a broad range of
cerebrovascular disease and cognitive function. METHODS: Subjects (n =
78) were recruited for a study of subcortical ischemic vascular disease
(SIVD) and Alzheimer disease (AD) contributions to dementia. A new
method was developed to define volumes of interest from high-resolution
three-dimensional T1-weighted MR images. Volumetric measures of MRI
segmented white matter signal hyperintensities (WMH) in five different
brain regions were related to regional PET glucose metabolism (rCMRglc)
in cerebral cortex, MRI measures of regional cortical atrophy, and
neuropsychological assessment of executive and memory function.
RESULTS: WMH was
significantly higher in the prefrontal region compared to the other
brain
regions. In all subjects, higher frontal and parietal WMH were
associated with reduced frontal rCMRglc, whereas occipitotemporal WMH
was only marginally associated with frontal rCMRglc. These associations
were stronger and more widely distributed in nondemented subjects where
reduced frontal rCMRglc was correlated with WMH for all regions
measured. In contrast, there was no relationship between WMH in any
brain region and rCMRglc in either parietal or occipitotemporal
regions. WMHs in all brain regions were associated with low executive
scores in nondemented subjects. CONCLUSIONS: The frontal lobes are most
severely affected by SIVD. WMHs are more abundant in the frontal
region. Regardless of where in the brain these WMHs are located, they
are associated with frontal hypometabolism and executive dysfunction.

PMID: 15277616 [PubMed - indexed for MEDLINE]

COMMENT:

First because PET/CT will show you a definite organic cause before
SPECT will, and certainly long before standard MRI or CT shows
anything. Thus you can save yourself the MRI and all the workup looking
for secondary causes. If all you have is a separate PET and a CT, you
can still do them both and save yourself the MRI and secondary cause
workup, if positive, and if negative, it can make you look for
secondary causes much more thoroughly.

This has a drastic effect on management. If you KNOW for certain that
your patient has early Alzheimers, you don't have to do a million
dollar workup every time they have a drastic cognitive change from a
UTI or flu or cold or whatever. You now have the guts to treat it and
wait it out without wondering of your patient is dying of meningitis or
stroke or whatever.

Second, it's getting more and more important to make a diagnosis of
cause of early dementia, because there's a lot you can do about the
diseases themselves. Certainly you can treat early vascular dementia
specifically to keep it from progressing, and probably wouldn't want to
do any of *that* (vigorous anti-stroke therapy and probably a statin)
to a patient with pure Alzheimer's.

We're beginning to get a glimmer of treatment option, even for
Alzheimer's disease. High dose vitamin E, fish oil, and
antinflamatories slow it a bit, and in the mouse model curcumen (from
the spice turmeric) actually disrupts AD plaques and stops the disease.
And Indians who eat a lot of turmeric (the main ingredient in curry)
have about quarter the AD incidence we have in the West. Google for a
lot more info. Too early to say if this will hold for humans, but if I
had early AD and knew it from PET, I would certainly be gulping E and
turmeric like crazy. It's benign (unlike antiplatelet therapy, or even
statins in the elderly without vascular risk factors). Surely other
more specific therapies for AD (though I dare say a lot more expensive
than an Indian spice) are just around the corner.

SBH