Greetings All,
There are a number of interesting articles in this month's Archives
Neurology. I enclose the abstracts below.
See http://archneur.ama-assn.org/current.dtl
R
Alex Mitchell
Neuropathologic Substrate of Mild Cognitive Impairment
William R. Markesbery, Frederick A. Schmitt, Richard J. Kryscio, Daron
G. Davis, Charles D. Smith, and David R. Wekstein
Arch Neurol. 2006;63:38-46.
Objective To define the neuropathologic findings in amnestic mild
cognitive impairment (MCI) and early Alzheimer disease (EAD).
Methods The mean numbers of diffuse plaques, neuritic plaques (NPs),
and neurofibrillary tangles (NFTs) in 4 neocortical regions and 4
ventromedial temporal lobe regions were counted in 10 patients with
amnestic MCI and compared with the mean numbers in 23 normal control
subjects and 10 patients with EAD, and then were compared with memory
performance. All of the controls and patients were followed
longitudinally.
Results Patients with MCI showed no significant difference (P>.05) in
the number of diffuse plaques from that in normal controls or patients
with EAD. In patients with MCI, the number of NPs was significantly
elevated in all 4 neocortical regions and amygdala compared with
controls (P<.01 to <.001). There were no significant differences (P>.05)
in the number of NPs between MCI and EAD cerebral cortex, but
significant increases were present for NPs in EAD amygdala and subiculum
compared with MCI (P<.01). In patients with MCI compared with controls,
the only significant increase in NFTs in the neocortex was in the
parietal lobe. However, the number of NFTs was significantly elevated in
MCI in all 4 ventromedial temporal lobe structures compared with
controls (P<.01 to <.001). In comparing MCI with EAD, there were
significant increases in NFTs in EAD in frontal and temporal lobes,
amygdala, and subiculum (P<.01). The numbers of NPs and NFTs were
significantly elevated in all of the neocortical regions and
ventromedial temporal lobe regions in patients with EAD compared with
controls (P<.001). Memory function was significantly correlated with
NFTs in CA1 of the hippocampus (P<.01) and the entorhinal cortex
(P<.05).
Conclusions In patients with amnestic MCI who were followed
longitudinally, the early changes of Alzheimer disease were present. The
NFTs were slightly more prominent than -amyloid peptide deposition in
the progression from normal to MCI to EAD. Ventromedial temporal lobe
NFTs probably represent the substrate for memory decline in MCI. From a
neuropathologic perspective, it appears that amnestic MCI is, in
reality, EAD.
Mild Cognitive Impairment Is Early-Stage Alzheimer Disease: Time to
Revise Diagnostic Criteria
John C. Morris
Arch Neurol. 2006;63:15-16.
Mild cognitive impairment (MCI) is the focus of intense research
interest as regards the early detection and treatment of Alzheimer
disease (AD). Although MCI can be a heterogeneous condition and may have
static or even reversible causes, the memory-predominant subtype,
amnestic MCI, is viewed as an important risk factor or prodrome for AD.
The characterization of amnestic MCI in large part comes from the
seminal work of Petersen and colleagues,1 who propose that it does not
constitute dementia but instead is a transitional stage between normal
aging and AD. Based on this premise, clinical trials of AD treatments
have been conducted in individuals with MCI to evaluate whether the
conversion to AD can be prevented or delayed.2
There is little evidence, however, to support the notion of a
transitional stage interposed between normal aging and AD. Alzheimer
disease is characterized by progressive synaptic and neuronal
dysfunction, and the . . . [Full Text of this Article]
Archives of Neurology Early Releases
for January 9, 2006
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Original Contributions
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Subjective Complaints Precede Parkinson Disease: The Rotterdam Study
Lonneke M. L. de Lau; Peter J. Koudstaal; Albert Hofman; Monique M.
B.
Breteler
Arch Neurol published 9 January 2006,
10.1001/archneur.63.3.noc50312
http://archneur.ama-assn.org/cgi/content/abstract/63.3.noc50312v1?etoc
Subjective Complaints Precede Parkinson Disease
The Rotterdam Study
Lonneke M. L. de Lau, MD; Peter J. Koudstaal, MD, PhD; Albert Hofman,
MD, PhD; Monique M. B. Breteler, MD, PhD
Arch Neurol. 2006;63:(doi:10.1001/archneur.63.3.noc50312).
Background Neuronal degeneration and dopamine loss in the preclinical
phase of Parkinson disease may produce subtle complaints before
clinically recognizable symptoms emerge.
Objective To examine whether subjective complaints of stiffness,
slowness, tremors, or postural imbalance in persons without clinical
signs of parkinsonism are related to an increased risk of future
Parkinson disease.
Design Population-based cohort study. We recorded subjective complaints
of stiffness, slowness of movement, tremors, falling, or a feeling of
imbalance in a standardized interview of 6038 participants without
dementia in whom no parkinsonian signs were found on physical
examination at baseline, and we studied them prospectively for the
occurrence of incident Parkinson disease.
Setting General population.
Participants A total of 6038 participants who were free of dementia and
parkinsonian signs.
Main Outcome Measures Incident Parkinson disease. Participants were
examined in person both at baseline (January 1990-June 1993) and at 2
follow-up visits (September 1993-December 1994 and April 1997-December
1999), and the cohort was continuously monitored through computerized
linkage of the study database to general practitioners' medical records.
We analyzed the data using Cox proportional hazards regression models.
Results Participants who reported stiffness, tremors, or imbalance at
baseline had a significantly increased risk of developing Parkinson
disease during follow-up (for stiffness, hazard ratio, 2.11; 95%
confidence interval, 1.25-3.55; P = .005; for tremors, hazard ratio,
2.09; 95% confidence interval, 1.12-3.90; P = .002; and for imbalance,
hazard ratio, 3.47; 95% confidence interval, 1.69-7.00; P = .001).
Conclusions Subjective complaints of stiffness, tremors, and imbalance
are associated with an increased risk of future Parkinson disease and
may reflect early effects of dopamine shortage, even when standard
neurological testing cannot yet demonstrate any motor symptoms.
Published online January 9, 2006 (doi:10.1001/archneur.63.3.noc50312).
Diagnostic Testing for Dementia
Asking the Right Questions
E. S. Roach, MD
Arch Neurol. 2006;63:146-147.
New techniques may give answers to questions that have not been asked.
When this occurs, physicians may have difficulty determining if the new
information is valuable to the patient or valuable in research. Both are
important, but it is essential to be able to identify which is which.-J.
Willis Hurst
Dementia is a symptom complex, not a disease. There are numerous causes
of dementia, and some individuals have more than 1 risk factor.1
Disappointingly, few people with dementia have treatable conditions like
vitamin deficiencies or chronic infections, and no one argues against
testing for these and other reversible disorders. Sadly, most
individuals with progressive dementia do not have reversible diseases,
and the debate centers on the value of tests with less obvious practical
value.2-3
If, as Van Gool2 believes, the usefulness of a diagnosis ultimately
hinges on whether it benefits the . . . [Full Text of this Article]
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