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Article ; Online: Cognitive Complications of COVID-19 Infection.

Warren, Scott / Drake, Jonathan / Wu, Chuang-Kuo

Rhode Island medical journal (2013)

2022 Volume 105, Issue 7, Page(s) 27–30

Abstract: SARS-CoV-2 is associated with a post-infectious neurocognitive syndrome characterized by fatigue and deficits in attention, memory, and executive function. As screening cognitive testing generally remains normal, the pathophysiologic basis of these ... ...

Abstract	SARS-CoV-2 is associated with a post-infectious neurocognitive syndrome characterized by fatigue and deficits in attention, memory, and executive function. As screening cognitive testing generally remains normal, the pathophysiologic basis of these symptoms remains controversial and there is no standardized treatment paradigm. We present a clinical case demonstrative of typical neurocognitive sequelae of SARS-CoV-2 infection, highlighting medical and social factors that may have contributed to the severity of symptoms. We discuss the pathophysiologic evidence for cognitive "brain fog" following COVID-19 infection as well as lifestyle changes and rehabilitation strategies that may improve recovery. As the benefits of pharmacologic therapy remain unproven, we close with a brief discussion of medication options that might be appropriate targets for future clinical trials in the context of rehabilitative treatment.
MeSH term(s)	COVID-19/complications ; Cognition ; Executive Function/physiology ; Humans ; Neuropsychological Tests ; SARS-CoV-2
Language	English
Publishing date	2022-09-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	419430-5
ISSN	2327-2228 ; 0363-7913
ISSN (online)	2327-2228
ISSN	0363-7913
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Article: Parkinson's disease with dementia, lewy-body disorders and alpha-synuclein: recent advances and a case report.

Wu, Chuang-Kuo

Acta neurologica Taiwanica

2011 Volume 20, Issue 1, Page(s) 4–14

Abstract: The advance in research on the dementia syndrome associated with Parkinson's disease recently gains momentum in part because Parkinson's disease inevitably causes declined cognition and then lead to poor quality of life. More importantly, dementia of ... ...

Abstract	The advance in research on the dementia syndrome associated with Parkinson's disease recently gains momentum in part because Parkinson's disease inevitably causes declined cognition and then lead to poor quality of life. More importantly, dementia of Lewy bodies, now known as the second most common neurodegenerative disorder, shares the common neuropathological hallmark with Parkinson's disease and yet exhibits a unique clinical syndrome. Recent genetic, neurochemical and neuropsychological experiments robustly confirm a link between dementia associated with Parkinson's disease and dementia with Lewy bodies. Meanwhile, controversial issues regarding diagnostic criteria and proper treatments remain unresolved. Here I review milestone research conclusions and report a typical case with pathological data in order to clarify different aspects of these two dementia disorders.
MeSH term(s)	Aged, 80 and over ; Cognition Disorders/etiology ; Dementia/complications ; Dementia/history ; Dementia/metabolism ; Female ; History, 18th Century ; History, 19th Century ; Humans ; Lewy Bodies/metabolism ; Lewy Bodies/pathology ; Lewy Body Disease/complications ; Lewy Body Disease/history ; Lewy Body Disease/metabolism ; Parkinson Disease/complications ; Parkinson Disease/history ; Parkinson Disease/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2011-03
Publishing country	China (Republic : 1949- )
Document type	Case Reports ; Historical Article ; Journal Article ; Review
ZDB-ID	2192417-X
ISSN	1028-768X ; 1019-6099
ISSN	1028-768X ; 1019-6099
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Article: Mild cognitive impairment, healthy aging and Alzheimer's disease.

Wu, Chuang-Kuo

Medicine and health, Rhode Island

2008 Volume 91, Issue 5, Page(s) 132–133

MeSH term(s)	Aged ; Aged, 80 and over ; Aging ; Alzheimer Disease/diagnosis ; Alzheimer Disease/drug therapy ; Alzheimer Disease/physiopathology ; Cognition ; Cognition Disorders/diagnosis ; Geriatric Assessment ; Health Status ; Humans ; Neuropsychological Tests ; Psychological Tests
Language	English
Publishing date	2008-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1317172-0
ISSN	2163-5730 ; 1086-5462
ISSN (online)	2163-5730
ISSN	1086-5462
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Article: Cholinergic neuronal and axonal abnormalities are present early in aging and in Alzheimer disease.

Geula, Changiz / Nagykery, Nicholas / Nicholas, Alexander / Wu, Chuang-Kuo

Journal of neuropathology and experimental neurology

2008 Volume 67, Issue 4, Page(s) 309–318

Abstract: A large body of evidence indicates that basal forebrain cholinergic neurons are selectively vulnerable to degeneration early in Alzheimer disease (AD). Recent studies, however, demonstrate reductions in cortical activity of the cholinergic enzyme choline ...

Abstract	A large body of evidence indicates that basal forebrain cholinergic neurons are selectively vulnerable to degeneration early in Alzheimer disease (AD). Recent studies, however, demonstrate reductions in cortical activity of the cholinergic enzyme choline acetyltransferase only in late stages of AD. To address this apparent contradiction, we compared abnormalities in magnocellular basal forebrain cholinergic neurons and their axons in nondemented young (<65 years; n = 6), nondemented old (>65 years; n = 7), pathologically mild (n = 5), and pathologically severe (n = 5) AD cases. Cholinergic axon abnormalities (i.e. thickened fibers and ballooned terminals) were evident in nondemented middle-aged cases, increased in nondemented old cases, and reduced in density in severe AD. This suggests that loss of cortical cholinergic axons in AD occurs preferentially in fibers with these abnormalities. Paired helical filament 1-immunoreactive pretangles and tangles were observed as early as the third decade prior to their appearance in entorhinal/perirhinal cortex; they were increased in mild and severe AD. These results indicate that basal forebrain cholinergic neuron abnormalities are present very early in aging and in the course of AD. Therefore, despite the morphologic alterations, choline acetyltransferase activity, but not necessarily normal neuron functions, may be preserved.
MeSH term(s)	Adult ; Age Factors ; Aged ; Aged, 80 and over ; Aging/pathology ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Axons/pathology ; Cell Count/methods ; Choline O-Acetyltransferase/metabolism ; DNA-Binding Proteins/metabolism ; Female ; Humans ; Male ; Middle Aged ; Neurons/metabolism ; Neurons/pathology ; Polycomb-Group Proteins ; Postmortem Changes ; Prosencephalon/pathology ; Transcription Factors/metabolism
Chemical Substances	Amyloid beta-Peptides ; DNA-Binding Proteins ; PHF1 protein, human ; Polycomb-Group Proteins ; Transcription Factors ; Choline O-Acetyltransferase (EC 2.3.1.6)
Language	English
Publishing date	2008-04-01
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1097/NEN.0b013e31816a1df3
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Article: Pharmacotherapy of dementia with Lewy bodies.

Fernandez, Hubert H / Wu, Chuang-Kuo / Ott, Brian R

Expert opinion on pharmacotherapy

2003 Volume 4, Issue 11, Page(s) 2027–2037

Abstract: The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical ...

Abstract	The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical syndrome separate from Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, a consensus workshop in 1995 established a new set of diagnostic criteria. Dementia that precedes or accompanies the onset of spontaneous (i.e., not neuroleptic-induced) Parkinsonism is termed DLB. In addition, fluctuations in alertness, cognition and function and visual hallucinations are emphasised and included as core features of DLB. The degree to which an individual patient exhibits cognitive impairment, behavioural problems and Parkinsonian features is variable. Therefore, treatment must be individualised. Although there are no officially approved drugs for DLB, limited experience from clinical trials, as well as past experience with the treatment of AD and PD patients, provide some basis for making drug choices. The cholinergic deficit seen in DLB makes cholinesterase inhibitor drugs the mainstay of treatment for cognitive impairment. This class of drugs has also shown therapeutic benefit in reducing hallucinations and other neuropsychiatric symptoms of the disease. Because of their relatively greater therapeutic window, cholinesterase inhibitors are also used as first-line therapy for the treatment of psychosis in DLB. Patients with DLB are extremely sensitive to the extrapyramidal side effects of neuroleptic medications. Thus, only atypical antipsychotic agents such as quetiapine, should be considered as alternative treatment for psychosis. Anxiety and depression are best treated with selective serotonin re-uptake inhibitors, whereas REM sleep behaviour disorder may be treated with low dose clonazepam. Parkinsonism responds to dopaminergic agents; however, precipitation or aggravation of hallucinosis may occur. Levodopa is preferred over dopamine agonists due to its lower propensity to cause hallucinations and somnolence. As the diagnostic criteria for DLB become more refined and validated by postmortem studies, it is hoped that rigorous, well-designed trials will be performed, aimed at alleviating the primary target symptoms of dementia, psychosis and Parkinsonism.
MeSH term(s)	Antipsychotic Agents/therapeutic use ; Autonomic Nervous System Diseases/drug therapy ; Autonomic Nervous System Diseases/etiology ; Behavior/drug effects ; Cognition/drug effects ; Cognition Disorders/drug therapy ; Cognition Disorders/etiology ; Humans ; Lewy Body Disease/complications ; Lewy Body Disease/drug therapy ; Lewy Body Disease/pathology ; Lewy Body Disease/psychology ; Parkinson Disease/drug therapy ; Parkinson Disease/etiology
Chemical Substances	Antipsychotic Agents
Language	English
Publishing date	2003-08-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2001535-5
ISSN	1465-6566
ISSN	1465-6566
DOI	10.1517/14656566.4.11.2027
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Zs.A 5130: Show issues

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Article: Amyloid-beta deposits in the cerebral cortex of the aged common marmoset (Callithrix jacchus): incidence and chemical composition.

Geula, Changiz / Nagykery, Nicholas / Wu, Chuang-Kuo

Acta neuropathologica

2002 Volume 103, Issue 1, Page(s) 48–58

Abstract: The incidence, distribution and chemical composition of amyloid-beta (A beta) peptide-positive deposits were investigated in the lower primate species common marmoset (Callithrix jacchus). No A beta deposits were observed in the brains of 7 marmosets ... ...

Abstract	The incidence, distribution and chemical composition of amyloid-beta (A beta) peptide-positive deposits were investigated in the lower primate species common marmoset (Callithrix jacchus). No A beta deposits were observed in the brains of 7 marmosets below 7 years of age. In 15 marmosets above 7 years, 60% displayed cortical A beta-immunoreactive plaques, 80% had A beta deposited in intracortical vessels and 87% displayed A beta deposits in meningeal vessels. The cerebral cortex of the oldest animal (15 years) contained a substantial density of deposits. A beta-immunoreactive plaques were found predominantly in association cortical zones followed by a lower density in paralimbic cortical areas. Deposits within vessels were most frequent in occipital cortex. A beta40 was found primarily in vascular deposits, while A beta42 was present in plaques. Approximately 20% of plaques and most vascular deposits displayed thioflavin S staining, indicative of the presence of fibrillar A beta. Varying proportions of A beta deposits contained acetylcholinesterase or butyrylcholinesterase activities and apolipoprotein E and alpha1-antichymotrypsin immunoreactivity. A few plaques contained immunoreactivity for amyloid precursor protein in swollen neurites. However, no abnormally phosphorylated tau immunoreactivity was present in these neurites. Survival analysis in a colony of marmosets indicated that only 6% of animals can be expected to survive beyond 7 years of age. These results indicate that the aged marmoset brain displays A beta deposits with a distribution and chemical composition similar to those found in the human. These similarities suggest that the aged marmoset may be a useful lower primate model for the study of the pathological effects of A beta. However, the relatively small number of animals which can be expected to reach old age severely limits the utility of this species as a model of A beta deposition.
MeSH term(s)	Aging/pathology ; Amyloid beta-Peptides/analysis ; Animals ; Apolipoproteins E/analysis ; Brain Diseases/epidemiology ; Brain Diseases/mortality ; Brain Diseases/pathology ; Callithrix ; Cerebral Cortex/chemistry ; Cerebral Cortex/enzymology ; Cerebral Cortex/pathology ; Cholinesterases/analysis ; Disease Models, Animal ; Female ; Incidence ; Male ; Neurites/chemistry ; Neurites/enzymology ; Neurites/pathology ; Peptide Fragments/analysis ; Plaque, Amyloid/chemistry ; Plaque, Amyloid/enzymology ; Plaque, Amyloid/pathology ; Survival Analysis ; Thiazoles/analysis ; alpha 1-Antichymotrypsin/analysis
Chemical Substances	Amyloid beta-Peptides ; Apolipoproteins E ; Peptide Fragments ; Thiazoles ; alpha 1-Antichymotrypsin ; amyloid beta-protein (1-40) ; amyloid beta-protein (1-42) ; thioflavin T (2390-54-7) ; Cholinesterases (EC 3.1.1.8)
Language	English
Publishing date	2002-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s004010100429
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Article ; Online: Age-related loss of calcium buffering and selective neuronal vulnerability in Alzheimer's disease.

Riascos, David / de Leon, Dianne / Baker-Nigh, Alaina / Nicholas, Alexander / Yukhananov, Rustam / Bu, Jing / Wu, Chuang-Kuo / Geula, Changiz

Acta neuropathologica

2011 Volume 122, Issue 5, Page(s) 565–576

Abstract: The reasons for the selective vulnerability of distinct neuronal populations in neurodegenerative disorders are unknown. The cholinergic neurons of the basal forebrain are vulnerable to pathology and loss early in Alzheimer's disease and in a number of ... ...

Abstract	The reasons for the selective vulnerability of distinct neuronal populations in neurodegenerative disorders are unknown. The cholinergic neurons of the basal forebrain are vulnerable to pathology and loss early in Alzheimer's disease and in a number of other neurodegenerative disorders of the elderly. In the primate, including man, these neurons are rich in the calcium buffer calbindin-D(28K). Here, we confirm that these neurons undergo a substantial loss of calbindin in the course of normal aging and report a further loss of calbindin in Alzheimer's disease both at the level of RNA and protein. Significantly, cholinergic neurons that had lost their calbindin in the course of normal aging were those that selectively degenerated in Alzheimer's disease. Furthermore, calbindin-containing neurons were virtually resistant to the process of tangle formation, a hallmark of the disease. We conclude that the loss of calcium buffering capacity in these neurons and the resultant pathological increase in intracellular calcium are permissive to tangle formation and degeneration.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Aging/metabolism ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Autopsy ; Calbindins ; Calcium/metabolism ; Cholinergic Neurons/metabolism ; Cholinergic Neurons/pathology ; Female ; Humans ; Male ; Middle Aged ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Neurofibrillary Tangles/metabolism ; Neurofibrillary Tangles/pathology ; Prosencephalon/metabolism ; Prosencephalon/pathology ; S100 Calcium Binding Protein G/metabolism
Chemical Substances	Calbindins ; S100 Calcium Binding Protein G ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-08-27
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-011-0865-4
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Article: Loss of calbindin-D28K from aging human cholinergic basal forebrain: relation to plaques and tangles.

Geula, Changiz / Nagykery, Nicholas / Wu, Chuang-Kuo / Bu, Jing

Journal of neuropathology and experimental neurology

2003 Volume 62, Issue 6, Page(s) 605–616

Abstract: Reports from our laboratory have indicated a substantial and specific loss of the calcium binding protein calbindin-D28K (CB) from the human basal forebrain cholinergic neurons (BFCN) in the course of normal aging. In the present set of experiments we ... ...

Abstract	Reports from our laboratory have indicated a substantial and specific loss of the calcium binding protein calbindin-D28K (CB) from the human basal forebrain cholinergic neurons (BFCN) in the course of normal aging. In the present set of experiments we determined the relationship between the age-related loss of CB and the presence and density of plaques and tangles in the brains of normal elderly. In 23 cases ranging in age from 20 to 93 years of age we observed plaques and tangles in the BFCN region and the cerebral cortex in a subset of cases. Plaques were seen in the basal forebrain in very few cases above 65 years. Plaque density in the basal forebrain and cortex displayed a significant negative correlation with the proportion of the BFCN, which contained CB immunoreactivity. However, the brains of 2 elderly cases that displayed a substantial loss of CB from the BFCN did not contain any plaques. Tangles were observed in the BFCN as early as 26 years of age. Only tangles in the entorhinal cortex showed a significant negative correlation with the loss of CB from the BFCN. It is likely that loss of CB from the BFCN and formation of plaques and tangles are part of general age-related processes that occur in parallel rather than being causally related.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Aging/metabolism ; Aging/pathology ; Amyloid beta-Peptides/metabolism ; Calbindin 1 ; Calbindins ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Choline O-Acetyltransferase/metabolism ; Female ; Humans ; Immunohistochemistry/methods ; Male ; Middle Aged ; Neurofibrillary Tangles/metabolism ; Neurofibrillary Tangles/pathology ; Neurons/metabolism ; Neurons/pathology ; Plaque, Amyloid/metabolism ; Plaque, Amyloid/pathology ; Prosencephalon/metabolism ; Prosencephalon/pathology ; S100 Calcium Binding Protein G/metabolism
Chemical Substances	Amyloid beta-Peptides ; CALB1 protein, human ; Calbindin 1 ; Calbindins ; S100 Calcium Binding Protein G ; Choline O-Acetyltransferase (EC 2.3.1.6)
Language	English
Publishing date	2003-05-16
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/62.6.605
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Article: Apoptotic signals within the basal forebrain cholinergic neurons in Alzheimer's disease.

Wu, Chuang-Kuo / Thal, Leon / Pizzo, Donald / Hansen, Lawrance / Masliah, Eliezer / Geula, Changiz

Experimental neurology

2005 Volume 195, Issue 2, Page(s) 484–496

Abstract: A relatively early and substantial loss of basal forebrain cholinergic neurons is a constant feature of Alzheimer's disease (AD). However, the mechanisms that contribute to the selective vulnerability of these neurons are not fully delineated. In the ... ...

Abstract	A relatively early and substantial loss of basal forebrain cholinergic neurons is a constant feature of Alzheimer's disease (AD). However, the mechanisms that contribute to the selective vulnerability of these neurons are not fully delineated. In the present series of experiments, we determined the possible contribution of apoptotic processes and other pathologic cascades to the degeneration of the cholinergic neurons of the nucleus basalis of Meynert (NBM) in AD. In contrast to neurons in the frontal cortex which showed prominent DNA fragmentation as detected by the TUNEL method, no DNA fragmentation was observed within the NBM in any of the AD or normal brains. Similarly, immunoreactivity for the apoptotic signals Fas, Fas-ligand, Bax, Bcl-x, caspase-8, caspase-9 and caspase-3 was absent from the NBM of AD and control brains. In contrast, a substantial subpopulation of cholinergic neurons within the NBM in AD displayed prominent immunoreactivity for the apoptotic signal Fas-associated death domain (FADD) in the form of tangles. FADD immunoreactivity was also present in dystrophic neurites. FADD-positive tangle-like structures were localized in neurons which contained immunoreactivity for the cholinergic marker choline acetyltransferase (ChAT) and the low affinity neurotrophin receptor p75NTR. While many of the NBM cholinergic neurons in control brains contained immunoreactivity for the calcium binding protein calbindin-D28K (CB), the NBM neurons in AD displayed a substantial loss of CB immunoreactivity. Importantly, most of FADD-immunoreactive cholinergic neurons were devoid of CB immunoreactivity, and, conversely, most CB-positive cholinergic neurons had no FADD immunoreactivity. FADD immunoreactivity within the basal forebrain was colocalized with phosphorylated tau immunoreactive tangles and dystrophic neurites. In contrast, FADD immunoreactivity did not appear to be related to the primarily diffuse amyloid-beta deposits intermingled between cholinergic neurons in AD NBM. Finally, many CD68-positive microglia were observed surrounding the NBM cholinergic neurons in AD. In conclusion, the findings of the present study indicate that, while the FADD apoptotic signaling pathway may be triggered within the basal forebrain cholinergic neurons in AD, the apoptotic cascade is most likely aborted as no DNA fragmentation was detected and the executioner caspase-3 was not up-regulated within these neurons. The findings also suggest possible relationships between loss of CB, FADD expression and phosphorylation of tau within the basal forebrain cholinergic neurons in AD.
MeSH term(s)	Acetylcholine/metabolism ; Adult ; Aged ; Aged, 80 and over ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Apoptosis/physiology ; Arabidopsis Proteins/metabolism ; Calbindin 1 ; Calbindins ; Choline O-Acetyltransferase/metabolism ; DNA Fragmentation/physiology ; Fatty Acid Desaturases/metabolism ; Female ; Humans ; Immunohistochemistry/methods ; In Situ Nick-End Labeling/methods ; Indoles ; Male ; Membrane Transport Proteins/metabolism ; Middle Aged ; Nerve Tissue Proteins/metabolism ; Neurons/cytology ; Neurons/metabolism ; Prosencephalon/pathology ; S100 Calcium Binding Protein G/metabolism ; Signal Transduction/physiology
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; Arabidopsis Proteins ; CALB1 protein, human ; CD68 antigen, human ; Calb1 protein, rat ; Calbindin 1 ; Calbindins ; Indoles ; Membrane Transport Proteins ; Nerve Tissue Proteins ; S100 Calcium Binding Protein G ; Slc15a4 protein, rat ; DAPI (47165-04-8) ; Fatty Acid Desaturases (EC 1.14.19.-) ; Fad7 protein, Arabidopsis (EC 1.14.99.-) ; Choline O-Acetyltransferase (EC 2.3.1.6) ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2005-10
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2005.06.020
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Article: Clinician assessment of the driving competence of patients with dementia.

Ott, Brian R / Anthony, David / Papandonatos, George D / D'Abreu, Anelyssa / Burock, Jeffrey / Curtin, Alicia / Wu, Chuang-Kuo / Morris, John C

Journal of the American Geriatrics Society

2005 Volume 53, Issue 5, Page(s) 829–833

Abstract: Objectives: To determine the validity and reliability of clinician ratings of the driving competence of patients with mild dementia.: Design: Observational study of a cross-section of drivers with mild dementia based on chart review by clinicians ... ...

Abstract	Objectives: To determine the validity and reliability of clinician ratings of the driving competence of patients with mild dementia. Design: Observational study of a cross-section of drivers with mild dementia based on chart review by clinicians with varying types of expertise and experience. Setting: Outpatient dementia clinic. Participants: Fifty dementia subjects from a longitudinal study of driving and dementia. Measurements: Each clinician reviewed information from the clinic charts and the first study visit. The clinician then rated the drivers as safe, marginal, or unsafe. A professional driving instructor compared these ratings with total driving scores on a standardized road test and categorical ratings of driving competence. Clinicians also completed a visual analog scale assessment of variables that led to their determinations of driving competence. Results: Accuracy of clinician ratings ranged from 62% to 78% for the instructor's global rating of safe versus marginal or unsafe. In general, there was moderate accuracy and interrater reliability. Accuracy could have been improved in the least-accurate raters by greater attention to dementia duration and severity ratings, as well as less reliance on the history and physical examination. The most accurate predictors were clinicians specially trained in dementia assessment, who were not necessarily the most experienced in their years of clinical experience. Conclusion: Although a clinician may be able to identify many potentially hazardous drivers, accuracy is insufficient to suggest that a clinician's assessment alone is adequate to determine driving competence in those with mild dementia.
MeSH term(s)	Aged ; Alzheimer Disease/psychology ; Automobile Driving ; Dementia/psychology ; Humans ; Longitudinal Studies ; Mental Competency ; Physicians
Language	English
Publishing date	2005-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80363-7
ISSN	1532-5415 ; 0002-8614
ISSN (online)	1532-5415
ISSN	0002-8614
DOI	10.1111/j.1532-5415.2005.53265.x
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