MCI as an entity is evolving and somewhat controversial. The MoCA is a brief cognitive screening tool with high sensitivity and specificity for detecting MCI as currently conceptualized in patients performing in the normal range on the MMSE.

Sir: Clinicians are often reluctant to use psychomotor stimulants in patients with disinhibition from frontal lobe dysfunction because of the concern that these medications will worsen behaviors or result in psychosis. 1 We contrasted the effects of dex-troamphetamine and quetiapine, an atypical antipsychotic often used to treat agitation in dementia patients with cognitive and behavioral symptoms, in 8 patients with behavioral-variant frontotemporal dementia (FTD) in a double-blind crossover trial. We were interested in testing a stimulant for several reasons: (1) there is autopsy, cerebrospinal fluid, and imaging evidence of dopaminergic deficiencies in FTD (reviewed in Huey et al. 2); (2) there is a clinical association between FTD and basal ganglia dopaminergic dysfunction (i.e., parkinsonism) 3 ; and (3) executive dysfunction associated with psychiatric illness (e.g., attention-deficit/hyperactivity disorder) can improve with do-pamine augmentation. 4 Method. All 8 patients had behavioral symptoms. Over 1 week, medication daily dosage was gradually increased to either 20 mg of dextroamphetamine or 150 mg of quetiapine in divided doses. The patients returned home on the target dose for 3 weeks before returning to our clinic for reevaluation. At this point, the patients were tapered to half the study medication for 2 days before discontinuation and then underwent washout for 1 week, and the process was then repeated with the other medication. Medication order was randomized, and the patients, care-givers, and clinicians were blinded to the order. The individuals assigned durable power of attorney by the patients provided written consent, and all patients gave assent. The study was approved by an institutional review board and was conducted from November 2004 to August 2006. The primary measure of behavioral symptoms was the Neuropsychiat-ric Inventory (NPI), 5 and the primary cognitive measure was the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). 6 Results. All patients were able to tolerate the full dose of dextroamphetamine. One patient experienced sedation on que-tiapine treatment and was unable to tolerate the full dose. The most common adverse effect of both medications was sleep disturbance. The results for the total NPI can be seen in Figure 1. Using nonparametric methods (a 2-tailed Friedman test), there was a significant effect of treatment on the total NPI (p = .05). Post hoc Wilcoxon signed-rank tests showed that the total NPI was significantly lower than pretreatment baseline on dextro-amphetamine (p = .02), but there was no significant difference between baseline and quetiapine, nor between quetiapine and dextroamphetamine. The NPI subscales that decreased the most on dextroamphetamine were apathy (2.8 points) and disinhibi-tion (2.4 points). There was no significant overall effect of treatment on the RBANS. The order of magnitude of this effect is large compared to that observed in pharmacologic trials for behavioral symptoms of Alzheimer's disease. A summary of ava...

The criteria ought to provide the foundation for research work into the neuropsychology, neuropathology, genetics, molecular biology, and epidemiology of these important clinical disorders that account for a substantial proportion of cases of primary degenerative dementia occurring before the age of 65 years.

The dementia with Lewy bodies (DLB) Consortium has revised criteria for the clinical and pathologic diagnosis of DLB incorporating new information about the core clinical features and suggesting improved methods to assess them. REM sleep behavior disorder, severe neuroleptic sensitivity, and reduced striatal dopamine transporter activity on functional neuroimaging are given greater diagnostic weighting as features suggestive of a DLB diagnosis. The 1-year rule distinguishing between DLB and Parkinson disease with dementia may be difficult to apply in clinical settings and in such cases the term most appropriate to each individual patient should be used. Generic terms such as Lewy body (LB) disease are often helpful. The authors propose a new scheme for the pathologic assessment of LBs and Lewy neurites (LN) using alpha-synuclein immunohistochemistry and semiquantitative grading of lesion density, with the pattern of regional involvement being more important than total LB count. The new criteria take into account both Lewy-related and Alzheimer disease (AD)-type pathology to allocate a probability that these are associated with the clinical DLB syndrome. Finally, the authors suggest patient management guidelines including the need for accurate diagnosis, a target symptom approach, and use of appropriate outcome measures. There is limited evidence about specific interventions but available data suggest only a partial response of motor symptoms to levodopa: severe sensitivity to typical and atypical antipsychotics in approximately 50%, and improvements in attention, visual hallucinations, and sleep disorders with cholinesterase inhibitors.

Criteria for the diagnosis of vascular dementia (VaD) that are reliable, valid, and readily applicable in a variety of settings are urgently needed for both clinical and research purposes. To address this need, the Neuroepidemiology Branch of the National Institute of Neurological Disorders and Stroke (NINDS) convened an International Workshop with support from the Association Internationale pour la Recherche et l'Enseignement en Neurosciences (AIREN), resulting in research criteria for the diagnosis of VaD. Compared with other current criteria, these guidelines emphasize (1) the heterogeneity of vascular dementia syndromes and pathologic subtypes including ischemic and hemorrhagic strokes, cerebral hypoxic-ischemic events, and senile leukoencephalopathic lesions; (2) the variability in clinical course, which may be static, remitting, or progressive; (3) specific clinical findings early in the course (eg, gait disorder, incontinence, or mood and personality changes) that support a vascular rather than a degenerative cause; (4) the need to establish a temporal relationship between stroke and dementia onset for a secure diagnosis; (5) the importance of brain imaging to support clinical findings; (6) the value of neuropsychological testing to document impairments in multiple cognitive domains; and (7) a protocol for neuropathologic evaluations and correlative studies of clinical, radiologic, and neuropsychological features. These criteria are intended as a guide for case definition in neuroepidemiologic studies, stratified by levels of certainty (definite, probable, and possible). They await testing and validation and will be revised as more information becomes available.

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Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. Specific criteria for the clinical diagnosis of dementia associated with PD (PD‐D), however, have been lacking. A Task Force, organized by the Movement Disorder Study, was charged with the development of clinical diagnostic criteria for PD‐D. The Task Force members were assigned to sub‐committees and performed a systematic review of the literature, based on pre‐defined selection criteria, in order to identify the epidemiological, clinical, auxillary, and pathological features of PD‐D. Clinical diagnostic criteria were then developed based on these findings and group consensus. The incidence of dementia in PD is increased up to six times, point‐prevelance is close to 30%, older age and akinetic‐rigid form are associated with higher risk. PD‐D is characterized by impairment in attention, memory, executive and visuo‐spatial functions, behavioral symptoms such as affective changes, hallucinations, and apathy are frequent. There are no specific ancillary investigations for the diagnosis; the main pathological correlate is Lewy body‐type degeneration in cerebral cortex and limbic structures. Based on the characteristic features associated with this condition, clinical diagnostic criteria for probable and possible PD‐D are proposed. © 2007 Movement Disorder Society