The role of the right inferior frontal gyrus in the pathogenesis of post-stroke psychosis.

Psychotic symptoms have previously been reported following right hemisphere brain injury. We sought to identify the specific neuroanatomical basis of delusions following stroke by studying a series of patients with post-stroke psychosis. Lesion overlap analysis was conducted on three individuals with delusions following right hemisphere stroke. These cases were compared with a control group of patients with similar anatomical damage. The main outcome measures were presence of delusions and presence of behavioural susceptibility. The right inferior frontal gyrus and underlying white matter, including the superior longitudinal fasciculus and anterior corona radiata, were involved in all three cases. All three had a preexisting untreated psychiatric disorder. In contrast, only one of nine control cases with equivalent lesions had evidence of previous psychiatric disorder (p = 0.0182, Fisher’s exact test), and this was being treated at the time of stroke. We provide clinical evidence from patients with structural brain lesions implicating damage to the right inferior frontal lobe in the generation of persistent psychosis following stroke. We suggest that preexisting psychiatric disease provided a behavioural susceptibility to develop delusions in these individuals. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00415-014-7242-x) contains supplementary material, which is available to authorized users

Study protocol: EXERcise and Cognition In Sedentary adults with Early-ONset dementia (EXERCISE-ON)

<p>Abstract</p> <p>Background</p> <p>Although the development of early-onset dementia is a radical and invalidating experience for both patient and family there are hardly any non-pharmacological studies that focus on this group of patients. One type of a non-pharmacological intervention that appears to have a beneficial effect on cognition in older persons without dementia and older persons at risk for dementia is exercise. In view of their younger age early-onset dementia patients may be well able to participate in an exercise program. The main aim of the EXERCISE-ON study is to assess whether exercise slows down the progressive course of the symptoms of dementia.</p> <p>Methods/Design</p> <p>One hundred and fifty patients with early-onset dementia are recruited. After completion of the baseline measurements, participants living within a 50 kilometre radius to one of the rehabilitation centres are randomly assigned to either an <it>aerobic exercise program in a rehabilitation centre</it> or a <it>flexibility and relaxation program in a rehabilitation centre</it>. Both programs are applied three times a week during 3 months. Participants living outside the 50 kilometre radius are included in a feasibility study where participants join in a <it>daily physical activity program set at home making use of pedometers</it>. Measurements take place at baseline (entry of the study), after three months (end of the exercise program) and after six months (follow-up). Primary outcomes are cognitive functioning; psychomotor speed and executive functioning; (instrumental) activities of daily living, and quality of life. Secondary outcomes include physical, neuropsychological, and rest-activity rhythm measures.</p> <p>Discussion</p> <p>The EXERCISE-ON study is the first study to offer exercise programs to patients with early-onset dementia. We expect this study to supply evidence regarding the effects of exercise on the symptoms of early-onset dementia, influencing quality of life.</p> <p>Trial registration</p> <p>The present study is registered within The Netherlands National Trial Register (ref: NTR2124)</p

Concordance and Discordance Between Brain Perfusion and Atrophy in Frontotemporal Dementia

The aim of this study was to determine if a dissociation between reduced cerebral perfusion and gray matter (GM) atrophy exists in frontotemporal dementia (FTD). The study included 28 patients with FTD and 29 cognitive normal (CN) subjects. All subjects had MRI at 1.5 T, including T1-weighted structural and arterial spin labeling (ASL) perfusion imaging. Non-parametric concordance/discordance tests revealed that GM atrophy without hypoperfusion occurs in the premotor cortex in FTD whereas concordant GM atrophy and hypoperfusion changes are found in the right prefrontal cortex and bilateral medial frontal lobe. The results suggest that damage of brain function in FTD, assessed by ASL perfusion, can vary regionally despite widespread atrophy. Detection of discordance between brain perfusion and structure in FTD might aid diagnosis and staging of the disease

Nuclear Imaging in Frontotemporal Dementia

Frontotemporal dementia (FTD) covers a range of heterogeneous neurodegenerative syndromes, predominantly affecting the frontal and temporal lobes (frontotemporal lobar degeneration or FTLD). Most patients present with behavioural deficits, executive dysfunction and language difficulties. FTD presents as clinically recognized subtypes with behavioural manifestation (FTD-b) and primary progressive aphasia (PPA), which can be divided into semantic dementia (SD), progressive nonfluent aphasia (PNFA) and logopenic aphasia (LPA). FTD is a common type of dementia, particularly at younger age. The underlying neuropathological process of FTLD leads to the clinical phenotype and can be characterized roughly in tauopathy (FTD-TAU) and TAR DNA-binding protein (TDP-43) pathology. Genetics is an important causal factor for FTD, and genetic heterogeneity is reflected by the identification of mutations in causative genes. Diagnostic criteria have modest sensitivity, and it may be challenging to differentiate FTD from psychiatric disorders or other types of dementia, especially AD. Advances in molecular imaging have increased the accuracy of FTD diagnosis, and nuclear imaging techniques improve the understanding of the molecular basis of FTD, which is important to develop rational therapies. Although currently no effective treatment is available for FTD, early and correct diagnosis is necessary for adequate clinical management, because of prognostic implications and for genetic counselling.</p

Neuroimaging in Psychiatric Disorders

In psychiatry, neuroimaging facilitates the diagnosis of psychiatric disorders and the development of new medications. It is used to detect structural lesions causing psychosis and to differentiate depression from neurodegenerative disorders or brain tumors. Functional neuroimaging, mostly in the form of molecular neuroimaging with positron emission tomography or single photon emission tomography, facilitates the identification of therapeutic targets, the determination of the dose of a new drug needed to occupy its target in the brain, and the selection of patients for clinical trials