Although the development of functional imaging techniques has established the implication of the amygdala in the emotional process, its specific role remains controversial. The aim of this study was to highlight the sensitivity of the amygdala to emotional intensity (arousal). We conducted an analysis of the modulation of amygdala activation according to variation in emotional intensity via an fMRI event-related protocol. Monitoring of electrodermal activity, a marker of psychophysiological emotional perception and which reflects the activation of the autonomic nervous system, was carried out concurrently. Eighteen subjects (10 men; aged from 22 to 29 years) looked at emotionally positive photographs. We demonstrated that the left and right amygdalae were sensitive to changes in emotional intensity, activating more in response to stimuli with higher intensity. Furthermore, electrodermal responses were more frequent for the most intense stimuli, demonstrating the concomitant activation of the autonomic nervous system. These results highlight the sensitivity of the amygdala to the intensity of positively-valenced visual stimuli, and in conjunction with results in the literature on negative emotions, reinforce the role of the amygdala in the perception of intensity.

We present a brain map of the areas supplied by various arteries in the brainstem, cerebellum and cerebral hemispheres. Arterial territories are depicted in a form that is directly applicable to neuroimaging slices in clinical practice. The arterial territories are outlined based on an extensive overview of anatomical studies of cerebral blood supply. For arterial territories of the hemispheres, we present the variability of the cortical territories of the three main cerebral arteries and define the minimal and maximal cortical supply areas.

Apathy is commonly defined as a loss of motivation leading to a reduction in goal-directed behaviors. This multidimensional syndrome, which includes cognitive, emotional and behavioral components, is one of the most prevalent neuropsychiatric features of Parkinson’s disease (PD). It has been established that the prevalence of apathy increases as PD progresses. However, the pathophysiology and anatomic substrate of this syndrome remain unclear. Apathy seems to be underpinned by impaired anatomical structures that link the prefrontal cortex with the limbic system. It can be encountered in the prodromal stage of the disease and in fluctuating PD patients receiving bilateral chronic subthalamic nucleus stimulation. In these stages, apathy may be considered as a disorder of motivation that embodies amotivational behavioral syndrome, is underpinned by combined dopaminergic and serotonergic denervation and is dopa-responsive. In contrast, in advanced PD patients, apathy may be considered as cognitive apathy that announces cognitive decline and PD dementia, is underpinned by diffuse neurotransmitter system dysfunction and Lewy pathology spreading and is no longer dopa-responsive. In this review, we discuss the clinical patterns of apathy and their treatment, the neurobiological basis of apathy, the potential role of the anatomical structures involved and the pathways in motivational and cognitive apathy.

The purpose of this study was to estimate the risk factors, early course, outcome and neuroimaging patterns in primary intracerebral hemorrhages (PIH). Using the Besançon Stroke Registry, 350 patients with first PIH documented by computed tomography (CT) between 1987 and 1993 were included in the present study. Patients with hemorrhage secondary to traumatism, brain tumor, thrombolytic treatment, vascular malformation or with hemorrhagic infarction were excluded. All CTs were evaluated to define the location, extension and volume of bleeding (55% of CT were performed within the first 12 h). Causes of death were classified and the 30-day outcome survival was evaluated with a modified Rankin scale (40 patients underwent a noncodified surgical procedure and were excluded from the outcome evaluation). Locations were lobar (36.5%), lenticular (32%), thalamic (15.7%), cerebellar (8.8%), midbrain and pons (2%), intraventricular (2%), caudate (1%) and multiple (2%). Risk factors included hypertension (54.8%), alcohol (18%) anticoagulant treatment (8.8%) and none (31.2%). The largest mean volume was in putaminal (41.7 ml) and lobar (39.8 ml) locations. Among 191 patients admitted before the 12th hour of evolution, 51 (26.7%) experienced an early clinical worsening. In this group, the percentage of patients with anticoagulant treatment (19.6%) was significantly higher (p < 0.0001). PIH enlargement was documented in 3 patients. Overall, the 30-day mortality rate was 24.2% with 48% of all deaths occurring in the first 3 days. Death and 30-day survival status were closely associated with PIH volume (p < 0.0001). Our study provides information on the natural history of PIH and especially on initial evolution. PIH volume seems to be an interesting indicator for death and functional status at 30 days.