Impairment of Parkinson's disease (PD) axial motor signs (AMS) has been described as a risk factor for dementia. Executive dysfunction is an important feature in recently proposed clinical diagnostic criteria for PD dementia. To clarify the relationship between AMS progression and executive cognitive performance, we conducted a 6-year prospective study in PD patients without AMS impairment at baseline. A hospital-based cohort of PD patients (n = 24) without dementia, in the initial motor stage (Hoehn-Yahr < or = 2), and matched controls (n = 20) were followed prospectively over a 6-year period. Neuropsychological tests were performed in both groups, and motor function (including AMS: speech, gait, postural instability) was evaluated in the PD group. The PD group had a significantly higher decline in neuropsychological test scores than did the controls. Most of the neuropsychological and motor decline occurred in the last 4 years. In UPDRS III, progression of AMS and especially speech were the most important motor variables related to dementia. There was a correlation between speech impairment progression and declines in MMSE (r = -0.598, p = 0.002), Clock Drawing (r = -0.671, p < 0.001), Semantic Verbal Fluency (r = -0.435, p = 0.034), Alternating Sequences (r = 0.497, p = 0.014), and Raven's Coloured Progressive Matrices (r = -0.735, p < 0.001). PD patients with higher speech impairment progression showed more rapid declines in some neuropsychological tests. Further studies are needed to clarify the different roles of speech, gait and postural instability on the initial phases of cognitive dysfunction.
According to some studies, 80% of subjects suffering from post-traumatic stress disorder (PTSD) present twice the risk of developing an insanity as they age because of the high level of stress that has been induced. Indeed, the triggered trauma has a deleterious effect on the establishment of the stress’ axis (the hypothalamic pituitary adrenal axis) which is then not able to regulate itself. As a consequence, the hippocampal neurons will be attacked by an excess of cortisol. Memory's dysfunction is central in the symptomatology of PTSD, particularly in respect to encoding and recall. The hippocampus is able to transfer information to the prefrontal cortex. Actually, subjects with PTSD present less activity in the prefrontal cortex triggered by a decrease of encoding and recall capacities. EMDR therapy (eye movement desensitization and recruitment) allow for a fast relief of symptoms by a bilateral alternate stimulation (SBA). Indeed, saccadic eye movements stem affect related to the traumatic event and process the associated cognitions. During the desensitization phase in EMDR, we noticed an increase in activity of the brain's prefrontal, ventromedial, amygdala and thalamic regions. Indeed, the recall of traumatic memories goes through implicit emotional valence regions and associative areas for which the experience is already deeply integrated. After comparing cerebral activity before and after the therapy, researches on EMDR shows that a reduction of stress’ symptoms has some sensitive link to PTSD (in prevention to dementia).Disclosure of interestThe authors have not supplied their declaration of competing interest.
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