Risk factors for vascular dementia: Hypotension as a key point

Physiologically, the cerebral autoregulation system allows maintenance of constant cerebral blood flow over a wide range of blood pressure. In old people, there is a progressive reshape of cerebral autoregulation from a sigmoid curve to a straight line. This implies that any abrupt change in blood pressure will result in a rapid and significant change in cerebral blood flow. Hypertension has often been observed to be a risk factor for vascular dementia (VaD) and sometimes for Alzheimer disease although not always. Indeed, high blood pressure may accelerate cerebral white matter lesions, but white matter lesions have been found to be facilitated by excessive fall in blood pressure, including orthostatic dysregulation and postprandial hypotension. Many recent studies observed among other data, that there was a correlation between systolic pressure reduction and cognitive decline in women, which was not accounted for by other factors. Baseline blood pressure level was not significantly related to cognitive decline with initial good cognition. Some researchers speculate that blood pressure reduction might be an early change of the dementing process. The most confounding factor is that low pressure by itself might be a predictor of death; nevertheless, the effect of low blood pressure on cognition is underestimated because of a survival bias. Another explanation is that clinically unrecognized vascular lesions in the brain or atherosclerosis are responsible for both cognitive decline and blood pressure reduction. We discuss the entire process, and try to define a possible mechanism that is able to explain the dynamic by which hypotension might be related to dementia

Statin-associated necrotizing autoimmune myopathy with concurrent myasthenia gravis

Statin treatment has been associated with necrotizing autoimmune myopathy and has been linked to myasthenia gravis. We present an unprecedented clinical challenge with both disorders occurring in a patient treated with statins few months earlier

Memantine: Reality and Potentiality

Memantine protects cultured neurons from excitotoxin-induced cell-death; it attenuated loss of cholinergic neurons in the CNS induced by injection of NMDA into the basal forebrain of rats. It has been shown that memantine induced production of brain-derived neurotrophic factor (BDNF), a substance shown to promote survival and differentiation of CNS neuron. Due to the preclinical effects of memantine owing to its anti-ischemic and anti-excitotoxic properties, recent clinical efficacy has been demonstrated in patients with advanced dementia of vascular origins. Therefore, it has been employed in different trials, in vascular dementia, showing a potential benefit and no unbearable side effects. Different studies underline the possible role of memantine in Parkinson Disease

Facial Emotion Recognition in Patients with Amnesic Mild Cognitive Impairment and Mild-Moderate Alzheimer's Disease

Background: Although several studies have found evidence of impairment in facial emotion recognition in Alzheimer's disease, current understanding regarding which specific emotions are preserved and disrupted is inconsistent. Moreover, facial emotion recognition has been little explored in subjects with amnesic mild cognitive impairment. Objective: To investigate processing of human faces identity and emotional expressions in patients with probable mild-moderate Alzheimer disease (AD), amnesic mild cognitive impairment (a-MCI) and healthy control subjects (CS). Methods: Thirty subjects were included in the study: 10 AD (mean MMSE corrected score=20.94; DS=1.96), 10 a-MCI (mean MMSE corrected score=25.98; DS=0.69), and 10 CS (mean MMSE corrected score=29.85; DS=0.4). The three groups did not differ for age and education. All patients underwent an extensive neuropsychological test battery. Geriatric Depression Scale was employed to exclude depressed patients. A new battery for assessing face emotion processing was developed. It included 48 faces pictures of 6 models balanced for sex and age (young, adult and old). For each model there were poses corresponding to seven emotions (anger, disgust, fear, happiness, sadness, surprise, boredom) as well as neutral expressions. Subjects had to perform four different tasks: 1) deciding the emotion label that best described the facial expression shown; 2) choosing the picture that matched the target emotion verbal label; 3) sorting the faces displaying the same facial expression; 4) sorting the faces displaying the same identity. Results: Recognition accuracy in all three groups was better for positive emotions and neutral expressions than negative emotions, consistent with previous studies. AD patients were more impaired in the recognition of overall emotions and neutral faces than a-MCI and CS subjects. Compared with CS, a-MCI did not differ significantly in their emotion recognition abilities. When segregated by emotions, we found significant differences in emotion recognition between the diagnostic groups for fearful and sad faces. In particular, AD patients and a-MCI subjects differed significantly from CS in fearful face recognition; AD patients also had impairment in recognizing facial expressions of sadness. Only patients with AD were impaired on the facial identity task. The predominant pattern across all groups and emotions was of a better recognition of emotions when displayed by young faces instead of either adult or old faces. Conclusions: A selective impairment in recognition of facial expressions of fear is already present in patients with a-MCI. An additional deficit in processing of sad faces emerge with AD progression and may be related to the degeneration progression towards structures implicated in emotional processing systems. An early detection of emotional impairment in MCI phases of dementia may have clinical impact and prognostic value