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Physiologically, the cerebral autoregulation system allows maintenance of constant cerebral blood fl ow 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 signifi cant change in cerebral blood fl ow. 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 signifi cantly 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 defi ne a possible mechanism that is able to explain the dynamic by which hypotension might be related to dementia. Keywords: vascular dementia, hypotension, low blood pressure, alzheimer disease As longevity increases worldwide, age-related dementias are burgeoning. Age-related cerebral degenerative changes are coupled therefore with decreased perfusion, usually assumed to be secondary to decreased cerebral metabolic demands (Meyer et al 1999). During aging, the declines in cerebral tissue densities of the gray cortex (polio-araiosis) and of the white matter (leuko-araiosis) refl ect neuronal degenerative changes, which progress concurrently with cerebral perfusion declines.In particular, leuko-araiosis correlates with advancing age, cerebral atrophy, hypoperfusion of white matter, and cognitive impairments (Meyer et al 2000). Leuko-araiosis is detectable in 9%-19% of older 'normal' subjects, but is virtually always present in vascular dementia (VaD). Of special interest are the data emerging from the study of Meyer and colleagues (2000): normative subjects destined for later cognitive decline had excessive leuko-araiosis at study entry, suggesting leuko-araiosis is, by itself, a risk factor for cognitive decline.Thus, the researchers are trying to defi ne the passage between normality, the so-called leuko-araiosis age-related and the excess of the response to the vascular damage, confi guring the dementia, as a clinical syndrome. White matter injury m...

Background The pupillary light reflex is the main mechanism that regulates the pupillary diameter; it is controlled by the autonomic system and mediated by subcortical pathways. In addition, cognitive and emotional processes influence pupillary function due to input from cortical innervation, but the exact circuits remain poorly understood. We performed a systematic review to evaluate the mechanisms behind pupillary changes associated with cognitive efforts and processing of emotions and to investigate the cerebral areas involved in cortical modulation of the pupillary light reflex. Methodology We searched multiple databases until November 2018 for studies on cortical modulation of pupillary function in humans and non-human primates. Of 8,809 papers screened, 258 studies were included. Results Most investigators focused on pupillary dilatation and/or constriction as an index of cognitive and emotional processing, evaluating how changes in pupillary diameter reflect levels of attention and arousal. Only few tried to correlate specific cerebral areas to pupillary changes, using either cortical activation models (employing micro-stimulation of cortical structures in non-human primates) or cortical lesion models (e.g., investigating patients with stroke and damage to salient cortical and/or subcortical areas). Results suggest the involvement of several cortical regions, including the insular cortex (Brodmann areas 13 and 16), the frontal eye field (Brodmann area 8) and the prefrontal cortex (Brodmann areas 11 and 25), and of subcortical structures such as the locus coeruleus and the superior colliculus. Conclusions Pupillary dilatation occurs with many kinds of mental or emotional processes, following sympathetic activation or parasympathetic inhibition. Conversely, pupillary constriction may occur with anticipation of a bright stimulus (even in its absence) and relies on a parasympathetic activation. All these reactions are controlled by subcortical and cortical structures that are directly or indirectly connected to the brainstem pupillary innervation system.

Sexual dysfunction affects a large part of patients suffering from multiple sclerosis, but some aspects of its clinical presentation and aetiology are not clearly defined yet. In an unselected sample of 108 patients with definite multiple sclerosis we investigated the relationship between symptoms of sexual dysfunctioning and sphincteric dysfunction, patients' and disease characteristics, disability and neurological impairment, psychological and cognitive functioning. Sexual dysfunction directly correlated with presence of physical disorders (r=0.37, P=0.0004), low educational level (r=0.32, P<0.002), disability (r=0.31, P<0.003), age at onset of symptoms (r=0.30, P<0.003), sphincteric dysfunction (r=0.30, P<0.003), age (r=0.30, P<0.004), depression (r=0.29, P<0.005), fatigue (r=0.29, P=0.005), cognitive deterioration (r=0.26, P<0.01), primary-progressive course of disease (r=0.25, P<0.02), neurological impairment (r=0.25, P<0.02), marriage (r=0.24, P<0.02), anxiety (r=0. 23, P<0.03), male gender (r=0.22, P=0.03) bladder dysfunction (r=0. 29, P<0.04), and unemployment (r=0.21, P<0.04). Sexual dysfunction correlated inversely with relapsing - remitting course of disease (r=-0.31, P<0.002). No correlation was found between sexual dysfunction and bowel dysfunction, duration of disease, secondary-progressive course of disease, number and frequency of sexual intercourses in the last year, number of partners, number of exacerbations in the last year, number of months since last exacerbation, masturbation, and fertility. In conclusion, the association between sexual dysfunction and sphincteric dysfunction indicates a common aetiology corresponding to the frequent involvement of the spinal cord in multiple sclerosis, but the concomitant correlation between sexual dysfunction and other variables suggests the possible aetiological role of physical, psychological and sociological factors as well.

Alzheimer's disease is the most frequent form of dementia, where behavioral and cognitive disruption symptoms coexist. Depression, apathy, anxiety, and other conduct disorders are the complaints most often reported by caregivers. Fifty subjects were referred to our Institute with a diagnosis of probable Alzheimer's disease. Cognitive impairment was equally distributed among the subjects. Patients, aged 68 to 76 years old, were randomized to receive inhibitors of cholinesterase (Donepezil, 5 mg/day) alone, or inhibitors of cholinesterase plus selective serotonin reuptake inhibitors (SSRIs) (citalopram HBr, 20 mg/day). We followed up all the patients for one year, with particular concern for neuropsychological aspects associated with eventual behavioral changes. Results indicate that SSRI intake seems to be effective for depression, decreasing it and improving quality of life for both patients and caregivers. Side effects in both groups were few, and there were no study withdrawals. This paper discusses the relationship between dementia and depression, and presents our finding that depressive symptoms, if specifically treated, tend to reduce caregiver stress and improve well-being in patients with Alzheimer's disease.