More men than women are diagnosed with Parkinson's disease (PD), and a number of gender differences have been documented in this disorder. Examples of clinical characteristics that appear in men more often than women include rigidity and rapid eye movement behavior disorder, whereas more women than men exhibit dyskinesias and depression. Differences between men and women in cognition have not been extensively examined, though there are reports of deficits in men in aspects of cognition that contribute to activities of daily living, in verbal fluency, and in the recognition of facial emotion, and deficits in women in visuospatial cognition. Side of disease onset may interact with gender to affect cognitive abilities. One possible source of male-female differences in the clinical and cognitive characteristics of PD is the effect of estrogen on dopaminergic neurons and pathways in the brain. This effect is not yet understood, as insight into how the fluctuation of estrogen over the lifetime affects the brain is currently limited. Further attention to this area of research will be important for accurate assessment and better management of PD. Attention should also be directed to multiple covariates that may affect clinical characteristics and cognition. Knowledge about differences in the presentation of PD symptoms in men and women and about the pathophysiology underlying those differences may enhance the accuracy and effectiveness of clinical assessment and treatment of the disease.

Emotion identification appears to decline with age, and deficient visual scanning may contribute to this effect. Eye movements of 20 older adults (OAs) and 20 younger adults (YAs) with normal saccades were recorded while viewing facial expressions. OAs made fewer fixations overall, and they made a higher proportion of fixations to the lower halves of faces. Topographical distribution of fixations predicted better OA accuracy for identifying disgust than other negative emotions. Impaired OA accuracy for fear and anger was specific to vision, with normal identification of these emotions in the auditory domain. Age-related frontal-lobe atrophy may affect the integrity of the frontal eye fields, with consequent scanning abnormalities that contribute to difficulties in identifying certain emotions.

The interaction of visual/visuospatial and motor symptoms in Parkinson's disease (PD) was investigated by means of a 31-item self-report questionnaire. The majority of 81 non-demented patients reported problems on non-motor tasks that depended on visual or visuospatial abilities. Over a third reported visual hallucinations, double vision and difficulty estimating spatial relations. Freezing of gait was associated with visual hallucinations, double vision and contrast sensitivity deficits. Visual strategies frequently were employed to overcome freezing. The results underscore the importance of investigating visual and visuospatial impairments in PD and their relation to motor symptoms, in order to help patients develop successful compensatory strategies.

In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). Critical flicker fusion thresholds were normal, relative to age-matched healthy subjects. For color, the majority of the errors were tritanomalous (blue axis). Color and stereoacuity deficits were unrelated to severity of dementia, in accordance with models of vision that describe these functions as modular rather than diffuse for cortical localization. Although contrast sensitivity was depressed throughout the frequency range in AD, more patients were impaired at low than at high spatial frequencies, contrasting with the observed normal aging pattern of high-frequency loss. Healthy elderly subjects showed depressed critical flicker fusion thresholds and reduced contrast sensitivity at high frequencies, relative to the young group; differences between these groups were not found for the other vision tests. A subset of the AD group received detailed neuro-ophthalmological examination, and no abnormalities were found. This finding, taken together with normal thresholds for critical flicker fusion, suggests that the widespread visual dysfunction reported here is more likely to be related to known pathological changes in primary visual and association cortex in AD than to changes in the retina or optic nerve.