There is evidence that shows the mild depressive symptoms, or even sub-syndromal symptoms, are responsible for the non-recovery of social functioning, which furthers the idea that residual depressive symptoms are detrimental for functional recovery in patients being treated for BP-II. It has been suggested that symptom interference in relation to social and interpersonal relationships in BP-II is worse than symptom interference in other chronic medical illnesses such as cancer. This social impairment can last for years, even after treatment that has resulted in a resolution of mood symptoms.The factors related to this persistent social impairment are residual depressive symptoms, limited illness insight (a very common occurrence in patients with BP-II), and impaired executive functioning. Impaired ability in executive functions is directly tied to poor psychosocial functioning, a common side-effect in patients with BP-II.The impact on a patients psychosocial functioning stems from the depressive symptoms (more common in BP-II than BP-I). An increase in these symptoms severity seems to correlate with a significant increase in psychosocial disability. Psychosocial disability can present itself in poor semantic memory, which in turn affects other cognitive domains like verbal memory and (as mentioned earlier) executive functioning leading to a direct and persisting impact on psychosocial functioning.An abnormal semantic memory organization can manipulate thoughts and lead to the formation of delusions and possibly affect speech and communication problems, which can lead to interpersonal issues.
Metamorphopsia is a type of distorted vision in which a grid of straight lines appears wavy and parts of the grid may appear blank. People can first notice they suffer with the condition when looking at mini-blinds in their home. For example, straight lines might be wavy or bendy. Things may appear closer or further than they are. Initially characterized in the 1800s, metamorphopsia was described as one of the primary and most notable indications of myopic and senile maculopathies. Metamorphopsia can present itself as unbalanced vision, resulting from small unintentional movements of the eye as it tries to stabilize the field of vision. Metamorphopsia can also lead to the misrepresentation of an object’s size or shape.It is mainly associated with macular degeneration, particularly age-related macular degeneration with choroidal neovascularization. Other conditions that can present with complaints of metamorphopsia include: pathological myopia, presumed ocular histoplasmosis syndrome, choroidal rupture and multifocal choroiditis. Pathology
The mechanisms that result in the development of metamorphopsia involve structural changes in the retina of the eye (retinal mechanism) as well as processing changes in the cerebral cortex of the brain (cortical mechanism). The retinal mechanism involves the displacement of retinal layers which results in the mislocation of light on the retina. The cortical mechanism, which was discovered after the retinal mechanism, is affected by perceptual “filling-in” and visual crowding effects. The cortical mechanism was found to work in combination with the retinal mechanism to contribute to metamorphopsia in long-standing maculopathy or after the treatment of macular disorders.