What may be expressed as post-traumatic stress disorder (PTSD) in adults may become DID when occurring in children, possibly due to their greater use of imagination as a form of coping.Possibly due to developmental changes and a more coherent sense of self past the age of six, the experience of extreme trauma may result in different, though also complex, dissociative symptoms and identity disturbances. A specific relationship between childhood abuse, disorganized attachment, and lack of social support are thought to be a necessary component of DID. Although what role a childs biological capacity to dissociate to an extreme level remains unclear, some evidence indicates a neurobiological impact of developmental stress.Delinking early trauma from the etiology of dissociation has been explicitly rejected by those supporting the early trauma model. However, a 2012 review article supports the hypothesis that current or recent trauma may affect an individuals assessment of the more distant past, changing the experience of the past and resulting in dissociative states. Giesbrecht et al. have suggested there is no actual empirical evidence linking early trauma to dissociation, and instead suggest that problems with neuropsychological functioning, such as increased distractibility in response to certain emotions and contexts, account for dissociative features. A middle position hypothesizes that trauma, in some situations, alters neuronal mechanisms related to memory. Evidence is increasing that dissociative disorders are related both to a trauma history and to "specific neural mechanisms".
Foster Kennedy syndrome is a constellation of findings associated with tumors of the frontal lobe.Although Foster Kennedy syndrome is sometimes called "Kennedy syndrome", it should not be confused with Kennedy disease, or spinal and bulbar muscular atrophy, which is named after William R. Kennedy. Pseudo-Foster Kennedy syndrome is defined as one-sided optic atrophy with papilledema in the other eye but with the absence of a mass. Presentation
The syndrome is defined as the following changes:
optic atrophy in the ipsilateral eye
disc edema in the contralateral eye
central scotoma (loss of vision in the middle of the visual fields) in the ipsilateral eye
anosmia (loss of smell) ipsilaterallyThis syndrome is due to optic nerve compression, olfactory nerve compression, and increased intracranial pressure (ICP) secondary to a mass (such as meningioma or plasmacytoma, usually an olfactory groove meningioma). There are other symptoms present in some cases such as nausea and vomiting, memory loss and emotional lability (i.e., frontal lobe signs). Diagnosis
Brain tumor can be visualized very well on CT scan, but MRI gives better detail and is the
preferred study. Clinical localization of brain tumors may be possible by virtue of specific neurologic deficits or
symptom patterns. Tumor at the base of the frontal lobe produces inappropriate behavior, optic nerve
atrophy on the side of the tumor, papilledema on the other side, and anosmia. Treatment
The treatment, and therefore prognosis, varies depending upon the underlying tumour. While awaiting surgical removal, treat any increased intracranial pressure
with high-dose steroids (i.e., dexamethasone).