We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Depression in epilepsy represents a frequently encountered psychiatric comorbidity that is likely to be related to a number of variables that are both biological and psychosocial. Current literature on the neurobiology of depression in epilepsy has focused on frontal lobe dysfunction. Modern studies of interictal psychiatric disorders of epilepsy have usually attempted to identify their similarities to the psychiatric disorders that meet current classificatory systems. In the interictal dysphoric disorder, eight key symptoms, grouped in three major categories, are identified: labile depressive symptoms, labile affective symptoms, and supposedly specific symptoms (paroxysmal irritability and euphoric moods). A specific instrument, named Interictal Dysphoric Disorder Inventory (IDDI), has been developed in the context of a collaborative German-Italian study. One of the most frequent methodological errors in studies of depression in epilepsy is the sole reliance on screening instruments for the diagnosis of depressive disorders.
By
Raúl de la Fuente-Fernández, Division of Neurology University of British Columbia Vancouver, BC, Canada,
A. Jon Stoessl, Division of Neurology University of British Columbia Vancouver, BC, Canada
This chapter discusses the recent neuroimaging studies that have started to unravel some of the mysteries behind the behavior and cognitive manifestations of Parkinson's disease (PD). In-vivo anatomical and functional confirmation of the cortico-striatal loops in humans comes from magnetic resonance imaging (MRI) techniques. In the early stages of PD, frontal lobe dysfunction most likely reflects deafferentation in relation to dopamine deficiency. In keeping with neuropathological studies, which have demonstrated Lewy bodies and cell loss in medial temporal lobe areas high-resolution MRI images have demonstrated hippocampal atrophy in PD. There is pathological and in-vivo positron emission tomography (PET) evidence that other neurotransmitters, particularly cholinergic pathways, are involved in PD dementia (PDD). In-vivo PET studies are currently investigating whether concomitant amyloid pathology may contribute to dementia in PD subjects, although at this point, it appears that amyloid deposition is associated more with dementia with Lewy bodies (DLB) than with PDD.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.