To send 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 sending content to .
To send content items to your Kindle, first ensure email@example.com
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 sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent 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.
This chapter reviews the neuroanatomy and neurochemistry of frontal-subcortical circuits (FSCs) and outlines the signature syndromes of FSC circuit dysfunction. The oculomotor circuit originates in the frontal eye field as well as prefrontal and posterior parietal cortex and connects sequentially to the central body of the caudate nucleus, dorsomedial GP interna (GPi) and ventrolateral SN pars reticulata (SNr), ventral anterior and medial dorsal thalamic nuclei, and back to the frontal eye field. Emotional, motivational, and affective information processed by the basal ganglia is represented in the rostromedial limbic circuitry arising from the orbital and medial prefrontal cortex. Processing of the detailed information contained in the FSCs is modulated by input from dopaminergic, cholinergic, noradrenergic, and serotonergic systems. The orbitofrontal (OF) cortex is the neocortical representation of the limbic system and involved in the determination of the appropriate time, place, and strategy for environmentally elicited behavioral responses.
Sleep-wake disturbances (SWD) are frequently (20%-50%) encountered in stroke patients. Clinical symptoms include hypersomnia, excessive daytime sleepiness, fatigue, and insomnia. The most dramatic forms of poststroke hypersomnia are observed in patients with bithalamic paramedian stroke. The presence of SWD after stroke is associated with cognitive and psychiatric (depression, anxiety) disturbances. The recognition and diagnosis of poststroke SWD occur primarily on clinical grounds. Validated questionnaires such as the Epworth Sleepiness Scale and the Fatigue Severity Scale may help in the recognition of poststroke sleepiness and fatigue. In patients with paramedian thalamic stroke, treatment with 20-40 mg of bromocriptine may improve apathy and presleep behavior. Changes in sleep architecture depend upon: patient and health characteristics present before the stroke, topography and extent of the lesion, associated complications of stroke (e.g. SDB, fever, infections, cardiovascular disturbances, depression, anxiety), drug treatment, and time after stroke onset.