Many different causes of<unk>  have been suggested. While there is some debate about the validity of<unk>  as a separate disease, experts mostly agree that<unk>  is the result of frontal lesions and not with cerebellar or brainstem lesions. As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward,<unk>  may be a dopamine-related dysfunction.<unk>  may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere. Damage to the basal ganglia Injuries to the frontal lobe and/or the basal ganglia can interfere with an individual's ability to initiate speech, movement, and social interaction. Studies have shown that 5-67% of all patients with traumatic brain injuries and 13% of patients with lesions on their basal ganglia suffer from some form of diminished motivation. It may complicate rehabilitation when a stroke patient is uninterested in performing tasks like walking despite being capable of doing so. It should be differentiated from apraxia, when a brain injured patient has impairment in comprehending the movements necessary to perform a motor task despite not having any paralysis that prevents performing the task; that condition can also result in lack of initiation of activity. Damage to the capsular genu A case study involving two patients who suffered from acute confusional state and<unk>  was conducted to see if these symptoms were the result of an infarct in the capsular genu. Using clinical neuropsychological and MRI evaluations at baseline and one year later showed that the cognitive impairment was still there one year after the stroke. Cognitive and behavioral alterations due to a genu infarct are most likely because the thalamo-cortical projection fibers that originate from the ventral-anterior and medial-dorsal nuclei traverse the internal capsule genu. These tracts are part of a complex system of cortical and subcortical frontal circuits through which the flow of information from the entire cortex takes place before reaching the basal ganglia. Cognitive deterioration could have occurred through the genu infarcts affecting the inferior and anterior thalamic peduncles. In this case study the patients did not show any functional deficits at the follow-up one year after the stroke and were not depressed but did show diminished motivations. This result supports the idea that<unk>  may exist independently of depression as its own syndrome. Damage to anterior cingulate circuit The anterior cingulate circuit consists of the anterior cingulate cortex, also referred to as Brodmann area 24, and its projections to the ventral striatum which includes the ventromedial caudate. The loop continues to connect to the ventral pallidum, which connects to the ventral anterior nucleus of the thalamus. This circuit is essential for the initiation of behavior, motivation and goal orientation, which are the very things missing from a patient with a disorder of diminished motivation. Unilateral injury or injury along any point in the circuit leads to<unk>  regardless of the side of the injury, but if there is bilateral damage, the patient will exhibit a more extreme case of diminished motivation, akinetic mutism. Acute caudate vascular lesions It is well documented that the caudate nucleus is involved in degenerative diseases of the central nervous system such as Huntington disease. In a case study of 32 acute caudate stroke patients, 48% were found to be experiencing<unk> . Most of the cases where<unk>  was present were when the patients had a left caudate infarct that extended into the putamen as seen through a CT or MRI scan.
Abulia
Iatrosophia
Equinovalgus
Pinguecula
Acalvaria
Epiblepharon
Liber pantegni
Prospero