The incidence of dementia is higher in the cancer patient population for the following reasons: 1. Occurrence of leukoencephalopathy secondary to chemotherapy such as intrathecal chemo-therapy, especially the combination of irradia-tion and methotrexate (Abrey et al., 1998) 2. Slowly progressing viral infections (Manuelidis et al., 1988) 3. Radiation-related dementia characterized either by dementia alone or by dementia with gait abnormalities and incontinence. A small num-ber of patients will also have hydrocephalus and benefit by ventricular-abdominal shunting (Asai et al., 1989) Parkinsonism The major clinical features of Parkinson’s disease are recognized as a symptom complex manifested by any combination of six cardinal features: tremor at rest, rigidity, bradykinesia-hypokinesia, flexed posture, loss of postural reflexes, and the freezing phenome-non. At least two of these features, with at least one being either tremor at rest or bradykinesia, must be present for a diagnosis of Parkinson’s disease. The biochemical pathology in this disorder is decreased dopaminergic neurotransmission in the basal ganglia. Parkinsonism can occur in cancer patients for the following reasons 1. Use of dopamine antagonists and depleting agents 2. Radiation injury, including radiation necrosis 3. Hydrocephalus/normal pressure hydro-cephalus 4. CNS hypoxia 5. Following encephalitis 6. Parathyroid dysfunction 7. Tumor 8. Multi-infarct state 9. Idiopathic Parkinson’s disease co-existing in the cancer population The clinical features of tremor, rigidity, and flexed posture are referred to as positive phenomena; bradykinesia, loss of postural reflexes, and freezing are negative phenomena. In general, the negative phe-nomena are more disabling. Bradykinesia results in difficulty with speech, swallowing, ADL, and mobility. Walking, transferring, and even bed mobility can be affected. Severe bradykinesia prevents these patients from driving due to slowed foot movement between the accelerator and the brake pedal. Loss of postural reflexes leads to increased risk of falls and a high in-cidence of hip fractures in parkinsonian patients. Af-fected patients also have cognitive and behavioral signs such as decreased attention span, visuospatial impairment, and personality changes. They are often more fearful, indecisive, and passive, as well as de-pressed, than is normal (Dropcho, 1991). Autonomic disturbances are also encountered. Patients may ex-perience constipation, urinary retention, hypoten-sion, and/or erectile dysfunction.Treatment is aimed at controlling symptoms through use of standard antiparkinsonian medica-tions and rehabilitation interventions. Physical and occupational therapies play an important role in maintaining ADL and muscle strength and slowing de-velopment of contractures and the accompanying characteristically stooped posture. Functional deficits often worsen disproportionately with periods of im-mobility; thus mobility should be preserved as much as possible despite intercurrent illnesses. Rehabilita-tion also involves treatment of dysphagia, manage-ment of bowel and bladder problems, and assistance with psychosocial difficulties caused by declining cognition. Psychological Issues Psychological symptoms can include reactive anxiety and depression, major depression, and organic brain disorder. The incidence of these disorders is gener-ally greater with higher levels of disability and ad-vanced illness (Breitbart et al., 1998). Symptoms of depression may include anorexia, insomnia, fatigue, weight loss, dysphoric mood, hopelessness, worthlessness, excessive guilt, and suicidal ideation (Massie and Holland, 1990). Symptoms are initially likely to be reactive to the diagnosis of a malignancy and then depressive as the functional deficits caused by neurologic impairments are manifested. Endicott (1984) suggested substitution criteria for making the diagnosis of depression, as somatic symptoms of de-pression might be unreliable and nonspecific in can-cer patients.