Hydrocephalus should be suspected when changes in mentation occur, when a patient fails to make expected functional gains, or when spasticity, seizures, and emotional problems are present. Work-up may include computed tomography (CT) scan, lumbar puncture, CT cisternography, and radionu-clide cisternography. Neurosurgical consultation for shunt placement should be obtained. Cranial Nerve Deficits Cranial nerve function should be routinely assessed in patients with brain tumors, as appropriate inter-vention may greatly improve functional status. Visual and hearing deficits are frequently seen in menin-giomas, acoustic neuromas, and pituitary adenomas. Ophthalmoplegia and facial pain may also present as symptoms of central nervous system (CNS) tumor (Rowland, 1995). Suprasellar lesions can cause bitemporal hemi-anopsia, but can also cause diminished visual acuity, scotomata, quadrantic deficits, and blindness of one or both eyes. When treating patients with visual deficits, rehabilitation management should include an ophthalmology consultation to quantify the extent of the visual field loss. Training the patient to utilize compensatory techniques such as scanning will im-prove visual spatial awareness. Driving recommen-dations should be given before discharge, with plans for further evaluations as vision improves. Vision im-pairment typically leads to adverse effects on inde-pendent living and must be considered in discharge planning. Patients with double vision can be treated with alternating-eye patching. Facial pain can be very debilitating and may be treated with tricyclic antidepressant, antiepileptic, or analgesic medications, alone or in combination or in combination with mild narcotic medications. Facial and eyelid paralysis may necessitate plastic surgery interventions for corneal protection or cosmesis. Hearing deficits may have a central or peripheral eti-ology. Audiology evaluations will differentiate sen-sorineural from conductive hearing loss. Speech pathology consultation is necessary to establish ap-propriate routes for communication. Balance Abnormalities The neurologic components of human balance are the visual, vestibular, and somatosensory systems. The brain stem and cerebellum process and integrate information about balance from various peripheral receptors, which is then sent onward through corti-cospinal and brain stem pathways. Balance abnor-malities may include dizziness, unsteadiness, vertigo, muscle weakness, and proprioceptive sensory loss. Injuries of the posterior columns of the spinal cord or of the parasagittal or sensory cortex of the brain can lead to these difficulties. Many cancer-related problems and treatments contribute to imbalance, in-cluding poor nutrition, anemia, anxiety, postural hy-potension, and dehydration. Medications such as antiemetics, tranquilizers, opiates, vestibulotoxic an-tibiotics (e.g., aminoglycosides), and diuretics may also cause loss of balance. Radiation therapy that in-cludes the temporal bone and/or the posterior fossa can also lead to intermittent vertigo. While brain tu-mors at many different locations may lead to a sense of vertigo, nystagmus occurs with vestibular or pos-terior cranial fossa tumors. Patients frequently com-pensate by tilting their head to decrease the nystag-mus. Acoustic neuromas can present as Ménière’s disease, where vertigo is associated with hearing loss and tinnitus. Tumors affecting the cerebellum may lead to ataxia and dysdiadochokinesis. Vestibular disturbance can be treated by habitua-tion, which leads to decreased sensitivity of the vestibular response. The goals of rehabilitation are to resolve reversible deficits and to learn compensatory and adaptive techniques for irreversible deficits, thereby improving safety and increasing indepen-dence. Rehabilitation may include training patients to effectively use other sensory input and habituation to control symptoms provoked by activity. Spontaneous resolution can occur and is often related to the sever-ity of the initial insult as well as the possible plastic-ity of the CNS. The Balance Master System is a medical device (NeuroCom International, Clackamas, Oregon) used to quantify and treat balance abnormalities. It utilizes a partially enclosed environment with a monitor screen that changes visual orientation input. It has platforms on which a patient stands (both outside and inside the environment) to measure movements and/or provide tilts or weight shifts. Harnesses are available for safety. Parameters measured include (1) amount of weight bearing on either foot, (2) sway with upper body movement, (3) rhythmic weight shift with body movement in all planes, (4) limits of sta-bility whereby patients are provided a mechanical force toward which they try to shift their weight to compensate to maintain balance, and (5) weight shifts during movements such as transfers from sit-ting to standing and walking. Visual feedback is then given regarding the patient’s position while the ther-apist can give verbal cues. The results are stored for quantitative and graphic analysis. Vestibular and vi-sual components can be isolated by the device’s en-vironment. A custom exercise program can then be developed based on the determined deficits. Propri-oceptive responses may be improved via controlled mobility, improved anterior-posterior weight shifts, increasing trunk strength and range of motion, as well as increasing midline symmetry and transitional movements. Pharmacologic treatments include meclizine and dimenhydrinate, which may cause sedation. Trans-dermal scopolamine patches can also be used and are believed to cause less sedation. Cognition/Speech Deficits Deficits in cognition and speech occur; they vary in type and severity by the location and type of tumor, anticancer treatment, pre-morbid cognitive baseline, and co-morbid medical conditions. Cognitive deficits arise from tissue injury caused by the tumor itself, surgical resection, and the acute effects of radiation and chemotherapy (Silberfarb, 1983). The neu-ropsychiatric side effects of both steroid and anti-convulsant therapy should also be considered in cog-nitive assessment (Lewis and Smith, 1983). Emotional sequelae such as depression and anxiety are com-mon, may worsen cognitive functions, or are over-looked in the presence of cognitive deficits. Coexist-ing medical conditions such as hypothyroidism are treatable and should be considered in the differential diagnosis of cognitive impairment.Cognitive deficits are most often seen in areas in-volving memory, attention, initiation, and psychomo-tor retardation. Primary interventions for memory im-pairment include memory aids and the use of visual imagery. Cognitive remediation programs teach pa-tients adaptive strategies and compensatory tech-niques. Psychostimulants have been reported to be useful in treating psychomotor retardation, depres-sion, and opioid-induced drowsiness (Bruera et al., 1989; Weitzner et al., 1996). Dopamine agonists and stimulating antidepressants improve attentional dys-function, particularly distractibility and difficulty fo-cusing, in higher level patients (Gualtieri et al., 1989). Bromocriptine can be effective for motor aphasias and neglect in some patients (Grujic et al., 1998). Carba-mazepine, tricyclic antidepressants, trazodone, aman-tadine, and -blockers have been prescribed to man-age agitation in patients with traumatic brain injury (Brooke et al., 1992; Mysiw et al., 1988; Whyte, 1988).Aphasia is a language disorder, whereas dysarthria is an articulation disorder. In contrast to aphasia, naming, fluency, repetition, and comprehension are normal in dysarthric conditions, and dysarthric pa-tients can read and write without errors. The sever-ity of aphasia correlates significantly with communi-cation difficulty. Other disorders such as apraxia, visual constructive difficulties, and neglect need to be considered in the differential diagnosis of communi-cation dysfunction.Myelopathy may occur due to tumor involvement, ir-radiation, and intrathecal chemotherapy. Metastatic tumors may involve the spine or spinal cord. Back pain is a frequent symptom and in 10% of cases may be due to spinal instability (Gilbert et al., 1977; Portenoy et al., 1987; Rodichok et al., 1981). Any tu-mor can metastasize to the spine and cause sufficient destruction to produce spinal instability. The thoracic spine is the segment most commonly involved, fol-lowed by lumbosacral and then cervical vertebral lev-els (Casciato and Lowitz, 1983; Schlicht and Smelz, 1994). Spinal cord compression eventually occurs in ap-proximately 5% of patients with cancer (Casciato and Lowitz, 1983). Abrupt neurologic deterioration from spinal cord involvement may occur from rapidly growing lesions in the extradural space. Infarction of the vertebral blood supply can cause cord injury. Radiculopathy at any level is also possible (Gilbert et al., 1977; Rodichok et al., 1981). By the time treat-ment is pursued, as many as 50% of patients may not be able to ambulate, and 10% to 30% may be para-plegic (Shapiro and Posner, 1983; Shaw et al., 1980). Symptoms include weakness, incoordination, gait abnormality, spinal or radicular pain, paresthesias, sensory disturbances, autonomic disturbances, as well as bowel or bladder problems. Pinprick and deep pain sensation is often retained until later in the course of the disease. Motor involvement typi-cally occurs before sensory involvement with epidural extension (Galasko, 1999). With radiation treatment alone, ambulation is maintained in 79% of patients if they were ambulatory before treatment and in 42% with paraparesis. In 20% to 25% of patients, significant neurologic deterioration was noted dur-ing the course of treatment with radiation alone (Findlay, 1984). Significant neurologic deterioration and progres-sive spinal instability require a neurosurgical con-sultation. High-dose steroids are used in the acute phase to control neurologic damage. Tetraplegia, whether complete or incomplete, occurs with spinal cord involvement at T1 or above. Below this level, injuries more commonly result in paraplegia, conus medullaris syndrome, or cauda equina syndrome. Local pain is typically described as constant and aching, whereas radicular pain is classically sharp and shooting. Referred pain can be either aching or sharp and at a location distant to the involved site. Pain can also occur with epidural involvement; this pain worsens with Valsalva maneuvers, coughing, and neck and back flexion (Gilbert et al., 1978; Ger-ber and Vargo, 1998). Functional prognostic factors are listed . With use of radiation treatment and posterior laminectomy, the overall results were that complete paraplegia patients rarely recovered, but those who were ambulatory remained ambulatory and approxi-mately one-half of patients with incomplete paraple-gia regained ambulation (Posner, 1995). Recovery tends to occur first in the area of sensory disturbance, followed by motor abnormalities (Casciato and Lowitz, 1983; Schlicht and Smelz, 1994). Radiation-Related Myelopathies The detrimental effects of radiation are multifactorial and cannot be entirely attributed to dosage, site, or technique. Such myelopathy may be transient or de-layed (Dropcho, 1991). With transient myelopathy, peak onset is at 4 to 6 months (Dropcho, 1991). Clin-ical onset may involve symmetric paresthesia or shock-like sensations in a nondermatomal pattern from spine to extremities (Leibel et al., 1991). Radi-ologic studies are usually normal. Symptoms typically resolve in 1 to 9 months (Dropcho, 1991). Con-versely, delayed myelopathy is irreversible, has a la-tency period of 9 to 18 months, and generally occurs within 30 months (Dropcho, 1991). The incidence is reported at 1% to 12%. The latency period is de-creased with increased radiation dose and in children (Leibel et al., 1991). The onset of symptoms begins with lower extremity paresthesias and is followed by sphincter disturbance.