Primary brain tumors are less than 2% of all malignancies but are the second leading cause of death from neurologic disorders after stroke (22). One-half to two-thirds of intracranial tumors have been reported to be primary tumors (23). Primary brain tumors are classified by cell of origin; the primary system of classification is that of the World Health Organization (WHO), which divides tumors into nine categories. The most common categories include tumors that displace brain parenchyma of the intracranial supratentorial compartment. Of these tumors, the most common in adults are the astrocytomas, in particular grade IV astrocytoma, otherwise known as glioblastoma multiforme (GBM) (24). The median survival for a patient with GBM has been reported between 7 and 17 months (25).
In addition to primary brain tumors, brain metastases are estimated to occur in 20% to 40% of patients with cancer. The most common mechanism of metastasis to the brain is through hematogenous spread. Most of the metastases are located in the cerebral hemispheres, followed by the cerebellum and then the brainstem. The incidence of brain tumor metastases is rising, possibly due to the increasing length of survival of a patient with cancer (26), increasing ability to diagnose a tumor with improved radiographic imaging (27), and possibly recent chemotherapy agents, which may weaken the blood-brain barrier (28).
Normal brain parenchyma can be destroyed or compressed by the tumor, and the location of the tumor determines the resultant neurologic deficit. Surgical resection may exacerbate these deficits by creating inflammation or peritumoral infarct (29). Radiation treatment has long been an integral part of brain tumor treatments and often results in collateral damage. Early acute radiation leukoencephalopathy is likely due to increased cerebral edema. Late delayed radiation reactions include focal cerebral radiation necrosis, diffuse cerebral radiation injury (DCRI), and combined-therapy diffuse white matter injury/leukoencephalopathy. Clinical DCRI has been reported in 2% to 5% of patients with metastases and 19% of 1-year survivors after whole-brain radiation (30,31).
The most common neurologic deficits include impaired cognition (80%), weakness (78%), visual-perceptual deficits (53%), sensory loss (38%), and bowel/bladder dysfunction (37%). Other deficits include cranial nerve palsy, dysarthria, dysphagia, aphasia, ataxia, and diplopia, which are less common. Approximately 75% of patients with a brain tumor have three or more neurologic deficits concurrently, and 39% have five or more deficits (32). Because of the diverse nature of these neurologic deficits, comprehensive multidisciplinary inpatient rehabilitation is often necessary for these patients. In rehabilitation medicine, the physical impairments that could result in functional deficits are primarily addressed.
Patients who have impairments resulting in functional decline that could affect bed mobility, ambulation, transferring from sitting or lying to a standing position, or activities of daily living (ADLs) (eg, eating, grooming, dressing, bathing, and toileting) can benefit from comprehensive inpatient rehabilitation. Comprehensive cancer rehabilitation services are not widely available for these patients (33). Because of this, many patients with a brain tumor receive their rehabilitation at general rehabilitation facilities alongside patients with stroke and traumatic brain injury. Patients with a brain tumor have similar efficiencies of improvement when compared to traumatic brain injury, stroke, and between brain tumor types. Lengths of stay tend to be shorter among patients with a brain tumor, possibly secondary to a need to return the patients home sooner given their shorter life expectancies (34,35,36,37,38). However, some notable differences between these populations should be noted (eg, physiatrists may need to be cognizant of the continued decline of patients with progressive tumors).
Neurologic Motor Impairment
Motor impairment can be due to hemiparesis, ataxia, and apraxia. Motor impairment may lead to an unsafe gait pattern creating a higher risk for falls and a need for inpatient rehabilitation transfer. In inpatient rehabilitation, the patient will be seen by physical and occupational therapists. Physical therapy would focus on gait and transfers. To address transfers, efforts could be focused on sliding board transfer or stand pivot transfers. With respect to mobility, physical therapists focus on wheelchair mobility and gait with or without an assistive device (eg, a single-point cane, quad cane, rolling walker, hemiwalker). Occupational therapy would focus on problems with ADLs. Commonly addressed basic ADLs include dressing, bathing, toileting, grooming, eating, and the like. The occupational therapist and physical therapist are also aware of the cognitive component necessary for mobility and ADLs. Once a patient is functionally safe using an assistive device such as a rolling walker, he or she can be discharged home. Then, the patient can continue with outpatient rehabilitation, gradually improving his or her ambulation with an assistive device and further strengthening weakened muscles by way of a progressive resistance exercise program.
The pattern of recovery of muscle strength and function does not always follow the pattern of recovery observed in patients with stroke. However, the stroke recovery pattern is often used as a guideline for patients with brain tumors. The recovery of strength occurs in a proximal-to-distal direction, with flaccidity and decreased muscle tone progressing to spasticity and increased muscle tone. The spasticity in the affected limbs can evolve into flexor or extensor synergy patterns. Recovery of muscle movement may plateau at any stage or may progress to isolated coordinated volitional motor movement (39,40).
Several techniques and exercises are used for neuromuscular facilitation in patients with stroke. Often, a combination of procedures and techniques from the various programs are used in patients with cancer with neuromuscular weakness. Proprioceptive neuromuscular facilitation developed by Kabat, Knott, and Voss relies on several mechanisms, such as spiral diagonal movement patterns of the extremities and quick stretch. Brunnstrom movement therapy facilitates the use of the synergy patterns mentioned as a means of developing voluntary control. Rood proposed that cutaneous sensory stimulation in the form of superficial stroking, tapping, brushing, vibrating, or icing provides facilitatory or inhibitory inputs (41).
In addition to the traditional range-of-motion and strengthening exercises as well as neuromuscular facilitation techniques, functional electrical stimulation can also be incorporated into the rehabilitation program for neuromuscular weakness. It uses a low-level electrical current that stimulates motor nerves or reflex sensory nerves to produce muscle contraction. The goal of functional electric stimulation is to produce purposeful, functional movements in paretic or paralytic muscles (42).
Sometimes, owing to weakness of the ankle dorsiflexors, it is necessary to use an ankle-foot orthosis (AFO) to improve hemiparetic gait. There are two major types of AFOs: the double metal upright AFO attached to an orthopedic shoe and the molded plastic AFO, which is more commonly used. With the plastic AFO, the footplate sits within the shoe and extends upward behind the calf. The advantages of a plastic AFO over a double metal upright AFO include better cosmesis, lighter weight, and the freedom to wear different shoes.
Shoulder subluxation, predominantly inferior, which is caused by the loss of normal motor control of the shoulder stabilizers, including the deltoid and supraspinatus muscle, is often seen in the hemiparetic patient (43). It can often be the cause of shoulder pain in hemiplegic patients (44,45). Other possible causes of shoulder pain in this patient population include complex regional pain syndrome, traction injury of the brachial plexus, rotator cuff tendinitis or tear, subacromial or subdeltoid bursitis, adhesive capsulitis, or heterotopic ossification. Diagnosis of glenohumeral subluxation is made through physical examination and radiographic evaluation. The acromiohumeral interval is compared on each side with the arms in an unsupported position during physical examination, and radiographic evaluation is used to quantify the amount of subluxation. Radiographic studies can provide an early evaluation for subluxation with slight gapping of the superior aspect of the glenohumeral joint (46).
Treatment of hemiparetic shoulder subluxation involves proper positioning of the arm, physical modalities, and exercise. The use of an arm sling can help maintain proper positioning and posture during ambulation. However, this is discouraged when the patient is seated, and its overuse may contribute to compromise of superficial blood flow as well as to joint contracture. Arm troughs and lapboards are used while patients are seated (47). Other interventions include biofeedback and functional electrical stimulation.
Hemisensory deficit and homonymous hemianopsia may be seen with hemiparesis. Visual or somatic hemineglect is more frequently seen when the nondominant cerebral hemisphere is affected. Hemispatial neglect has a negative effect on sitting balance, visual perception, wheelchair mobility safety awareness, and risk of falling (42). Patients with neglect have difficulty with hygiene and self-care activities on the affected side. Rehabilitation programs must address the issue of hemispatial neglect through focused measures led by speech therapists, occupational therapists, and physical therapists. Family training and education are important in this setting as well.
Cerebellar ataxia may be seen with mass effect within the posterior fossa. Of note, cerebellar ataxia can also be seen in paraneoplastic cerebellar degeneration and with high-dose administration of cytarabine (ara-C) or 5-fluorouracil (5-FU) (48,49). Involvement of the cerebellum can produce intention tremors, dysmetria, and dysdiadochokinesis as patients lose the ability to coordinate the agonist and antagonist muscle groups (50). The response to pharmaceutical management has been poor; consequently, physical and occupational therapy has been the mainstay of treatment for ataxia. This includes the teaching of compensatory techniques for performing basic self-care and occupational activities and the possible use of weighted bracelets or similar devices to help decrease the oscillations. Physical therapy directed at gait training with the use of assistive devices can help improve mobility in ataxic individuals (51).
Depending on its location, a tumor may be associated with deficits in speech, which can vary in severity and type. Often, one can diagnose the type of aphasia from a comprehensive neurologic examination, including speech comprehension, fluency, and repetition. These include Broca’s aphasia, Wernicke’s aphasia, anomic aphasia, global aphasia, conduction aphasia, and the transcortical motor and sensory aphasias.
A speech pathologist will implement treatment approaches, including melodic intonation therapy, Amer-Ind Code treatment, functional communication treatment, stimulation approach, and Promoting Aphasics’ Communication Effectiveness (PACE) therapy (52).
Cognitive deficits often are more problematic than motor deficits. They can arise from direct injury to the brain tissue due to the tumor itself, from surgical resection, radiation, chemotherapy, depression/anxiety, as well as medications, particularly steroids and anticonvulsants (28). Impairments most commonly seen involve limited memory and attention, decreased initiation, and psychomotor retardation (53).
The rehabilitation physician will assess the patient’s cognitive status as part of the physical examination. This assessment is needed to formulate a rehabilitation program involving speech pathologists. Specific deficits in language and cognition can further be delineated through specific testing performed by a speech pathologist. However, it is sometimes necessary to have formal neuropsychological testing done, especially if the patient wishes to return to work.
A disruption in the swallowing process can also occur in patients with brain tumors or following craniotomies. It is important to determine, through clinical assessment, whether dysphagia is present because there is the potential for serious complications, such as malnutrition and aspiration pneumonia, if dysphagia remains undetected. Often, its presence can be established from a history and neurologic examination. If dysphagia is suspected, a speech pathologist is consulted; then, daily swallowing therapy and exercises are incorporated into the therapeutic milieu.
Treatments include dietary modifications and dysphagia exercise and facilitation techniques (54). Depending on the results from a clinical swallowing evaluation or videofluoroscopic evaluation, food can be modified to different consistencies, including puree, semisolid, or solid. Liquids may also have to be thickened using various thickening (55).
Exercises and facilitation techniques are employed to aid and strengthen various components of the swallowing process. These include exercises employed for treatment for the lips to facilitate the ability to prevent food or liquid from leaking out of the oral cavity. There are exercises to assist the pharyngeal swallow by improving tongue base retraction. Vocal cord adduction exercises are instituted to strengthen weak cords to prevent aspiration.
Compensatory strategies include proper head and trunk positioning, which for most patients is to be seated upright with head midline, trunk erect, and the neck slightly flexed forward. Other techniques include the chin-tuck method and head turning and tilting during swallowing.
After dysphagia has been identified and measures are implemented for its treatment, regular follow-up to assess for improvement is required. This again can be done through clinical examination or radiographically. If improvement is noted, the diet may be advanced appropriately.
Spasticity is defined as velocity-dependent resistance to passive movement across a joint. It is an abnormality involving increased muscle tone and is one of the positive findings of the upper motor neuron syndrome. Spasticity must be distinguished from soft tissue contractures. Soft tissue contractures result from scar tissue formation and may be the result of a number of causes, including uncontrolled spasticity.
Often, brain tumors can cause muscle spasticity. This can affect the gait pattern or ADLs and, in severe cases, can cause pain and joint contractures as well as being a detriment to hygiene of the involved areas. Sometimes, spasticity may be beneficial, as when a patient may use knee extensor spasticity to assist in transferring from a sitting to a standing position. Indications for the treatment of spasticity include the need to decrease pain, improve hygiene, improve gait and transfers, minimize contractures, and improve self-care.
Treatment measures for spasticity include physical and medical interventions. Proper positioning, passive range-of-motion exercises, serial casting, splints, and braces are some of the physical interventions used in treating spasticity. Oral medications may also be used, including tizanidine, dantrolene sodium, and baclofen. Because these medications work systemically, the most common limiting side effects are excessive drowsiness and cognitive changes. Tizanidine or dantrolene is recommended by most clinicians for treating spasticity stemming from primary brain pathology (55). Often, because of the cognitive side effects of these oral medications, botulinum toxin injections, phenol injections, or intrathecal baclofen pumps may be useful. These medications act locally but are harder to administer and more invasive.
As in patients with stroke, bladder incontinence may be present in patients with brain tumors. The causes of bladder incontinence can be multifactorial and include an untreated urinary tract infection, inability to ambulate to the bathroom, and altered cognitive status. If the pontine micturition center is preserved, patients with brain tumors can have upper motor neuron bladder dysfunction, which is characterized by bladder hyperreflexia with reflex or urge incontinence and complete emptying (56). Postvoid residual volumes are generally low in the absence of bladder outlet obstruction. Persistent areflexia and retention may occur with bilateral lesions (57).
Treatment first involves identifying the cause of the bladder dysfunction. Obtaining a urinalysis with cultures and sensitivities and then starting appropriate antibiotics is the treatment for urinary tract infections. Using a bedside commode or a urinal is of benefit for patients who have weakness or inability to safely ambulate to the bathroom. A timed voiding program that has the patient urinate at set times throughout the day, before the bladder can contract, can be of help for patients with hyperreflexic urgency. Anticholinergic medications such as oxybutynin (Ditropan) or tolterodine tartrate (Detrol) can be used for persistent incontinence in this setting of a hyperreflexic detrusor (57). If the patient’s blood pressure can tolerate it, a trial of an alpha-adrenergic agent (eg, tamsulosin, terazosin) may be useful in reducing urinary resistance in older male patients who are experiencing symptoms of urinary retention.