Parkinson disease

Parkinson disease is a degenerative disorder involving a progressive loss of dopaminergic neurons in the substantia nigra, with the appearance of intracellular inclusions know as Lewy bodies. A loss of 70% to 80% of dopaminergic function accompanies symptomatic Parkinson disease, causing a resting tremor and difficulty in the control of voluntary movement. Olfaction, sleep, cardiovascular function, bowel motility, and cognitive function are all often compromised. Although not directly associated with motor system pathology, the functional deficits are emotionally devastating to the patient, resulting in depression and other mood disorders. The predominant pharmacological approach in the management of Parkinson disease is the enhancement of dopaminergic function in the affected brain regions. Among the earliest successful approaches was the use of levodopa (L-dopa), a precursor of the neurotransmitter dopamine in the central nervous system (CNS). The use of this agent (and most agents to date) only enhances dopaminergic function in the remaining neurons but has no effect on the progressive loss of neurons. In addition to central conversion of L-dopa to dopamine in the substantia nigra pars compacta, a similar conversion occurs in the limbic system, a brain center associated with the regulation of behavior. Excessive dopaminergic influence in the limbic system has been associated with aberrant disease manifestations including paranoia, delusions, hallucinations, and related psychiatric disturbances, all of which may influence sleep and mood. These behavioral changes are obviously antagonistic to any therapeutic plan. In addition to L-dopa, a dopamine precursor, agents that inhibit the breakdown of dopamine, enhance the release of dopamine, or have dopaminergic agonist activity will have similar behavioral effects ( Box 36.1 ). Dopaminergic agents may produce postural hypotension and syncope because of their ability to produce vasodilation based on CNS and peripheral actions. ^, If patients are unable to take their medication, an increasing danger exists (with extended therapy) that movement may become impossible and normal chest wall expansion and contraction may be compromised.

Because Parkinson disease is progressive in nature, patients may have different presentations depending on the stage of the disease and the presence of pharmacological interventions. In the early months of the disease, the motor signs may be particularly subtle, and patients may report only slowness, stiffness, and trouble with handwriting. Attention to the history of tremor, slowness of fine motor control, a hunched and slightly flexed posture, and micrographia may lead the physician to diagnose Parkinson disease in its early phases. As the disease advances, patients have increasing difficulty in activities of daily living and gait as well as bradykinesia and distal tremor.

Once a definitive diagnosis has been made, the control of symptoms and the side effects of medications is balanced with the level of functional involvement. The physician and patient may discuss the option of several medications (see Box 36.1 ) but must determine the best approach based on the clinical presentation. One limitation is the side effect of involuntary movements (dyskinesias). These dyskinesias can be difficult to control and are different from the involuntary movements caused by the disease itself. As mentioned earlier, dopamine agonist regimens that do not cause dyskinesias can also be prescribed, but their effect on symptoms is not as potent. Often physicians may begin treatment with a dopamine agonist (Ropinirole) and continue with the agonist as long as symptoms are satisfactorily controlled. Later the physician can initiate treatment with L-dopa when the disease is in the advanced stages. With the elderly patient who has cognitive deficits, combination therapy may be the initial choice. Once a medication regimen has been initiated, the patient and therapist may notice improvements in symptoms and therefore also in functional abilities. After taking a medication over time, patients may find that the effect of the medication begins to wear off before the next dose is scheduled. At this point consultation with the rehabilitation team is recommended to potentially change the timing of the medication release ability (extended release), or they may combine the treatment with other antiparkinsonian medications.

Great emphasis is placed on treating the motor features of Parkinson disease, but patients may have nonmotor manifestations, including depression, anxiety, cognitive impairment, and dementia. Often the patient does not mention these difficulties because he or she does not link them with Parkinson disease. Patients may demonstrate some of these difficulties, and the therapist should recognize the symptoms and refer the patient for further follow-up.

The major problems that patients have after 5 years of treatment for Parkinson disease are fluctuations (both motor and nonmotor), dyskinesias, and behavioral or cognitive changes. ^, The mechanisms behind these complications relate both to the underlying disease and the effects of medications. Motor fluctuations take several forms. Most commonly, a predictable decline in motor performance occurs near the end of each medication dose (“wearing off”). Patients change gradually from “on,” with a good medication response, into an “off” period 30 minutes to 1 hour before the next medication dose is due. Often patients have involuntary movements (dyskinesias) as a peak-dose complication, and sometimes similar movements occur at the end of the dose. Sudden and severe cataclysms of motor fluctuation occur rarely, with ambulatory patients becoming immobilized over a period of seconds (“sudden on-off”). Because these fluctuations occur throughout the day, accurate detection requires the cooperation of the patient, who must be trained to keep and complete a diary recording function. These journals generally divide the 24-hour day into 30-minute segments to detect good medication response (“on”), poor medication response (“off”), disabling dyskinesias, and sleep. Recently two new formulations of L-dopa intended to address wearing off have been approved. Rytary carbidopa-levodopa extended-release capsules contain both immediate- and extended-release beads that provide reduced off time in patients with motor fluctuations. DUOPA carbidopa-levodopa intestinal gel is administered through a gastrostomy tube into the jejunum using a pump and can have a dramatic effect in reducing “off” time.

In general, to meet functional goals and outcomes effectively, therapists working with patients taking antiparkinsonian medication must be aware of both the positive and negative side effects of medications. Learning the difference between tremor and dyskinesia is crucial. The therapist must coordinate therapy sessions during good medication response times to facilitate optimal outcomes. In addition, patients should be monitored for postural hypotension, dizziness, and cognitive changes. Therapists have the unique opportunity to determine the best timing, frequency, and duration of the treatment; understanding the impact of a patient’s drug regimen will only enhance the outcome. Therapists must also be aware that exercise increases metabolism. Increased metabolism may use up the medication faster; thus an individual who generally remains symptom-free (no off times between doses) and whose metabolism is increased will again exhibit signs of the disease (distal tremors and axial or proximal rigidity). These increases in symptoms may stem from a problem of drug dosage, not being signs of further degeneration of the basal ganglia. All changes in symptoms should be discussed with both the pharmacist and the physician.

Cancer

Cancer is a general term for disorders associated with abnormal and uncontrolled cell proliferation. Virtually any organ system can be affected, either as the primary site of disease or as a secondary site associated with metastasis. Cancer pharmacology has improved significantly during the recent past with an expanded understanding of cancer biology and newly developed drugs that target cancer vulnerabilities. Effective early treatments, adjuvant chemotherapy, and hormonal therapy can extend overall survival and prevent disease reoccurrence. In the past 5 years the ability to harness the power of the immune system in the treatment of cancer has brought about a paradigm shift whereby some of the most feared diseases—such as melanoma, lung cancer, and even late-stage metastatic disease—can be eradicated. Cancer may interfere with neurological rehabilitation in various ways. Tumors within the brain may interfere with cognitive, motor and sensory function as well as autonomic and metabolic control (see Chapter 25 ). Peripherally tumors may interfere with nerve function and associated motor control or may produce pain. In addition, drugs that reduce cancer pain may interfere with cognitive and motor function. Among such drugs, morphine and related opiate derivatives ( Box 36.2 ) are notable. A significant degree of tolerance to the CNS depressant effects will develop with long-term administration. Currently cannabinoids are being studied not only for the treatment of cancer symptoms but also for their anticancer effects. Cannabinoids are considered useful in combating anorexia, chemotherapy-induced nausea and vomiting, pain, insomnia, and depression. ^, Nabiximols (Sativex), a cannabinoid drug, is still under study. An oral mucosal spray made up of a whole-plant extract with tetrahydrocannabinol (THC)/cannabidiol (CBD) is available in Canada and parts of Europe to treat pain linked to cancer as well as muscle spasms and pain from MS. In cancer chemotherapeutic regimens, many antiemetic agents are used. These include dopaminergic antagonists (which may produce motor deficits similar to those of Parkinson disease), dronabinol (a chemical component of marijuana, which can affect cognitive function), and nabilone (a synthetic cannabinoid) as well as high-dose corticosteroids (which affect mood). Some antitumor agents may be neurotoxic; reduced deep tendon reflexes, paresthesias, and demyelination are associated with vincristine (Oncovin) and oxaliplatin (Eloxatin). ^, Naturally any change in drugs involving cancer treatment (directly or indirectly) requires the approval of the patient’s oncologist.

The main role of rehabilitation specialists is to help patients with cancer recover from the physical changes that accompany their illness, promote function in activities of daily living, and help provide adaptations to activities within the limits of each patient’s function and the illness. Clinicians should be aware of chemotherapy side effects and the side effects of medications given to treat the toxic effects of chemotherapy. The importance of recognizing toxic effects early in the treatment regimen cannot be overstated and will help the oncologist to alter the dose or discontinue the offending medication.

A number of chemotherapeutic and nonchemotherapeutic medications are used to fight cancer. Most anticancer therapies operate on the simple principle that because cells in tumors are actively dividing, agents that kill dividing cells will kill tumor cells. Tissue cells that divide rapidly are therefore at risk, including hair, mucosal linings, bone marrow, immune cells, and skin epithelial cells. Nonchemotherapy medications called biological response modifiers (BRMs) are naturally made by the body but in anticancer treatment are delivered in large quantities and at higher doses than those produced by the body. Interferon and interleukin are two of the most commonly used medications. Monoclonal antibodies that target oncogenic pathways are also used as chemotherapy to suppress the immune system.

Chemotherapy often has side effects that affect the integumentary, GI, hematological, and neurological systems. Each type of therapy has potential side effects along with the more general side effects of the treatment regimen. Because of their chemotherapeutic treatment of cancer, patients often have muscular weakness, neuropathy, fatigue, pain, immobility, and reduced flexibility. Often the therapist will have to be supportive and flexible with treatment plans to accommodate for changing physiological, psychological, and social factors during treatment.

GI symptoms such as nausea and vomiting may occur; medications such as Compazine and Reglan may be given to help control these episodes. Symptoms of diarrhea may be addressed through prescriptions or the use of over-the-counter (OTC) medications including milk of magnesia and magnesium citrate. The development of mucositis or esophagitis is also possible. A prescription solution of three medications (diphenhydramine [Benadryl], nystatin, and viscous lidocaine) can help to relieve pain, inflammation, and potential associated fungal infections. Bone marrow suppression from chemotherapeutic regimens may lead to an increased risk of infection, risk of bleeding, and fatigue as well as a lack of exercise capacity and musculoskeletal weakness. Patients undergoing chemotherapy may receive one or more medications to signal the bone marrow to increase its output of white blood cells (filgrastim [Neupogen]), stimulate the production of red blood cells (epoetin alfa [Epogen]), and stimulate increased production of platelets (oprelvekin [Neumega]). These therapies may be instituted to help the patient more quickly reverse suppression of bone marrow and allow the chemotherapy to continue without interruption. Generalized symptoms include fever, body aches and pains, and feelings of ill health and fatigue. No specific medications are used to improve these symptoms. In general taking medications such as acetaminophen, ibuprofen, or narcotics for fever and pain may help. The use of exercise as an adjunctive therapy for cancer treatment–related symptoms has gained favor in oncology rehabilitation as a promising intervention. Exercise is thought to help improve endurance, functional ability, and quality of life. ^{, ,} The major side effects associated with BRMs and monoclonal antibodies are generalized as well and include fever and flulike symptoms with associated arthralgia and myalgia. Other side effects include lymphedema, which is characterized by fluid retention caused by disruption of lymphatic drainage or the removal of lymph nodes. As mentioned earlier, neurological changes may occur, with the development of neurological signs as well as forgetfulness, suicidal ideation, and depression.

In treating cancers, selection of the most appropriate treatment or treatments, dose, and dose intervals as well as the management of adverse effects requires specialized knowledge and a team effort. In addition, cancer treatment regimens undergo frequent updates due to findings of ongoing clinical trials. The availability of drugs with new mechanisms of action (e.g., immune checkpoint inhibitors), good target selectivity (e.g., kinase inhibitors), efficacy in specific cancers, and different adverse-effect profiles permits the use of new drug combinations and regimens. The rehabilitation professional is an important team member in oncology because his or her actions potentially affect quality of life.

Seizure disorders (epilepsy)

Epilepsy is associated with a diverse group of neurological disorders resulting in motor, psychic, and autonomic manifestations. Many antiseizure medications may produce drowsiness, ataxia, and vertigo ( Box 36.3 ). Some may produce cognitive disorders in children and adults. ^, Although these adverse effects may be exhibited throughout therapy, they are most troublesome during its initiation, the addition of a drug, and the escalation of dosage. Sudden discontinuation of antiseizure medications may result in status epilepticus, which can be fatal. Many antiseizure medications are finding successful applications outside epilepsy, especially in the area of pain management. As with cancer, clinical evidence has shown that cannabinoids such as CBD can be used to reduce seizures effectively, particularly in patients with treatment-resistant epilepsy. However, many questions remain regarding the mechanism, safety, and efficacy of cannabinoids in short- and long-term use.

The practicing clinician working with patients who have a history of seizure disorders must be prepared for the onset of a seizure and be aware of any adverse side effects of medications. Adverse side effects are typically determined on a clinical basis, signifying the importance of recognition by the health care provider. Many of the common side effects can also have negative implications for motor learning, especially while the patient is getting used to the medication or the dosage is being elevated or tapered.

The treatment of seizure disorders with pharmacotherapy is typically intended to control the seizure activity completely without producing unwanted side effects. Pharmacological intervention usually begins with one medication (monotherapy); if this drug is unsuccessful, a second is added while dosage of the first is tapered. Or a combination may be needed. The effects of the medications vary and may include enhancing the inhibitory effects of γ-aminobutyric acid (GABA) (benzodiazepines); reducing posttetanic potentiation, thereby reducing seizure spread (iminostilbenes); or modulating neuronal voltage-dependent sodium and calcium channels (hydantoin). The overall result is a reduction in abnormal electrical impulses in the brain. The choice of antiseizure drugs primarily depends on the seizure type and, if possible, the diagnosis of a specific syndrome. If seizures are recurrent and occur during critical periods of childhood, adolescence, and early adulthood, they may result in significant impairments in function and increased disability.

Some side effects may be slow to develop and difficult to diagnose because seizures can often be mistaken for sedation or cognitive dysfunction, especially in children, who may not report drug side effects. Practitioners can also mistakenly accept reversible drug toxicity as a necessary consequence of a seizure disorder. The number of seizures occurring during physical or occupational therapy should be tracked to assist in determining appropriate pharmacotherapy.

One common antiseizure medication, valproic acid (Depakene), may cause nausea, vomiting, hair loss, tremor, tiredness, dizziness, and headache. Valproic acid has also been reported to aggravate absence seizure in patients with absence epilepsy. Metabolic side effects may include an increase in glucose-stimulated pancreatic insulin secretion, which may be followed by an increase in body weight. Long-term use of valproic acid is known to increase bone resorption in adult epileptic patients and can decrease the mineral density of bone.

Another seizure medication, carbamazepine (Tegretol), is considered a safe drug, but it has a long list of adverse effects, most commonly ataxia and nystagmus. Other systems frequently involved are the skin, the hematopoietic system, and the cardiovascular system. Gabapentin (Neurontin) is another well-tolerated antiseizure medication with proven clinical efficacy and a low incidence of adverse events in clinical trials. Common side effects include dizziness, fatigue, and headache. Phenytoin (Dilantin) has adverse effects including ataxia, nystagmus, slurred speech, confusion, dizziness, and, at high doses, peripheral neuropathy.

Benzodiazepines (e.g., diazepam) are useful in managing status epilepticus, but their effects are not long-lasting, so they are often used along with a primary anticonvulsant. The most frequent side effects are dose-related sedation, difficulty with concentration, dizziness, and difficulty walking.

Pharmacological adverse events that occur under the influence of seizure medications must be recognized by the rehabilitation specialist to participate in a team approach to patient care. Therapists can assist in determining the effectiveness of a specific treatment regimen, appropriate timing of rehabilitation interventions, and the overall progress of the patient during rehabilitation.

Stroke, hypertension, and related disorders

Stroke, by virtue of its interference with blood flow and oxygenation, produces both reversible and irreversible neurological deficits. The loss of function associated with stroke has at least two major causes. The first involves loss of oxygenation to a critical brain region, followed by glutaminergic rebound and excessive calcium influx with apoptosis (programmed cell death). Current drugs and those under development are aimed at restoring blood flow and inhibiting glutaminergic hyperexcitability and intracellular apoptotic mechanisms. The second pathogenic issue is related to reperfusion injury associated with oxygen free radicals and associated cellular damage. In this case, free radical scavengers have shown some promise in animal models of stroke. To reduce the damage associated with thromboembolism in such cases, tissue plasminogen activator (tPA) has been recommended. However, this agent is most effective when given within an hour and up to 4.5 hours after the vascular insult. Currently some studies have provided strong evidence to support the efficacy of endovascular therapy with intravenous thrombolytic treatment in patients with acute ischemic strokes due to large vessel occlusions. Speed of delivery, multidisciplinary care, and access to specialized teams with endovascular capability is required to achieve results similar to those seen in these trials.

Drugs with other mechanisms used to improve the prognosis of stroke are under development, ^, showing variable promise. However, drugs used for concurrent conditions (atherosclerosis and hypertension) before and after a stroke are complicating factors for optimal outcomes from rehabilitation. These drugs include β-adrenergic antagonists, which reduce heart rate and correspondingly alter exercise tolerance. Occasionally calcium channel blockers, α-adrenergic blockers, and related agents may cause similar effects, including weakness, dizziness, syncope, and cognitive disorders. Changes in serum electrolytes induced by diuretics and the angiotensin-converting enzyme inhibitors may affect the heart, the vasculature, and skeletal muscle and ultimately cause impairments in areas such as strength of contraction. Box 36.4 lists many of these drugs. Many of the cholesterol synthesis inhibitors (agents used to reduce serum cholesterol) may induce muscle weakness, which may impact rehabilitation ( Box 36.5 ), but this adverse effect is considered rare despite the increase in prescribing. Abrupt discontinuation of antihypertensive medications may result in a hypertensive crisis, dramatically increasing the risk of stroke and related disorders.

Clinicians caring for patients with stroke, hypertension, and cardiac disorders will benefit from understanding the impact of any medication on the therapeutic plan. These patients may be taking any number of medications to manage the acute and subacute complications of cardiovascular impairments and their resulting sequelae. Other complications after stroke that may require pharmacological intervention include urinary tract infections, musculoskeletal pain, deep vein thrombosis, pressure sores, shoulder subluxation, and depression. All these medications have their own issues, and health care providers must be aware of adverse events and any alteration in function of the heart that may occur in relation to exercise.

Anticoagulants such as heparin, warfarin, and aspirin (so-called blood thinners ) are used to prevent another stroke after the first one has occurred. Side effects may include bleeding, allergic reactions, thrombocytopenia, and, in the case of aspirin, stomach irritation. New oral anticoagulants have been development for stroke prevention in atrial fibrillation. These newer agents such as dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa) have a predictable pharmacological profile so that international normalized ratio (INR) monitoring and dose modifications are not required. Their main advantages, apart from their treatment efficacy, include the reduced rate of intracranial hemorrhage, the lack of need for routine coagulation monitoring, the predictable anticoagulation response, and the limited interaction with food and drugs. Blood thinners make the patient more susceptible to bruising; therefore care must be taken in patient handling and choice of activity. Antiarrhythmics are used to restore the heart’s normal conduction patterns. Antiarrhythmic drugs may make some patients experience lightheadedness, dizziness, or faintness when they get up after sitting or lying down (orthostatic hypotension). Antiarrhythmic drugs may also cause low blood sugar or changes in thermoregulation. The most common side effects are dry mouth and throat, diarrhea, and loss of appetite. These problems usually go away as the body adjusts to the drug and do not require medical treatment. Therapists must be prepared for hypotensive events and the need to educate patients on positions that will reduce the effects of orthostatic hypotension.

Hypertension is a common disorder that is frequently encountered when treating patients in the rehabilitation environment. Antihypertensive medications are used to lower blood pressure (see Box 36.4 ) by limiting plasma volume expansion, decreasing peripheral resistance, and decreasing plasma volume. Often patients under medical management will undergo changes in dose and additions or deletions of medication, which may lead to problems during rehabilitation. Side effects of these medications may include increased frequency of urination, increased urinary excretion of potassium, orthostatic hypotension, hypotension, dehydration, tiredness, fatigue, cold hands and feet, and dizziness. Health care providers working with a patient who is taking antihypertensive medications should monitor for side effects, clinical signs, and the patient’s perceived exertion. Generally people on antihypertensive medications require careful cardiovascular monitoring during any physical activity.

Many patients tend to become depressed after experiencing a stroke, a cardiac event, or another neurological disorder. Such changes in mood may be attributable to a natural loss of physical function or a neurochemical response to changes in brain chemistry. Patients with signs and symptoms of depression (sadness, anxiety, hopelessness, suicidal ideation) should be referred for further follow-up by the physician. Many antidepressant medications take at least 2 weeks to achieve a therapeutic level. Antidepressants may cause temporary side effects (sometimes referred to as adverse effects ) in some people. These effects are generally mild. Any unusual reactions, side effects, or behaviors that interfere with functioning should be reported to the physician immediately. The most common side effects of tricyclic antidepressants (TCAs) are dry mouth, constipation, bladder problems, sexual problems, blurred vision, dizziness, and drowsiness. The newer antidepressants have different types of side effects, including headache, nausea, nervousness, insomnia, agitation, and sexual problems. Therapists working with patients who are depressed may have to delay rehabilitation until the depression is well managed.

Hyperlipidemia is considered a modifiable risk factor for heart disease and stroke. Many patients may be receiving pharmacological treatment to reduce their cardiovascular risk. Several types of drugs are available for cholesterol lowering, including statins, bile acid sequestrants, nicotinic acid, and fibric acids. The statins are considered first-line drugs and are generally well tolerated, but they can produce myopathy under some circumstances. An elevation of creatine kinase level is the best indicator of statin-induced myopathy and should be checked for when patients report leg pain. Bile acid sequestrants also produce moderate reductions in cholesterol. Sequestrant therapy can produce a variety of GI symptoms, including constipation, abdominal pain, bloating, fullness, nausea, and flatulence. Nicotinic acid (niacin) therapy can be accompanied by a number of side effects. Flushing of the skin is common with the crystalline form and is intolerable for some persons. However, most persons have tolerance to the flushing after more prolonged use of the drug. The fibrates have the ability to lower serum triglycerides and are generally well tolerated in most persons. GI symptoms are the most commonly reported, and fibrates appear to increase the likelihood of cholesterol gallstones.

Overall, patients taking cardiovascular medications need careful monitoring for any drug impact on cardiorespiratory or metabolic responses in relation to rehabilitation activities. Thus the effects of drugs must be considered in developing the rehabilitation plan.

Anxiety and depression

Agents used in the management of anxiety, whether from acute or chronic disease, must be carefully titrated. Among these agents are the benzodiazepines, whose anxiolytic (anxiety-reducing) dosage range immediately precedes a dose that may affect motor skills and cognitive function ( Box 36.6 ). In subjects of all ages but especially the geriatric population, the administration of benzodiazepines may produce paradoxical excitement, confusion, and behavioral changes. Geriatric subjects also have an increased incidence of injury from falls concurrent with use of benzodiazepines and other sedative-hypnotic drugs. Although benzodiazepines may have variable effects on learning and declarative memory, these effects may differ among the benzodiazepines; there may also be considerable variation in individual responses. If producing sleep alone is desired, zolpidem (Ambien) and zaleplon (Sonata) are attractive alternatives because these agents do not have anxiolytic effects. Although the anxiolytic agent buspirone (Buspar) is relatively free of benzodiazepine-like effects, the onset time for the desired anxiolytic effect is characteristically delayed. Lack of compliance with anxiolytic agents may increase panic attacks and reduce effective interactions with a therapist.

The emergence of the selective serotonin reuptake inhibitors (SSRIs) has revolutionized the treatment of depression. The older agents, such as the TCAs, are just as effective in the management of several forms of depression; however, their adverse effect profile is somewhat different. TCAs often produce drowsiness and orthostatic hypotension, effects that complicate any rehabilitation regimen. Although these effects may also be produced by SSRIs, their incidence is much reduced. Certain TCAs, by virtue of their ability to inhibit the reuptake of norepinephrine in adrenergic nerve terminals, may be used at lower doses for neuralgia. Although these low-dose regimens are usually not associated with the side effects previously mentioned, some patients may be more sensitive to these effects than others. This requires increased vigilance for the care team in determining iatrogenic versus pathological sources of somnolence and syncope. A partial list of antidepressants is presented in Box 36.7 . Noncompliance with antidepressant therapy may result in lack of interest in any therapeutic regimen.

Patients with stroke and other neurological diagnoses often have depression, which reduces motivation and decreases compliance with a therapeutic regimen. Although obviously linked, the degree of functional restoration after a stroke does not always correlate with resolution of depression.

Many patients with neurological disorders are diagnosed with or experience anxiety and depression. Affective symptomatology can be the result of cognitive and emotional deficits or impairment of brain function from the existing pathology. In the rehabilitation environment, many patients may show signs and symptoms of anxiety or depression that can make the process of recovery more difficult. The rehabilitation professional must recognize the manifestations of both anxiety and depression, such as fear of dying or “going crazy,” heart palpitations, shortness of breath, difficulty concentrating, depressed mood, diminished interest or pleasure in activities, sleep disturbance, changes in appetite, psychomotor retardation and agitation, and suicidal ideation. Anxiety and depression may limit the patient’s full participation in recovery of function and are associated with poorer outcomes. ^,

Anxiety and depression can be managed well when treated with the medications discussed previously, but some drugs—including centrally acting hypotensives (methyldopa), lipid-soluble β-blockers (propranolol), benzodiazepines, and other CNS depressants—may cause a depressed mood. Therefore in the case of a patient with depression, review of the medication regimen can be useful as it can help to determine whether one of the medications is implicated.

Pharmacological treatments for anxiety and depression should be administered at a dosage and time that ensure the best patient response during treatment. Antianxiety medications (see Box 36.6 ) act within a short time after ingestion, producing their effects of sedation and relaxation and thereby reducing anxiety. Higher levels may cause drowsiness, sleep, and anesthesia and are associated with falls, which may not be ideal when the aim of treatment is to promote recovery of function. Antidepressant medications (see Box 36.7 ) typically take weeks for therapeutic levels to be achieved in the brain and an improvement in mood to be demonstrated. Rehabilitation may be appropriate for a patient taking these medications when they have improved the patient’s mood and outlook. Side effects of antidepressants can also cause some difficulties, including lightheadedness, drowsiness, short-term memory loss, disturbed sleep, clumsiness, sedation, and low blood pressure.

Some evidence has shown that recovery from brain injury may be positively influenced by antidepressants ^, and that antidepressants can play a role in brain plasticity. These studies suggest that recovery of function after brain injury can be influenced by experience and pharmacological intervention. Rehabilitation specialists must be prepared to assess responses to pharmacotherapy, recognize adverse effects, manage minor side effects, and seek appropriate assistance for adverse events.

Arthritis and autoimmune disorders

Autoimmune mechanisms play an important role in the inflammatory process and progressive joint destruction of rheumatoid arthritis (RA). Because of the constant pain associated with movement, patients tend to seek nonprescription drugs (including dietary supplements) that often escape prescription drug monitoring programs in pharmacies. It is important for all health professionals to recognize this issue, particularly with RA. In the management of RA, the therapeutic approach may influence the progress of rehabilitation. Pharmacological agents that reduce RA symptoms and impede joint damage can be categorized as either nonbiological disease-modifying antirheumatic agents (DMARDs) or biological DMARDs, which include inhibitors of tumor necrosis factor (TNF)-alpha biologics or non-TNF biologics. DMARDs are the key mediations that should be initiated as soon as possible after disease onset. Nonsteroidal antiinflammatory drugs (NSAIDs) and/or corticosteroids can be used for symptomatic improvement as they provide rapid relief of symptoms compared with DMARDs, which may take weeks to months to have an effect.

Treatment with glucocorticoids may reduce joint pain and facilitate movement, but it may also produce changes in mood and muscle wasting. Although this is reversible and limited to systemic administration of high-dose corticosteroids, its impact cannot be overlooked and certainly affects the prognosis of physical or occupational therapy. Corticosteroids should not be used as monotherapy; they are valuable in controlling symptoms before DMARDs can take effect and are used in acute RA flares as burst therapy. Continuous low doses of corticosteroids may be used as adjunctive therapy when DMARDs do not provide adequate disease control. Some data suggest that they have disease-modifying activity ; however, it is preferable to avoid chronic use when possible so as to avoid long-term complications. NSAIDs and DMARDs have steroid-sparing properties that permit reductions in corticosteroid dose. Prednisone and related glucocorticoids may often produce a false sense of well-being that may exceed the ability of the patients to engage safely in certain exercise regimens. From the patient’s perspective, this pharmacological effect is perceived as a “cure” and does not provide the motivation to continue with exercise therapy. The same problems may exist with the use of corticosteroids in other autoimmune disorders.

NSAIDs ( Box 36.8 ) have long been used for the relief of pain due to arthritis; however, depletion of prostaglandins in the gastric mucosa produces bleeding, which has limited their usefulness. NSAIDs should seldom be used as monotherapy for RA because they do not alter the course of the disease; instead, they should be viewed as adjuncts to DMARDs. The development of newer agents that are more selective for isoforms of cyclooxygenase (COX-2 inhibitors), which are involved in joint inflammation, is a major advance. An example is celecoxib. Although bleeding disorders are dramatically reduced, the incidence of ataxia with these agents may be increased. Unfortunately cardiovascular toxicity risk has led to the withdrawal of most of the COX-2 inhibitors from the market. Patients with neurological diseases or pathological processes with problems requiring anti-inflammatory medications may develop side effects that interact with and complicate existing motor deficits. Failure to comply with the arthritis medication regimen will likewise reduce effective movement.

BOX 36.8

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