eMedicine Specialties > Physical Medicine and Rehabilitation > Upper Limb Musculoskeletal Conditions

Shoulder and Hemiplegia: Treatment & Medication

Author: Robert Gould, DO, Physiatrist, Interventional Pain Care, LLC
Coauthor(s): Susan S Barnes, DO, Assistant Professor, Department of Physical Medicine and Rehabilitation, Michigan State University
Contributor Information and Disclosures

Updated: Feb 5, 2009

Treatment

Rehabilitation Program

Physical Therapy

Therapy during the flaccid stage

In patients with hemiplegia, ROM of the shoulder is usually lost early, so Hanger and colleagues recommended that preventive treatments begin as soon as possible, usually within the first 1-2 days poststroke.3 Arm support and preservation of joint ROM is performed through early passive motion. Before active rehabilitation exercises of the extremities are started, Cailliet suggests initiating trunk motions with side-to-side rolling.6 As the patient progresses from the supine to the prone position, attempt to maintain the patient in reflex-inhibiting positions. Gradually implement exercises to raise the arm overhead. Upon regaining the seated position, the patient begins gentle weight-bearing exercises through the impaired arm with the elbow and wrist extended, causing glenohumeral joint reduction and proprioceptive stimulation to the shoulder.

Cailliet has also contended that ROM should be evaluated often because of the almost daily progression or regression of the completed stroke.6 Full ROM does not need to be a therapeutic objective but a means for preventing contractures. Also, during passive exercises, the patient should try to assist with motions and hold positions in hopes of encouraging active control of the extremity. Sensory stimulation, as well as NMES, can be used to initiate sensory-motor reeducation. However, if functional gains plateau because of persistent weakness, then attention may need to focus on functional retraining of the unaffected limb or, through the use of assistive devices, on achieving independence with ADL. Forced extremity use or constraint therapy also may be considered.

Therapy during the spastic stage

A major goal of early stroke management is the prevention of muscle spasticity that could interfere with the patient's potential for regaining function. As muscle tone returns to the hemiplegic limb, spasticity may progressively increase. Carr and Kenney proposed the use of reflex-inhibiting postures that tend to discourage the development of spasticity, contractures, and other undesirable sequela.38 Even with proper positioning, spasticity may evolve, thus requiring frequent slow stretching, along with the use of splints, to help reduce tone. Overly aggressive stretching should be avoided since it can have a deleterious effect on the treated shoulder by inducing a worsened synergy.

Development of motor control

As hemiparetic limb movements evolve, they show a combination of hypertonicity and weakness, features typical of an upper motor neuron lesion. The recruitment patterns of individual motor units in these affected muscles are slow and inconsistent. Brandstater has related that the variable degrees of cocontraction of the agonist and antagonist muscle groups cause movements to be slow and clumsy.39 Because of the importance in coordinating these movements during recovery, multiple approaches have been developed in an attempt to improve functional outcome. More conventional rehabilitation methods involve reeducating weak muscles by strengthening and stretching. But because these methods have produced marginal results, other techniques that attempt to counter the evolution of normal pathological processes and encourage the use of sensory inputs to facilitate muscle activity have been developed.

Neurodevelopmental technique

Developed by the Bobaths for the treatment of cerebral palsy, the neurodevelopmental technique (NDT) is probably the most widely accepted method used in the development of motor control in patients with hemiplegia. Brennan relates that exercises that promote normal muscle tone and diminish excessive spasticity through the use of reflex-inhibiting postures are performed and allow the patient to feel normal movements while preventing the use of compensatory motions.40 As Lorish and colleagues indicate, this facilitates higher-level reactions and patterns in order to attain normal automatic motor responses that eventually allow the performance of skilled voluntary movement.35 Brandstater suggests that reciprocal inhibition also be used to temporarily reduce tone in spastic antagonist muscles through the use of a vibratory stimulus.39

Sensorimotor integration

Advocated by Rood, the sensory integration system, as described by Brandstater, involves superficial sensory stimulation and feedback to the affected extremity by means of brushing, stroking, tapping, icing, vibration, sudden or gentle stretching of the muscle, and even electrical stimulation to facilitate muscle activation.39 The use of robot-aided sensorimotor stimulation also has been implemented. Volpe and coauthors researched the effects of using a robotic device that interacts with the patient in real-time to enhance motor outcome.41 The robot was able to guide the powerless limb and provided a sensorimotor experience that responds quickly, just like hand-over-hand therapy. In their randomized blinded study, robot-trained subjects demonstrated improved motor outcome of the shoulder and elbow, as well as improved function.

So theoretically, if motor recovery does in fact depend on motor relearning, then optimal therapies can be tailored for individual patient needs through treatments performed by robotic devices. Overall, Volpe believes that "focused sensorimotor exercise appears to produce better motor outcome."41

Functional utilization of evolving synergies

Assuming normal stages of recovery following stroke, Brunnstrom encouraged reflex tensing in order to develop flexor and extensor synergies during early recovery. According to Reding, induced synergistic reflexes transition into voluntary activation through central facilitation when applied to physiotherapy.42 Functional utilization uses techniques such as tonic stretches and voice commands to elicit muscle contractions.

Motor relearning program

Developed by Carr and Shephard, this practical method emphasizes motor relearning by practicing task-specific motor activities while sitting, standing, or walking.43 Therapists analyze each task, determine which components the patient cannot perform or has difficulty performing, trains the patient in those components of the task, and ensures carryover of this training during daily activities. Brennan has maintained that ultimately, treatment focuses on eliminating unnecessary muscle activity, subsequently expediting skilled motor activities.40 Lorish and colleagues have contended that the use of task-specific training programs tends to be more consistent with modern theories of motor relearning.35

Biofeedback

Biofeedback is based on muscular relaxation and/or reeducation by verbal, visual, sensory, or auditory responses. Biofeedback is used in an attempt to relax the antagonist muscles, subsequently allowing the opposed agonists to function more effectively. In order to reeducate the UE, the spastic scapular and glenohumeral antagonist muscles need to be released in order for the agonists to work more proficiently. A common type of biofeedback, which was first introduced in 1960, involves the use of EMG for neuromuscular reeducation. Overall, trials involving EMG biofeedback have shown mixed results, and its cost-effectiveness is uncertain. However, a meta-analysis by Schleenbaker and Mainous showed it to be an effective tool for neuromuscular reeducation and improving functional outcomes in stroke patients with hemiplegia.44

Proprioceptive neuromuscular facilitation

Developed by Kabat, Knott, and Voss, proprioceptive neuromuscular facilitation (PNF) involves repeated muscle activation of the limbs by quick stretching, traction, approximation, and maximal manual resistance in functional directions (ie, spiral and diagonal patterns) to assist with motor relearning and increasing sensory input. Brennan asserts that it is based on the principles of normal human development (ie, mass movements precede individual movements, reflexive movements precede volitional movements, developments occur cephalically to caudally, control is gained proximally prior to distally, the timing of normal movements is distal to proximal).40 Lorish and coauthors have considered it to be an optimal method of stretching in patients with hemiplegia.35

In an attempt to relax spastic antagonist muscle groups, rhythmic stabilization can be used, which involves alternating voluntary contractions of agonist and antagonist muscles. However, Brandstater revealed PNF to be more effective when muscle weakness is not due to upper motor neuron lesions.39

Active repetition

Chae and colleagues revealed that the use of active repetition has been shown to maximize motor relearning when used in the appropriate candidate.4,5 Parry and coworkers found that stroke patients who were less severely impaired (ie, possessed some early volitional arm movement) prior to treatment benefited from the use of early additional therapies that involved repetitive movements and functional tasks.45 However, patients with severe arm impairment showed very little improvement in function irrespective of receiving additional therapies. This data supports previous clinical trials that suggest there is no current physical therapy approach that results in sustained improvements of upper limb function in patients who are severely impaired. In patients who are severely impaired, the use of adaptive techniques and equipment may be an appropriate rehabilitation strategy.

As of yet, numerous clinical trials have not proven that application of any of these facilitative approaches improves patient outcome over conventional therapy.46,47,48,49,50,51  They have also not yet proven that one of these approaches is clearly superior to the others.4,35,39  Currently, common clinical practice involves implementing elements of various techniques, with Cailliet suggesting that the following basic concepts be used during muscle reeducation6 :

  • Patient should visualize (ie, mirror) specific movements.
  • Verbally reinforce intended movements and encourage the feel of specific motions.
  • Copy similar motions performed simultaneously by the contralateral arm.
  • Position the UE to decrease scapular depression and retraction.
  • Apply sensory stimulation simultaneously to movements.
  • Use prone exercises to stimulate righting reflexes that tend to imitate primitive motor function.
  • Start seated and standing stimulation exercises to help decrease subluxation and modify synergy patterns.
  • Attempt to increase passive range of motion (PROM) with gentle slow motion, rhythmic stabilization, or voluntary contraction followed by relaxation or gentle stretching.
  • Avoid vigorous traction on the arm when stretching connective tissue around the spastic joint.
  • Use of electric stimulation can enhance muscle relaxation.
  • Use the functional arm to simultaneously train the paretic arm to improve ROM and proprioceptive stimulation.
  • Use modalities (eg, ice, transcutaneous electrical nerve stimulation [TENS], vibration) to diminish spasticity.

Related eMedicine articles:
Motor Recovery In Stroke
Stroke Motor Impairment
Transcutaneous Electrical Nerve Stimulation

Surgical Intervention

In the past, surgical release of tendons and muscle was commonly performed on patients experiencing prolonged spasticity and synergy. For patients experiencing a painful spastic shoulder, surgical transection of the subscapularis and pectoralis tendons was performed to eliminate internal rotation and adduction forces. Hecht reported that following treatment, up to 88% of these patients had improved pain and increased ROM, with some developing active abduction.52 Today, this form of treatment rarely is used.

Other Treatment

Constraint-induced movement therapy

Constraint-induced movement therapy (CIT) is a family of therapies that induce patients who have had a stroke to greatly increase the amount and quality of movement of their paretic limb, in turn improving function. CIT is based on the theory of "learned nonuse," first described by Wolf and colleagues53  and later by Taub and coauthors.54 Following substantial neurological injury, a shocklike phenomenon, called diaschisis, results in a dramatically depressed condition of motor neuron function. During this shock period, the patient is unable to move the affected limb and subsequently learns to compensate with the functional limb. As the shock resolves and function starts to improve, attempts to use the affected limb result in clumsy and ineffective movements that positively reinforce continued compensation.

Treatment begins by restraining the functional limb during all waking hours, except for specified activities, and then forcing the patient to perform tasks almost exclusively with their paretic limb for up to 2 weeks. This usually produces measurable improvement of function in the paretic limb, as well as increases in speed and strength of contraction, provided some selective hand movement (slight wrist and finger extension), good balance, and good cognitive and communication skills are present.

As reported by Morris, a behavioral training technique called shaping often is used in conjunction with CIT.55 Shaping has resulted in substantial improvement of motor function. Shaping approaches a desired motor outcome in small successive steps through explicit positively reinforced feedback by the therapist. This allows subjects to experience successful gains in performance with relatively small amounts of motor improvement. A battery of approximately 60 tasks has been developed with a preliminary shaping plan for each task. Each task can be broken down into subtasks. Performance regressions are never punished and usually are ignored. If performance continues to exhibit no improvement after approximately 3 trials, the subject is encouraged to improve further at a later time, a simpler subtask is attempted, or an entirely different task is substituted. Eventually, an individualized task-oriented home program that emphasizes the use of the most impaired movements and joints is established.

Researchers report that patients tend to reach a plateau in motor recovery within 6-12 months following stroke. Taub and coauthors refuted this by studying the effectiveness of CIT in overcoming learned nonuse in chronic hemiplegic stroke patients.54 Compared with an attention-comparison group, the restrained subjects improved on each measure of motor function (ie, performance time, quality of movement, range of activities); in most cases, patients improved markedly. Two-year follow-up revealed that ADL functions had been maintained or increased. Researchers subsequently concluded that the use of CIT proved to be an effective means of restoring substantial motor function in chronic stroke patients.

Intra-articular triamcinolone acetonide injection

Some speculate that the use of a triamcinolone injection into the glenohumeral joint is effective in relieving shoulder pain experienced by patients with hemiplegia. Typically, 3 injections of 40 mg of triamcinolone are given via the posterior route. Dekker and colleagues demonstrated significant reduction in pain (5 of 7 patients) and improved ROM (4 of 7 patients) that did not reach a level of significance.56 None of the secondary outcome parameters (eg, spasticity, motor function, signs and symptoms of shoulder-hand syndrome) showed statistically significant changes either. Dekker concluded that careful positioning, adequate support, and proper handling remain the key actions to prevent hemiplegic shoulder pain.
 
Another study, a randomized placebo-controlled trial by Snels and coauthors involving intra-articular triamcinolone injections, concluded that treatment effect seemed to decrease shoulder pain and accelerate recovery but was also not found to be statistically significant when compared with placebo.34

Subscapularis motor point nerve block

Many authors, including Wanklyn and colleagues, believe that shoulder pain relates significantly to restriction of external rotation secondary to spasticity.21 For this reason, Chironna and Hecht felt that motor block to nerves innervating internal rotators would help relieve the pain caused by internal rotation synergy.57 Using a medial scapular approach, the 2 authors identified the motor points of the nerves to the subscapularis (upper and lower subscapular nerves) via electrical stimulation; then they injected phenol in these points.57 An immediate improvement in external rotation, abduction, and flexion was noted, as well as a reduction in pain.

Hecht followed this up with a larger study that showed similar results in pain control and ROM, with the greatest improvement in external rotation.52,58 Hecht also reported on a subset of patients with a more spastic pectoralis major than subscapularis. These patients present with greater limitations and pain in abduction and flexion compared with external rotation.

A major complication reported with phenol motor point blocks and neurolysis of mixed nerves is the onset of delayed or chronic neuropathic pain. Fortunately, as reported by Chironna and Hecht, the subscapularis has no sensory nerve component, making the onset of true neuropathic pain unlikely.57 The effect of the block generally lasts from 3-9 months, with the procedure found to be a safe and effective adjunct to conservative treatment. The block is probably most efficacious if performed prior to the development of soft tissue contractures.

Botulinum toxin

Botulinum toxin can be used as a replacement for phenol nerve block if the patient does not tolerate the phenol or if the injection is too painful. BOTOX® also is preferred when the desired outcome is for slower onset with shorter duration.59,60 This procedure is sometimes used when the subscapularis and pectoralis major muscles require nerve block.

Neurolysis of the musculocutaneous nerve

Elbow flexor spasticity is a common poststroke complication of the flexor synergy pattern. Regular stretching of this muscle group has been suggested as only being effective for a very short period of time before the spastic shortened muscle returns. Kong and Chua found that neurolysis (50% ethyl alcohol) of the musculocutaneous nerve can be an effective treatment.61 Subjects experienced significant improvement in elbow flexion spasticity and PROM, without it affecting their strength. These improvements were maintained during the 6-month follow-up period. A small percentage of patients even experienced improved walking balance, decreased finger flexor spasticity, and pain relief of the shoulder. The only significant complication reported was a temporary dysesthetic pain in the distribution of the lateral antebrachial cutaneous nerve, a branch of the musculocutaneous nerve.

Neuromuscular electrical stimulation

Since no sling design definitively prevents or treats shoulder subluxation, an effective alternative available is NMES. Chantraine and colleagues reported that the aim of NMES is to reduce subluxation of the hemiplegic shoulder without the use of restrictive splints.62 NMES may even elicit strong sedative effects on pain by acting on sensory nerves. Faghri and coauthors believed that it also could be used prophylactically as a temporary means of splinting the shoulder until recovery of motor function is sufficient enough to support the glenohumeral joint.8 Numerous other studies have suggested that it also improves spasticity and enhances muscle strength of the hemiparetic limb.

A study by Chantraine and colleagues found that patients with hemiplegia and subluxation who received 5 weeks of NMES had significantly more improvement in pain relief, reduced subluxation, quicker motor recovery, and possibly facilitated recovery of shoulder function. These results were maintained for up to 2 years.62 However, it was recommended that patients continue exercising to maintain control of their pain.

In patients with chronic hemiplegic stroke and TBI, Yu and coauthors used percutaneous NMES (perc-NMES) in the posterior deltoid and supraspinatus muscles 6 hours a day for 6 weeks.17 This resulted in reduced subluxation and improvements in pain and disability. These results were maintained during 3 months of follow-up. Yu and coworkers subsequently followed this up with a study comparing transcutaneous NMES with perc-NMES. They found that perc-NMES is less painful, has a much easier application, and has potential for long-term use. This study also found a reduction of shoulder subluxation, with possible enhancement of recovery and improvement in shoulder pain.18

In another study, Chae and coauthors treated chronic stroke survivors who had shoulder pain and subluxation with intramuscular electric stimulation to the supraspinatus, posterior and middle deltoid, and upper trapezius for 6 hours a day for 6 weeks.5 They compared this treatment group with the cuff-style sling-wearing controls over a similar 6 week time frame. Results showed better pain control in the patients receiving electric stimulation versus controls (63% vs 21%) with an effect that was even maintained through 12 months posttreatment.

At this point, the optimal muscles and number to stimulate has not been established. Yu and coauthors believe that using muscles with strong superior and medially directed forces, as well as those stabilizing the scapula, may significantly enhance the efficacy of this intervention.17,18

Even after 6 months poststroke, forced active repetitive movements of the paretic limb through the use of NMES appears to enhance motor and functional recovery. This has been clinically proven to occur as a result of neuroplasticity, in which active repetitive training of the hemiparetic limb causes functional reorganization in the adjacent intact cortex, subsequently allowing for maximum motor recovery. Chae and colleagues treated the extensor digitorum communis (EDC) and extensor carpi radialis (ECR) by combining neuromuscular stimulation with active repetitive wrist and finger extension exercises for 1 hour per day for a total of 15 sessions, subsequently producing significantly enhanced motor recovery that was maintained for up to 12 weeks.4 However, no significant functional effect was proven.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Skeletal muscle relaxants

Modulate muscle contractions.


Baclofen (Lioresal)

Muscle relaxant (central), presynaptic GABA-B receptor agonist that works on inhibitory synapses in the brain and spinal cord. Lessens flexor spasticity and hyperactive stretch reflexes of upper motor neuron origin. Eliminated through renal excretion.

Adult

5 mg PO bid/tid, titrate to affect q3d; not to exceed 80-120 mg qd divided

Pediatric

<12 years: Not established; 2.5-5 mg PO qd suggested; not to exceed 30 mg (ages 2-7 y) to 60 mg (8 y or older)
>12 years: Administer as in adults

Opiate analgesics, benzodiazepines, alcohol, tricyclic antidepressants, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase baclofen effects

Documented hypersensitivity; history of seizures

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include hallucinations, confusion, sedation, hypotonia, dizziness, weakness, fatigue, unsteadiness, headache, hypotension, nausea, increased urinary frequency, paresthesias, and ataxia; sudden withdrawal can lead to seizures and hallucinations; caution in impaired renal function, pregnancy, and breastfeeding mothers


Diazepam (Valium)

Modulates postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. Also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders. Elimination is via hepatic and renal excretion.

Adult

2 mg PO bid; not to exceed 60 mg/d divided doses

Pediatric

0.12-0.8 mg/kg/d PO divided doses

Phenothiazines, barbiturates, alcohols, and MAOIs increase CNS toxicity when administered concurrently

Acute narrow-angle glaucoma; breastfeeding

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Adverse effects include sedative effect, decreased attention, decreased memory, decreased motor coordination, drowsiness, fatigue, confusion constipation, depression, diplopia, dysarthria, coma, tremor, ataxia, respiratory depression, headache, hypotension, incontinence, change in libido, nausea, vomiting, rash, vertigo, blurred vision, paradoxical excitement, anxiety, hallucinations, sleep disturbances, increased salivation, and neutropenia; true physiological addiction may occur; withdrawal symptoms may occur if tapered too quickly
Patients should avoid jobs or tasks that require full mental alertness, such as operating machinery and driving; caution in patients who are elderly, in those who are debilitated, and in those with hepatic and renal disease


Dantrolene sodium (Dantrium)

Induces release of Ca++ into sarcoplasmic reticulum, subsequently decreasing the force of excitation coupling. Only drug that intervenes at a muscular level. Preferred for the cerebral form of spasticity. Less likely to cause lethargy or cognitive changes like baclofen or diazepam. Eliminated in the urine and bile.

Adult

25 mg/d PO; slowly increase by 25 mg PO q4-7d; not to exceed 400 mg/d divided doses

Pediatric

0.5 mg/kg PO bid; not to exceed 3 mg/kg qid or <100 mg qid

Toxicity may increase with the coadministration of clofibrate and warfarin; coadministration with estrogen may increase hepatotoxicity in women older than 35 years

Documented hypersensitivity; active hepatic disease (hepatitis and cirrhosis)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Long-term safety has not been established; adverse effects include sedation, malaise, fatigue, diarrhea, nausea, vomiting, constipation, GI bleed, anorexia, dizziness, weakness, photosensitivity, urinary changes, tachycardia, labile blood pressure, aplastic anemia, leukopenia, seizures, speech disturbances, headache, depression, rash, pruritus, hepatotoxicity, myalgia, chills, and fever; monitor liver function tests periodically, especially in patients older than 35 years and in females; caution in impaired pulmonary and cardiac function; liver metabolism can lead to hepatotoxicity


Tizanidine (Zanaflex, Sirdalud)

Agonist action at alpha2-adrenergic receptors. Facilitates the action of glycine (inhibitory neurotransmitter) and prevents the release of L-glutamate and L-aspartate (excitatory amino acids) from the presynaptic terminal of spinal interneurons, thus reducing spasticity. Elimination is hepatic and renal.

Adult

4 mg PO tid, start with low dose and titrate; average dose 12-24 mg/d divided doses; not to exceed 36 mg/d divided doses

Pediatric

Not recommended

May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance), and can cause increased hypotensive effects when administered concurrently with diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include hypotension, bradycardia, dry mouth, daytime somnolence, nighttime insomnia, dizziness, UTI, constipation, diarrhea, dyspepsia, vomiting, hepatocellular injury, jaundice, speech disorder, blurred vision, dyskinesia, nervousness, pharyngitis, hallucinations, psychosis, depression, anxiety, weakness, fever, rash, and sweating; monitor ophthalmic and hepatic function; caution in elderly patients, breastfeeding women, prolonged QT interval, and renal disease


Clonidine (Catapres)

Centrally acting alpha2-adrenergic receptor agonist developed as an antihypertensive agent. Acts by reducing sympathetic outflow from CNS. Also has been found to be effective in improving spasticity. Metabolized in liver. Has renal elimination.

Adult

0.1 mg PO bid, slowly titrate up to 0.3 mg bid; not to exceed 0.6 mg (or 2.4 mg) qd divided doses
Catapres-TTS (transdermal patch): 0.1 mg qwk; titrate up to 0.3 mg qwk

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Tricyclic antidepressants inhibit hypotensive effects; coadministration with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects are enhanced by narcotic analgesics

Documented hypersensitivity; severe coronary artery insufficiency, conduction disturbances, cerebral vascular disease, and renal failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include syncope, orthostatic hypotension, nausea, vomiting, anorexia, malaise, dry mouth, nervousness, agitation, drowsiness, weakness, headache, constipation, rash, pruritus, myalgia, urticaria, insomnia, impotence, decreased libido, arrhythmia, and weight gain; caution in breastfeeding women
Sudden withdrawal produces a rebound effect, including nervousness, agitation, headache, tremor, and a rapid elevation of blood pressure, rarely causing hypertensive encephalopathy and stroke

Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They block the active re-uptake of norepinephrine and serotonin.


Amitriptyline (Elavil)

Representative member of the tricyclic family that is commonly used as an antidepressant with sedative effects. Used in some cases for the treatment of thalamic syndrome and CRPS. Mechanism of action involves inhibition of membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Metabolized by the P450 2D6 of the liver. Has renal elimination.

Adult

25 mg PO qhs, increase weekly; not to exceed 300 mg qd; reduce dose in elderly patients or adolescents

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine and quinidine) may increase amitriptyline levels; amitriptyline inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; patient has taken MAOIs in past 14 d; has history of seizures, cardiac arrhythmias, glaucoma, and urinary retention; acute post MI

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include drowsiness, anticholinergic effects, CNS overstimulation, arrhythmias, stroke, myocardial infarct, coma, seizures, hallucinations, confusion, delusions, ataxia, tremors, extrapyramidal symptoms, hypotension, hypertension, nausea, fatigue, increased perspiration, paralytic ileus, constipation, urinary frequency, nausea, vomiting, blurred vision, headache, photosensitivity, rash, urticaria, alopecia, edema, blood dyscrasias, libido changes, and blood sugar changes
In women, breast enlargement and galactorrhea may occur; in men, testicular swelling and gynecomastia may occur
Caution in patients with history of seizures, urinary retention, closed-angle glaucoma, cardiovascular disease, suicidal tendencies, surgery, electroconvulsive therapy, psychosis, manic depression, hyperthyroidism, liver dysfunction, or diabetes; caution in elderly patients

Antiepileptic drugs (AEDs)

Use of certain AEDs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in muscle spasm.


Gabapentin (Neurontin)

Class of medication that was developed as an adjunct treatment of partial seizures with or without secondary generalization. Structurally related to the GABA neurotransmitter, but it does not interact with GABA receptors, and its mechanism of action is unknown. Used in some cases for the treatment of thalamic syndrome and CRPS. Does not appear to be appreciably metabolized in humans. Has renal elimination.

Adult

300 mg PO qhs, increase over few days to 300-600 mg tid; not to exceed 3600 mg/d divided doses

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may increase norethindrone levels significantly

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include somnolence, dizziness, hyperkinesia, paresthesia, decreased or absent reflexes, anxiety, ataxia, fatigue, nystagmus, visual disturbances, dysarthria, anemia, nausea, vomiting, malaise, headache, anorexia, dry mouth or throat, dyspepsia, flatulence, diarrhea, constipation, gingivitis, hypertension, purpura, arthralgia, alopecia, eczema, pruritus, increased perspiration, hirsutism, dysuria, angioedema, and blood glucose fluctuation; possible seizures during withdrawal; because of dizziness, somnolence, and CNS depression, avoid driving or using complicated machinery until patients have gained sufficient experience with the drug's use
Caution in compromised renal function and elderly patients; caution in breastfeeding women

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.


Ibuprofen (Advil, Motrin)

Representative member of the propionic acid class of NSAIDs. In case of shoulder problems with hemiplegia, it is used in some cases for the treatment of CRPS, bursitis, tendonitis, soft tissue injury, thalamic pain syndrome, arthritis, and general pain control, including headache and muscle aches. Metabolized and eliminated in the urine.

Adult

200-800 mg PO tid/qid

Pediatric

5-10 mg/kg PO tid/qid; not to exceed 40 mg/kg/d

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Adverse effects include GI toxicity (eg, ulceration, bleed, perforation), diarrhea, nausea, vomiting, renal toxicity (eg, acute interstitial nephritis, renal papillary necrosis, hematuria), hepatic toxicity (eg, jaundice, hepatitis), anaphylactoid reactions, edema, aseptic meningitis, blurred vision, dizziness, headache, rash, pruritus, and tinnitus; caution in patients with history of upper GI disease, impaired renal or hepatic function, bronchospastic reactivity, nasal polyps, angioedema, renal disease, hypertension, cardiac failure, anticoagulation therapy, coagulation defects, or diabetes


Ketoprofen (Oruvail, Orudis)

For relief of mild to moderate pain and inflammation.
Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.
Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

More on Shoulder and Hemiplegia

Overview: Shoulder and Hemiplegia
Differential Diagnoses & Workup: Shoulder and Hemiplegia
Treatment & Medication: Shoulder and Hemiplegia
Follow-up: Shoulder and Hemiplegia
References
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References

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Further Reading

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Keywords

shoulder, hemiplegia, stroke, shoulder pain, shoulders, subluxation, pain in shoulder, rotator cuff injury, hemiplegic, complex regional pain syndrome, CRPS, NMES, neuromuscular electrical stimulation, shoulder pain after stroke, contractures, spastic muscle imbalance of the glenohumeral joint

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Contributor Information and Disclosures

Author

Robert Gould, DO, Physiatrist, Interventional Pain Care, LLC
Robert Gould, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, International Spine Intervention Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Coauthor(s)

Susan S Barnes, DO, Assistant Professor, Department of Physical Medicine and Rehabilitation, Michigan State University
Susan S Barnes, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, and American Osteopathic College of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Robert J Kaplan, MD, James E Van Zandt VA Medical Center, Staff Physician, Department of Rehabilitation Medicine
Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service (www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.

 
 
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