Now let's talk about stroke side effects. Learning objective number six. Determine the cause of shoulder pain in your stroke patient in your outpatient clinic post-acute care. Post-stroke shoulder pain is encountered commonly, particularly during the spastic phase of recovery. But the differential diagnosis is large, and it can include complex regional pain syndrome, shoulder subluxation, brachial plexopathy, peripheral nerve injury, bicipital tendinopathy, rotator cuff tendinopathy, adhesive capsulitis, and heterotopic ossification. Complex regional pain syndrome, or CRPS, type 1, is also known as reflex sympathetic dystrophy. It may occur in up to 25% of stroke patients, characterized by shoulder pain, hand pain, hyperesthesia, vasomotor changes, wrist and or hand edema, skin and or muscle atrophy in the shoulder and hand. Type 1 CRPS is also known as shoulder hand syndrome. Ultimately, it is a clinical diagnosis. The most sensitive and specific diagnostic test for this is a triple phase bone scan that can reveal, in select cases, periarticular uptake in the shoulder, wrist, and or metacarpophalangeal joints. Treatment modalities for CRPS are varied with varying degrees of success. This can include, for the upper extremity, stellate ganglion block, oral steroids, nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, anticonvulsants, alpha adrenergic blockers, beta blockers, and other interventions, such as calcium channel blockers, topical capsaicin, transdermal lidocaine, calcitonin, biphosphonates, and intraarticular corticosteroid injections. Non-pharmacologic management of CRPS includes range of motion exercises, desensitization techniques, edema control, transcutaneous electric nerve stimulation, or TENS, contrast baths between hot and cold, and ultrasound. Shoulder subluxation can occur commonly post-stroke. That's an abnormally increased space between the humeral head and the acromion of the shoulder, and this can be measured in finger breaths. Treatment for shoulder subluxation include acrylic lap trays or lap trays of other materials, wheelchair arm boards, kinesio taping, functional electric stimulation, and slings. In brachial plexus endoperiphal nerve injury, this is thought to be due to traction injury, and this can be investigated with electrodiagnostic studies, and management of this is similar to that of shoulder subluxation, including range of motion exercise, proper static and dynamic positioning, and judicious use of slings. Bicipital tendinitis, or tendinopathy, is characterized by pain in the interior and lateral aspects of the shoulder. Yergesen signs may be positive, which is pain with resisted external rotation of the arm with the elbow inflection. Treatment options include stretching exercises of the biceps brachii muscle, strengthening exercises of the biceps brachial muscle, if feasible, oral analgesics, and injections. With lidocaine and or steroid. Rotator cuff tendon tear and or tendinopathy may be caused by impaired glenohumeral joint biomechanics post-stroke with positive impingement signs. Treatment options include range of motion exercises, subacromial steroid injection, and or anesthetic injection, and reduction of internal rotator muscle tone. Adhesive capsulitis or frozen shoulder is defined by a decreased mobility post-stroke of the upper limb with decreased range of motions, especially abduction and external rotation associated with discomfort. Treatment of adhesive capsulitis includes range of motion exercise, passive and, if feasible, active-assisted, to terminal stretch, preceded by modalities such as moist-warm, moist-cool, ultrasound, and TENS. In selected cases, an intracapsule steroid injection may play a role. Fortunately, in stroke patients, heterotopic ossification is relatively uncommon. It is more common in traumatic brain injury patients. Often it affects shoulder or elbow. The first line of treatment is range of motion exercise. A preventative drug could be aditrinate disodium, but it cannot remove existing heterotopic bone. Post-stroke spasticity. It is defined as a velocity-dependent increase in muscle resistance against passive lengthening. It arises from involvement of pyramidal tract and nearby motor pathways with increased alpha-motor neuron excitability. Post-stroke spasticity is hard to quantify, but it has been thought to be at least 40% of stroke patients. It can be painful and negatively impact function. The upper limb usually involves shoulder adduction, shoulder internal rotation, elbow flexion, wrist flexion, and finger flexion. Lower limb spasticity usually involves extension of the hip, extension and reflection of the knee, and extension of the ankle, but it can involve others. Management of post-stroke spasticity. Positioning to prevent contractures and to decrease spasticity, the use of static and dynamic splints, and the use daily, if possible, of range of motion and stretching exercises to all affected joints in the upper and lower limbs. Oral agents for spasticity include baclofen, a GABA-B agonist, diazepam, a GABA-A agonist, dantrolene sodium to block calcium release from the sarcoplasm reticulum, tizanidine, an alpha-2 agonist. The side effects include muscle weakness and decreased alertness and cognition. The evidence base for these agents in stroke patients is not very strong. Chemoneurolysis for spasticity. Phenol, an aromatic alcohol, is a neurolytic agent that can be effective, but its use is limited by the high incidence of painful dysesthesias. When effective, phenol can decrease spasticity for up to a year or more, and the cost of phenol is relatively inexpensive. Probably the most common chemoneurolytic agent for spasticity is botulinum toxin A and B. There are other agents, including hyaluronic acid. Botulinum toxin works by blocking acetylcholine release from the presynaptic membrane. There are lower incidence of side effects than the oral agents, relatively easier to use than a phenol block. You tend to be able to inject into or near the motor point of the affected muscle with nerve stimulator for guidance. Some people use ultrasound guidance instead. The downside of botulinum toxin is that there's a shorter duration of effect than with phenol. Intrathecal baclofen. This is delivered via an implantable infusion pump with less CNS depressant effects than with oral baclofen. One can use a lower dose than when given orally. Physiatrists can provide outpatient care for the pumps and be vigilant to avoid overdose or withdrawal. Other treatments for post-stroke spasticity include surgery involving the brain, spinal cord, nerve, and muscle, not used quite as much, acupuncture, and probably a combination of non-pharmacologic and pharmacologic treatments is often a more effective approach. Question. A patient one year post-stroke presents with severe lower limb spasticity. He has tolerated oral baclofen and tazanidine poorly due to sedation. Which treatment options should not be considered? A. Dantrolene. B. Botulinum toxin injection. C. Intrathecal baclofen. D. Diazepam. The answer is D, diazepam. The administration of baclofen, a GABA-B agonist, tazanidine, an alpha-2 agonist, and diazepam, a GABA-A agonist, can result in central nervous system depression. Targeted injection of intramuscular botulinum toxin type A in patients with stroke-related spasticity may effectively reduce spasticity. Intrathecal baclofen is associated with less central nervous system depression and fewer side effects because of its direct delivery past the blood-brain barrier, although it is generally more effective for lower limb spasticity. Use of intrathecal baclofen for stroke patients with spastic hypertonia resulted in improved quality of life. Dantrolene is the only peripherally acting oral antispasticity medication that functions by proxying calcium released from the sarcoplasmic reticulum. Deep venous thrombosis, or DVT. Stroke patients can have at least two out of three elements of Verckau's triad, the triad being immobility, endothelial injury, and venous stasis. The prevalence of DVT post-stroke can be as high as 20% to 75%, and about 25% of all DVTs are proximal. How do we prophylax against DVT? With venous gradient compression hose, intermittent pneumatic compression devices, and heparin subcutaneously, unfractionated or low molecular weight. How do you diagnose DVT? History often includes calf pain and limb pain. However, DVT can often be asymptomatic. Physical examination can include limb edema and a positive Holman sign, but also physical examination in patients with DVT can often be normal. Diagnosing it can include a venous duplex ultrasonography and a D-dimer assay. In very rare cases, in inconclusive cases, a venogram can be prescribed. How do you treat DVTs? With anticoagulation, with warfarin, with low molecular weight heparin, and with other devices. There's differences in opinion. Some physicians will only treat proximal DVTs in the thigh. Some physicians will say you should treat all DVTs, even if it's more distal. Vena cava filters when anticoagulants are contraindicated, such as if you have a hemorrhage or you're at a falls risk, and you want to early mobilize patients whenever possible. Pulmonary embolism. Fortunately, it seems to occur in only 1% to 2% of stroke patients. History could be dyspnea, chest discomfort, examination, tachypnea, pain upon deep inspiration, tachycardia. Diagnosis of pulmonary embolism generally is with a spiral chest CT scan or a ventilation perfusion scan, and rarely pulmonary angiography. Generally, treatment for pulmonary emboli is an anticoagulant for about six months. If that cannot occur, vena cava filter, and sometimes removal of the clot if that can be done. Bladder dysfunction post-stroke. It occurs in 50% to 70% of stroke patients within the first month, but exists in only about 15% of patients at six months and about 10% of patients at two years. Bladder dysfunction can include failure to empty and failure to store. Bladder dysfunction post-stroke may result in urinary tract infection, skin breakdown, and social embarrassment. This seems to occur by injury to the central descending pathways that leads to the loss of voluntary inhibition of the detrusor muscle, leading to a hyperactive bladder, but also you can have an areflexic or hyperflexic bladder or outlet obstruction. Contributing extrinsic factors for bladder dysfunction post-stroke include diabetes, existence of a urinary tract infection, aphasia, cognitive dysfunction, and impaired mobility. In an inpatient rehab setting, bladder scans by nursing staff should be done to see if there is any high post-void residual. If that does exist, then bladder catheterization intermittently is the preferred mode unless if there's a contraindication to that and one needs to have a more permanent catheterization. Urodynamic testing can be very, very helpful, but unfortunately in recent years is not being covered by insurance in the inpatient setting and only is being covered in the outpatient setting. Management of bladder dysfunction should include fluid intake regulation, a scheduled toiling bladder routine, treatment of UTI if it exists, training of the family, mobility and toilet transfer training, and the possible role of transcutaneous electrical stimulation. Medications for bladder dysfunction include oxybutynine for hyperreflexic bladder, corticol for hypoactive bladder, Tamsulosin, an alpha blocker for sphincter hyperactivity, and the role of botulinum toxin injections into the urinary sphincter for dyssynergia. Bowel dysfunction occurs in about 30% of patients, usually involved with incontinence. If there's any infectious causes, you should treat that. Timed toiling with bowel routine and toilet transfer training should be done.

post-stroke shoulder pain

spasticity

treatment options

deep venous thrombosis

bladder and bowel dysfunction