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10 Articles in Volume 9, Issue #5
Dextrose Prolotherapy for Recurring Headache and Migraine Pain
Diagnosis of Low Back Pain
Ethics, Education, and Policy: Relationship and Mutual Reliance
Human Chorionic Gonadotropin in Pain Treatment
Musculoskeletal Ultrasound
Painful Herpetic Reactivation and Degenerative Musculoskeletal Injury
Post-stroke Pain
Preventive Medications for Chronic Daily Headache
The Pathophysiology of Neuropathic Pain
Use of Pulsed Radiofrequency in Clinical Practice

Post-stroke Pain

A clinical history and physical examination with judicious use of appropriate diagnostic modalities are mandatory in identifying what is the likely pain in stroke survivors.

It is well recognized that the recovery and long-term health of stroke survivors can be adversely affected by a number of medical complications, including chronic pain. The medical literature estimate of the prevalence of chronic post-stroke pain ranges from 32-42% at four to six months and 11-21% at twelve to sixteen months after a stroke.1-3 Shoulder pain alone has been found to affect up to 72% of post-stroke survivors.4 If one were to include other causes of post-stroke pain, this number could be significantly higher.

The Post-Stroke Rehabilitation Out-comes Project studied the prescription of pain medications by providers at seven distinct inpatient rehabilitation facilities (six in the United States and one in New Zealand) for 1,122 stroke patients.4 The results of this study revealed the complexity of post-stroke pain: twelve distinct areas of pain in the human body were identified, eight distinct classes of medications used to treat pain were utilized, and twenty-nine different pain medications were prescribed.

Properly identifying the potential causes of pain should be a major focus in post-stroke care because the correct evaluation and treatment will be of significant benefit for the patient. The objective of this article is to provide a review in the available medical literature of potential causes and treatment of chronic post stroke pain, including neuropathic and musculoskeletal causes.

Neuropathic Pain Central Post-stroke Pain

Central post-stroke pain (CPSP) has been referred to as thalamic pain and was once thought to be synonymous with thalamic injury. However, it is now believed that the key factor in developing central post-stroke pain is a lesion in the spino-thalamo-cortical pathway and that this syndrome actually arises more often from non-thalamic than thalamic lesions.5 The condition is actually not as rare as once thought and has been reported at an 8% incidence in the first year after stroke, 63% of which develop pain within the first month.6

CPSP is characterized by an intense spontaneous or evoked pain localized in the affected extremities and can affect the entire side of the body with an aching and burning quality.7 Sensory disturbance is a major component of CPSP, including abnormal temperature sensation, dysesthesia and hypersensitivity to cutaneous stimuli.7 In contrast, there is often a normal response to light touch and vibration. The pain appears to be alleviated with relaxation and worsened with emotional and physical stress.7

Commonly prescribed oral medications for use in post-stroke pain include antidepressants and anticonvulsants, while opioids are not felt to be effective.4,8

The tricyclic antidepressant amitriptyline given at 75mg/day was found to be effective in improving the pain scores in 10 out of 15 patients with CPSP versus 1 of 15 in a placebo group of a double blinded placebo-controlled crossover study at 2 weeks and 4 weeks from the start of treatment.9 Amitriptyline is usually started at 10 or 25mg/day and titrated up to 75mg/day. The medication is commonly given at nighttime as it can cause sedation and thus interfere with daytime activities. Amitriptyline has a variety of adverse reactions including anti-cholinergic side effects and should be carefully considered and monitored when prescribing—especially for elderly patients.

Anticonvulsants have been used in clinical practice for a variety of neuropathic pain syndromes since the 1960s. Gabapentin has become commonly used for treating a variety of neuropathic pain conditions and was the most prescribed anti-convulsant in the Post-Stroke Rehabilitation Outcomes Project pain study which looked at medication usage for stroke patients at seven inpatient rehabilitation facilities.4 Gabapentin is a structural analog of the neurotransmitter gamma-aminobutyric acid (GABA), but its exact mechanism of action in the treatment of central neuropathic pain is unclear. Gabapentin is relatively safe, with the most common side effects being dizziness and sedation.

Specific research on gabapentin to treat CPSP is limited to case series and not large, randomized, well-controlled studies.4,8 One report described gaba-pentin as being effective for thalamic pain starting at 300mg two times/day and titrating up to 300mg three times/day, while a second case found effective treatment starting at 100mg three times/day and titrating up to 300mg three times/day lasting at least one year.12,13 There are no randomized clinical trials examining the effectiveness of gabapentin for CPSP on a larger scale at the present time, nor is there any literature on the use of gabapentin at higher doses such as 2400mg/day or 3600mg/day. Further study is recommended before justifying the wide-spread use of gabapentin for this condition.

Lamotrigine is an anti-epileptic medication with non-NMDA anti-glutamatergic activity and is relatively well-tolerated, although there is documented potential for severe dermatologic adverse reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis. It was found to be moderately effective and achieve greater reduction of pain than a placebo at maximum doses of 200mg/day.10 Higher doses of lamotrigine have been thought to provide even better relief of pain but have not been tested with larger controlled studies.11

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) type 1 is a sympathetically mediated pain disorder presenting with the qualities of neuropathic pain. CRPS type 1 is differentiated from CRPS type 2 in that type 1 cannot be defined by a peripheral nerve injury. Although established as a wellknown complication after stroke, it remains unclear exactly how common it is. Estimates of its prevalence have ranged from 12.5% to 30.5%.14-16 CRPS type 1 is most commonly seen one to three months after stroke and less often after five months. The exact mechanisms that precipitate the onset of CRPS after stroke are not precisely understood at this time. Spasticity and limited range of motion of the shoulder, especially external rotation, appear to be influential factors towards development of this condition.17 Conversely, adequate range of motion in the shoulder is felt to be a protective mechanism against the development of CRPS type 1.

The most common presentation of post-stroke CRPS is severe shoulder and hand pain with sparing of the elbow together with swelling, especially in the hand. CRPS is unique from other forms of neuropathic pain in that it is associated with vasomotor, sudomotor, and trophic changes. The diagnosis of CRPS is based on clinical criteria adopted by the International Association for the Study of Pain (see Table 1).

Table 1. Clinical Criteria for the Diagnosis of Complex Regional Pain Syndrome (CRPS)
  1. Continuing pain which is disproportionate to any inciting event.
  2. Must report at least one symptom in three of the four following categories:
    • Sensory— reports of hyperesthesia and/or allodynia
    • Vasomotor— reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry
    • Sudomotor/Edema— reports of edema and/or sweating changes and/or sweating asymmetry
    • Motor/Trophic— reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Must display at least one sign at time of evaluation in two or more of the following categories:
    • Sensory— evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement)
    • Vasomotor— evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    • Sudomotor/Edema— evidence of edema and/or sweating changes and/or sweating asymmetry
    • Motor/Trophic— evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. There is no other diagnosis that better explains the signs and symptoms
Adopted form the International Association for the Study of Pain

The clinical course of CRPS can progress through three stages.18 Stage 1, the acute stage, lasts a few weeks to six months after stroke and is characterized by pain, hypersensitivity, edema, swelling and, possibly, hyperhydrosis. Stage 2, the dystrophic stage, is characterized by decreased blood flow and temperature in the limb, with the development of decreased joint range of motion. The pain may be severe and persistent by this stage. Hyperhydrosis may become more prominent, as can dermatologic findings such as hair and nail changes. Areas of osteoporosis may be seen on plain radiography at this stage. Stage 3, the atrophic stage, is end stage and characterized by severe loss of function. While the pain may be less severe, there are now irreversible atrophic changes to soft tissue, muscle and bone, and almost invariably involving joint contractures. In this stage the skin may appear glossy, cool and dry.

Treatment of this condition can be frustrating and multi-modal approaches are frequently used. Physical and occupational therapy is a mainstay of treatment by decreasing the pain and improving function of the affected limb.18,19 Desensitization of the affected limb through sensory overload using various types of stimuli, contrast baths and massage are among the techniques and modalities that can help the patient overcome the pain.18 At the same time, a concerted effort should be made to restore as much range of motion and motor strength to prevent limb dysfunction as possible. Physical and occupational therapy are valuable adjuncts in treatment and are generally safe. However, therapy does require effort and commitment on the part of the patient to participate but, sometimes, access or transportation to see a therapist can be a barrier to treatment.

There are several pharmacologic treatments for CRPS, but definitive evidence-based recommendations developed from large well-designed controlled studies are lacking. Tricyclic antidepressants, as described previously, are used for various types of neuropathic pain but there are no specific studies in the literature on the efficacy of this medication class in treating CRPS type 1.

“Musculoskeletal causes of shoulder pain are often a result of biomechanical changes to the upper extremity after a stroke. Spasticity can retract the scapula and depress, adduct, and internally rotate the shoulder—all of which can eventually cause pain.”

Oral corticosteroids have shown success in treating post-stroke CRPS type 1, although their exact mechanism of action is unclear for this condition. A study comparing prednisolone to the non-steroidal anti-inflammatory drug piroxicam found the prednisolone group to have an 83% improvement in the symptoms compared to 17% for piroxicam.20 However, this study was not tested against a control group receiving a placebo.20 Prednisone at up to 100mg/day, tapered over two weeks, has also been used with success.18,21 While not enough studies exist to put forth an agreed-upon corticosteroid, dosing, or duration, we feel these results warrant consideration of oral corticosteroids as a safe and potentially effective treatment option for CRPS type 1, barring contra-indications to the medication.

As described previously for central post-stroke pain syndrome, anticonvulsants have been used to treat for neuropathic pain and gabapentin, in particular, has been found to be frequently used in post-stroke pain.4 Limited research on gabapentin in the treatment of CRPS type 1 post-stroke has been done. One study evaluated patients in a pain center who had been diagnosed with CRPS type 1 for years, many of whom had failed other types of treatments. This study showed mild benefits of gabapentin in pain relief.22 A second study of gabapentin in early stage CRPS type 1 showed reductions in pain scores by six weeks of treatment, but was not controlled against a placebo group.23 Both studies started patients on gabapentin at 600mg/day and titrated upwards to 1800mg/day maximum. It is not known if higher doses than those used in the studies would offer greater benefit (gabapentin can be prescribed at doses of up to 2400 or 3600mg/day). Neither study showed gabapentin to be beneficial for the other complications of CRPS, most notably limb dysfunction, although van de Susse’s study did show some reduction of sensory deficits in the affected limb.22,23

Thus, while commonly prescribed, the current literature suggests that gabapentin may not be as effective in treating CRPS type 1 as its frequency of use indicates. There are both older and new anti-epileptics which are available on the market which have not had any supporting literature in the treatment of CRPS. Pregabalin is a newer anti-epileptic which is molecularly-related to gabapentin but, at the present time, there are no specific studies of this medication in treating CRPS. High quality randomized studies of these various anti-epileptics versus placebo control and each other during all stages of CRPS type 1 need to be done to help develop evidence-based treatment guidelines and best, safe practices.

Musculoskeletal Pain Hemiplegic Shoulder Pain

Musculoskeletal causes of shoulder pain are often a result of biomechanical changes to the upper extremity after a stroke. Spasticity can retract the scapula and depress, adduct and internally rotate the shoulder—all of which can eventually cause pain. In particular, pain with external rotation is thought to be a significant factor in the development of persistent shoulder pain after stroke.24-26 Loss of motor control can prevent the patient from countering these forces and thus perpetuate this cycle. Adhesive capsulitis, glenohumeral subluxation and rotator cuff injury are three of the major underlying pathologies seen in hemiplegic shoulder pain, among others. Other causes of shoulder pain can include neck pathologies such as cervical radiculopathy, brachial plexus injury and myofascial pain. These conditions are by no means mutually exclusive and can be seen in combination with each other.

Adhesive capsulitis, affecting up to an estimated 50% of patients, is a major cause of post-stroke shoulder pain.27 It is actually unclear why adhesive shoulder capsulitis develops, but the condition is characterized by the insidious global loss of shoulder movement in multiple planes of movement, but especially external rotation and abduction. Loss of shoulder complex motion eventually leads to decreased soft tissue elasticity and then to joint contracture.

Gleno-humeral subluxation after a stroke most commonly occurs in the anterior and inferior directions. In the hemiplegic shoulder, the rotator cuff muscles—in particular, the supraspinatus—are ineffective in supporting the humerus. Consequently the soft tissues supporting gleno-humeral joint become over-stretched. While shoulder subluxation is associated with pain, it is not clear that the subluxation itself is the direct cause of pain.25 Subluxation though can predispose the patient to painful tendon, soft tissue, or even brachial plexus injury through improper handling or movements. Prevention of this condition is difficult but can be done through proper positioning of the affected upper extremity. Interventions can include proper bed and wheelchair positioning, arm support via devices such as a lap tray, taping or a shoulder sling. Caretakers and medical staff should be educated on proper handling technique such as avoiding sudden traction on the limb.

Hemiplegia itself can be a contributing factor to rotator cuff injury, as the humeral head is unable to glide downwards naturally, thus predisposing the rotator cuff to become impinged.27 This situation can further be exacerbated if spasticity develops, as the normal scapulo-humeral rhythm is disrupted and results in increased stress on the gleno-humeral complex. Poor handling of the shoulder can exacerbate tendon injury and pain or precipitate more serious structural damage. One study of hemiplegic shoulder pain found a rotator cuff tear—not just impingement—in 22% of patients studied.27

While exercise and therapy are mainstays of treatment for musculoskeletal shoulder conditions in the normal adult population, in the stroke population this can be a major challenge as the patient may have little or no voluntary movement along with the presence of spasticity. Transcutaneous functional electrical stimulation applied to the supraspinatus and posterior deltoid is a modality that has shown some effectiveness in not only reducing pain but also addressing glenohumeral subluxation.28

No studies were found in the literature that evaluated the effectiveness of specific oral medications in the treatment of hemiplegic shoulder pain. However, corticosteroid injection into the painful hemiplegic shoulder has been studied as a means of treatment. A study by Dekker et al of the effects of a series of three triamcinolone 40mg injections into a painful hemiplegic shoulder found beneficial gains in pain reduction after one or two injections in 56% of the patients, although this study was not done with a placebo control.29 A later study looking at a series of three 40mg triamcinolone injections into a painful hemiplegic shoulder versus a saline placebo control found saw a reduction in pain on a visual analog score of 2.3 from triamcinolone versus 0.2 for the placebo, but this was not statistically significant.30 Based on this, it is unclear whether corticosteroid injections should be broadly performed for hemiplegic shoulder pain, but the use of this treatment may be more effective when considered on a case by case basis.

A different approach to the treatment of hemiplegic shoulder pain was studied by Lim et al on the premise that spastic shoulder muscles were the cause of hemiplegic shoulder pain.31 This idea is based on the hypothesis that intra-muscular botulinum toxin A (BTA) injections may provide targeted muscle relaxation and inhibit sensory neuron neurotransmitter release. This study compared the injection of BTA into the infraspinatus, subscapularis and pectoralis muscles (maximum 50 units per muscle, 100 units per patient) with a placebo intra-articular shoulder injection to saline intra-muscular injections in the same muscles with 40mg triamcinolone intra-articular injection. At 12 weeks, the BTA group achieved better relief of pain and shoulder range of motion than the intra-articular corticosteroid group. This study did not compare against a control group receiving both placebo intra-muscular and intra-articular injections.

It appears that the treatment of hemiplegic shoulder pain with injections has some promise. More research needs to be done in evaluating the effects of different agents in the articular space or muscles, dosing strengths, as well as combination therapy of different types of injections. Major consideration needs to be given to the fact that these studies did not make mention of separating out the various subtypes of potential shoulder pathologies. Lo et al demonstrated that the causes of hemiplegic shoulder pain can be complex and it was actually uncommon for patients to have a singular identifiable pathology.27 We believe this is a factor that needs to be clearly defined in future studies and thus may lead to more precise treatments.

Degenerative Joint Disease

Degenerative joint disease is estimated to affect over 40 million people in the United States and is the most common disease of the joints worldwide, commonly affecting the knee and hip in the elderly population.31 The presence of osteoarthritis is associated with poorer functional outcome in the inpatient rehabilitation setting of stroke patients.32

The clinical presentation of osteoarthritis is pain in the involved joint that is initially relieved by rest but present during rest in advanced stages along with morning stiffness of less than 30 minutes. X-ray is an important diagnostic tool in showing decreased joint space, osteophytes and subchondral sclerosis and cysts, but it can be difficult to correlate radiographic severity with the clinical presentation.33,34 As the condition progresses, decreased range of motion at the joint with resultant muscle weakness may occur as well. Symptoms can be exacerbated by spasticity, increased activity, overuse or poor positioning.

Conservative management may include exercise, pharmacologic modalities, and weight loss. An assistive device for ambulation may be able to offload the ground-reactive force through the arthritic limb. Exercise, both aerobic and resistive, is recommended in the treatment of osteoarthritis of both the hip and knee and has been found to provide modest but significant reduction of pain in the hip and the knee.35-37

Pharmacologic treatments are more effective when combined with non-pharmacologic treatment such as exercise.38 Acetaminophen is a well-tolerated and effective analgesic and is considered a first line medication, especially for mild to moderate pain. Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are also effective, although their side effects must be closely monitored. Serious adverse reactions of NSAIDs include gastrointestinal bleeding, renal failure and hypertension.

Tramadol is an atypical synthetic oral analgesic which binds to the µ-opioid receptor and has weak reuptake of norepinephrine and serotonin.39 One advantage of tramadol is that it does not have the renal or gastrointestinal concerns of NSAIDs, although it can potentially lower the seizure threshold which is of special concern in stroke patients. While tramadol has been approved for more moderate to severe pain, a meta-analysis of tramadol’s effectiveness in treating pain from osteoarthritis concluded that while it is effective at reducing pain intensity and function, the benefits are considered small.40

Opioids can be considered for patients with moderate to severe pain who find tramadol, NSAIDs or acetaminophen ineffective.35 While potentially more powerful, opioid therapy does carry its share of adverse side effects such as constipation, nausea, sedation and cognitive side effects.

Femur Fracture

Stroke is associated with a significant decrease in bone mass on the paretic side, as immobility and decreased weight bearing through the limb decrease weight-bearing forces needed to maintain bone density. The risk of femur fracture can be increased four-fold after a stroke, with significantly increased mortality.41,42 Stroke is associated with a significantly increased risk of falls due to motor, cognitive and perceptual deficits, making femur fracture a serious cause of lower extremity of pain.43 Fractures can occur at any time after stroke but have statistically been shown to occur more often several years after the initial stroke.42

Presentation of femur fracture includes pain and tenderness in the hip or thigh, ecchymosis, weakness, deformity and shortening of the leg. Initial treatment involves verification with imaging, immediate orthopedic surgery consultation, cessation of weight-bearing activity and proper positioning of the limb, as well as pain management followed by the appropriate reduction and treatment of the fracture.

Genu Recurvatum

Genu recurvatum is a dynamic posterior hyperextension of the knee during the standing and stance phase of gait. The biomechanical mechanisms that lead to genu recurvatum vary. These causes can include quadriceps weakness, ankle plantar flexor spasticity, Achilles’ tendon contracture, quadriceps spasticity and ankle plantar flexor weakness.44 These biomechanical factors alone, or in combination, cause the ground reactive force to fall farther in front of the knee than normal, pushing the knee into extension and straining the anterior cruciate ligament and posterior capsule. While knee extension is associated with a position of joint stability, excessive extension can lead to pain and eventual deformity if left unopposed. Without the normal cushioning and stabilizing forces of knee flexion seen in the normal stance phase of gait, recurvatum can force direct transfer of weight from the femur onto the tibia, leading to pain from both compression of the medial tibiofemoral joint and tension on the posterolateral ligaments.45

Treatment of genu recurvatum starts by identifying and correcting the biomechanical factors leading to the knee hyperextension. This can include physical therapy for quadriceps strengthening, gait training, proprioceptive exercises, plantarflexor strengthening and treatment of plantarflexion contracture. Orthotics can also be used such as an ankle-foot orthoses (AFO) or a knee cage.46 A common solution is to use an AFO set at a slight degree (e.g., 5°) of dorsiflexion which helps promote knee flexion.

“Stroke is associated with a significantly increased risk of falls due to motor, cognitive and perceptual deficits, making femur fracture a serious cause of lower extremity of pain.”43

Orthoses are generally safe although they can cause some complications.46,47 An orthosis that places the patient into excessive knee flexion can lead to falls—especially in patients with knee extensor weakness—and quadriceps strengthening is encouraged to help counter this. Skin breakdown is another complication for patients with conditions causing edema or fluctuating volume such as congestive heart failure or end stage renal disease, especially when using a plastic AFO. In these situations, a traditional metal upright brace may be a better solution. Compliance can be an issue as patients may find a brace difficult to don or doff, or may be reluctant to wear an orthosis because of their appearance.

Equinovarus Foot

The equinovarus foot is a condition characterized by excessive ankle plantarflexion and inversion which can be accompanied by toe curling. This condition can arise due to spasticity and other upper motor neuron conditions.18 It is caused by the mechanical pull of spastic plantarflexors (gastrocnemius and soleus) and ankle invertors (tibialis anterior, flexor hallucis longus, flexor digitorum longus and tibialis posterior). This can subsequently lead to soft tissue contracture and joint deformity, making treatment and improved function even more difficult. Equinovarus can be painful during the gait cycle as initial contact would occur on the anterolateral foot instead of the heel and also lead to skin breakdown. Excessive plantar flexion from this condition can lead to genu recurvatum and knee pain.

The treatment for equinovarus, similar to genu recurvatum, should address underlying biomechanical abnormalities. Physical therapy can improve range of motion and motor retraining of the muscles of the foot and ankle. Bracing provides stabilization and corrective biomechanical forces. In subjects with spas-ticity, intramuscular injection of botulinum toxin A (BTA) is an effective and relatively safe treatment for equinovarus.48-50 To provide better economy of use, injecting BTA at lower doses in combination with continued passive stretching may produce similar results as higher doses.50

Surgical options are available for severe cases of equinovarus if the joint is contracted. The SPLATT (split anterior tibial transfer) decreases inversion by splitting the spastic tibialis anterior and creating an eversion vector while Achilles tendon lengthening can be done to help treat plantar flexion contractures.18 The SPLATT procedure is considered relatively safe and can increase function, especially in ambulatory stroke patients, although bracing may still be required after the surgery.51,52

Heterotopic Ossification

Heterotopic ossification (HO) is the abnormal deposition of bony tissue outside of, or beyond, normal areas of bone. It can occur from a number of causes including trauma, orthopedic surgery, burns, spinal cord injury and traumatic brain injury. Most commonly, it affects the shoulder, elbow or hip. Neurogenic heterotopic ossification typically develops between one to three months from the time of the initial insult.53 There is extensive literature on neurogenic HO after spinal cord and traumatic brain injuries. In contrast, heterotopic ossification after stroke has been not been nearly as extensively documented.54 An orthopedic study suggests an increased risk of heterotopic ossification for post-stroke survivors who undergo total hip arthroplasty.55 It is unclear exactly how common this condition is post-cerebrovascular accident.

Diagnosis of heterotopic ossification by clinical presentation alone is difficult. Symptoms include pain in the affected joint, decreased range of motion, tenderness, swelling, skin warmth and low grade fever. The clinical presentation of heterotopic ossification can be confused for deep vein thrombosis and cellulitis. Laboratory studies that may help with diagnosis include serum alkaline phos-phatase, erythrocyte sedimentation and C-reactive protein—all of which can be elevated. Alkaline phosphatase can be serially measured to determine activity.56 Alkaline phosphatase is elevated during active formation of bone tissue and gradually decreases to normal as bone formation slows and eventually halts.

Imaging studies include plain radiography, triple phase bone scan, computed tomography (CT) and magnetic resonance imaging (MRI). Triple phase bone scan has excellent sensitivity for diagnosing HO as early as two to four weeks, although it may not be specific in differentiating from other sources of inflammation or skeletal pathologies.57 Therefore, an x-ray is still useful as a relatively specific and low cost test to identify ectopic bone formation. CT is useful in differentiating immature from mature bone and is helpful when surgery is a serious consideration for treatment.58

Radiation therapy has been used both as a prophylactic to neurogenic HO development and as secondary prevention after surgical resection. While showing some promise in retarding the progression of HO, it has thus far been studied for use after spinal cord injuries but not strokes.59 Indomethacin, a non-steroidal anti-inflammatory medicine, has also been studied as a prophylactic agent for heterotopic ossification. It is unclear which treatment is more successful, although there is evidence to suggest radiation therapy may be superior.60 Neither has been advocated for routine use after stroke.

The treatment of neurogenic heterotopic ossification includes pharmacologic and surgical options. The primary agents are bisphosphonates—particularly sodium etidronate which is the most widely-studied agent for this condition. Bisphosphonates work by preventing bone crystallization through inhibiting calcium phosphate precipitation, inhibiting calcium phos-phate transformation to hydroxyapatite and preventing hydroxyapatite crystal aggregation.61

Surgical resection of HO may be indicated for cases where the deformity causes severe functional limitations such as the inability to sit properly in a chair, increased risk of pressure ulcers, or hindering mobilization and activities of daily living, and the heterotopic bone tissue is mature. Surgical risks can include post-operative infections, DVT/PE, and anemia. There is also evidence that after resection of heterotopic bone, radiologic recurrence can be seen in 82-100% of cases, with 17-58% of cases becoming clinically significant.62

Conclusion

Post-stroke survivors are susceptible to a many potential sources of pain. It is important to remember that aside from the causes described in this article, stroke survivors are no less susceptible to other medical causes of pain such as gout and deep vein thrombosis. Clinical history and physical examination with judicious use of appropriate diagnostic modalities in stroke survivors are mandatory in identifying what is the likely pain source. Clinicians must identify these causes early on to develop a comprehensive treatment plan to improve quality of life.

In neuropathic post-stroke pain syndromes, treatment is directed towards addressing the symptoms through pharmacologic means, although the medications that are commonly used to treat neuropathic pain have had surprisingly few studies to back their use. In fact, physicians are treating neuropathic post-stroke pain conditions using medications that need more studies (such is the case of gabapentin), while other medications are being used with no formal studies having been done on their effectiveness in post-stroke pain. For example, duloxetine is a selective serotonin reuptake inhibitor class anti-depressant which has been shown to be effective for certain forms of neuropathic pain, however no studies exist looking at using this medication in various forms of post-stroke pain. Better understanding of the mechanisms in the development of central post-stroke pain and complex regional pain syndrome may provide valuable clues in the future treatment of these conditions.

For the various musculoskeletal causes of pain, it is crucial to try and understand the underlying biomechanical causes of pain from motor function changes after stroke rather than just try to address the pain with medications. Unfortunately, correcting biomechanical deficits or dysfunctions can be difficult as this is intimately linked to motor recovery after stroke and can be a primary barrier to recovery and treatment.

It was clear in the research for this review that the overall quantity of large, high quality studies of the treatment of most causes of post-stroke pain is very limited, both for neuropathic and musculoskeletal origins. Further high quality research on post-stroke pain is needed to help develop future evidence-based standards of care.

Last updated on: December 22, 2011
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