CPR Overview

Cardiopulmonary resuscitation (CPR) is performed when a person is not breathing, has no pulse, or both.
Rescue Breathing and Chest Compressions

Rescuers are strongly advised to complete a first aid/CPR course before attempting this procedure.
• Ask the person needing help if he or she is OK. If there is no response, seek
medical care.
• Then, open the airway by moving the chin; avoid neck movement.
• Once the airway is open, look, listen, and feel for breathing.
• If breathing is absent, give 2 slow breaths. If breath does not go in, see
choking.
o For adults, give 1 breath every 5 seconds.
o For children, give 1 breath every 3 seconds.

• Check for pulse. If pulse is present, continue rescue breathing. If there is
no pulse, begin chest compressions.
o For adults, give 1.5-2 inch compressions of the sternum at a rate of 80-100
per minute using 2 hands, then give 2 breaths.
o For children, give 0.5-1 inch compressions of the sternum at a rate of 80-100
per minute using 1 hand, then give 1 breath.
o For infants, give 0.5-1 inch compressions of the sternum at a rate of 100 per
minute using 3 fingers, then give 1 breath.

Transcutaneous Electrical Nerve Stimulation

Transcutaneous Electrical Nerve Stimulation INTRODUCTION Transcutaneous electrical nerve stimulation (TENS) currently is one of the most commonly used forms of electroanalgesia. Hundreds of clinical reports exist concerning the use of TENS for various types of conditions such as low back pain (LBP), myofascial and arthritic pain, sympathetically mediated pain, bladder incontinence, neurogenic pain, visceral pain, and postsurgical pain. Because many of these studies were uncontrolled, there has been ongoing debate about the degree to which TENS is more effective than placebo in reducing pain. The currently proposed mechanisms by which TENS produces neuromodulation include the following: Presynaptic inhibition in the dorsal horn of the spinal cord Endogenous pain control (via endorphins, enkephalins, and dynorphins) Direct inhibition of an abnormally excited nerve Restoration of afferent input The results of laboratory studies suggest that electrical stimulation delivered by a TENS unit reduces pain through nociceptive inhibition at the presynaptic level in the dorsal horn, thus limiting its central transmission. The electrical stimuli on the skin preferentially activate low- threshold myelinated nerve fibers. The afferent input from these fibers inhibits propagation of nociception carried in the small unmyelinated C fibers by blocking transmission along these fibers to the target or T cells located in the substantia gelatinosa (laminae 2 and 3) of the dorsal horn. The mechanism of the analgesia produced by TENS is explained by the gate control theory proposed by Melzack and Wall in 1965. The gate usually is closed, inhibiting constant nociceptive transmission via C fibers from the periphery to the T cell. When painful peripheral stimulation does occur, the information carried by C fibers reaches the T cells and opens the gate, allowing pain transmission centrally to the thalamus and cortex, where it is interpreted as pain. The gate control theory postulated a mechanism by which the gate is closed again, preventing further central transmission of the nociceptive information to the cortex. The proposed mechanism for closing the gate is inhibition of the C-fiber nociception by impulses in activated myelinated fibers.   TECHNICAL CONSIDERATIONS A TENS unit consists of one or more electric signal generators, a battery, and a set of electrodes. The units are small and programmable, and the generators can deliver trains of stimuli with variable current strengths, pulse rates, and pulse widths. The preferred waveform is biphasic, to avoid the electrolytic and iontophoretic effects of a unidirectional current. The usual settings for the stimulus parameters used clinically are the following: Amplitude - Current at low intensity, comfortable level, just above threshold Pulse width (duration) - 10-1000 microseconds Pulse rate (frequency) - 80-100 impulses per second (Hz); 0.5-10 Hz when stimulus intensity is set high When TENS is used for pain control, patients are instructed to try different frequencies and intensities to find those that provide the best pain control for that individual. Optimal settings of stimulus parameters are subjective and are determined by trial and error. Electrode positioning is quite important. Usually, the electrodes are placed initially on the skin over the painful area, but other locations (eg, over cutaneous nerves, trigger points, acupuncture sites) may give comparable or even better pain relief. The 3 options for the standard settings used in different therapeutic methods of TENS application include the following: Conventional TENS has a high stimulation frequency (40-150 Hz) and low intensity, just above threshold, with the current set between 10-30 mA. The pulse duration is short (up to 50 microseconds). The onset of analgesia with this setup is virtually immediate. Pain relief lasts while the stimulus is turned on, but it usually abates when the stimulation stops. Patients customarily apply the electrodes and leave them in place all day, turning the stimulus on for approximately 30-minute intervals throughout the day. In individuals who respond well, analgesia persists for a variable time after the stimulation stops. In acupuncturelike settings, the TENS unit delivers low frequency stimulus trains at 1-10 Hz, at a high stimulus intensity, close to the tolerance limit of the patient. Although this method sometimes may be more effective than conventional TENS, it is uncomfortable, and not many patients can tolerate it. This method often is considered for patients who do not respond to conventional TENS. Pulsed (burst) TENS uses low-intensity stimuli firing in high frequency bursts. The recurrent bursts discharge at 1-2 Hz, and the frequency of impulses within each burst is at 100 Hz. No particular advantage has been established for the pulsed method over the conventional TENS method. Patient comfort is a very important determinant of compliance and, consequently, the overall success of treatment. The intensity of the impulse is a function of both pulse duration and amplitude. Greater pulse widths tend to be more painful. The acupuncturelike method is less tolerable because the impulse intensity is higher. The amount of output current depends on the combined impedance of the electrodes, skin, and tissues. With repetitive electrical stimuli applied to the same location on the skin, the skin impedance is reduced, which could result in greater current flow as stimulation continues. A constant current stimulator, therefore, is preferred to minimize sudden uncontrolled fluctuations of current intensity related to changes in impedance. An electroconductive gel applied between the electrode and skin serves to minimize the skin impedance. Skin irritation can occur in as many as 33% of patients, at least in part, due to drying out of the electrode gel. Patients need to be instructed in the use and care of TENS equipment, with particular attention to the electrodes. Medical complications arising from use of TENS are rare; however, skin irritation is a frequent problem and often is due partly to the drying out of the electrodes. Sometimes individuals react to the tape used to secure the electrodes. Skin irritation is minimized by using self-adhesive disposable electrodes and repositioning them slightly for repeated applications. The use of TENS is contraindicated in patients with demand-type pacemakers because their stimulus outputs may drive or inhibit the pacemaker. A variety of newer transcutaneous or percutaneous electrical stimulation modalities recently has emerged. Interferential current therapy (IFC) is based on summation of 2 alternating current signals of slightly different frequency. The resultant current consists of cyclical modulation of amplitude, based on the difference in frequency between the 2 signals. When the signals are in phase, they summate to an amplitude sufficient to stimulate, but no stimulation occurs when they are out of phase. The beat frequency of IFC is equal to the difference in the frequencies of the 2 signals. For example, the beat frequency and, hence, the stimulation rate of a dual channel IFC unit with signals set at 4200 and 4100 Hz is 100 Hz. IFC therapy can deliver higher currents than TENS. IFC can use 2, 4, or 6 applicators, arranged in either the same plane for use on regions such as the back or in different planes in complex regions (eg, the shoulder). Percutaneous electrical nerve stimulation (PENS) combines advantages of both electroacupuncture and TENS. Rather than using surface electrodes, PENS uses acupuncturelike needle probes as electrodes, placed at dermatomal levels corresponding to local pathology. The main advantage of PENS over TENS is that it bypasses the local skin resistance and delivers electrical stimuli at the precisely desired level in close proximity to the nerve endings located in soft tissue, muscle, or periosteum.   APPLICATIONS OF TENS IN CLINICAL PRACTICE Literature on the use of TENS in a variety of medical conditions reports a wide range of outcomes, from very positive to negative effectiveness. Currently, there is an overall consensus favoring the use of TENS, with authorities differing on its value in different clinical situations. Generally, TENS provides initial relief of pain in 70-80% of patients, but the success rate decreases after a few months or longer to around 20-30%. To exclude a false-negative response, a trial of TENS for at least 1 hour should be given to confirm potential benefit from subsequent continuous use. According to Johnson, the time from the start of stimulation to the onset of analgesia varies from almost immediate to hours (on average 20-30 minutes in over 75% of patients and 1 hour in 95% of patients). The duration of analgesia also varies considerably, continuing only for the duration of stimulation in some patients and providing considerable prolonged poststimulation relief in others. The same TENS protocol may have different degrees of antinociception in acute experimental pain compared with chronic clinical pain in patients with chronic LBP. Patients differ in their stimulus preferences and in their rates of compliance. In Johnson's study of compliance in patients who benefited from TENS, 75% used the device on a daily basis. Patients showed individual preferences for particular pulse frequencies and patterns and consistently adjusted their stimulators to these settings on subsequent treatment sessions.   Indications for the use of TENS Neurogenic pain (eg, deafferentation pain, phantom pain), sympathetically mediated pain, postherpetic neuralgia, trigeminal neuralgia, atypical facial pain, brachial plexus avulsion, pain after spinal cord injury (SCI) Musculoskeletal pain: Examples of specific diagnoses include joint pain from rheumatoid arthritis and osteoarthritis, acute postoperative pain (eg, postthoracotomy), and acute posttraumatic pain. After surgery, TENS is most effective for mild-to-moderate levels of pain, and it is ineffective for severe pain. The use of TENS in chronic LBP and myofascial pain is controversial, as placebo-controlled studies fail to show statistically significant beneficial results. Uncertainty also exists about the value of TENS in tension headache. Visceral pain and dysmenorrhea are other conditions in which TENS has been applied successfully. Other disorders: TENS has been used successfully in patients with angina pectoris and urge incontinence, as well as in patients requiring dental anesthesia. Reports discuss use of TENS to assist patients in regaining motor function following stroke, to control nausea in patients on chemotherapy, as an opioid-sparing modality in postoperative recovery, and in postfracture pain. Contraindications for the use of TENS TENS should not be used in patients with a pacemaker (especially of the demand type). TENS should not be used during pregnancy because it may induce premature labor. TENS should not be applied over the carotid sinuses due to the risk of acute hypotension through a vasovagal reflex. TENS should not be placed over the anterior neck because of possible laryngospasm due to laryngeal muscle contraction. The electrodes should not be placed in an area of sensory impairment (eg, in cases of nerve lesions, neuropathies), where the possibility of burns exists. A TENS unit should be used cautiously in patients with a spinal cord stimulator or intrathecal pump.

 

Shoulder and Hemiplegia

 

Shoulder and Hemiplegia         INTRODUCTION Background: Good shoulder function is a prerequisite for effective hand function, as well as for performing multiple tasks involving mobility, ambulation, and activities of daily living (ADL). A common sequela of stroke is hemiplegic shoulder pain that can hamper functional recovery and subsequently lead to disability. Poduri et al report that hemiplegic shoulder pain can begin as early as 2 weeks poststroke but typically occurs within 2-3 months poststroke. Most studies have speculated about the etiology of shoulder pain in hemiplegia but have failed to establish a cause-and-effect relationship. Some of the most frequently suspected factors contributing to shoulder pain include subluxation, contractures, complex regional pain syndrome (CRPS), rotator cuff injury, and spastic muscle imbalance of the glenohumeral joint (Teasell, 1998). However, identifying the exact mechanism(s) of shoulder pain can be inherently difficult, with many of the current treatment regimens varying according to assumptions made about its cause. Hanger et al suggest that it is highly probable that the cause is multifactorial with different factors contributing at different stages of recovery (ie, flaccidity contributing to subluxation and subsequent capsular stretch, abnormal tonal and synergy patterns contributing to rotator cuff or scapular instability). Because of the difficulty in treating shoulder pain once established, initiate treatment early. For individuals who have had strokes with resultant hemiplegia, motor and functional recovery also are important steps in the treatment process. Chae et al indicate that the amount of motor recovery is related to the degree of initial severity and the amount of time before voluntary movements are initiated. Numerous neurofacilitative treatments have been developed in hopes of improving the quality and decreasing the amount of time to recovery. Unfortunately, Chae et al have found that the length of stay at most acute inpatient rehabilitation facilities is shortening, with restoration of maximal function involving the use of compensatory strategies as the primary means for treatment rather than the restoration of motor control. Pathophysiology: In order to understand the pathologic processes and changes that occur in the hemiplegic shoulder, the factors that contribute to normal shoulder position need to be understood. As proposed by Cailliet, normal anatomic position involves a well-approximated glenohumeral joint, proper glenoid fossa angle (forward and upward), and proper scapular alignment with the vertebral column. The joint is stabilized by musculature (ie, supraspinatus, deltoid, latissimus) and, to a smaller degree, the shoulder capsule, which supports the humerus. The trapezius, serratus anterior, and rhomboids provide proper scapular alignment. The latissimus also works to depress the scapula. Erector spinae muscle tone, along with the righting reflex, maintains the vertebral column in an upright alignment. If any of these components are disrupted during the recovery process, then shoulder function may be compromised or a painful shoulder may result. Following a stroke, the brain and body progress through the following series of stages, which are discussed in detail by Cailliet: (1) transischemic attack, (2) flaccidity, (3) spasticity, and (4) synergy. A gradual progression from one stage to the next usually occurs, but they are not mutually exclusive of one another, and they can occur simultaneously in the affected limb. Flaccid stage Once the inciting injury to the brain occurs, the flaccid stage evolves with a state of areflexia. This stage of areflexia includes loss of muscle tone and volitional motor activity, variable sensory loss, and loss of muscle stretch reflexes. Muscular support of the humeral head in the glenoid fossa by the supraspinatus and deltoid muscles is lost. This leads to downward and outward subluxation of the humeral head, with the only support coming from the joint capsule. The shoulder capsule is thin and is composed of 2 tissue layers. The inner synovial layer, the stratum synovium, is highly vascular but poorly innervated, making it insensitive to pain but highly reactive to heat and cold. The outer layer, the stratum fibrosum, is poorly vascularized but richly innervated, predisposing it to pain from stretch. For this reason, Faghri et al suggest that added capsular stretch in a flaccid shoulder may predispose the capsule to irreversible damage and the shoulder to pain. Flaccidity of the trapezius, rhomboids, and serratus anterior muscles leads to depression, protraction, and downward rotation of the scapula, which Cailliet believes leads to significant angular changes of the glenoid fossa, subsequently contributing to subluxation. Also, the spine begins to flex laterally toward the hemiparetic side because of the elimination of the righting reflex, further altering the scapulothoracic relationship. However, Prevost et al compared the affected and unaffected shoulders by using a 3-dimensional radiographic technique that determines the true position of the humeral head in relation to the scapula. This technique revealed less downward rotation of the glenoid fossa than originally expected, and no significant relationship was found between the extent of scapular orientation and the severity of subluxation (Prevost, 1987; Culham, 1995). Subsequently, it was concluded that scapular position does not contribute as much to inferior subluxation as was originally thought. Teasell points out that this now appears to be the most widely accepted viewpoint. Spastic stage As stroke recovery evolves, flaccidity may progress to spasticity. Cailliet explains that normally, the brainstem contains upper extremity (UE) flexor patterns and lower extremity (LE) extensor patterns that are refined and coordinated by the premotor and neocortexes. Following a stroke, the connections that control these reflexes can be interrupted, resulting in the release of these basic patterns and the evolution of spasticity and synergy patterns. If the neurologic deficits become severe enough, primitive tonic neck reflexes may develop. When primitive tonic neck reflexes are present, the elbow extends when the head turns toward the affected side, and the elbow flexes when the head turns away. The presence of primitive tonic neck reflexes is considered prognostically unfavorable for motor recovery. The first evidence of UE spasticity is internal rotation of the humerus from the subscapularis and pectoralis major, with a debate as to which muscle contributes stronger to this pattern. This pattern may then progress into the forearm pronators (ie, pronator quadratus, pronator teres, flexor carpi radialis). Spastic involvement of the rhomboids leads to scapular depression and downward rotation, while the latissimus dorsi contributes to adduction, extension, and internal rotation of the humerus. Biceps brachii spasticity further depresses the head of the humerus and flexes the elbow. As spasticity and synergy evolve, Teasell notes there is a failure of the antagonist muscles to relax when the agonist muscles contract, thus creating cocontraction. For example, during internal rotation, excessive spasticity of the internal rotators of the humerus (ie, subscapularis, pectoralis major, latissimus, teres major) overwhelms the external rotators (ie, supraspinatus, infraspinatus, teres minor). The muscles causing downward and outward rotation of the scapula, the rhomboids, overwhelm the trapezius and serratus anterior muscles. Spastic unilateral paraspinal muscles overwhelm those on the contralateral side, causing lateral flexion of the spine toward the affected side. Synergy stage If neurologic impairment of the completed stroke progresses, synergy patterns, which tend to worsen with initiated efforts, may emerge. Cailliet proposes that the synergy component that usually occurs first is spastic elbow flexion; the shoulder phase is weaker and usually requires a more reflexive status to occur. The restrictions created by the synergy patterns create therapeutic challenges to attaining meaningful UE function. Upper extremity flexor synergy patterns include (1) shoulder/scapular depression (downward rotation and retraction), (2) humeral adduction/internal rotation, (3) elbow flexion, (4) forearm pronation (rarely supination), and (5) wrist/finger flexion (thumb-in-hand position). When treating patients in flexion synergy, aim therapy at retraining the overwhelmed agonists, stressing the desired components of function, and releasing the uninhibited flexion patterns by initiating opposite movements at the “key points of control.” Frequency: In the US: According to Van Ouwenaller et al, shoulder pathology with resulting pain is relatively common in individuals who develop hemiplegia after stroke and/or brain injury. Van Ouwenaller reports shoulder pathology occurs in up to 85% of patients with spastic symptoms and in up to 18% of patients with flaccid symptoms. Other clinical trials report a general incidence of shoulder pain in patients with hemiplegic stroke as 16-84% (Forster, 1994; Najenson, 1971), while that for shoulder subluxation has been found to be as high as 81% (Najenson, 1971). Reflex sympathetic dystrophy (RSD) also appears to be a relatively common complication of hemiplegia, with Van Ouwenaller reporting an incidence of 27% in patients with spasticity versus 7% of those with flaccidity. Other sources report an incidence of 12.5-61%.   CLINICAL History: Obtaining an accurate and detailed history is an important part of the examination. For those patients who have difficulty with communication, the history may be provided by a family member. Common symptoms of the shoulder/UE reported by patients with hemiplegia may include the following: Reduced mobility of the shoulder Tenderness Swelling/edema Pain with movement Decreased coordination Physical: The physical examination of a patient with shoulder dysfunction associated with hemiplegia is extensive, as the physician is required to assess the involved musculoskeletal and neurological conditions. Suggested clinical tests and evaluations include the following: Observation Atrophy Asymmetry Swelling/edema Tenderness Pain with motion Decreased range of motion (ROM) Decreased coordination Decreased reflexes Palpation Anatomical variation Palpable gap between acromion and humeral head (use fingerbreadths or calipers) External and clinical methods for measuring subluxation (Boyd, 1992) include the following: Palpate and/or measure the subacromial space using calipers or a thermoplastic jig. Compare these findings to those of the opposite shoulder. Measure the distance separating the acromial angle and the lateral epicondyle of the humerus using a sliding caliper (anthropometric measure). Assess pulses Peripheral circulation Adson maneuver Assess arm function - Action Research Arm Test Evaluation of shoulder pain Ritchie Articular Index (ordinal measurement) Shoulder lateral rotation ROM to the point of pain (SROMP) Precise ratio measurement Requires the use of a goniometer Evaluate for complex regional pain syndrome (CRPS) Neurologic examination Cognition Orientation Memory Attention span Manual muscle testing Assess strength and tone Evaluate spasticity (Modified Ashworth scale) Sensory evaluation Light touch Pin-prick Vibration Proprioception Two-point discrimination Stereognosis Reflexes Coordination Cranial nerves and visual fields Evaluate for neglect Letter cancellation test Line bisection test Evaluate for apraxia Fugl-Meyer index to test motor performance Causes: Glenohumeral subluxation Glenohumeral subluxation basically is defined as a partial or incomplete dislocation that usually stems from changes in the mechanical integrity of the joint. Subluxation is a common problem in patients with hemiplegia, especially during the flaccid stage, and often occurs within 3 weeks poststroke. Subluxation appears to be caused by the weight of the flaccid arm applying direct mechanical stretch to the joint capsule as well as traction to unsupportive muscles of the shoulder. Teasell suggests that other factors contributing to subluxation include improper positioning, lack of support in the upright position, and pulling on the hemiplegic arm when transferring the patient. Controversy exists as to an association between shoulder subluxation and pain. Subluxation has been a commonly sited cause of shoulder pain and disability, with Yu et al reporting that longitudinal data suggests a correlation between early subluxation and shoulder pain. However, Bohannon et al have found no significant correlation between the presence of subluxation and the occurrence of pain, while Wanklyn et al have found no association between the severity of subluxation and the degree of pain. Numerous cases of subluxation without pain have been documented, as well as cases of a painful shoulder without subluxation. A correlation between subluxation and RSD also has been studied. Dursun et al found that subluxation was present in 74.3% of patients with RSD and 40% of patients without RSD; of these same patients, 78.6% with subluxation and 38.1% without subluxation reported shoulder pain. Dursun concluded that shoulder subluxation might be a causative factor of RSD as well as shoulder pain. Physicians usually can diagnose subluxation by palpating and measuring anatomical landmarks (fingerbreadths and calipers, respectively) during physical examination. Bohannon et al found that performing shoulder palpation to help diagnose subluxation can be reliably graded, with good interrater reliability and good correlation with more precise radiographic measurements. Other authors believe that there are no precise clinical means to measure the degree of subluxation, and if one could be devised, then the benefit of treatment would be validated. Several radiographic methods that give a reliable measure of subluxation have been proposed, but some require specialized equipment that is not widely available. Treatment of subluxation by reduction remains a controversial means of controlling shoulder pain. Slings, arm boards, troughs, and lap trays have not proven to be effective and may result in overcorrection in some cases. Sling use also may cause lateral subluxation, impair proprioception, interfere with functional activities, or promote undesirable synergy patterns; furthermore, sling use may not prove beneficial in preventing shoulder subluxation. Strapping also has been attempted with variable results. Even though sling use and other supportive devices remain controversial, Yu et al report that treatment of shoulder subluxation continues to be the standard of care for several reasons, including the following: Painful shoulder subluxation most commonly is present when the UE is in a dependent position. Painful shoulder subluxation improves with joint reduction. Subluxation may have a role in the pathogenesis of other painful conditions by stretching local neurovascular and musculoskeletal tissues. Early prevention is warranted since chronic shoulder pain often is refractory to treatment. Subluxation may inhibit functional recovery by limiting shoulder ROM. Because of the unproven effectiveness of support devices, a newer form of treatment, neuromuscular electrical stimulation (NMES), has provided some moderate success in the prevention and treatment of subluxation. Yu et al demonstrated substantial reduction in subluxation, and possibly enhancement of motor recovery and reduction of shoulder pain. However, it is debated whether NMES should be used prophylactically or whether its use should be held until subluxation develops. NMES is discussed further in the treatment section (see Neuromuscular electrical stimulation). Spasticity Spasticity is defined as a velocity-sensitive disorder of motor function causing increased resistance to passive stretch of muscles and hyperactive muscle stretch reflexes. Following stroke, Teasell reports that supraspinal suppressor areas (pyramidal and extrapyramidal motor systems) that are normally responsible for maintaining the delicate balance between the facilitative and inhibiting influences of both alpha and gamma motor neurons are decreased or eliminated, resulting in spasticity, flexor tone, and synergy. Van Ouwenaller identified spasticity as a prime factor and one of the most common causes of shoulder pain in patients with hemiplegia. Compared to patients with flaccidity, patients with spasticity seem to experience a much higher incidence of shoulder pain, which is thought to be the result of muscle imbalance. The muscles found to predominate the synergy pattern in the shoulder include the adductors (ie, teres major, latissimus dorsi), and to a greater extent, the internal rotators (ie, subscapularis, pectoralis major). Bohannon et al reports finding external rotation to correlate most with hemiplegic shoulder pain. The mainstay of treatment for spasticity begins with physical therapy and the use of ROM and stretching exercises, although overly aggressive stretching should be avoided. Proper positioning also is used as a means of controlling spasticity by suppressing the evolution of synergy patterns. Antispasticity medications, as well casting and orthotics, also should be considered. If conservative treatment fails, then the use of motor point blocks have been advocated as an effective means for improving pain, ROM, and possibly function. Complex regional pain syndrome (shoulder-hand syndrome, RSD, causalgia, sympathetically maintained pain, Sudeck atrophy, minor dystrophy) The International Association for the Study of Pain has advocated using the terms complex regional pain syndromes (CRPS) type 1 (RSD) and type 2 (causalgia). The International Association for the Study of Pain categorization states that RSD develops secondary to noxious stimuli that are not limited to the distribution of a single peripheral nerve, while causalgia starts after a nerve injury. The incidence of CRPS varies in the literature. Davis et al report that CRPS occurs in 12.5% of patients who have had a stroke, while Chalsen et al report the incidence as 61%. CRPS usually presents within 3 months poststroke and rarely after 5 months poststroke. Davis et al demonstrated that of those patients developing CRPS, 65% had done so by 3 months poststroke, and 98% had done so by 5 months poststroke. CRPS most commonly precipitates in bone or soft tissue injuries, but in up to 30% of the cases, the injury is innocuous and the patient does not remember the injury. Snider reports that about 5-8% of patients have an incomplete nerve injury. Other factors may include UE immobilization, myocardial infarction, stroke, rotator cuff tear, shoulder spasticity, and glenohumeral joint subluxation. CRPS more commonly affects the UE, with Tepperman et al reporting metacarpophalangeal (MCP) joint tenderness to be the best diagnostic indicator, having a sensitivity and specificity of 85.7% and 100%, respectively. However, intuitively it is questionable whether any one physical examination maneuver could have such high sensitivity and specificity for a syndrome as complex as RSD. Using electromyography (EMG), Cheng et al found a significant correlation between the presence of spontaneous activity and the development of clinical RSD in 65% of subjects, whereas only 4% of those without spontaneous activity developed RSD. However, this is not consistent with the definition of RSD set forth by The International Association for the Study of Pain, since the IASP criteria would dictate that patients with identifiable nerve lesions may have causalgia, but not RSD. For the best prognosis, early recognition and prompt treatment are essential for patients with CRPS. Vasomotor instability (eg, hand edema, MCP tenderness, dystrophic skin changes) should be sought upon examination. Evaluation with a triple-phase bone scan showing periarticular uptake in the wrist and MCP joints of the involved hand can also help with the diagnosis. Treatment options are numerous, with physical therapy as the cornerstone. ROM exercises, optimal positioning of the limb, and avoiding painful stimuli are all suggested. Other treatments might include nonsteroidal anti-inflammatory drugs (NSAIDs), modalities (eg, electric nerve stimulation, ultrasound), short course of oral steroids, or a ganglion block. Kingery reports that the prognosis for resolution with preserved ROM is better in patients with some voluntary movements, with less spasticity, and without significant sensory loss. Nearly 35% of patients with CRPS type 1 have symptom resolution in one year.   Adhesive capsulitis Glenohumeral capsulitis is postulated to play an important role in hemiplegic shoulder pain. Patients usually present with pain and limited passive movement of the shoulder, especially external rotation and abduction. Joynt et al report that adhesive changes may reflect a later stage in the recovery process when chronic irritation or injury, inflammation, or lack of movement eventually results in adhesions. When Rizk et al performed shoulder arthrography in 30 patients with hemiplegic shoulder pain, they found changes consistent only with capsular restriction typical of adhesive capsulitis in 77% of subjects. This finding suggests an association between adhesive changes and shoulder pain. A study by Wanklyn et al also found an association between reduced ROM (specifically external rotation) and hemiplegic shoulder pain, with an incidence as high as 66%. This association was believed to be due to abnormal muscle tone or structural changes, namely adhesions. Because diminished ROM of shoulder spasticity and adhesive capsulitis present similarly, it is often difficult to distinguish between pain in the limited hemiplegic shoulder based on capsulitis, spasticity, or a combination. Treatment for adhesive capsulitis usually involves manual mobilization exercises, analgesics, and possibly steroid injections. If conservative management fails, then the use of distention arthrography or manipulation while the patient is under anesthesia may be indicated. Subacromial bursitis Some patients with hemiplegia complain of lateral shoulder pain that radiates down the arm when moved. This radiating pain seems to correlate with a diagnosis of subacromial bursitis. Joynt et al demonstrated that injecting 10 mL of 1% lidocaine into the subjective pain sites related to at least moderate pain relief at the subacromial injection site and improved ROM in 50% of the patients. This finding suggests that the subacromial bursitis can contribute to pain and poor ROM in a significant number of cases. Early treatment with physical modalities, NSAIDs, steroid injections, and ROM exercises is advocated for the reduction of symptoms and prevention of later complications. Brachial plexus traction neuropathies/injury Patients with hemiplegia who have their flaccid arm in an unsupported dependent position, or patients who have been inappropriately transferred by pulling on the arm, tend to be at increased risk for traction neuropathy. Wanklyn et al reported a 27% increased incidence of shoulder pain in dependent patients after discharge, which may reflect improper handling at home by caregivers. For this reason, patient and caregiver education regarding proper transfer techniques and correct handling of the hemiplegic arm should be stressed. Severe sensory loss or neglect tends to increase the risk for such injuries as well. Kaplan suggests that plexus injury should be considered in a patient who has atypical return of distal function. Treatment for traction injuries is limited to the use of supportive care until the return of function. Heterotopic ossification Heterotopic ossification (HO) presents as calcification of soft tissue around traumatic or neurologically affected joints. Currently, the etiology of HO is unknown. Patients typically are asymptomatic, and the problem usually is incidentally discovered on radiographs of a joint that is losing ROM. Clinically, HO can present with local erythema, warmth, induration, and swelling. Cailliet reports that onset can occur as early as 2 weeks or as late as 3-6 months poststroke. Treatment begins with ROM exercises, followed by medications (eg, Didronel, Indocin) and irradiation. In severe cases, surgery is necessary to resect the extra-articular bone once it is mature. Neglect Joynt et al reports that neglect may lead to increased trauma or disturbed perception of the quality of the pain, thereby producing a sensation of pain without the usual pathology. Snels et al have found that on numerous occasions, patients with sensory deficits, visual field deficits, or neglect more commonly experience recurrent injuries of the shoulder, possibly contributing to capsulitis. Treatment options suggested by Lorish et al include caloric stimulation, prism glasses, visuospatial cueing, computer-assisted training, and compensatory strategies. Thalamic syndrome (central poststroke pain, analgesia dolorosa, Dejerine-Roussy syndrome) Thalamic syndrome usually occurs in less than 5% of stroke survivors, but it is found in 50% of those who have had a thalamic stroke. The pain can evolve spontaneously or can be evoked by touch and is often severe, diffuse, and disabling. Patients describe the pain as burning, tingling ("pins and needles"), sharp, shooting, stabbing, gnawing, dull, or achy. This pain often is refractory to treatment. The patient also relates experiencing hyperpathia (an exaggerated pain reaction to mild external cutaneous stimulation). Treatment includes medications such as analgesics, antidepressants (ie, tricyclic antidepressants), and anticonvulsants. Other treatment alternatives include sympathetic blockade, guanethidine block, as well as psychological evaluation and treatment. Rarely, surgery is necessary. Soft tissue injury/trauma Soft tissue trauma often is a result of uncontrolled ROM exercises, poor positioning of the hemiplegic patient, or improper transfer technique. Kumar et al showed that 62% of their patients using an overhead pulley system for therapy and performing ROM exercises experienced shoulder pain irrespective of other pathology, thus demonstrating that overaggressive stretching or ROM should be avoided during the rehabilitation process. Patients with poor cognition, neglect, and other sensory deficits tend to be predisposed to traumatic injuries to the affected extremity. Rotator cuff inflammation/rupture Because rotator cuff tears are prevalent in the general population, it is often difficult to determine if a tear was present premorbidly or if it occurred poststroke. Through the use of shoulder arthrography, Najenson et al demonstrated an incidence of rotator cuff tear in patients who were poststroke and were experiencing shoulder pain to be as high as 40% on the affected side, compared to only 16% on the unaffected side. Other studies, including one by Joynt et al, have revealed no incidence of rotator cuff tear with hemiplegic shoulder pain. Teasell reports that hemiplegic shoulder pain is not commonly associated with a rotator cuff disorder.     DIFFERENTIALS Adhesive Capsulitis Chronic Pain Syndrome Fibromyalgia Heterotopic Ossification Osteoarthritis Rheumatoid Arthritis Spasticity Other Problems to be Considered: Glenohumeral subluxation Trauma/soft tissue injury Fractures Brachial plexus traction neuropathies/injury Neglect (increased trauma risk) Shoulder capsule stretch and tears secondary to disuse/flaccidity Bursitis and tendonitis Thalamic syndrome (central poststroke pain, analgesia dolorosa, Dejerine-Roussy syndrome) Spasticity and synergy (muscle imbalance) Complex regional pain syndrome (shoulder-hand syndrome, reflex sympathetic dystrophy, causalgia, sympathetically maintained pain, Sudeck atrophy, minor dystrophy) Impingement syndromes Rotator cuff inflammation/rupture Prior musculoskeletal injury Bicipital tendonitis/rupture Osteoporosis Suprascapular neuropathy Median neuropathy Radiculopathy Contractures Vascular compromise Thoracic outlet syndrome Myofascial pain syndrome/fibromyalgia

Piriformis Syndrome

Piriformis Syndrome   INTRODUCTION Background: Piriformis syndrome has remained a controversial diagnosis since its initial description in 1928. Piriformis syndrome usually is caused by a neuritis of the proximal sciatic nerve. The piriformis muscle can either irritate or compress the proximal sciatic nerve due to spasm and/or contracture, and this problem can mimic a discogenic sciatica (pseudosciatica). Pathophysiology: The piriformis muscle is flat, pyramid-shaped, and oblique. This muscle originates to the anterior of the S2-S4 vertebrae, the sacrotuberous ligament, and the upper margin of the greater sciatic foramen (see Image 1). This muscle passes through the greater sciatic notch and inserts on the superior surface of the greater trochanter of the femur. With the hip extended, the piriformis muscle is the primary external rotator; however, with the hip flexed, the piriformis muscle itself becomes a hip abductor. This muscle is innervated by branches from L5, S1, and S2. A lower lumbar radiculopathy also may cause secondary irritation of the piriformis muscle, which may complicate the diagnosis and hinder patient progress. Many developmental variations of the relationship between the sciatic nerve in the pelvis and piriformis muscle have been observed. In approximately 20% of the population, the muscle belly is split with one or more parts of the sciatica nerve dividing the muscle belly itself. In 10% of the population, the tibial/peroneal divisions are not enclosed in a common sheath. Usually, the peroneal portion splits the piriformis muscle belly; the tibial division rarely splits the muscle belly. Involvement of the superior gluteal nerve usually is not seen in cases of piriformis syndrome. This nerve leaves the sciatic nerve trunk and passes through the canal above the piriformis muscle. Blunt injury may cause hematoma formation and subsequent scarring between the sciatic nerve and short external rotators. Nerve injury can occur with prolonged pressure on the nerve or vasa nervorum. Etiology can be subdivided into a few categories as follows: Hyperlordosis Muscle anomalies with hypertrophy Fibrosis (due to trauma) Partial or total nerve anatomical abnormalities Other causes can include the following: Pseudoaneurysms of the inferior gluteal artery adjacent to the piriformis syndrome Bilateral piriformis syndrome due to prolonged sitting during an extended neurosurgical procedure Cerebral palsy Total hip arthroplasty Myositis ossificans Vigorous physical activity This syndrome remains controversial because, in most cases, the diagnosis is clinical, and no confirmatory tests exist to support the clinical findings. Frequency: In the US: Given the lack of agreement on exactly how to diagnose this condition, estimates of frequency of sciatica caused by piriformis syndrome vary from rare to approximately 6% of sciatica cases seen in a general family practice. Approximately 90% of adults have had at least one episode of disabling LBP in their lifetime. Mortality/Morbidity: Piriformis syndrome is not life-threatening, but it can have significant associated morbidity. The total cost of low back pain (LBP) and sciatica is significant, exceeding $16 billion in both direct and indirect costs. Sex: Some reports suggest a 6:1 female-to-male predominance.   CLINICAL History: Piriformis syndrome often is not recognized as a cause of LBP and associated sciatica. This clinical syndrome is due to a compression of the sciatic nerve by the piriformis muscle. This condition is identical in clinical presentation to LBP with associated L5, S1 radiculopathy due to discogenic and/or lower lumbar facet arthropathy with foraminal narrowing. Not uncommonly, patients demonstrate both of these clinical entities simultaneously. This diagnostic dilemma highlights the need for patients with LBP and associated radicular pain to undergo a complete history and physical examination, including a digital rectal examination. Many cases of refractory trochanteric bursitis are observed to have an underlying occult piriformis syndrome due to the insertion of the piriformis muscle on the greater trochanter of the hip. If both the trochanteric bursitis and the piriformis syndrome are treated inadequately, both conditions remain resistant to medical management. Physical: Examination findings may include the following: Piriformis muscle spasm often is detected by careful deep palpation. Digital rectal examination may reveal tenderness on lateral pelvic wall that reproduces symptoms. Reproduction of sciatica type pain with weakness is noted by resisted abduction/external rotation (Pace test). The Freiberg test is another diagnostic sign that elicits pain upon forced internal rotation of the extended thigh. The Beatty maneuver reproduces buttock pain by selectively contracting the piriformis muscle. The patient lies on the uninvolved side and abducts the involved thigh upward; this activates the ipsilateral piriformis muscle, which is both a hip external rotator and abductor with the hip flexed. A painful point may be present at the lateral margin of the sacrum. Shortening of the involved lower extremity may be seen. The patient may have difficulty sitting due to an intolerance of weight bearing on the buttock. The patient may have the tendency to demonstrate a splayed foot on the involved side when in the supine position. Piriformis syndrome alone is rarely a cause of a focal neuromuscular impairment; either a sciatic mononeuropathy or an L5-S1 radiculopathy can mimic both of these conditions, obscuring diagnosis of piriformis syndrome. A Morton foot may predispose the patient to developing piriformis syndrome. The prominent second metatarsal head destabilizes the foot during the push-off phase of the gait cycle, causing foot pronation and internal rotation of the lower limb. The piriformis muscle (external hip rotator) reactively contracts repetitively during each push-off phase of the gait cycle as a compensatory mechanism, leading to piriformis syndrome. Causes: Approximately 50% of patients with piriformis syndrome have a history of trauma, with either a direct buttock contusion or hip/lower back torsional injury. The remaining 50% of cases are of spontaneous onset, so the treating physician must have a high index of suspicion for this problem, lest it be overlooked.   DIFFERENTIALS Lumbar Degenerative Disc Disease Lumbar Facet Arthropathy Lumbar Spondylolysis and Spondylolisthesis Myofascial Pain Trochanteric Bursitis Other Problems to be Considered: Lumbosacral radiculopathy Buttock pain Ischial tuberosity bursitis Sciatica

WORKUP Lab Studies: Laboratory studies generally are not indicated in diagnosing piriformis syndrome. Imaging Studies: Diagnostic imaging of the lumbar spine is mandatory to exclude associated discogenic and/or osteoarthritic contributing pathology. Reports in the literature on piriformis muscle describe imaging by nuclear diagnostic studies and MRI of the pelvis, but these tests are neither practical nor reliable diagnostic approaches to this problem. The history and clinical diagnostic examination provide the greatest and most specific diagnostic yield for this problem. Other Tests: Results of electrodiagnostic testing for piriformis syndrome usually are normal. Reports of positional H-reflex abnormalities can be found in the literature; however, such findings have not been widely accepted or reproduced.   TREATMENT Rehabilitation Program: Physical Therapy: Because a definitive method to accurately diagnose this problem is not available, treatment regimens are controversial and have not been subjected to randomized blind clinical trials. Despite this fact, numerous treatment strategies exist for patients with piriformis syndrome. Functional biomechanical deficits may include the following: Tight piriformis muscle Tight hip external rotators and adductors Hip abductor weakness Lower lumbar spine dysfunction Sacroiliac joint hypomobility Functional adaptations to these deficits include the following: Ambulation with thigh in external rotation Functional limb length shortening Shortened stride length Once the diagnosis has been made, these underlying perpetuating biomechanical factors must be corrected. Consider the use of ultrasound and other heat modalities prior to physical therapy sessions. Prior to performing piriformis stretches, the hip joint capsule should be mobilized anteriorly and posteriorly to allow for more effective stretching. Soft tissue therapies of the piriformis muscle can be helpful, including longitudinal gliding with passive internal hip rotation, as well as transverse gliding and sustained longitudinal release with the patient lying on his/her side. Addressing sacroiliac joint and low back dysfunction also is important. A home stretching program should be provided to the patient. These stretches are an essential component of the treatment program. During the acute phase of treatment, stretching every 2-3 hours (while awake) is a key to the success of nonoperative treatment. Prolonged stretching of the piriformis muscle is accomplished in either a supine or orthostatic position with the involved hip flexed and passively adducted/internally rotated. Medical Issues/Complications: No consensus exists on overall treatment of piriformis syndrome due to lack of objective clinical trials. Conservative treatment (eg, stretching, manual techniques, injections, activity modifications, modalities like heat or ultrasound, natural healing) is successful in most cases. Injection therapy can be incorporated if the situation is refractory to the aforementioned treatment program. For effective injection, the piriformis muscle must be localized manually by digital rectal examination. Then the piriformis muscle is injected using a 3.5-inch (8.9-cm) spinal needle. Care must be taken to avoid direct injection of the sciatic nerve. Surgical Intervention: Surgical management is the treatment of last resort. Surgery for this condition involves resection of the muscle itself or the muscle tendon near its insertion at the superior aspect of the greater trochanter of the femur (as described by Mizuguchi). These surgical procedures are described as effective, and they do not cause any associated superimposed postoperative disability. Consultations: Because of the enigmatic nature of piriformis syndrome, initial consultation obtained from an orthopedic surgeon or similar specialist usually is nonspecific. This disorder is considered to be a soft tissue problem that presents as low back or buttock pain with sciatica. After all differential diagnoses have been excluded, consider piriformis syndrome. Due to the traumatic etiology of most cases, piriformis syndrome usually is associated with other more proximal causes of LBP, sciatica, and buttock pain (thereby further clouding the diagnosis). Other Treatment (injection, manipulation, etc.): The Spray N' Stretch myofascial treatment and ultrasound modality preceding physical therapy sessions are useful. Manual muscle medicine, including facilitated positional release, may be helpful. Injections with steroids, local anesthetics, and botulinum toxin have been reported in the literature for this condition. No single technique is universally accepted. Localization techniques include manual localization of muscle with fluoroscopic and electromyographic guidance. The piriformis muscle, after localization with a digital rectal examination, can be injected with a 3.5-inch (8.9-cm) spinal needle. Care should be taken to avoid direct injection of the sciatic nerve.   FOLLOW-UP Further Inpatient Care: Inpatient care would be necessary only if surgical intervention is warranted. Surgery is the last resort treatment for severe cases of piriformis syndrome. Further Outpatient Care: Piriformis syndrome usually is treated effectively with conservative measures. Please refer to the Treatment section for a discussion of treatment recommendations. Deterrence/Prevention: No method has been demonstrated to prevent piriformis syndrome. The best prevention is to maintain biomechanical balance by restoration of a more physiologic weight bearing distribution with a level pelvis/sacral base and equal leg lengths, achieved by heel lift therapy if necessary. This treatment approach also prevents recurrences of piriformis syndrome, especially if the underlying etiology is a leg-length discrepancy. The patient also must engage in a general stretching program that includes bilateral piriformis muscles. Complications: The most significant complication is failure to recognize, diagnose, and treat this disabling condition. If left untreated, a patient may undergo unsuccessful back surgery for a disc herniation; however, a coexisting occult piriformis syndrome can result in a failed back syndrome. Another complication is inadvertent direct injection of the sciatic nerve, which usually results in a nondisabling and temporary sciatic mononeuropathy. Prognosis: The prognosis depends upon early recognition and treatment. As this is a soft tissue syndrome, it has a tendency to be chronic, usually due to late diagnosis and treatment and has a less favorable prognosis. Patient Education: For conservative measures to be effective, the patient must be educated with an aggressive home-based stretching program to maintain piriformis muscle flexibility. He or she must comply with the program even beyond the point of discontinuation of formal medical treatment.   MISCELLANEOUS Medical/Legal Pitfalls: The greatest medical/legal concern is either misdiagnosis or failure to diagnose piriformis syndrome. In most cases, the diagnosis is one of exclusion. Therefore, if piriformis syndrome is not in the differential diagnosis list, it may be overlooked. The patient becomes a chronic pain patient doomed to a lifetime of disability and chronic management with medication. Because the diagnosis usually is elusive, missing the diagnosis does not constitute malicious negligence and, therefore, rarely would be sufficient grounds alone for a medical malpractice lawsuit. Piriformis syndrome may be a secondary perpetuating factor underlying chronic posttraumatic intractable LBP. Negligent misdiagnosis or delayed diagnosis of this condition has caused a significant degree of unnecessary disability and financial loss. Special Concerns: In female patients, piriformis syndrome may be a cause of dyspareunia, but, again, this connection becomes impossible to prove. Diagnosis of piriformis syndrome requires a high index of suspicion by either the primary care physician or the obstetric/gynecologic specialist/surgeon. A bimanual simultaneous vaginal-rectal examination of female patients to determine this soft tissue diagnosis helps the physician to prescribe appropriate treatment. Although it is a misdiagnosed etiology of LBP/sciatica, piriformis syndrome can be a significant cause of soft tissue pain and disability. This problem requires a skillful, attentive physician to conduct a thorough history/physical examination that provides an accurate diagnosis. Once the clinical diagnosis has been made, a specific treatment can be formulated to provide the best outcome with a minimal degree of long-term disability.