Monday, September 29, 2008

Shoulder and Hemiplegia


Shoulder and Hemiplegia






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.”


  • 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%.



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


  • 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.




Adhesive Capsulitis
Chronic Pain Syndrome
Heterotopic Ossification
Rheumatoid Arthritis

Other Problems to be Considered:

Glenohumeral subluxation
Trauma/soft tissue injury
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
Suprascapular neuropathy
Median neuropathy
Vascular compromise
Thoracic outlet syndrome
Myofascial pain syndrome/fibromyalgia

1 comment:

Anonymous said...

12 years stroke (hemiplegia) survivor.
I had the greatest shock of my life when i had a cardiac arrest 12 years ago and slumped into comma. I was in comma for a year and three months before i was able to open my eyes. I stuttered with speech and and i noticed i could not move the full right side of my body my hands and legs this was when the doctor told me i had stroke (hemiplegia). I was bedridden and kept in a wheel chair when i need to move for 10 years more and it became worse because i started having memory failure i hardly remember anything. The condition was debilitating and even my neurologist could not help me with his several therapy. My wife came in one day with a medicine she got from a herbal doctor she wanted me to start taking that i will be okay, i was reluctant because i had given up already and was waiting for my death day. she talked me into taking it telling me how much she love and cares about me and how she and the kids are gonna miss me. I took the medicine for 3 months as recommended and my condition improved i was able to walk and move those parts affected by the stroke and today i have fully recovered after 12 years of horror. Do not die because of ignorance you too can be well again. just contact him on for more information on about it and how to get his medicine. thanks for allowing me share my story.