Phenobarbital-Induced Fibromyalgia As the Cause of Bilateral Shoulder Pain
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Phenobarbital-induced fibromyalgia as the cause of bilateral shoulder pain STEPHEN 1. GOLDMAN, DO MICHELLE S. KRINGS, MS, PT, ATC 1« A female swimming instructor swimming strokes; in fact, it had affected all her normal, was seen with chronic bilateral shoulder pain active lifestyle as she could not raise her arms above and loss of range of motion. Intensive physi shoulder level. She had no history of arm or shoulder pain, cal therapy significantly improved the range and she denied having paresthesia, other joint pain, of motion but did not alleviate the pain. Osteo swelling, or taking any new meclications. She had under gone multiple meclical evaluations before this referral was pathic manipulative treatment produced no made. Previous medical records were unavailable. further improvement in pain or function. The patient's medical history was remarkable for Results of laboratory tests were all within hypertension, mitral valve prolapse, and tonic/clonic normal limits. Four months after the initial con seizures, which had been completely controlled with sultation, the patient, who was taking med phenobarbital, 120 mg/d, for the previous 10 months. ication for tonic/clonic seizures, recalled that She had previously taken hydantoin sodium, which was her symptoms began after her anticonvulsant discontinued because of "liver toxicity." She did not medication was switched from hydantoin remember her previous dosage of hydantoin sodium. sodium to phenobarbital. Therefore, pheno barbital-induced fibromyalgia was diagnosed. Physical examination In 4 months, pain had completely disappeared. Physical examination revealed the patient to be in excel The authors discuss several theories regard lent physical condition. Musculoskeletal examination ing the cause of fibromyalgia and the mech revealed a high right iliac crest with the patient in the standing position, with an S-shaped scoliosis convex left anism of action of phenobarbital, including in the lumbar region (apex L-2) and convex right in the its relationship to sleep disturbance, a prob thoracic region (apex T-8). The left lower extremity was able contributor to pain and dysfunction in the longer by V2 inch with the patient in the supine position. patient described. Bilaterally, the shoulders were rolled forward. Bilater (Key words: Shoulder pain, phenobarbi al Adson's sign with subclavian bruit was present. The tal, fibromyalgia, seizure disorder) upper portion of the rib cage was also markedly rolled for ward, with decreased respiratory motion. Manual mus Diagnosing the cause of shoulder pain is often cle testing revealed upper extremity strength to be 4- difficult. This article describes chronic shoulder to 4/5 in all groups, except for weakness bilaterally in exter nal rotators. The patient had no decreased sensation to pain resulting from an unusual cause-phenobar light touch, and her cranial rhythmic impulse was marked bital-induced fibromyalgia. ly depressed. Multiple tender points (> 11) were present bilaterally across the trapezius mechanisms, wrists, and Report of case elbows, and across multiple costochondral junctions. A 47-year-old woman was seen in consultation for the gradual onset of shoulder pain and loss of motion. The pain Treatment course began without any inciting event and increased at night, Physical therapy evaluation showed significant loss of especially in the medial aspect of the upper arms bilat both active and passive range of motion in the shoulder erally. girdles, with minimal loss of ventral and dorsal joint play The patient was employed as a swimming instruc in the right glenohumeral joint (Table 1). Weakness was tor, and the pain limited her ability to demonstrate seen grossly in the bilateral abductors and external rota tors. Results of the impingement, drop-arm, and supraspina From the Total Rehabilitation and Athletic Conditioning Cen tus tests inclicated no abnormality. ter, Botsford General Hospital, Farmington Hills, Mich, where The patient underwent a 3-month program of intense Dr Goldman was medical coordinator; Ms Krings is a staffphys ical therapist. physical therapy with the goal of restoring pain-free Correspondence to Stephen 1. Goldman, DO, 23995 Novi Rd, range of motion to within functional limits. Treatment Suite CI03, Novi, MI 48375. consisted of moist heat applied bilaterally to the shoul- Case report· Goldman and Krings JAOA • Vol 95 • No 8 · August 1995·487 tion of motion in the thoracic inlet and upper portion of Table 1 the chest cage. No further increased function or decreased Active Range of Glenohumeral Motion at pain was achieved, however, in spite of improved upper Start of Physical Therapy (Baseline) and body mechanics, resolution of bilateral Adson's sign, and Six Months Mter Physical Therapy correction of the scoliosis. Four months after the initial consultation, the patient Range of motion, degrees recalled that her symptoms began after her anticonvul sant medication was switched from hydantoin sodium to Baseline After 6 months phenobarbital. The possibility of phenobarbital-induced fibromyalgia was discussed with the patient's neurolo • Flexion gist, who did not agree with the tentative diagnosis. The Right 138 152 patient then requested another neurologic opinion. In Left 135 160 the interim, she was given amitriptyline hydrochloride, 10 mg 1 hour before bedtime, which resulted in some • Abduction decrease in pain. A second neurologist confirmed the Right 128 140 diagnosis of phenobarbital-induced fibromyalgia and sug Left 125 145 gested switching the patient to carbamazepine, which • Internal rotation the patient refused because of concerns about long-term Right 46 50 side effects. She agreed to a trial change back to hydan Left 60 55 toin sodium, 100 mg daily for 2 days, then twice a day for 2 days, then three capsules daily beginning on day 4, • External rotation with subsequent monitoring of serum hydantoin sodium Right 78 90 and liver enzyme levels. Left 38 80 One week later, serum hydantoin sodium levels were therapeutic and the phenobarbital therapy was discontinued. The patient subsequently had a greatly improved cra ders for 20 minutes, followed by continuous ultrasonog nial rhythmic impulse. Two weeks later, she reported raphy to the anterior inferior capsule, joint mobilization, marked pain reduction and marked improvement in range and active and passive stretching. The patient was guid of motion (Table 3). Physical therapy and OMT were con ed progressively through a functional conditioning program tinued. Within 4 months of the change of medication, the and a home flexibility and strengthening program, with patient reported that she had no residual shoulder pain, concentration on the rotator cuff and scapular stabilizer was sleeping well, and was able to play volleyball. She still muscle groups. On completion of this program, the patient had decreased internal rotation of the right glenohumeral showed significant objective improvement in range of joint. Magnetic resonance imaging (MRI) of the right motion (Table 1). However, the patient continued to com shoulder revealed a slight tear of the anterior inferior plain of bilateral shoulder pain that did not decrease throughout the therapy pro Table 2 gram. Results of Patient's Laboratory Studies Osteopathic manipula tive treatment (OMT) ses Reference sions were scheduled every laboratory 2 weeks and the patient was Test Value normal range restarted on physical therapy. Several weeks la ter, the White blood cell count, X 1091L 4.9 4.0-10.0 patient had no improvement Red blood cell count, x 10121L 4.1 3.5-5.5 in function or relief from pain. Results of multiple lab Hemoglobin concentration, gldL 13.6 12.0- 15.0 oratory tests (Table 2) were Hematocrit, % 39.3 36.0-48.0 all within normal limits. A 9 3/8-inch left heel wedge was Platelets, X 10 1L 286.0 150.0-450.0 prescribed to level the pelvis Erythrocyte sedimentation and help to correct her func rate, mmlh 2.0 0.0-10.0 tional scoliosis. Continued treatment with physical Thyroid-stimulating hormone, /-lUlL 2.7 0.4- 5.5 therapy and OMT using com Antinuclear antibody titer <1:40 <1:40 binations of high-velocity, low-amplitude thrust, Aspartate transaminase (SGOT), IUIL 36.0 17.0-37.0 myofascial release, and cran Alanine transaminase (SGPT), lUlL 42.0 30.0-65.0 iosacral techniques result ed in total resolution of the Lactate dehydrogenase, lUlL 185.0 80.0-191.0 scoliosis. Attention was then Alkaline phosphokinase, lUlL 120.0 50.0-136.0 directed toward normaliza- 488 · JAOA • Vol 95 • No 8 · August 1995 Case report · Goldman and Krings es to pain may be related Table 3 to theories regarding non Active Range of Glenohumeral Motion in Relation to restorative sleep and poor Anticonvulsant Medication physical fitness causing Range of motion, degrees pronounced fatigue, decreased will to exercise, At 2 weeks At 1 month and resultant decreased after start of after resumption slow-wave sleep, causing amitrip tyline of hydantoin Three months a positive feedback loop. therapy therapy later Fatigue may also be the result of an ill-defined • Flexion "muscle-derived fatigue Right 155 145 175 factor."4 Left 168 165 175 Physical examination reveals an absence of • Abduction edema; multiple tender 145 125 160 Right points, usually at mus Left 163 160 170 culotendinous junctions with hyperemia to deep • Internal rotation palpation; normal find Right 50 10 45 ings on joint examina Left 60 45 70 tions; and normal results of laboratory studies • External rotation Right 90 80 90 (including complete blood Left 90 90 90 cell count, erythrocyte sedimentation rate, and rheumatoid antibody, with glenoid labrum. Bilateral shoulder MRI was not per occasional elevated antinuclear antibody). The dif formed because the patient's left shoulder was now asymp ferential diagnosis includes temporomandibular tomatic. Amitriptyline therapy was gradually discontin joint syndrome, polymyalgia rheumatica, polymyosi ued. The patient decided not to pursue arthroscopic tis, neuroses, chronic fatigue syndrome, hypothy examination of the labrum tear. roidism, and myofascial pain.