朱毛 gibberish

Patient, 52 year-old white female housewife living with her husband, complained of right hip and leg pain for 2 years. She could not recall the onset of the symptom, but her symptoms had increased over the past 2 years. Pt complained of dull pain or pressure around the right hip joint, pain usually got worse at night and relieved some by taking over counter ibuprofen. However, pain was not relieved through rest. Recently her pain had radiated to the right low back and leg and she also complained of numbness in the posterior thigh, calf and onto the foot. She visited her primary care physician. She was diagnosed with sciatica and was referred to physical therapy. Upon evaluation, patient AROM of the back was WFL and did not provoke pain. However, patient complain of pain with AROM of hip in all plane with empty end feel secondary to muscle guarding. Joint mobility was not tested at this point. SLR was positive. No other neurological findings were positive. It was revealed that patient had tenderness upon palpation on the R hip joint with some trigger points on the right piriformis and hamstrings. Slight decreased in lordosis was observed. No other findings were positive and vital signs were normal.

Patient received some AAROM exercises to right hip, postural re-education and trigger point release for piriformis and hamstrings. Due to patient’s pain, E-Stim IFC was used on the right hip. After 4 weeks of treatment, patient’s symptom has not decreased and started to complain of bladder symptoms. Therapist decided to refer patient back to the physician secondary to unknown cause of pain and symptoms inconsistent with musculoskeletal conditions.

Result: primary care physician ordered hip x-ray for patient and revealed conventional intramedullary chondrosarcoma of the right acetabulum on radiography (similar to reference 2). Patient underwent surgery to remove the tumor and referred back to physical therapy to regain strength and use of the affected area after surgery.

This case was chosen because a lot of times chondrosarcoma in the pelvis may arise sciatica, back and leg pain which mimic musculoskeletal symptoms. Therapist must aware of patient’s condition and progress and refer patient back to physician when appropriate. If the therapist in this case knew the patient had chondrosacrcoma, he/she would not have use E-stim, which is contraindicated to tumor.

Questions:

1)       Why, do you think, chrondrosacrcoma would cause sciatica and bladder symptoms?

2)       As a therapist, how do we determine whether or not to use E-stim for pain in such cases?

Reference:

1.  Goodman CC, Snyder TEK. Differential Diagnosis for Physical Therapists, 4 ^th ed. Philadelphia, PA: Saunders. 2007.

2.   http://radiographics.rsnajnls.org/cgi/content-nw/full/23/5/1245/F11A

3.  Dutton, Mark. Orthopedic Examination,Evaluation, and Intervention, The McGraw Hill Companies, Inc. 2004.

This is a fake case..

After reading the case study by Walsh and Sadowski [1], one can conclude that the therapist described in the article made several assumptions that led to dismissing the non-musculoskeletal diseases. First of all, patient presented with excruciating pain and severe limitation to movement, however, the therapist did not consider the degree and nature of limitation atypical and assume it was due to prolonged history of shoulder pain. This could be a justifiable assumption because severe pain often occurs after surgery and it is not unusual for patient to present with capsular restriction to accessory motions. On the other hand, the constant nature of patient’s pain and her history of cancer might have been indicated as a red flag. Yet, the therapist was not suspicious of cancer recurrence because the MRI, bone scan and arthroscopy did not reveal metastatic disease. This assumption was not justifiable because the MRI or bone scan may not have targeted the problematic organ. Negative results on those exams may not rule out systemic diseases. Therefore, when patient has a history of cancer, it is wise to assume that their symptoms have a pathological origin until proven otherwise. Third, at the evaluation, therapist had already assumed that there would be an extended recovery due to connective tissue of the shoulder might have been compromised by 7 corticosteroid injections. After 4 weeks, when the patient still presented with same amount of pain, a slow rate of improvement in strength and range of movement which did not correlate well with a musculoskeletal shoulder condition alone, yet the therapist was not suspicious and thought the slow progress was just due to a maladaptive state producing hyperalgesia from central pain sensitization [1]. After 7 weeks of therapy, therapist thought that patient did show some functional improvement during the course of physical therapy secondary to patient’s disability index (from disability questionnaire) reduced from 52% to 42%. Nonetheless, the disability measure used in this case has not undergone scientific validation and could not be assumed to be indicative of real functional changes. The unexpectedly poor improvements after 4-7 weeks should raise another red flag.

From my point of view, I believe therapists should be aware that they might be treating  patients with systemic disease along with musculoskeletal condition.

Hides et al [1] explained the multifidus atrophy in patients with low back pain was not due to disuse atrophy or reflex inhibition. Yet, they believed the atrophy was caused by inhibition due to perceived pain, through a long loop reflex, which targeted the vertebral level of pathology to protect the damaged tissues.

Disuse atrophy of muscle is often defined as loss of mass and strength, which can occur after prolonged immobility, such as extended bed rest, or having a body part in a cast for a period of time [2]. Subjects recruited from this research was experiencing first episode of acute and subacute low back pain with no known bed rest or immobilizer and the mean duration of symptoms was less than 15 days (men: 12.1days, women: 14.6days)[1]. The rapidity onset suggested that disuse atrophy was not the cause. Multifidus consists of five separate bands, which receive their own innervations. These bands spread caudolaterally from the midline; each originates from one lumbar vertebra and attaches to mamillary processes, the iliac crest and the sacrum, so they are polysegmental [1]. If disuse atrophy of muscle occurs, one may expect to see reduction in muscle size throughout the entire length of the muscle over different levels of lumbar spine. However, the ultrasound scanning revealed marked cross-sectional area (CSA) asymmetry of multifidus and the wasting of the muscle in each patient was only isolated to one vertebral level instead of the entire length of the muscle. The localized distribution of muscle wasting further suggested that disuse atrophy was not the cause.

Hides et al [1] also pointed out that the wasting of multifidus was not caused by reflex inhabitation. Hides and co-workers, with support findings from deAndrade et al [3], suggested that reflex inhibition can occur in the absence of pain, and has a more specific pattern of wasting. They used the knee joint as an example. With knee joint damage, afferent stimuli from the joint inhibit activation of alpha motor neurons to quadriceps via a spinal reflex mechanism and caused quadriceps wasting [1]. According to the segmental anatomical arrangement and innervations of multifidus fascicles, Hides et al further suggested that if wasting from low back pain patient was due to reflex inhibitions, the site of greatest wasting would be below the vertebral level of pathology and symptoms, where the bulk of these segmental fascicles is situated. The wasting of multifidus was measured by CSA in this study. The asymmetry of CSA at the level of symptoms was found significantly different from other levels with P<0.05 by Duncan’s multiple-range test, which suggested that multifidus wasting only occurred at the level of symptoms but not below. Therefore, reflex inhibition was not the cause of multifidus wasting either.

Reference:

1. Hides JA, Stokes MJ, Saide M, Jull GA, Cooper DH. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute / subacute low back pain. Spine. 1994; 19:165-172.

2. Campellone, Joseph V. 05-22-2007. Muscle atrophy. http://www.nlm.nih.gov/medlineplus/ency/ article/003188.htm. MedlinePlus.

3. deAndrade JR, Grant C., Dixon AstJ. Joint distension and reflex muscle inhibition in the knee. J Bone Joint Surg 1965; 47A:313-322.