Neuromusculoskeletal Disorders
Following SARS: A Case Series

This section is compiled by Frank M. Painter, D.C.
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FROM:   J Can Chiropr Assoc. 2011 (Mar);   55 (1):   32-39 ~ FULL TEXT

Brynne Stainsby BA, DC,   Scott Howitt BA, CK, CSCS, DC, FCCSS(C), FCCRS(C),
Jason Porr BSc

Graduate Student,
Clinical Sciences,
Canadian Memorial Chiropractic College,
6100 Leslie Street,
Toronto, Ontario M2H 3J1. ext. 208

OBJECTIVE:   To detail the presentation of three health care workers diagnosed with sudden acute respiratory syndrome (SARS) who later presented to a CMCC teaching clinic with neuromusculoskeletal sequelae and underwent conservative treatments. This case series aims to inform practitioners of the potential pathogenesis of these neuromuscular complaints and describes their treatment in a chiropractic practice.

CLINICAL FEATURES:   Three patients presented with a variety of neurological, muscular and joint findings. Conservative treatment was aimed at decreasing hypertonic muscles, increasing joint mobility, and improving ability to perform activities of daily living.

INTERVENTION AND OUTCOME:   The conservative treatment approach utilized in these cases involved spinal manipulative therapy, soft tissue therapy, modalities, and rehabilitation. Outcome measures included subjective pain ratings, disability indices, and return to work.

CONCLUSION:   Three patients previously diagnosed with SARS presented with neuromusculoskeletal complaints and subjectively experienced intermittent relief of pain and improvement in disability status after conservative treatments.

From the Full-Text Article:


The number of chiropractors treating patients previously diagnosed with SARS is unknown, however, with over 8000 cases reported during the global outbreak, it is certainly possible these patients may present in a chiropractic office. Readers should be aware of the limited body of knowledge regarding neuromusculoskeletal complaints associated with SARS and therefore, the difficulties in the determination of prognosis. Furthermore, other viral infections may present as neuromuscular disorders, and practitioners should be educated regarding the potential mechanisms of pathogenesis including direct action (viral myositis or neuritis), infl ammatory reaction (immune mimicry), or via a systemic infl ammatory response syndrome. [12]


Muscle weakness and an elevated serum CK level have been documented in patients infected by the SARS-CoV, however, little is understood about the mechanism of injury. [2, 10] Though clinical trials to examine the pathogenesis of SARS-associated myopathy are currently not available in the literature, the findings of case reports and series suggest it may be a common sequela of the infection. [2, 10] A number of potential causes have been identified and warrant further investigation.

Cachetic myopathy has been suspected due to disuse following bed rest. [2, 5, 13] Patients commonly suffered from acute respiratory failure during the second phase of SARS and required bed rest which may have lead to deconditioning and muscle wasting. [5] While disuse is likely to play a role in muscle atrophy, it does not fully explain the necrosis and histochemical changes reported in the literature.

Due to the number of patients presenting with myalgia and an elevated serum CK level, a viral-induced myositis has been suggested. [10] During in situ hybridization and viral culture for SARS-CoV, the negative fi ndings suggest the necrosis may be due to cytokine release which caused immune damage rather than viral infection of the skeletal muscles. [13] This theory was reinforced by the absence of viral particles observed during electron microscopy. [13]

The use of systemic corticosteroids as treatment for acute respiratory failure during the second phase of SARS has also been suggested as a potential contribution to the development of myopathy. [2, 5] Corticosteroids have been purported to alter electrical excitability of muscle fi bres, decrease the number of thick filaments, and/or inhibit protein synthesis. [5] Interestingly, patients who did not receive steroid therapy were not found to experience myofi ber atrophy, further indicating the potential role of corticosteroid therapy in the development of myopathy. [2] It must be noted however, authors believe three to 10 days of steroid therapy (typical dose) alone was not adequate to explain the pathogenesis of myopathy, and stressed the need for investigation of other (or combined) causes. [2]

One such cause may be the development of critical illness myopathy (CIM), an acquired myopathy following acute or chronic disease. This disorder has frequently been observed in conditions requiring mechanical ventilation and high-dose steroid treatment. [2] It is believed to be caused by activated leukocytes infiltrating skeletal muscle and causing the release of pro- and anti-inflammatory cytokines, leading to axonal degeneration with preservation of the myelin sheath. [13] This disorder is characterized by a normal cerebrospinal fluid protein level, preservation of cranial nerve and autonomic function and a lack of lymphocyte infiltration of neurons. [13] Clinically, patients maintain sensation (via peripheral nerves), and testing reveals elevated serum CK and decreased thick filaments with fi ber atrophy and necrosis on biopsy. [2, 13]


Similarly, neurologic manifestations of SARS have not been well described in the literature. [12] A relationship between the SARS-CoV and neurological symptoms has not been established; it is currently unknown if the virus has the potential to damage peripheral nerves directly or if the observed neuropathy is an immune mediated process. [12]

Critical illness polyneuropathy (CIP) has been suggested most commonly to explain the neurologic presentation following a diagnosis of SARS. [11, 13] CIP develops as an acute neuropathy during severe illness and typically remits when the underlying illness is controlled. [11] An illness such as SARS could have produced elevated levels of proinfl ammatory cytokines, platelet activating factor, arachidonic acid, free radicals and proteases. [13] These factors could create a neurotoxic environment and lead to neuropathy. [13] If acute, practitioners must ensure the underlying systemic inflammatory response (sepsis) is medically managed and other causes (neurotoxic drugs, poisoning and nutritional deficiencies) are ruled out as there is no specific treatment for CIP. [13] Prognosis is unknown and may vary depending on the severity of the disease. It has been suggested that symptoms (especially weakness) may persist in those patients with a long duration of sepsis or those requiring long-term care in intensive care, however, actual durations of illness or treatment are not defined. [13] Chao et al. reported rapid improvement in neurologic status following extubation in a patient with severe respiratory symptoms. [11]

Clinical considerations

In the cases one and two, the patients were diagnosed with a psoas contracture. The psoas major may be related to the respiratory system due to its anatomical relationship with diaphragm. The psoas originates on the transverse processes and lateral aspects of the vertebral bodies of T12-L5 (and associated intervertebral discs). At its most superior attachment, the psoas is related to the medial and lateral arcuate ligaments, and the central tendon of the diaphragm. [14] In case three, the jump sign elicited during palpation of the scalenes highlights a more apparent involvement of accessory respiratory muscles. Though this has yet to be discussed in the literature, the involvement of muscles related with respiration in all three cases is an interesting finding following a respiratory illness. The respiratory difficulties reported by the patients in this case series may have required increased involvement of accessory muscles and resultant muscular pain. Future clinical or anatomical studies may be warranted to examine the relationship between viral respiratory infections and related muscular complaints.

Interestingly, all three patients complained of easy bruising following SARS. In a review by Yang et al., thrombocytopenia was a common haematological change reported in patients with SARS, though the exact cause was not well understood. [15] Increased destruction and/or decreased production of platelets in damaged lungs may be a mechanism resulting in thrombocytopenia in severe pulmonary conditions. [15] Clinicians should be aware of this possibility and educate patients and/or modify treatment plans accordingly.


As indicated above, the long-term prognosis of SARS and its associated complications are unknown. Practitioners must be prudent to re-evaluate frequently and ensure patients are improving or maintaining pain/disability status. Certainly, any deterioration in health status requires further investigation and co-management as appropriate.

Law et al. presented a case series to examine factors affecting return to work in 128 health care workers in Hong Kong with musculoskeletal complaints two years following in the SARS outbreak. [8] These authors noted patients continued to experience difficulties in performing activities of daily living and work tasks despite receiving acute treatment and rehabilitation. Return to work (RTW) has been suggested as an important measure of prognosis; however, it is known that pain does not correlate well with RTW. [8] A number of important considerations beyond pain and functional ability impact a worker’s ability and desire to return. [7, 8] Factors such as support in the workplace, feasibility of providing alternate duties, and the worker’s beliefs on the effects of return-to-work on their injury progression must be considered. [8]

The lack of evidence regarding prognosis of neuromuscular complaints in patients previously diagnosed with SARS must be clearly communicated to patients, however, it does not preclude treatment of conditions within the chiropractic scope. The current case series suggests the importance of appropriate use of outcome measures, both generic and disease-specifi c. Althou gh patients may report short-term pain relief and positive effects on health related quality of life, outcome measures (VAS, NDI, OBDI) may not demonstrate clinically relevant changes. The inclusion of an outcome measure that allows the patient to identify specific limitations (such as the MYMOP [16]) or addresses overall health related quality of life (such as the SF-36 [17, 18]) may allow for the measurement of subjective improvement.


Myopathic and neuropathic complications in patients diagnosed with SARS have been reported previously; however, to our knowledge, this is the first case series to describe patient presentation in a chiropractic clinic. Furthermore, we believe this case series represents a longer follow-up period (up to six years following SARS diagnosis) than was previously available in the literature. Little is known regarding the cause of these neuromuscular symptoms, and even less is known regarding treatment options for these patients, particularly after the acute illness has been controlled. [2, 5, 11, 13] Follow-up research should be conducted to obtain more information about the long-term outcomes of SARS.

Clinicians should be aware of the proposed pathogenesis of neuromuscular complaints with a previous SARS or other severe respiratory infections and ensure any differential causes have been ruled out prior to commencing a plan of management focused on conservative therapies.

In this case series, three patients with varied neuromuscular complaints reported short-term subjective improvements in their pain experience and quality of life, and two were able to return to work. Future research should investigate the role of conservative care and manual therapies for this type of patient population using subjective outcome measures.


The researchers gratefully acknowledge St John’s Rehab Hospital for providing data and interprofessional collaboration. Gratitude is expressed to the Canadian Memorial Chiropractic College for their continued support of chiropractic research.

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