Acute or subacute thoracic back pain is a symptom that raises a differential diagnosis including multiple potential life threatening conditions. In the presence of raised creatine kinase (CK) activity, myocardial injury will be an immediate concern. I encountered a patient who presented with severe thoracic back pain and raised CK that resulted in a diagnostic challenge. This case illustrates how subtle physical findings, even when apparently unrelated to the presenting problem, could represent an important clue to reach a final diagnosis.

CASE REPORT

A 59 year old man gradually developed severe sharp interscapular pain with occasional descending radiation, prompting a visit to the emergency room. Initial evaluation included a diminished muscle stretch reflex at the left ankle and an absent reflex on the right with otherwise unremarkable general and neurological examinations. Haemogram, electrolytes, liver and pancreatic enzymes were normal, but CK was 615 IU/l (normal 40–200 IU/l), with a normal cardiac (MB) fraction. Because of appropriate concerns about life threatening conditions such as myocardial infarction, aortic dissection, acute pancreatitis, or spinal cord compression, a range of emergent diagnostic investigations was obtained. An electrocardiogram showed sinus tachycardia. Chest radiograph, chest computed tomography with contrast, and abdominal ultrasound were normal. Magnetic resonance imaging of the cervical and thoracic spinal cord was unrevealing. He was treated with meperidine resulting in short lasting pain relief. Three days later he developed distal lower extremity hypesthesia and was transferred to our institution. On admission, his vital signs were remarkable only for a sinus tachychardia. Neurological examination showed mild distal hypesthesia in a stocking and glove distribution, slightly impaired vibratory sense in the feet, diffuse areflexia, and mild gait ataxia. He was treated with gabapentin, amitriptyline, and diazepam, achieving pain relief within 24 hours. Brain and thoracic spine magnetic resonance imaging, serial CK determinations, and troponin were normal. Nerve conduction velocities were generally slow with no changes in compound motor unit amplitude, supporting the diagnosis of a demyelinating peripheral neuropathy. The cerebrospinal fluid analysis showed 0 cells/mm and a protein of 790 mg/l (normal 150–450). His clinical presentation and diagnostic studies met the proposed diagnostic criteria for sensory Guillain-Barre syndrome (GBS).¹ One month later he suffered a relapse with worsening ataxia, mild distal lower extremity weakness, diffuse areflexia and more prominent sensory loss, and ataxia. Repeated nerve conduction studies showed diffuse slowing with increased latency and temporal dispersion, increased F wave latency and conduction block, further supporting the diagnosis of an acquired demyelinating process. He was treated with a course of intravenous immunoglobulin G with remarkable improvement. In the following three years, there were no additional relapses and his neurological examination reverted to normal.

DISCUSSION

GBS is an immune based, acquired inflammatory demyelinating polyradiculoneuropathy. The classic presentation of this syndrome consists of a monophasic acute ascending paralysis associated with areflexia, but many clinical variants have been described.² Sensory GBS is an unusual presentation characterised by symmetric sensory loss, diminished or absent reflexes and normal motor strength, associated with conduction abnormalities in motor nerves shown by electrodiagnostic studies.¹ The main differential factor between both forms of GBS is the presence of progressive weakness in more than one extremity as a required diagnostic criteria for typical GBS, a clinical finding that rules out the diagnosis of sensory GBS. The rest of the diagnostic criteria are very similar, with minor differences, as shown in table 1.

Although the presence of pain is a common feature of GBS, occurring in up to 50% of patients, it is typically severe low back or leg pain, and often is the presenting symptom.^3,4 Raised CK can be occasionally seen in GBS but its origin in this syndrome is still unclear.^4,5 The combination of severe interscapular pain and increased CK at presentation in our patient is unusual, and appropriately raised the concern of various other life threatening conditions such as aortic dissection, myocardial infarction, pulmonary embolism, or acute pancreatitis, prompting an extensive emergent work up. Weakness, sensory loss, and nerve conduction abnormalities may be subtle or absent at the onset of GBS. The subsequent development of distal hypesthesia, hyporeflexia, and ataxia unmasked the acquired acute demyelinating neuropathic process that was confirmed by the unequivocal findings of the nerve conduction studies during the acute and relapse phase of the illness. This case suggests that GBS should be included in the differential diagnosis of severe interscapular pain associated with raised CK activity. A careful evaluation for subtle clinical signs of early GBS, such as decreased or absent ankle muscle stretch reflexes, may help redirect the diagnostic evaluation, avoid unnecessary tests, and prompt appropriate treatment of this disabling and occasionally fatal illness.