Guillain-Barré syndrome after an operation on the spine. A case report.

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Abstract
Postoperative Guillain-Barre syndrome has been reported infrequently in the literature [1-4,13,15,16,20,21]. We managed a patient in whom Guillain-Barre syndrome developed after an operation on the lumbar spine. We are reporting this case to illustrate the importance of determining the exact cause of a new neurological deficit that occurs after an operation. A sixty-two-year-old woman was seen because of progressively disabling symptoms that were due to degenerative lumbar scoliosis and spinal stenosis. When the symptoms did not respond to appropriate non-operative treatment, the patient had lumbar decompression from the twelfth thoracic vertebra to the sacrum and segmental spinal instrumentation and arthrodesis from the eleventh thoracic vertebra to the sacrum. Somatosensory evoked potentials were monitored intraoperatively. No complications were apparent during the procedure. Postoperatively, the initial medical course seemed unremarkable. However, in retrospect, we realized that the patient had reported more diffuse pain in the body than would normally be expected after the operation. She had also noted increased paresthesias in the feet, but they were not investigated because she did not have a new motor or reflex deficit. The patient became independent in the activities of daily living and was discharged home. On the twenty-fifth postoperative day, the patient came to the emergency room because of progressive numbness and weakness of all four extremities. The symptoms in the lower extremities had evolved insidiously since the time of discharge, until she was not able to walk. The weakness and numbness of the upper extremities had occurred within the previous three days. She had no constitutional symptoms of infection. Physical examination revealed areflexic paresis of all four extremities, with the symptoms worse in the distal part of the extremities than in the proximal part, as well as sensory loss in the distal part of the extremities. The rectal tone and perianal sensation were normal. The second through twelfth cranial nerves were also normal. A myelogram of the entire spine showed normal findings, but examination of cerebrospinal fluid revealed five nucleated cells per cubic millimeter and a markedly elevated level of protein of 3.17 grams per liter (normal, 0.15 to 0.45 gram per liter). The patient was admitted for further evaluation and observation. Nerve-conduction studies showed slowing and prolonged latencies in the median, ulnar, and sural nerves. Electromyography did not demonstrate any fibrillations, but a reduction in the number of potentials was revealed. On the basis of these results and in the context of the history and the findings of the physical examination and the analysis of the cerebrospinal fluid, a diagnosis of acute inflammatory demyelinating polyradiculoneuropathy, or Guillain-Barre syndrome, was established [2,5]. Treatment with high doses of corticosteroids and of human immunoglobulin was not successful. The patient subsequently had a plasmapheresis, which was followed by notable improvement. Within six months, the neurological deficits, except for minor weakness of the intrinsic muscles of the hands, had completely resolved. The original symptoms in the spine were considerably decreased. However, eighteen months after the operation, there was a concern that a solid fusion would not be obtained at the level between the fifth lumbar vertebra and the sacrum. The patient was satisfied with the improvement of her condition, and she continued to be followed. The onset of progressive sensory and motor deficits after an operation on the spine is alarming and demands urgent and thorough investigation. The differential diagnosis is broad and includes not only treatable complications that are related to the procedure but also primary neurological diseases.