A 62-year old underwent a ventral discectomy of C7/Th1, cage interposition and decompression of the spinal canal due to a pure sensory cervical syndrome caused by osteochondrosis and foraminal stenosis of C7/Th1 on both sides. During surgery a dural leakage was sealed with a TachoSilO-Patch. The following day the patient reported a lack of strength in his right leg and facial asymmetry. On the 2nd postoperative day the physical examination showed an incomplete palsy of the right facial nerve, of the iliopsoas, the tibialis anterior and the extensor digitorum comm. Moreover, the patient felt pain in his left shoulder. Apart from those findings, no other paralyses or sensory losses were detected, muscle reflexes were symmetrical and normal. The cerebral and spinal MRI showed a vague pathology of the spinal cord at C8 but to the dorsal left. Facial MEP showed a canalicular conduction block of the right facial nerve. MEP of the upper and lower limb were hardly evocable from the cortex and showed prolonged latencies when evoking cervically and lumbally. Initially, we assumed these findings to be due to a central palsy of the right leg and a peripheral facial nerve palsy. Steroid treatment with Prednisolon 50 mg/d was started. The following day the patient worsened: palsy of the right hypoglossal nerve, paralyses of both arms regarding muscles innervated by C5/C6/C8 radices, areflexia. The MEPs were still pathological. Electrophysiological findings: Motor neurography of Nn. tibiales: distal latencies 6.7–7.2 ms, CNV 33–36 m/s, lowering CMAP distally and chronodispersion proximally; moreover, symmetrical demyelinating neuropathy of the upper limb was detected. Assuming this to be due to an atypical Guillain–Barre-Syndrome (GBS), we started treatment with ivIg (0.4 g PrivigenO/kg for 5 days). CSF (on 4th postoperative day): 243 cells/μl, monocytes (50%), protein (total) 468 mg/dl. One day after starting ivIg treatment the patient complained about loss of hearing and a tinnitus of both ears. Sensorineural hearing loss was found. As recommended by the ENT-colleagues, a steroid treatment (Prednisolon 250 mg i.v./d for 3 days) was added. The patient’s condition improved and he was sent on the 12th postoperative day to rehabilitation. Postoperative neuropathies are usually caused by pressure or by trauma during the procedure itself. In this case we presume that the asymmetrical, demyelinating polyradiculoneuropathy is to be interpreted as an atypical GBS. The aetiology of these unusual clinical findings was finally detected by simple motor nerve conduction studies. There are only few case reports on immune neuropathies following surgery that include a wide range of time of onset and symptoms. The extraordinary aspects of the above case are the very early appearance of symptoms, within 48 h after surgery, and the asymmetric dissemination including cranial nerves. In conclusion, even though a postoperative GBS is a very rare condition, the diagnosis of an immune neuropathy at the appearance of unusual patterns of palsies should be considered.
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