Case 81 -- New Rapidly Progressive Weakness

Contributed by Gloria Galloway, MD*, Michael J. Giuliani, MD**, and David Lacomis, MD***
Published on line in November 1996

Department of Neurology* Louisiana State University, Shreveport, LA;
Departments of Neurology**,*** and Pathology (Neuropathology)***
University of Pittsburgh School of Medicine, Pittsburgh, PA


A previously healthy 51-year-old woman developed arm and leg weakness without paresthesias one week after a flu-like illness. One week after the weakness occurred, difficulty ambulating necessitated hospitalization. Neurologic examination revealed mild asymmetric upper greater than lower extremity weakness with normal cranial nerves, deep tendon reflexes, and sensation. Creatine kinase, ESR, and cerebrospinal fluid (CSF) cell count and protein were normal. An edrophonium test was negative. Nerve conduction studies revealed low motor amplitudes and normal sensory responses. Needle examination revealed reduced recruitment of normal motor unit potentials, but there was no spontaneous activity.

Over another week, her weakness worsened and respiratory failure occurred. She underwent tracheal intubation and mechanical ventilation. There was facial and palatal weakness in addition to only a flicker of upper extremity movement and barely antigravity strength in the legs. Deep tendon reflexes were absent, but sensation remained normal. A brain CT scan was normal. The CSF contained 2 WBCs (1 PMN), and the protein rose to 54 mg/dl (normal less than 45). Nerve conduction studies revealed low motor and normal sensory responses in an arm and leg. There was no conduction block. An EMG needle examination was refused.

Five days after intubation, sudden mental status deterioration occurred, and an intracerebral hemorrhage was identified on CT scan. The patient succumbed to brain herniation. She had received intravenous heparin for venous thrombosis prophylaxis due to a history of thrombophlebitis.




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