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Depression of spinal motoneurons may underlie weakness associated with severe anemia
A Arturo Leis1, Dobrivoje S Stokic, Jinna M Shepherd
1Center for Neuroscience and Neurological Recovery, Methodist Rehabilitation Center, 1350 East Woodrow Wilson, Suite 2, Jackson, Mississippi 39216, USA. artleis@aol.com
A 37-year-old woman had a 2-week history of progressive weakness, muscle hypotonia, and absent or hypoactive deep tendon reflexes. Nerve conduction studies showed diminished H-reflexes and absent or decreased persistence of F-waves in all limbs. The patient was admitted to the hospital with a diagnosis of Guillain-Barré syndrome. Laboratory studies revealed severe anemia with a hemoglobin level of 4.1 g/dl and hematocrit of 15.1%. Immediate blood transfusion resulted in a hemoglobin of 13.2 g/dl and hematocrit of 40.2%, associated with rapid neurological recovery (normal stretch reflexes and muscle strength) and normalization of F-waves and H-reflexes. This case demonstrates that severe anemia may be associated with signs and symptoms that mimic Guillain-Barré syndrome, both clinically and electrophysiologically. It also suggests that a relative depression of spinal motoneuron excitability may be a possible mechanism for the weakness that is commonly observed in severe anemia.
A 37-year-old woman had a 2-week history of progressive weakness, muscle hypotonia, and absent or hypoactive deep tendon reflexes. Nerve conduction studies showed diminished H-reflexes and absent or decreased persistence of F-waves in all limbs. The patient was admitted to the hospital with a diagnosis of Guillain-Barré syndrome. Laboratory studies revealed severe anemia with a hemoglobin level of 4.1 g/dl and hematocrit of 15.1%. Immediate blood transfusion resulted in a hemoglobin of 13.2 g/dl and hematocrit of 40.2%, associated with rapid neurological recovery (normal stretch reflexes and muscle strength) and normalization of F-waves and H-reflexes. This case demonstrates that severe anemia may be associated with signs and symptoms that mimic Guillain-Barré syndrome, both clinically and electrophysiologically. It also suggests that a relative depression of spinal motoneuron excitability may be a possible mechanism for the weakness that is commonly observed in severe anemia.