The Hidden Danger: Dysautonomia in Guillain-Barré Syndrome Leading to Hemorrhagic Stroke
Clare Lambert1, Vanessa Dias Veloso2, Emily Gilmore3, Rachel Forman4
1Department of Neurology, Yale New Haven Hospital, 2Yale New Haven Hospital, 3Department of Neurology, Yale University School of Medicine, 4Department of Neurology, Yale School of Medicine
Objective:
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Background:

Guillain-Barré syndrome (GBS) is associated with dysautonomia due to demyelination of nerves in the autonomic system. We present a case of ataxic GBS, a rare variant often including bladder dysfunction and hemodynamic lability, whose illness was complicated by intracerebral hemorrhage (ICH).  ICH is a rare complication of GBS that has only been reported in the literature a handful of times. It has been hypothesized that autonomic dysregulation, particularly in patients with underlying vascular risk factors or vasculopathy secondary to treatment with intravenous immunoglobulin (IVIG), could play a role in blood vessel wall integrity. 

Case Presentation: A 63-year-old man with no significant medical history presented with weakness and urinary retention after a gastrointestinal illness. Examination revealed absent deep tendon reflexes, reduced vibratory sensation, and sensory ataxia, with blood pressure fluctuating from 90/70 to 150/70. Cerebrospinal fluid showed cytoalbuminologic dissociation. Brain and spine MRI showed no nerve root enhancement or microhemorrhages suggestive of cerebral amyloid angiopathy. He received IVIG and was discharged to rehabilitation. Four days later, he returned with altered mental status and right-sided weakness; CT revealed a large left frontal ICH, leading to craniotomy and hematoma evacuation. Blood pressure continued to fluctuate between 80/60 and 170/80, and he re-bled five days later, requiring a second decompression. Clot pathology ruled out vascular malformation, inflammation, or amyloid. He has since shown partial motor and cognitive improvement. 

Design/Methods:
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Results:
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Conclusions:
After excluding other causes, such as inflammatory vasculopathy secondary to IVIG, dysautonomia, as a complicatin of GBS was determined to be the cause of hypertensive ICH, in the context of labile blood pressures. This case underscores an exceedingly rare, but potentially devastating, complication of dysautonomia in GBS. Close monitoring for the development of dysautonomia and a good understanding of this complication is important.  
10.1212/WNL.0000000000212110
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