Case Presentation: This is an otherwise healthy 28-year-old female who presented with sudden, atraumatic left lower extremity paresis. With the same onset, she noted left-sided paresthesia and left upper extremity weakness. She additionally had a history of two episodes of transient, unilateral blurred vision. On admission, her examination revealed intact cranial nerves. Strength was intact on the right side. Left-sided strength was 4/5 in the upper extremity and 2/5 in the lower extremity. Reflexes were 2+ on the right and 3+ on the left. Her right-sided sensation was intact with a 25% decrease in sensation on the left. MRI/MRA of the head revealed an acute infarct of the right posterior superior frontal gyrus. There was also multifocal gliosis and encephalomalacia involving the bilateral parietal lobes and right cerebellum, suggestive of prior infarcts vs sequela of metabolic or mitochondrial disorders. There were no MR findings of vasculitis. A workup of her stroke including bubble study, telemetry, coagulopathy testing, autoimmune panels of serum/plasma and cerebral spinal fluid, infectious etiologies, and mitochondrial and metabolic disorders were all unremarkable. Additional laboratory evaluation revealed an erythrocyte sedimentation rate of 28 mm/hr and a C-reactive protein of 39.5 mg/L. She was initiated on stroke secondary preventative treatment. On follow-up, she was noted to have multiple inflamed cysts in various stages of development and healing in her bilateral axillae and right groin. She reports having similar lesions in past but never sought treatment. She was referred to dermatology, diagnosed with Hurley stage 3 HS, and initiated on clindamycin 300mg twice daily, rifampin 300mg twice daily, and chlorhexidine wash with expected escalation to adalimumab given severity of disease. On follow-up, her weakness had almost resolved with physical therapy.
Discussion: HS is a relatively uncommon disease, affecting 0.10% of the American population with increased incidence in women, those aged 30-39, African-American and biracial groups. The pathophysiology of HS is thought to be multifactorial, with genetic mutations and environmental factors creating an environment conducive to epidermal cyst formation that rupture, leading to systemic inflammation. While the mechanism that leads to systemic inflammation is still being investigated, there is growing evidence of inflammatory sequela related to HS in young, otherwise healthy individuals. This case of stroke in an otherwise healthy 28-year-old adds to the growing evidence of systemic inflammation secondary to HS and highlights the importance of a thorough review of systems and physical exam for early recognition of HS as a potential risk factor for stroke or heart attack.
Conclusions: Hidradenitis suppurativa (HS) is a chronic inflammatory condition that has recently been shown to have increased systemic implications. Care should be given to identifying this risk factor in otherwise healthy, young individuals presenting with stroke-like symptoms.