Background:The incidence of subarachnoid hemorrhage (SAH) in young adults is relatively rare. Kawasaki disease is a systemic vasculopathy that is known to cause coronary artery aneurysms; however, its effect on cerebral arteries remains largely unclear.Case Description:We report the case of a 20-year-old male with a history of Kawasaki disease who presented with SAH caused by the rupture of a nonbranching middle cerebral artery aneurysm. This is the third report of SAH associated with Kawasaki disease. Preoperative echocardiography of the patient rejected the presence of bacterial endocarditis and other heart abnormalities. An emergency craniotomy and clip occlusion of the aneurysm was successfully performed without obstructing the parent artery. Two weeks later, the patient was discharged without any apparent neurological deficit. We also performed a circumstantial pathological study on specimens obtained from the aneurysm wall. Our histological findings suggest that the elastic lamina and tunica intima were completely destroyed during the acute vasculitis phase of Kawasaki disease, which possibly led to the aneurysmal formation.Conclusions:Lack of active inflammatory changes and atherosclerotic lesions may explain the chronic feature of Kawasaki disease, not a typical aneurysmal formation.

The fibrogenic action of PSCs seems to be more strongly associated with activation of the toll-like receptor-dependent pathway than it is with phagocytosis of bacteria by PSCs.

This case showed evidence suggesting that olfactory dysfunction was probably related to limbic TDP-43 pathology and was possibly independent of her Alzheimer pathology. Olfactory dysfunction does not necessarily indicate the presence of tau or α-synuclein pathology and could be an early sign of ALS with the limbic involvement of TDP-43 pathology even when cognitive functions are preserved.

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