Reversible Parkinsonism Caused by Bilateral Subdural Hematomas in an Elderly Male

Introduction/Purpose Parkinsonism is most often associated with neurodegenerative disease, but structural lesions can rarely produce a secondary and potentially reversible syndrome. Bilateral subdural hematomas (SDHs) are an uncommon cause of rapidly progressive parkinsonism thought to result from compression of basal ganglia‐thalamocortical circuits. With increasing adoption of middle meningeal artery (MMA) embolization, treatment paradigms for SDH are evolving. We present a case of rapidly progressive parkinsonism that fully resolved following combined MMA embolization and surgical evacuation. Materials/Methods A previously independent 69 year old male with a history of hyperlipidemia and gastric reflux presented with 2 weeks of rapidly progressive gait instability and recurrent falls after an initial mechanical fall with head trauma. His symptoms progressed to severe shuffling gait, tremor, rigidity, and wheelchair dependence. He had no history of Parkinson's disease, dopamine‐blocking medications, or prodromal parkinsonian features. He did not take anticoagulants. Neurological exam demonstrated severe symmetric parkinsonism with marked postural instability, bilateral upper extremity rigidity, and a bilateral resting tremor. Non‐contrast head CT revealed large bilateral SDHs up to 26 mm traversing the superior frontal and parietal lobes. There was significant mass effect on the basal ganglia without midline shift. MRI suggested late subacute hematomas. The patient underwent bilateral MMA embolization with Onyx, a non‐adhesive liquid embolic agent, to reduce the vascular supply to the hematoma membranes. Following embolization, he underwent bilateral craniotomy and hematoma evacuation for decompression. The combined approach was chosen to both relieve acute mass effect and minimize long‐term recurrence risk. Results The patient showed marked neurological recovery shortly after intervention. Within 3 days post‐procedure, the patient's gait instability, rigidity, and tremor had significantly improved. The post‐procedure course was uncomplicated. By 2 weeks he had no residual parkinsonian features and did not sustain any further falls. At 6 weeks, CT demonstrated only small residual bilateral SDHs (≤9 mm) without recurrence. As the patient was asymptomatic, shared decision making was employed to develop the ongoing plan of care: routine surveillance for 3 months and monitoring for return of symptoms. Conclusion This case illustrates an uncommon and important secondary cause of parkinsonism. Bilateral SDHs can compress the basal ganglia and related pathways, leading to rapidly progressive motor features that may closely mimic idiopathic Parkinson's disease. Unlike neurodegenerative parkinsonism, symptoms due to structural compression may be fully reversible with appropriate intervention. Our case highlights several key points: (1) Secondary parkinsonism should be considered in patients with rapid onset or atypical features, particularly when imaging reveals structural lesions. (2) MMA embolization is an emerging therapy for SDH, and when combined with surgical evacuation, it may provide both immediate relief and reduced risk of recurrence. (3) Early recognition and prompt intervention can result in complete neurological recovery, underscoring the importance of collaboration between vascular neurologists, interventionalists, and neurosurgeons. This case reinforces the limited literature supporting a combined neuroendovascular and neurosurgical approach as an effective strategy to treat a secondary and reversible form of parkinsonism.