Objective: To describe two cases of parkinsonism caused by anoxic brain injury.

Background: Movement disorders occur in about 40% of patients following anoxic brain injury, with myoclonus being the most common [1]. Although the basal ganglia is a region vulnerable to anoxia, parkinsonism remains a rare manifestation of anoxic brain injury.

Method: We report two cases of patients who developed parkinsonism following cardiac arrest with anoxic brain injury. Case 1: A 56-year-old man presented with freezing of gait (FOG). Seven months prior, he experienced a cardiac arrest with prolonged ICU and rehab course. MRI Brain revealed bilateral symmetric restricted diffusion in the basal ganglia as well as cerebellar hemispheres along with frontal, temporal, parietal and occipital cortices. Examination showed bradykinesia, dysarthria, and FOG but with normal muscle tone and no tremor. Carbidopa-levodopa and istradefylline offered little benefit for FOG. Patient experienced partial improvement in gait with amantadine.

Case 2: A 46-year-old man presented for stiffness and slowness.  Four months earlier he experienced cardiac arrest with prolonged ICU and rehab course. MRI brain showed bilateral diffusion restriction and corresponding increased bilateral FLAIR hyperintensity in bilateral globus pallidus, thalami, and parietal and occipital lobes.  On exam, he had bilateral but left-side predominant bradykinesia and cogwheeling, as well as hypomimia, hypophonia, and slower gait. DaT scan showed decreased radiotracer uptake in the bilateral putamen and caudate. He was started on carbidopa-levodopa and had mild improvement in symptoms.

Results: Both cases demonstrated akinetic-rigid parkinsonism following anoxic brain injury but also differed in predominant symptoms and response to medication. Post-anoxic parkinsonism with akinetic-rigid subtype typically occurs 3 months after anoxic injury [2]. The involvement of freezing of gait may point to more extensive cerebral structures being damaged, including the cerebellum [3].

Conclusion: Parkinsonism is a rare manifestation that may be encountered in post-anoxic patients with basal ganglia injury. Differences in symptoms and response to medications may be due to extent of basal ganglia damage. DaT scan may be considered for further verification of parkinsonism in anoxia.

References: [1] Khot S, Tirschwell DL (2006) Long-term neurological complications after hypoxic-ischemic encephalopathy. Sem Neurol 26:422–431

[2] Bhatt MH, Obeso JA, Marsden CD. Time course of postanoxic akinetic-rigid and dystonic syndromes. Neurology. 1993 Feb;43(2):314-7.

[3] Yoon SY, Lee SC, Kim NY, An YS, Kim YW. Brain metabolism in patients with freezing of gait after hypoxic-ischemic brain injury: A pilot study. Medicine (Baltimore). 2017 Nov;96(45):e8212.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/parkinsonism-after-post-anoxic-brain-injury/