Objective: To describe a case of post-hypoxic postural instability associated with bilateral internal globus pallidi (GP) infarcts.

Background: A variety of movement disorders, including parkinsonism, have been described following hypoxic injury involving the GP. We present a rare case of postural instability in a patient who suffered hypoxia secondary to drug-induced respiratory failure.

Method: A 36 year-old man with depression, anxiety, ADHD, and polysubstance abuse lost consciousness following the use of amphetamine, cocaine, and heroin. EMS was called, and he responded to naloxone. The following day, he developed reduced speech output, bradykinesia, and postural instability (score 3 on MDS-UPDRS part III)—which was out of proportion to the remainder of his exam (overall score 9). MRI revealed isolated acute infarcts of the bilateral internal globus pallidi (GPi) without other signs of hypoxic injury. Bradykinesia was responsive to 600mg per day of levodopa; postural instability was recalcitrant.

Results: Cerebral hypoxia with subsequent GP infarction has been reported to cause parkinsonism, postural instability, and freezing of gait (1,2). Parkinsonism is the most likely post-stroke movement disorder occurring after GP infarction (3). “Lower extremity parkinsonism” is a common description of the clinical picture following bilateral basal ganglia infarcts (4). Given the GPi role in classic basal ganglia functional anatomy, we would expect hyperkinetic movement disorders, as the lesioned nuclei would release their inhibition on the excitatory thalamic-cortical signals. Despite MRI abnormalities being limited to GPi in our patient, we cannot assume that other susceptible areas were not affected by the hypoxic insult. The GPi projects to the mesencephalic locomotor region (including the pedunculopontinue nucleus) as part of a circuit involved in postural stability (5,6). GPi lesions likely cause network dysfunction leading to a phenotype not explained by classic basal ganglia functional anatomy.

Conclusion: This case demonstrates the essential role of the GPi in postural stability. Improved understanding of this role may help guide the development of better therapies for patients with underlying basal ganglia disorders.

References: 1. Fève AP, Fénelon G, Wallays C, Rémy P, Guillard A. Axial motor disturbances after hypoxic lesions of the globus pallidus. Mov Disord. 1993 Jul;8(3):321-326 2. Yoshii F, Kozuma R, Takahashi W, Haida M, Takagi S, Shinohara Y. Magnetic resonance imaging and 11C-N-methylspiperone/positron emission tomography studies in a patient with the interval form of carbon monoxide poisoning. J Neurol Sci. 1998 Sep 18;160(1):87-91 3. Suri R, Rodriguez-Porcel F, Donohue K, Jesse E, Lovera L, Dwivedi AK, Espay AJ. Post-stroke Movement Disorders: The Clinical, Neuroanatomic, and Demographic Portrait of 284 Published Cases. J Stroke Cerebrovasc Dis. 2018 Sep;27(9):2388-2397 4. Winikates J, Jankovic J. Clinical correlates of vascular parkinsonism. Arch Neurol. 1999 Jan;56(1):98-102 5. Morita H, Hass CJ, Moro E, Sudhyadhom A, Kumar R, Okun MS. Pedunculopontine Nucleus Stimulation: Where are We Now and What Needs to be Done to Move the Field Forward? Front Neurol. 2014 Dec 4;5:243 6. Nutt JG, Bloem BR, Giladi N, Hallett M, Horak FB, Nieuwboer A. Freezing of gait: moving forward on a mysterious clinical phenomenon. Lancet Neurol. 2011 Aug;10(8):734-44

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MDS Abstracts - https://www.mdsabstracts.org/abstract/postural-instability-secondary-to-hypoxic-injury-to-the-bilateral-globus-pallidi/