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AGR-1: Disentangling Post-Hypoxic Cognitive Impairment From Parkinsonian Syndromes: A Neuropsychological Case of Lance-Adams Syndrome

Oct 2026 · Archives of Clinical Neuropsychology · 0 citations

Abstract

Objective: This case highlights the neuropsychological profile of mild neurocognitive disorder following hypoxic injury in the context of COVID-19–related hospitalization, characterized by executive inefficiencies and post-hypoxic myoclonus. It aims to illustrate the role of neuropsychological evaluation in differentiating post-hypoxic cognitive and motor sequelae from neurodegenerative conditions such as Parkinsonian syndromes. Method/Data Selection: The patient is a 66-year-old, right-handed White male with 12 years of education who presented to neurology with memory concerns, tremor, imbalance, and insomnia in the context of normal imaging findings. Evaluation included a clinical interview with the patient and his wife, as well as standardized neuropsychological measures assessing premorbid functioning, attention, processing speed, executive functioning, language, visuospatial abilities, memory, motor functioning, and mood. This case study will be conducted following approval from the Institutional Review Board (IRB). Results/Data Synthesis: The patient and his wife reported persistent cognitive symptoms (e.g., forgetfulness, word-finding difficulty, slowed thinking) following hospitalization for COVID-19 with documented hypoxic events. Motor symptoms included intermittent tremor, imbalance, and episodic involuntary upper extremity movements. Testing was valid and revealed impaired verbal memory along with weaknesses in executive functioning and language. Attention, processing speed, visuospatial abilities, and visual memory were intact. Conclusions: Findings are most consistent with a chronic post-hypoxic condition (e.g., Lance-Adams Syndrome). The pattern of executive inefficiencies and isolated verbal memory impairment, alongside preserved core cognitive domains and normal DaTScan supports a post-hypoxic etiology rather than a primary neurodegenerative process.

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