Post-Stroke Athetosis and Hyperacute Strength Reacquisition as Unrecognized Contributors to Hemiplegic Shoulder Pain: A Case Report

Case Diagnosis: A 68-year-old female with flaccid right hemiparesis secondary to acute left thalamic and posterior hippocampal infarcts developed significant athetosis and rapid strength reacquisition within 3 days, likely the cause of new rotator cuff impingement.

Case Description or Program Description: On day 0, a 68-year-old female with history of hypertension, hyperlipidemia, and type 2 diabetes presented with right hemibody flaccid paralysis and aphasia consistent with radiographically-supported infarctions in the left thalamic and posterior hippocampal regions. She was outside of the time window for tPA and was loaded with aspirin and Plavix, later isolated to only aspirin after a small hemorrhagic conversion. By day 3, strength had improved to 4/5 and she was admitted to inpatient rehabilitation. On day 7, she complained of right shoulder pain inhibiting therapy and was observed to have significant RUE athetosis, Modified Ashworth Spasticity of 2 and positive Hawkins test. On day 9, shoulder films confirmed a high riding humerus and 2.5 mm subacromial space with scalloping of the undersurface of the acromion. On day 11, patient received subacromial triamcinolone injection.

Setting: Inpatient rehabilitation facility associated with a Tertiary Care Hospital

Assessment/Results: Following steroid injection for rapidly-developed impingement symptoms, her shoulder pain improved significantly and she was able to meaningfully engage in therapies utilizing adaptive equipment. She was discharged on day 21 after satisfactory improvement.

Discussion (relevance): Although hemiplegic shoulder pain is a common complication of stroke, its etiology remains variable and debated, and typically occurs in weeks to months post-stroke rather than days. This is an unusual case where rapid resolution of weakness compounded with athetoid movements seems to have caused hyperacute spastic elevation of glenohumeral components and development of acute impingement not experienced by the patient premorbidly.

Conclusions: Hyperacute hemiplegic shoulder pain may develop outside of the typically anticipated timeline in the unique setting of rapid return to strength, athetosis, and spasticity.