Albuminocytologic Dissociation and Intravenous Immunoglobulin Therapy in Parsonage-Turner Syndrome With Bilateral Involvement: A Case Report.

Parsonage-Turner syndrome (PTS) is a rare neurological disorder characterized by acute neuropathic pain followed by motor and sensory deficits, typically affecting the brachial plexus. While often self-limiting, atypical presentations can complicate diagnosis and management. We present a case of a 53-year-old male patient with a history of cervical foraminal stenosis and progressive left upper extremity (LUE) flaccid paralysis for over 14 months, with no clear cause for worsening symptoms. Diagnostic evaluation, including magnetic resonance imaging (MRI) and computed tomography (CT) of the brain, cervical spine, and brachial plexus, revealed grossly normal findings. Initial electromyography (EMG) studies demonstrated worsening motor response in the LUE without the typical dermatomal distribution of cervical radiculopathy, leading to the diagnosis of PTS. Additionally, shoulder subluxation and triceps tendon insertional enthesopathy were noted due to muscular instability. The patient was followed by outpatient neurology and physical medicine and rehabilitation departments when, 14 months later, he developed similar weakness in the contralateral right upper extremity (RUE). In the outpatient clinic, repeat EMG demonstrated severe axonal denervation with no motor or sensory response in the LUE, along with new-onset RUE weakness in the digits, prompting hospital admission. During a week-long hospitalization, all blood tests were normal, and infectious causes were ruled out. Notably, cerebrospinal fluid (CSF) analysis revealed albuminocytologic dissociation (ACD), a unique finding in the patient with a history of PTS. Given the conflicting presence of ACD and the potential for an underlying autoimmune inflammatory neuropathy, the patient was treated off-label with intravenous immunoglobulin (IVIG). IVIG was selected over corticosteroids due to the chronic and worsening nature of the condition, as there is limited clinical evidence supporting steroid efficacy in long-term cases. Physical therapy was initiated during hospitalization, leading to modest improvement in the RUE motor strength. This case highlights the diagnostic challenges of PTS, particularly in patients with bilateral involvement, atypical progression, and severe symptoms. A multidisciplinary approach, including the exclusion of other neuromuscular and structural pathologies, is essential. Early recognition and intervention may help mitigate long-term morbidity. Further research into early diagnostic markers and targeted treatments is warranted to improve patient outcomes and restore neuromuscular function.