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Paraneoplastic Limbic Encephalitis as the Initial Presentation of Small Cell Lung Cancer FREE TO VIEW

Amina Saqib, MBBS; Uroosa Ibrahim, MBBS; Alina Bhat, MBBS; Vahid Ghiasian, MD; Dany El-Sayegh, MD
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Staten Island University Hospital, Staten Island, NY

Chest. 2014;146(4_MeetingAbstracts):647A. doi:10.1378/chest.1995262
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SESSION TITLE: Cancer Student/Resident Case Report Posters I

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Paraneoplastic syndromes (PNS) are distinctive diseases caused by a remote rather than a direct effect of invasion and/or metastasis of malignant neoplasms. [1] The syndrome may present as paraneoplastic cerebellar degeneration, limbic encephalitis, paraneoplastic sensory neuropathy, Lambert-Eaton myasthenic syndrome, and occasionally autonomic failure. The most prevalent underlying malignant neoplasm, although it might be sometimes undetected in the early stage, is small-cell lung cancer (SCLC).

CASE PRESENTATION: Paraneoplastic syndrome (PNS) with distinct neurological features is reported in a 67 year old man presenting with new onset facial numbness and seizures followed by acute psychosis and neurobehavioral symptoms of aggression and paranoid ideation. The patient had no other medical problems and had a smoking history of one pack per day for fifty years. An MRI of the brain was normal. His clinical presentation suggestive of a left hemispheric focus prompted a video electroencephalogram, the results of which failed to establish definite lateralization. The finding of an opacity on a chest x-ray prompted a chest CT followed by a transbronchial biopsy and a PET scan leading to the diagnosis of Stage III B small cell lung cancer. A positive anti-Hu antibody titer established the diagnosis of PNS associated with Stage IIIB SCLC. However, the diagnosis was confounded by the presence of anti-glutamate decarboxylase (GAD) antibodies. The patient underwent chemotherapy with cisplatin and etoposide, concurrent radiotherapy and prophylactic brain irradiation which resulted in resolution to non-FDG avid status of all previously FDG avid sites in the right lung, right hilum, mediastinum, and right supraclavicular region consistent with good treatment response. This was associated with complete recovery of his neurological symptoms. Relapse of SCLC Stage IV with extensive bone metastasis four months later required additional radiation therapy. The patient developed thrombocytopenia and leukopenia following radiotherapy and died within 8 days of hospitalization.

DISCUSSION: Our case of PNS was unique in that it was associated with the presence of both anti-Hu and anti-GAD antibodies in the setting of SCLC. Anti-GAD antibodies are mostly found in the setting of autoimmune limbic encephalitis. Appropriate chemotherapy and radiotherapy resulted in remission of small cell lung cancer and resolution of PNS.

CONCLUSIONS: Our case highlights limbic encephalitis as an atypical presentation of small cell lung cancer and the importance of diagnosing the underlying etiology of neuropsychiatric symptoms for appropriate treatment choices. It also illustrates how treatment of the underlying cancer can reverse limbic encephalitis in small cell lung cancer.

Reference #1: 1. Henson RA & Urich H. Cancer and the Nervous System.The Neurological Manifestation of Systemic Malignant Disease. Oxford: Blackwell Scientific, 1982

DISCLOSURE: The following authors have nothing to disclose: Amina Saqib, Uroosa Ibrahim, Alina Bhat, Vahid Ghiasian, Dany El-Sayegh

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