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Abstract Details

From Lacrimal Sarcoid to Status Epilepticus: A Pathway Through the Sinuses
Autoimmune Neurology
P2 - Poster Session 2 (2:45 PM-3:45 PM)
049

The mechanism of spread of sarcoidosis through the nervous system is an area of active study; the most reported being leptomeningeal focus with centripetal spread. We present a case of a patient with lacrimal sarcoidosis and potential travel from the lacrimal glands into the ethmoidal sinuses, through the cribriform plate into the inferior frontal gyrus, causing new onset seizures.

A 32-year-old female with biopsy-proven sarcoidosis of bilateral lacrimal glands presents with first time seizures and no return to baseline.  Laboratory workup was notable for elevated angiotensin converting enzyme, electroencephalogram captured bilateral frontal discharges and magnetic resonance imaging of the brain demonstrated FLAIR hyperintensities in the anterior-superior frontal lobes and enlarged FLAIR signal in bilateral lacrimal glands concerning for neurosarcoidosis. Sinonasal biopsy showed granulomatous changes.  

 

N/A

Postmortem studies revealed granulomatous propagation of sarcoidosis by hematogenous and lymphatic routes along with local extension in the heart and lung. Neurosarcoidosis has been presumed to be hematogenous, given the preferential perivascular distribution and paucity of a well-defined intracranial lymphatic system. Perineural spread to the cranial nerves has been described from sinonasal disease, which could be associated with vasa-nervorum, since small arterial perforators are affected more frequently than larger vessels.

Conversely, our patient presented with dissemination that originated in the lacrimal glands, demonstrated to have invaded the nasal septum and ethmoidal sinus, and subsequent meningeal and parenchymal spread, which does not obey the hematogenous theory, and rather opens the possibility of a contiguous spread, such as that evidenced in other organs.

 

This case raises questions about the contiguous spread of neurosarcoidosis, of which the pathophysiology has not been keenly studied thus far. Likely, the dissemination of neurosarcoidosis is multifactorial, and we propose an alternate theory, yet to be investigated.

Authors/Disclosures
Gabriela Mata, MD
PRESENTER
Dr. Mata has nothing to disclose.
Kaushik Gokul Kaushik Gokul has nothing to disclose.
Navreet T. Chennu, MD Mr. Chennu has nothing to disclose.
Adam Awad, MD Dr. Awad has nothing to disclose.
Jafar Kafaie, MD, PhD, FAAN (Saint Louis University) Dr. Kafaie has nothing to disclose.