Peripheral facial nerve palsy

Abstract

(A) Neurosarcoidosis. Addition information on work up includes blood work showing unremarkable basic metabolic panel, liver function, complete blood count with differential, and serum calcium levels. A serum angiotensin converting enzyme (ACE) level was 109 U/L (9–67 U/L). CSF ACE was 9 U/L (<15 U/L). The diagnosis of Neurosarcoidosis was made. Sarcoidosis is a multi-systemic granulomatous inflammatory disease of unknown etiology. Neurological involvement can occur in up to 5% of patients with sarcoidosis. The neurological manifestation can vary widely from cranial neuropathies such as optic neuritis and peripheral seventh nerve palsy to spinal cord involvement to meningeal disease [1Spiegel D. Morris K. Rayamajhi U. Neurosarcoidosis and the complexity in its differential diagnosis: a review.Innovat Clin Neurosci. 2012; 9: 10-16PubMed Google Scholar, 2Hoyle J.C. Jablonski C. Newton H. Neurosarcoidosis: clinical review of a disorder with challenging inpatient presentations and diagnostic considerations.Neurohospitalist. 2014; 4: 94-101Crossref PubMed Scopus (32) Google Scholar]. The diagnosis of neurosarcoidosis should be suspected in a patient with neurological symptoms who already has an established diagnosis of systemic or pulmonary sarcoid. MRI of the brain may show nonspecific white matter changes or hydrocephalus; however, with the administration of gadolinium contrast, enhancement of the cranial nerves, meninges or the hypothalamic-pituitary axis may be observed [[2]Hoyle J.C. Jablonski C. Newton H. Neurosarcoidosis: clinical review of a disorder with challenging inpatient presentations and diagnostic considerations.Neurohospitalist. 2014; 4: 94-101Crossref PubMed Scopus (32) Google Scholar]. Lastly, biopsy should be considered to confirm the diagnosis. In patients with neurological disease only, biopsy of the meninges or other enhancing lesions would be considered. In patients with systemic disease, biopsy can be obtained from involved skin, lymph node or lung using direct guidance, transbronchial biopsy, or CT-guided biopsy. CSF analysis consistent with neurosarcoidosis includes lymphocytic pleocytosis, elevated protein, oligoclonal bands, and elevated angiotensin converting enzyme (ACE) levels. CSF lymphocytic pleocytosis may occur in 31–83% of patients, elevated protein may be seen in 41–83%, and oligoclonal bands may be found in 27–37% of patients with neurosarcoidosis. An elevated CSF angiotensin converting enzyme (ACE) levels is not highly sensitive but is relatively specific: it also can be elevated in carcinomatosis and infections of the central nervous system [[3]Ibitoye R.T. Wilkins A. Scolding N.J. Neurosarcoidosis: a clinical approach to diagnosis and management.J Neurol. 2017; 264: 1023-1028Crossref PubMed Scopus (48) Google Scholar]. Fluorodeoxyglucose positron emission tomography scan may also be considered to rule out systemic areas of involvement in patients who have not manifested with systemic symptoms. Patient’s history and symptoms were most consistent with the diagnosis of neurosarcoidosis especially considering the results discussed above. In this case, Bell’s palsy, multiple sclerosis, neuroborreliosis, and Ramsay-Hunt were less likely given patient’s presenting symptoms and diagnostic workup. Bell’s palsy is a diagnosis of idiopathic peripheral facial nerve palsy. Serum and CSF Lyme testing was negative and patient had denied exposure to tick bite thus ruling out peripheral facial nerve palsy secondary to lyme. Similarly, Ramsay-Hunt was unlikely as there was no ear pain and CSF was negative for VZV and HSV PCR. MRI findings of the brain did not reveal FLAIR-T2 hyperintensities to support diagnosis of multiple sclerosis. The following are the Supplementary data to this article: Download .xml (.0 MB) Help with xml files Supplementary data 1 Peripheral facial nerve palsyJournal of Clinical NeuroscienceVol. 69PreviewA 44 year-old right-handed female with a past medical history of hypothyroidism presented with a left facial droop and dysgeusia. In the weeks prior, she had experienced intermittent diplopia, transient decreased left eye visual acuity, frontal headache, and nausea without vomiting. The patient’s history was also notable for dyspnea, fever, night-sweats, myalgia, nonproductive cough, and wheezing for two months, with unintentional 10 lb weight loss. The patient was undergoing workup for these symptoms that to date had revealed 3 sub-centimeter right upper lobe lung nodules and mediastinal and hilar lymphadenopathy. Full-Text PDF