Cranial Neuropathy in patients with Peripheral Nerve Disorders. (P5.115)

Objective: To review the diagnosis and clinical features in patients with cranial neuropathy and peripheral nerve disorders. Background: Cranial nerve involvement has been well described in patients with Acute Inflammatory Demyelinating Polyneuropathy (AIDP). The literature on cranial nerve involvement in patients with more sub-acute to chronic peripheral nerve disorders is limited to case reports and review articles. Design/Methods: 87 patients were identified from the EMG database (Mayo Clinic, Rochester) with diagnostic codes for peripheral nerve disorders and a diagnosis of cranial neuropathy. Patients with clinical diagnosis of AIDP were excluded from the study. The relevant laboratory tests, electrodiagnostic findings and pathology results were reviewed. Results: In our cohort of 87 patients, lymphoma was the most common diagnosis (29%) followed by Sjogrens syndrome (8.5%) and Inflammatory / Immune mediated causes (8.5%). Amyloid and Sarcoidosis each accounted for 6% of the patients. In some patients the final diagnosis was Diabetes (5%) and Chronic Meningitis (5%). Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP), Multiple Myeloma, Facial Onset Sensory Motor Neuronopathy (FOSMN) and Non Diabetic Lumbosacral Radiculoplexusneuropathy (NDLSRPN) each accounted for 4% of the patients. A few patients were diagnosed with Vasculitis (2%), post infectious (2%), Paraneoplastic neuropathy (1%) and Hereditary Neuropathy (1%). 10% of patients in our cohort did not have a final diagnosis despite extensive investigations. Cranial nerves 5 and 7 were the most frequently involved, followed by cranial nerve 3 and 6. The peripheral nerve disorder localised to the root level in 45% of patients and the peripheral nerve level in 34% of patients. Conclusions: Inflammatory neuropathies especially Lymphoma followed by Sjogrens syndrome was the most common diagnosis in patients with cranial neuropathy and peripheral nerve disorders. The peripheral nerve disorder localised to the root level in a majority of the patients in our cohort. This is likely secondary to blood–nerve barrier being most vulnerable at this level. Disclosure: Dr. Rodrigues has nothing to disclose. Dr. Dyck has nothing to disclose. Dr. Kao has nothing to disclose.