Case Presentation: 84 year old previously healthy female with history of hypertension, Diabetes and chronic kidney disease stage 2 presented to the ER with dizziness. She reported light headedness with frequent room spinning while ambulating. She denied any other associated symptoms. In the ER she was noted to have a Blood pressure of 208/103 and therefore was admitted to our observation unit for further blood pressure management and symptom control.  Over the next few days, her blood pressure was improving however her severe vertigo persisted. She failed Epley Maneuvers and did not respond to meclizine. Her symptoms were extreme and she could no longer walk secondary to nausea and imbalance. She had a full neurological examination and had no focal physical exam findings to suggest either a peripheral or central cause of vertigo. Her laboratory findings were benign except for a hypercalcemia of 10.8 mg/dl, a creatinine of 1.78 mg/dl (baseline 1.4) and a protein gap of 8.1 (TP 10.6 g/dl, Albumin 2.5 g/dl). An MRI brain was preformed showing T1-2 hyperintensities consistent with lytic lesions and a subsequent protein electrophoresis was positive for IgA monoclonal protein (5231 mg/dl). She had a bone marrow biopsy preformed confirming Multiple Myeloma. Given these new findings, hyperviscosity syndrome was thought to be a cause of her symptoms. A serum viscosity was checked and noted to be 4.3 centipoises (expected <1.5) and later it rose to >5.6 centipoises.  She subsequently was started on chemotherapy and received plasmapheresis.

Discussion:  Vertigo is a common complaint in the ER setting often requiring an inpatient hospital stay for symptom management, however it is rarely the initial presenting symptom of Multiple Myeloma secondary to hyperviscosity syndrome. Hyperviscosity is related to the greatly elevated monoclonal protein levels.  Accroding to a review article published in Thrombosis and Hemostasis in 2003, symptomatic hyperviscosity is only present in about 2-6% of Multiple Myeloma patients being much more common in Waldenstroms Macroglobinemia. Its hallmark features include bleeding, ocular symptoms and neurological findings which include vertigo like our patient.  Most patients do not exhibit symptoms until viscosity is greater than 4 centipoises and those symptoms can be subtle until viscosity is greater than 5.  Hyperviscosity is thought to cause Vertigo by peripheral vestibular involvement causing vascular obstruction in the venules. Initial therapy is directed at reducing blood viscosity by plasmapheresis and long term management is related to treating the underlying disease to reduce monoclonal protein production.

Conclusions:  This case reminds hospitalists that although rare, hyperviscosity should be considered in a patient with persistent vertigo and can be the initial presenting sign in making the early diagnosis of Multiple Myeloma or other plasma cell dyscrasias if even if more classic signs and symptoms are absent.