A woman in her 50s was seen by her physician with a 1-month history of gait unsteadiness and imbalance and was suspected to have neuropathy, but she then went to the emergency department reporting 2 successive transient episodes, each lasting less than 1 hour, of acute dizziness, disorientation, gait dysfunction, and confusion. Urinalysis revealed a urinary tract infection, but computed tomography (CT) of the head showed extensive mass lesions with bilateral edema. Magnetic resonance imaging (MRI) of the brain delineated expansile mass lesions of the splenium of the corpus callosum, with T2–fluid-attenuated inversion recovery hyperintensity in the bilateral parietal lobes, left thalamus, and midbrain (Figure, A); administration of contrast revealed multiple ring-enhancing lesions (Figure, B). The woman’s medical history was significant for type 2 diabetes mellitus (DM), hypertension, recurrent urinary tract infections, onychomycosis, end-stage renal failure, and a history of living, unrelated donor renal transplant 12 years earlier, kidney transplant rejection, and prior episodes of syncope. Medications included tacrolimus, mycophenolate mofetil hydrochloride, prednisone (1 mg/d), losartan potassium, and insulin. Family history was notable for her father having died of lung cancer and her mother had heart disease and DM. Social history did not reveal any unusual exposures. Physical examination results showed a transplant surgical scar and onychomycosis. Neurologic findings revealed reasonably preserved mental status, with bedside examination revealing normal attention, language, and orientation but mild memory deficits for short-term recall (2 of 3 words recalled at a 5-minute delay) and long-term fund of knowledge. Cranial nerve, motor, sensory, and reflex examination results were significant only for gait ataxia, with an inability to perform tandem gait. Blood test results were consistent with DM. Findings from cerebrospinal fluid (CSF) examination included a white blood cell count of 9/µL, with differential examination showing 84% lymphocytes, 13% monocytes, and 3% neutrophils; red blood cell count of 1080/µL; protein level, 180 mg/dL; and glucose level, 87 mg/dL. Flow cytometry revealed B and T lymphocytes but no monoclonal populations of cells. Polymerase chain reaction amplification tests on CSF revealed no evidence of cytomegalovirus or herpes simplex virus 1 or 2 genetic material. Serum and CSF serologic test results were negative for antibodies to toxoplasma; testing using polymerase chain reaction on blood for Epstein-Barr virus (EBV) revealed minimal (very low positive) viral DNA at 52 IU/mL. A CT scan of the chest, abdomen, and pelvis showed a small, subpleural nodule; fatty liver; diverticulosis; failed native kidneys; and normal transplanted kidney. Whole-body positron emission tomography revealed hypermetabolic regions in the brain. Dexamethasone sodium phosphate and levetiracetam were administered. The patient underwent a diagnostic procedure.
Honig LS. Subacute Imbalance in a Renal Transplant Patient. JAMA Neurol. 2015;72(11):1367–1368. doi:10.1001/jamaneurol.2015.1904
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