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Binocular diplopia and right hemifacial numbness developed in a 52-year-old woman after resection of a right temporal lobe glioblastoma. Based on the Parks-Bielschowsky 3-step test, she was diagnosed with a right cranial nerve (CN) IV palsy in addition to right CN V dysfunction. Iatrogenic diplopia may result from temporal lobe surgery due to the intimate relationship of CN IV and CN III to the mesial temporal lobe. In addition, injury to CN V within Meckel cave is believed to be the cause of facial numbness in some patients after temporal lobe surgery. The anatomy of the intracranial portion of CN IV is reviewed, and the etiologies of CN IV palsy are discussed.

Opsoclonus is a pathological eye movement phenomenon in hich the eyes experience involuntary, arrhythmic, rapid, multidiectional, conjugate movements. It occurs in all eye positions and uring smooth pursuit, and can also persist during sleep. It is diferentiated from nystagmus in that there is no slow eye movement hase, and it differs from ocular flutter because the eye movement s multidirectional and not confined to the horizontal. Opsoclonus an be accompanied by tremors, cerebellar ataxia, myoclonic jerks, r encephalopathy. In addition to paraneoplastic etiologies, it is ometimes autoimmune, but frequently without an identifiable ntibody [1].

In September 2015, a Wyoming woman was admitted to a local hospital with a 5-day history of progressive weakness, ataxia, dysarthria, and dysphagia. Because of respiratory failure, she was transferred to a referral hospital in Utah, where she developed progressive encephalitis. On day 8 of hospitalization, the patient's family told clinicians they recalled that, 1 month before admission, the woman had found a bat on her neck upon waking, but had not sought medical care. The patient's husband subsequently had contacted county invasive species authorities about the incident, but he was not advised to seek health care for evaluation of his wife's risk for rabies. On October 2, CDC confirmed the patient was infected with a rabies virus variant that was enzootic to the silver-haired bat (Lasionycteris noctivagans). The patient died on October 3. Public understanding of rabies risk from bat contact needs to be improved; cooperation among public health and other agencies can aid in referring persons with possible bat exposure for assessment of rabies risk.

A 74-year-old woman with a history of asthma, Crohn disease, and osteoporosis presented with acute onset, constant sharp pain in the dorsal and plantar aspects of her bilateral feet. She endorsed associated paresthesias, but denied weakness. Several weeks after the onset of the pain, she developed pruritic palmar erythema. She denied dry eyes, dry mouth, or having had a rash like this before, but did endorse scaling on her hands following her biannual injection of denosumab for osteoporosis. The authors thank Kristin Leiferman, MD, of the immunodermatology laboratory at the University of Utah.

Neurodegeneration with brain iron accumulation (NBIA) is a group of genetic diseases characterized by progressive extrapyramidal symptoms and focal iron accumulation in the basal ganglia. β-Propeller protein-associated neurodegeneration (BPAN), also known as static encephalopathy of childhood with neurodegeneration in adulthood or NBIA 5, is an X-linked dominant subtype of NBIA.1 Brain MRI studies consistently demonstrate iron accumulation in the globus pallidus and substantia nigra with a subset of patients also demonstrating a halo of hyperintense signal surrounding a thin region of hypointense signal in the substantia nigra on T1-weighted imaging.2 The majority of patients with BPAN are female, but several affected males with identical phenotypes have been described, most likely harboring postzygotic mutations leading to somatic mosaicism.3 BPAN has been shown to be caused by heterozygous mutations in WDR45 at Xp11.23. To date, all mutations have been de novo, with no affected relatives.1,3,4 We report here on a patient with BPAN with a novel c.597_598 deletion mutation in WDR45.

A woman aged 77 years was transferred to our neurocritical care unit for evaluation and treatment of rapidly progressive motor weakness and encephalopathy. Examination revealed an ability to follow simple commands only and abnormal movements, including myoclonus, tongue and orofacial dyskinesias, and opsoclonus. Imaging study findings were initially unremarkable, but when repeated, they demonstrated enhancement of the cauda equina nerve roots, trigeminal nerve, and pachymeninges. Cerebrospinal fluid examination revealed mildly elevated white blood cell count and protein levels. Serial electrodiagnostic testing demonstrated a rapidly progressive diffuse sensory motor axonopathy, and electroencephalogram findings progressed from generalized slowing to bilateral periodic lateralized epileptiform discharges. Critical details of her recent history prompted a diagnostic biopsy. Over time, the patient became completely unresponsive with no further abnormal movements and ultimately died. The differential diagnosis, pathological findings, and diagnosis are discussed with a brief review of a well-known yet rare diagnosis.