A Case of Hypercalcemic-Type Stage IVB Small-Cell Carcinoma of the Ovary in a Young Woman.

A 38-year-old nulliparous woman with severe obesity (BMI 66) and hypertension presented with constipation, fatigue, weakness, and poor appetite that had progressively worsened over the prior two to three weeks. Upon admission, the patient was found to have significant hypercalcemia, leukocytosis, and lactic acidosis. Computed tomography (CT) scan of the chest, abdomen, and pelvis revealed an adnexal mass with extensive lesions throughout her pelvis, abdomen, and chest. An ultrasound-guided omental core biopsy was performed, which was confirmatory for metastatic ovarian small cell carcinoma. Given her poor prognosis and clinical status, chemotherapy was likely to provide minimal benefit and ultimately the patient decided to pursue a comfort-oriented plan of care and passed away on day 9 of admission.

A Case of Distal Common Bile Duct Obstruction Due to a Neuroendocrine Tumor.

Neuroendocrine tumors (NETs) are a rare subset of malignancies in the biliary tract that may have an aggressive and initially asymptomatic course. A 93-year-old female presented with four days of abdominal pain with associated nausea, jaundice, and brown-colored urine. A CT scan revealed a soft-tissue lesion measuring 1.9 x 1.5 x 1.9 cm within the distal-most aspect of the common bile duct and papilla with marked bile duct dilatation, pancreatic duct dilatation, and multiple hepatic lesions of varying sizes. The biliary stricture was palliated with a stent via endoscopic retrograde cholangiopancreatography. Biopsies taken from the biliary mass were consistent with a well-differentiated NET: World Health Organization, Grade 3. The patient was minimally symptomatic after stenting and was discharged home. She ultimately decided not to pursue further treatment and passed away two months after the initial presentation. Currently, surgical excision is considered the main and only curative treatment for localized NETs, although chemotherapy and radiation therapy may be suitable. Early detection and treatment of these rare NETs in the biliary tree can potentially result in curative treatment.

Prophylactic Spinal Cord Untethering in Children with Spinal Dysraphism Undergoing Thoracolumbar Fusion for Scoliosis.

BACKGROUND: It remains unclear whether spinal cord untethering is necessary to reduce the chances of neurologic decline in children with myelomeningocele and complex closed spinal dysraphism who undergo thoracolumbar fusion for scoliosis. We sought to determine the neurologic and functional outcomes of children with spinal dysraphism undergoing spinal fusion for scoliosis with and without prophylactic spinal cord untethering. METHODS: Retrospective, single-center review of patients with spinal dysraphism treated with thoracolumbar fusion over the last 10 years (2009-2019) with or without prophylactic spinal cord untethering. RESULTS: Seventeen patients with myelomeningocele and complex closed spinal dysraphism underwent spinal fusion for scoliosis. Mean age at time of surgery was 13.9 years. Prophylactic spinal cord untethering was performed in 8 of 17 (47%) patients. The change in Cobb angle after surgery was similar between the 2 groups (19.4° untethered vs. 19.9° no untethering). The ambulatory status was similar between the groups, with 37% of the untethered cohort and 44% of the non-untethered cohort being community or household ambulators. There were no changes in intraoperative motor or sensory evoked potentials in any patient during fusion surgery. No patient had a change in motor level or ambulatory status after scoliosis surgery. CONCLUSIONS: Our data suggest that prophylactic spinal cord untethering in children with spinal dysraphism undergoing thoracolumbar fusion for scoliosis may not be necessary in patients with moderate curvatures. Our conclusions are limited by the small sample size. A larger review of registry data may yield more powerful conclusions on the necessity of prophylactic spinal cord untethering in this patient population.

Acute Fever of Unknown Origin: A Presentation of West Nile Encephalitis.

INTRODUCTION: West Nile virus is an asymptomatic infection in most cases, but it can present with a rare complication of deadly neuroinvasive disease. CASE PRESENTATION: A 81-year-old White man presented with altered mental status and fever of unknown origin. After extensive workup, he was diagnosed with West Nile encephalitis based on positive serology, lumbar puncture, and clinical presentation. DISCUSSION: West Nile virus is a mosquito-borne RNA arbovirus that, in rare cases, can lead to encephalitis, which is a challenging diagnosis. There is no current treatment; however, a 5-day course of intravenous immunoglobulin seemed to show acute clinical improvement in both mentation and magnetic resonance imaging of the head and no long-term effects. CONCLUSION: We report this case to increase awareness among clinicians to include West Nile virus in the differential diagnosis of encephalitis with fever of unknown origin, particularly in endemic areas.

SARS-CoV-2-Associated Guillain-Barre Syndrome Obscured by Diabetes Mellitus Peripheral Neuropathy.

Multiple neurological complications, including Guillain-Barre syndrome (GBS), have been reported in association with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak. GBS has well-known associations with viruses such as influenza, human immunodeficiency virus, Zika, severe acute respiratory syndrome, Middle East respiratory syndrome, Epstein-Barr virus, and cytomegalovirus. Till date, there have been around 50 distinct published cases of GBS occurring concurrently or shortly after SARS-CoV-2 infection. This report describes the case of a 53-year-old male who presented with bilateral extremity paresthesias two weeks after a positive SARS-CoV-2 test. His symptoms were originally thought to be due to underlying diabetic peripheral neuropathy, but as they progressed, he was eventually diagnosed with SARS-CoV-2-associated GBS. Though GBS may not be a common sequelae of SARS-CoV-2 infection, the prevalence of diabetes mellitus-associated peripheral neuropathy is high enough to warrant awareness and prompt recognition of neurological symptoms that deviate from the baseline in individuals with recent, confirmed SARS-CoV-2 infection.

Peripheral Neuropathy as a Complication of SARS-Cov-2.

Previous reports have shown various neurological manifestations in about 36.4% of patients infected with SARS-Cov-2. However, peripheral neuropathy was only reported once before. A 40-year-old healthy woman presented with two weeks of cough, nasal congestion, sore throat, intermittent fevers, fatigue, and myalgia but no weakness. She tested positive for the SARS-Cov-2. Physical exam showed no neurologic deficit. Two weeks later, respiratory symptoms were improving but she developed sudden leg pain, numbness, and weakness. She described it as a "pain crisis". Neurological exam showed bilateral symmetrical, non-ascending lower extremity weakness and normal, symmetric reflexes. She had normal magnetic resonance imaging of the brain and spine, spinal fluid analysis, serum studies including creatinine kinase and C-reactive protein. She had elevated lactate dehydrogenase, low serum copper (72.9 (ref: 80.0-155.0 ug/dL)) and low vitamin B6 (14.6 (ref: 20.0-125.0 nmol/L)). A diagnosis of SARS-Cov-2-associated peripheral neuropathy was considered. We pursued empiric treatment with intravenous steroids (1000 mg methylprednisolone for three days), followed by a total of 2 g/kg of intravenous immunoglobulins (IVIG) given over five days. Pain management was done with gabapentin and ketorolac. We replaced copper and vitamin B6. Six weeks later, she reported improvement and was closer to baseline, but she endorsed residual, exertional, mild bilateral lower extremity pain, numbness, and weakness. Previous reports of treatment of SARS-Cov-2-associated neuropathy included corticosteroids and IVIG. Our patient saw the most symptomatic improvement with gabapentin. In our case, the preserved reflexes, lack of ascending pattern, sudden onset of symptoms, and normal cerebrospinal fluid (CSF) argued against Guillain-Barre syndrome. Copper deficiency can result in myelopathy but not peripheral neuropathy, so is unlikely the sole explanation. Awareness and early treatment of peripheral neuropathy in SARS-Cov-2 can result in improved clinical outcomes for patients.

Early ophthalmologic features of Parkinson's disease: a review of preceding clinical and diagnostic markers.

Non-motor symptoms in Parkinson's disease are an important cause of morbidity and may even precede the onset of the motor features of the disease. Visual abnormalities are among the most frequent non-motor symptoms observed during the early stages of the disease. Some of the visual symptoms of Parkinson's disease can likely be explained by the presence of dopaminergic neurons within the retina, where the progressive loss of dopamine and the accumulation of α-synuclein within the retinal layers leads to visual dysfunction, while some are caused by abnormalities in cortical visual processing. Many of these visual symptoms can be overlooked or go unrecognized. We review the visual symptoms in Parkinson's disease, including visual-processing and ocular motility abnormalities, stereopsis deficits, and visual hallucinations, focusing on the early stages of the disease. We focus on the reciprocal influence between the visual symptoms and the progression of the disease, analyzing the influence of dopaminergic therapy on the visual abnormalities. Finally, we discuss the possible role of some of these visual symptoms as possible markers or early diagnostic signs of the disease.

Amantadine Use for Postconcussion Syndrome.

The development of postconcussion syndrome after traumatic brain injury can result in a wide range of potentially debilitating symptoms that includes headaches, cognitive dysfunction, and mood disorders. Unfortunately, data on helpful medications are quite limited, particularly on the treatment of persistent headaches attributed to trauma. This retrospective medical record review used data collected from patients with a diagnosis of postconcussion syndrome in Mayo Clinic's Neurology and Physical Medicine and Rehabilitation outpatient clinics to evaluate the response of postconcussive symptoms to amantadine. A complete trial of amantadine was defined as 100 mg twice per day for 2 months. Thirty-three patients were prescribed amantadine for postconcussive syndrome after traumatic brain injury. One-third of patients discontinued the medication because of adverse effects. However, posttraumatic headaches were improved in 80% of patients who completed a full trial of amantadine. Surprisingly, patients had improvement in headaches even if the medication was prescribed years after the initial trauma. Little improvement was noted in other symptoms such as poor memory, dizziness, and personality changes. Although additional research is certainly needed, amantadine may be a reasonable medication to consider for the treatment of persistent headaches attributed to trauma, even if the initial injury is remote.