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.

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.

Objective: To determine whether Parkinson disease (PD) patients with (VH) have different clinical characteristics and gray-matter volume than those with visual misperceptions (VM) or other visual symptoms (OvS).Background: The spectrum of visual complaints in PD is broad and complex.Methods: We conducted a retrospective chart review of 525 PD patients to identify the frequency of visual symptoms and the association with clinical and radiological features. Brain volumetric MRI data was analyzed using multivariate logistic regression to differentiate cases with and without visual symptoms.Results: Among 525 PD cases, visual complaints were documented in 177 (33.7%). Among these, 83 (46.9%) had VH, 31 (17.5%) had VM, and 63 (35.6%) had OvS (diplopia, blurry vision, photophobia, dry eyes, and eye pain or soreness). When compared to OvS, patients with VH had significantly higher age, duration of disease, rate of REM sleep behavior disorder, and cognitive impairment. Visual hallucinations patients had decreased age-adjusted volumetric averages in 28/30 gray-matter regions when compared to PD without visual symptoms and 30/30 gray-matter regions when compared to VM patients.Conclusions: Visual symptoms in PD may represent a spectrum from OvS to VM to VH, with progression of the latter associated with older age, duration of disease, presence of REM sleep behavior disorder, cognitive impairment, and decreased gray-matter volume.

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OBJECTIVES 1. To report a variation of Numb Chin Syndrome (NCS) 2. Raise awareness and early localization of NCS to more efficiently develop a targeted treatment plan to prevent tumor spread and potentially improve clinical outcomes and survival. INTRODUCTION/BACKGROUND NCS is an uncommon but known complication of cancer. Prompt recognition is imperative to directed treatment. In some instances, numb chin may be complicated by other findings. CASE REPORT A 53-year-old female with past medical history of estrogen receptor positive invasive ductal breast carcinoma underwent partial mastectomy, chemotherapy, and radiation. After 6 years remission, new lung and liver metastases occurred, and chemotherapy resumed. Imaging was negative. Eight weeks later, she developed left chin numbness followed by progressive difficulty retaining food and drink. Her left lower lip weakened. Neurological examination revealed left lower lip weakness (showing a “droop” with attempted smile). The area of decreased sensation to sharp touch had expanded from the left chin to the nasolabial fold. The remainder of her neurological examination was unremarkable. Contrast-enhanced MRI was repeated which revealed a 1.9 cm enhancing left parotid mass. SUMMARY/ CONCLUSION NCS is defined as an ipsilateral loss of chin sensation. If there is no history of trauma or dental injury and especially if the presentation is atypical, then cancer is the most likely etiology. This case began as an uncomplicated NCS that rapidly expanded to involve a greater portion of the trigeminal nerve distribution, in addition to a branch of the facial nerve. Thus, each focal deficit was not the result of separate distal nerve lesions, but rather partial proximal cranial neuropathies at their parotid gland propinquity.