Rationale: Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is an infection-associated encephalitis/encephalopathy syndrome that is predominately caused by a virus. MERS has no direct association with central nervous system (CNS) infections or inflammation. Non-CNS infections may cause reversible lesion in the splenium of corpus callosum. Recently, there have been reports of many patients with hyponatremia related MERS. Interleukin-6 (IL-6) was also found elevated in serum and in cerebrospinal fluid (CSF) in patients with MERS. The role of IL-6 in the non-osmotic release of vasopressin is crucial. Persistent hyponatremia may be linked to this effect. The following is a case report of MERS secondary to encephalitis, complicated by hyponatremia. We will summarize the latest research and progress regarding MERS. Patient concerns: A 31-year-old man was admitted to our department with a 5-day history of fever and headache. His initial diagnosis was encephalitis and hyponatremia; during this period the patient also developed MERS secondary to the encephalitis. Diagnoses: Encephalitis was diagnosed by reviewing the history of fever, headache, neck rigidity and Kerning sign (+) on clinical examination. Lab tests revealed: serum VCA IgG (+), EBNA-1 IgG (−), EBV IgM (−), and inflammation in the analysis of CSF. Cranial MRI+C showed that the blood vessels on the surface of the brain were obviously increasing and thickening and diffuse slow waves were detected on the electroencephalogram (EEG). The patient's hyponatremia aggravated on the third day of hospitalization. On the fourth day of hospitalization, the patient was somnolent, apathetic, and slow. Magnetic resonance imaging (MRI) of the brain, with a T2-weighted fluid attenuated inversion recovery image, showed high-signal intensity in the splenium of the corpus callosum (SCC) on the fifth day of hospitalization. Diffusion-weighted imaging (DWI) showed splenial hyperintensity as a “boomerang sign” and reduced diffusion on apparent diffusion coefficient (ADC) maps. Cranial MRI findings returned to normal after 1 month. The diagnosis of MERS was confirmed. Interventions: We administered an intravenous drip infusion of acyclovir and prescribed oral sodium supplementation. Outcomes: The patient's neurological symptoms gradually improved. The MRI lesion in the SCC disappeared on the 30th day. Lessons: In patients with encephalitis accompanied by hyponatremia, elevated IL-6 or urinary β2-microglobulin (β2MG), and exacerbations such as sudden somnolence, delirium, confusion, and seizures, the possibility of secondary MERS should be investigated, in addition to the progression of encephalitis.

Background: Recreational N 2 O abuse is an important etiology of neurological impairment in young patients, which may easily be ignored clinically. Few current studies have investigated the characteristics or the effects experienced by its users. We aimed to explore any correlation between the clinical severity and biomarkers and spinal magnetic resonance imaging (MRI) abnormalities, identify independent factors associated with spinal MRI abnormalities, and ascertain factors affecting depression/anxiety in patients with N 2 O-related neurological disorders.Methods: Patients with N 2 O-related neurological disorders were enrolled retrospectively between February 2017 and July 2020. Their demographic, clinical, laboratory, neuroimaging, electrophysiological, and neuropsychological findings were analyzed.Correlation analyses were conducted using Spearman's or Pearson's correlation and linear regression analysis. Independent factors associated with spinal MRI abnormalities were identified using univariate and multivariate analyses. Results:The principal clinical manifestations of N 2 O-related neurological disorders (n = 63; 38 men, 25 women; mean age ± SD: 22.60 ± 4.46 years) were sensory disturbance, followed by gait disturbance and pyramidal tract damage. A significant negative correlation existed between serum vitamin B 12 levels and clinical severity (r = −0.309, p = .014), which disappeared after linear regression. An interval of less than 6 months between initial N 2 O abuse and hospitalization was independently associated with spinal MRI abnormalities (39.47% vs. 72.00%, respectively; χ 2 = 6.40, p = .01). Thirtyeight (60.32%) and 40 (63.49%) patients experienced anxiety and depression, respectively. Moreover, the higher the clinical scores/serum homocysteine levels, the greater the severity of anxiety/depression (r = 0.442, p < .01; r = 0.346, p < .01; r = 0.477, p < .01; r = 0.324, p < .01). Conclusions:The significant inverse correlation between initial vitamin B 12 levels and clinical severity could aid prognosis prediction in patients with N 2 O-related neurological disorders. Spinal MRI abnormalities were not related to clinical severity butThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Background: Several recent studies have reported subacute combined degeneration (SCD) induced by nitrous oxide (N 2 O) abuse. However, the association between the evolution of dynamic neuroimaging and clinical manifestations has not been reported in patients with N 2 O-induced SCD. Case presentation: We described the case of a 24-year-old man who developed SCD with inverted V-sign hyperintensities over the posterior aspect of the spinal cord caused by frequent, excessive N 2 O inhalation. One month after treatment, his weakness and paresthesia resolved and serum vitamin B 12 levels exceeded the normal levels. However, the hyperintensities had extended horizontally and longitudinally on T2-weighted magnetic resonance imaging (MRI), compared to those on the initial scan. Two months after treatment, the patient experienced some residual numbness in the distal limbs, and his serum homocysteine levels were normal, but the abnormal signals seen on cervical T2-weighted MRI had decreased only slightly compared to those seen on the one-month follow-up MRI. The evolution of conventional MRI findings lagged compared to the clinical manifestation, which was suggestive of a clinical-radiological dissociation. Conclusions: Clinical-radiological dissociation might have occurred in this case because T2-weighted imaging was not sensitive enough to reveal cytotoxic edema. Moreover, the serum vitamin B 12 level is not a good indicator of cellular vitamin B 12. Thus, clinicians should recognize this phenomenon, comprehensively assess the condition of patients with N 2 O-induced SCD, and avoid terminating treatment based on the resolution of clinical symptoms and serological results.

Background: We aimed to examine the differences between the clinical characteristics of patients with ischemic stroke and active cancer and those without cancer and develop a clinical score for predicting occult cancer in patients with ischemic stroke.Methods: This retrospective study enrolled consecutive adult patients with acute ischemic stroke, who were admitted to our department between December 2017 and January 2019. The demographic, clinical, laboratory, and neuroimaging characteristics of patients with ischemic stroke with active cancer and those without cancer were compared. Multivariate analysis was performed to identify independent factors associated with active cancer. Subsequently, a predictive cancer-risk score was developed using the area under the receiver operating characteristic curve.Results: Fifty-three (6.63%) of 799 patients with ischemic stroke had active cancer. The absence of a history of hyperlipidemia [odds ratio (OR)=0.17, 95% confidence interval (CI): 0.06–0.48, P<0.01], elevated serum fibrinogen (OR=1.72, 95% CI: 1.33–2.22, P<0.01) and D-dimer levels (OR=1.43, 95% CI: 1.24–1.64, P<0.01), and stroke of undetermined etiology (OR=22.87, 95% CI: 9.91–52.78, P<0.01) were independently associated with active cancer. Thus, a score based on the absence of hyperlipidemia and serum fibrinogen ≥4.00 g/L and D-dimer ≥2.00 μg/mL predicted active cancer with an area under the curve of 0.83 (95% CI: 0.77–0.89, P<0.01). The probability of active cancer was 59% at a supposed prevalence of 6.63%, if all three independent factors were present in a patient with ischemic stroke.Conclusions: We devised a score to predict active cancer in patients with ischemic stroke based on the absence of a history of hyperlipidemia and elevated serum D-dimer and fibrinogen that highlights the importance of hypercoagulability in these patients and may help determine early intervention and management.

Late-Onset Epilepsy (LOE), with onset in adult life, is often attributed to cerebrovascular disease and intracranial tumor. Herein we present a LOE patient with history of Linear Scleroderma en Coup de Sabre (LScs) and abnormal cranial MRI signs. Curiously, his band-like skin lesion, presenting on the forehead, was in line with the surface projection of the intracranial focus shown in MRI. This gave a clue of the link between the skin lesion and the intracranial focus and the epilepsy. To sum up, it exposed a rare cause of LOE. Moreover, it underlined the significance of recognizing the cause to be associated with a substantially increased risk of developing epilepsy.

Background Isolated peripheral facial palsy (P-FP) can lead to lesions involving the inferomedial tegmentum of the pons. However, cases with P-FP in result of a medullary lesion have rarely been reported and result from a paraventricular lesion have never been reported before. Cases presentation We described a 63-year-old man presenting with isolated P-FP due to ipsilateral pontomedullary infarction. Brain diffusion MRI revealed a hyper-intense signal on the left dorsolateral portion of the upper medulla and pontomedullary junction. And then we experienced a 77-year-old man presenting with lateral paraventricular infarction who showed contralateral peripheral type facial palsy. Brain diffusion-weighted image(DWI) showed a high-signal intensity lesion in the right lateral paraventricule and part of the posterior limb of the right internal capsule. Conclusions These two cases caution that a central nervous etiology should be considered in patients with P-FP, especially if they have high risk factors of cerebral infarction.

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