Our observation of a distinctive extrapyramidal syndrome, changes in the MRI signal in the basal ganglia, and elevated blood manganese levels in methcathinone users suggests that manganese in the methcathinone solution causes a persistent neurologic disorder.

We examined white matter abnormalities in patients with a distinctive extrapyramidal syndrome due to intravenous methcathinone (ephedrone) abuse. We performed diffusion tensor imaging in 10 patients and 15 age-matched controls to assess white matter structure across the whole brain. Diffuse significant decreases in white matter fractional anisotropy, a diffusion tensor imaging metric reflecting microstructural integrity, occurred in patients compared with controls. In addition, we identified two foci of severe white matter abnormality underlying the right ventral premotor cortex and the medial frontal cortex, two cortical regions involved in higher-level executive control of motor function. Paths connecting different cortical regions with the globus pallidus, the nucleus previously shown to be abnormal on structural imaging in these patients, were generated using probabilistic tractography. The fractional anisotropy within all these tracts was lower in the patient group than in controls. Finally, we tested for a relationship between white matter integrity and clinical outcome. We identified a region within the left corticospinal tract in which lower fractional anisotropy was associated with greater functional deficit, but this region did not show reduced fractional anisotropy in the overall patient group compared to controls. These patients have widespread white matter damage with greatest severity of damage underlying executive motor areas.

Recent studies have focused on the associations between human herpesvirus 6 (HHV-6) and human herpesvirus 7 (HHV-7), and multiple sclerosis (MS). The aim of this study was to investigate the associations between HHV-6 and HHV-7 reactivation and MS disease activity, and interleukin 12 (IL-12) and tumor necrosis factor α (TNF-α) production. Material and Methods. The frequency of plasma viremia by nested polymerase chain reaction and transcription of viral mRNA in peripheral blood mononuclear cells by reverse transcriptasepolymerase chain reaction (RT-PCR) of 14 relapsing/remitting (RR) and 14 secondary progressive (SP) MS patients were studied in comparison with clinical manifestation of the disease. Serum concentrations of cytokines IL-12 and TNF-α were analyzed by enzyme-linked immunosorbent assay. Results. Plasma samples from 25 of the 28 MS patients with estimated latent/persistent HHV-6 and/or HHV-7 infection were examined during relapse and remission/relative remission. HHV-6 reactivation was found in 4 of the 7 RRMS and 4 of the 7 SPMS patients, and HHV-7 reactivation was identified in 3 of the 7 RRMS and 1 of the 7 SPMS patients (all in relapse). In 2 of the 3 RRMS patients without viremia in relapse, HHV-6 mRNA transcription was detected. In RRMS and SPMS patients with active HHV-6 and HHV-7 infection in relapse, the serum concentrations of IL-12 and TNF-α were significantly higher than in those with latent virus infection. Conclusions. HHV-6 and HHV-7 reactivation could be implicated in the exacerbation of MS via activation of Th1 lymphocyte subsets.

Objectives This study aimed to define patterns of liver injury after severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection using multiparametric ultrasound (mpUS) in a variable patient population with differing severities of COVID‐19. Methods Ninety patients were enrolled into the study: 56 had SARS‐CoV‐2 3–9 months prior to enrolment; 34 served as a clinically healthy control group. All patients underwent an mpUS evaluation of the liver (elastography, dispersion and attenuation imaging). Seventy‐six patients had abdominal magnetic resonance (MR) and noncontrast enhanced thoracic computed tomography (CT) scans performed at the same day. All patients were screened for biochemical markers of liver injury. Results Liver elasticity, viscosity, and steatosis values were significantly altered in patients after COVID‐19, with particularly higher fibrosis scores compared to the control group ( P < .001). Increased biochemical markers of liver injury correlated with changes in mpUS ( P < .05), but not with findings on CT or MR findings. Seventeen of 34 hospitalized patients had a moderate or severe course of the disease course with more pronounced changes in mpUS. Increased body mass index was found to influence liver injury and correlated with more severe forms of COVID‐19 ( P < .001). Conclusions COVID‐19 can cause liver injury observable using mpUS. More severe forms of COVID‐19 and patient obesity are related to increased values of liver damage observed. In comparison to MRI and CT, mpUS appears to be more sensitive to involvement of liver parenchyma. Further research is warranted to establish this promising method for evaluating post‐COVID‐19 liver involvement in the aftermath of the pandemic.