IntroductionAlpha-synucleinopathy constituting a characteristic feature of Parkinson’s disease (PD) occurs at all levels of the brain-gut axis including the enteric nervous system (ENS). Lesions in the ENS may be connected with gut inflammation, increased intestinal permeability and dysmotility contributing to the pathogenesis of PD and its gastrointestinal manifestations.AimsTo evaluate fecal calprotectin and zonulin as biomarkers of gut inflammation and intestinal barrier dysfunction in PD patients.MethodsQuantitative evaluation of fecal biomarkers was performed by ELISA tests in 35 PD patients and 20 healthy controls. Additionally, patients filled out a short questionnaire concerning gastrointestinal symptoms.ResultsMedian fecal calprotectin level (μg/g) was significantly higher in PD patients compared to the controls: 54.5 (29.0–137.9) vs. 9.7 (5.2–23.3), p < 0.0001. Applying age-related reference ranges, the increased fecal calprotectin level was found in 43% of PD patients and in none of the control subjects (p < 0.001). No correlation between fecal calprotectin level and PD duration was observed. No statistically significant difference between the groups regarding zonulin level was found. The most frequent bowel symptoms reported by PD patients included constipation (69% of subjects), feeling of incomplete evacuation (51%), bloating (51%), abdominal pain (20%), and alternating bowel movement pattern (17%).ConclusionThe evaluation of fecal calprotectin level may be a useful tool to detect the signs of gut immune system activation present in a remarkable number of PD patients, also in the early stage of the disease. Calprotectin may constitute a critical link between amyloid formation and neuroinflammatory cascades serving as a prospective diagnostic and therapeutic target.

It is open to debate whether nigrostriatal pathway damage is crucial for the phenomenology of HT. Alternative hypothesis is presented that HT represents the heterogeneous spectrum of tremors with similar phenomenology, but different pathophysiology.

Background: This study examined the generalized effects of cycle ergometer aerobic interval training (AIT) on psychomotor behaviors in individuals with Parkinson’s disease (PD), including bimanual motor control, cognitive function, and neurological motor and non-motor parkinsonian signs. Methods: Twenty mild to moderate PD patients were randomly allocated to the following groups: (1) trained group (PD-TR, n = 10), which besides receiving usual care, underwent an 8-week moderate intensity AIT program; or (2) control group (PD-CO, n = 10) which received usual care, including participation in conventional physical therapy. Both groups were tested before and after the 8-week AIT program period with the following assessments: (1) laboratory analyses of bimanual motor control, (2) psychological evaluation of cognitive function, and (3) an evaluation of neurological parkinsonian signs. Results: The PD-TR group exhibited improved (1) bimanual motor control, reflected by a decreased time (p = 0.013) and increased rate of grip force development (p = 0.013) in the manipulating hand and a decreased time delay between grip force initiation in the manipulating and stabilizing hand (p = 0.020); (2) executive function, reflected by decreased performance time in part II of the Stroop Test (p = 0.007); and (3) neurological parkinsonian signs, reflected by an amelioration of upper-extremity bradykinesia (p = 0.015) and improvement in daily life manual functions (p = 0.004), mood, and intellectual function (p = 0.005). Conclusions: Following an 8-week moderate intensity AIT program, patients with PD exhibited improved psychomotor behaviors, reflected by bimanual motor control, executive function, and neurological parkinsonian signs.

Patients with Parkinson's disease have higher passive stiffness of the muscle belly and tendon than healthy matched controls.

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Summary Cytotoxic T‐lymphocyte antigen‐4 (CTLA‐4) is an important molecule in the down‐regulation of T‐cell activation. A study was undertaken to evaluate the association of the CTLA‐4 gene polymorphisms −319C/T, +49A/G, (AT)n, CT60A/G and Jo31G/T with the levels of membrane CTLA‐4 (mCTLA‐4) and cytoplasmic CTLA‐4 (cCTLA‐4) in CD4+ T lymphocytes from patients with multiple sclerosis (MS) and with susceptibility to MS, and the course of the disease. It was found that the Jo31GG and CT60GG genotypes were associated with decreased mean fluorescence intensity (MFI) of total CTLA‐4 (mCTLA‐4 + cCTLA‐4) molecules in CD4+ T cells from both relapsing‐remitting (RR) and secondary progressive (SP) MS patients compared with others. Consequently, possessing the Jo31G allele and/or the CT60G allele were associated with susceptibility to MS. The percentages of cells expressing mCTLA‐4 and cCTLA‐4 in RR patients were higher in carriers of the alleles non‐predisposing to MS (namely CT60A and Jo31T), but the percentages of corresponding cells were unexpectedly significantly lower in SP patients than in RR patients. Increased risk of paresthesia and pyramidal signs as a first manifestation of disease, and earlier transition to the SP form in those patients, was also noted. It is hypothesized that the decreasing frequencies of cells expressing immunosuppressive mCTLA‐4 and cCTLA‐4 in carriers of alleles non‐predisposing to MS (i.e. CT60A and Jo31T) may lead to inadequate down‐regulation of ongoing T‐cell responses in these patients and, as a consequence, earlier progression of disease from the RR form to the SP form.

Parry–Romberg syndrome (PRS) is a rare disorder, described in the nineteenth century by Caleb Parry and Moritz Romberg, characterized by acquired and slowly progressive atrophy of one side of the face. The pathogenesis of PRS is still unclear. Immune-mediated processes are thought to be a basic factor in PRS etiology, but autonomic nervous system might also be impaired. A case of PRS in a 26-year-old woman with coexisting disturbances in the lower left limb is presented. The multimodal electrophysiological studies were done, including electroencephalography, visual, brain auditory, somatosensory and trigeminal somatosensory evoked potentials, blink reflex, standard neurographic and electromyographic examinations, quantitative sensory tests and autonomic tests. Neuroimaging studies consisted of brain MR, single voxel proton MR spectroscopy, diffusion tensor imaging with fiber tractography. Based on multimodal electrophysiological and neuroimaging studies, it was concluded that the impairment in PRS is multisystemic, i.e., motor, sensory, and autonomic. A cortical origin of the symptoms is possible.

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