BACKGROUND:Astrocyte pathology is a defining feature of progressive supranuclear palsy (PSP), yet the relevance of fluid glial fibrillary acidic protein (GFAP) remains uncertain. OBJECTIVE:To determine whether mean GFAP concentrations differ between PSP and healthy controls or other parkinsonian disorders, particularly Parkinson's disease (PD) and multiple system atrophy (MSA). METHODS:PubMed and Scopus were searched from inception to 24 January 2026. Original human studies that measured GFAP in plasma, serum, or cerebrospinal fluid (CSF) and included a PSP group were eligible. Standardized mean differences were pooled using random-effects meta-analysis and interpreted as group-level separation rather than individual diagnostic accuracy. RESULTS:Of 1917 records, 1590 were screened after deduplication; 19 studies were included qualitatively and 12 quantitatively. Seven blood studies contributed to the primary PSP versus healthy-control analysis (PSP n = 283; controls n = 312). Blood GFAP was moderately higher in PSP (Hedges' g = 0.63, 95% CI 0.30 to 0.97; p = 0.003; I2 = 53.4%). The estimate persisted in leave-one-out and in a sensitivity analysis adding three studies with median-derived means (k = 10; g = 0.72, 95% CI 0.36 to 1.08). CSF GFAP was directionally concordant. Group-level separation between PSP and PD or MSA was limited and inconsistent. CONCLUSIONS:Mean blood GFAP concentrations are higher in clinically diagnosed PSP than in healthy controls, although the biological basis and disease specificity of this finding remain uncertain. However, these analyses do not establish sensitivity, specificity, or individual-level diagnostic performance, and GFAP should not be considered a stand-alone diagnostic marker.

Introduction:olfactory impairment is a clinical feature of Parkinson's disease (PD) even in the early phases. Diffusion tensor imaging fiber tracking analysis (DTI-FTA) has been able to highlight changes in the olfactory tract in PD, however in early phases of PD this analysis has not been investigated. We investigated the olfactory tract by DTI-FTA in early stages of PD (ePD). Methods:All patients were assessed using the Italian Olfactory Identification Test (IOIT), the Movement Disorder Society-Unified Parkinson's Disease Rating Scale-Part III (MDS-UPDRS-III) and the Hoehn and Yahr (H&Y) scale. Diffusion imaging was conducted by 3 T MRI. Results:Overall, 26 PD patients and 20 healthy subject were recruited. Hyposmia was observed in all PD patients. DTI-FTA of the olfactory tract showed significant mean diffusivity (MD) increases and a tract volume decrease for PD group. MD and age, only in the PD group, were significant for multiple correlations. Conclusion:DTI-FTA identified microstructural changes in the olfactory tract even in hyposmic ePD patients.

Background Olfactory dysfunction is a non-motor symptom and an important biomarker of Parkinson’s disease (PD) because of its high prevalence (> 90%). Whether hyposmia correlates with motor symptoms is unclear. In the present study, we aim to investigate the relationship between olfactory impairment with both motor and non-motor features and disease variables (disease duration, stage, and severity). Methods One-hundred fifty-four PD patients were evaluated. Odor identification ability was tested using Italian Olfactory Identification Test (IOIT). A comprehensive spectrum of motor and non-motor features was assessed. Cognitive function was investigated through MMSE. Patients were divided into 3 different clinical phenotypes using UPDRS-III: tremor-dominant type (TDT), akinetic-rigid type (ART), and mixed type (MXT). Results Three of the 33 IOIT items were most frequently misidentified: basil (74.3%), coffee (66.9%), and mushroom (59.6%). Hyposmia was found in 93%. Hyposmic patients were older than controls ( p = 0.01). Hoehn & Yahr (H&Y) score of 2 or greater was associated with higher probability of being hyposmic (OR = 5.2, p = 0.01). IOIT score did not significantly differ between TDT, ART, and MXT of analyzed PD patients. Performance to IOIT inversely correlated with age ( p < 0.01), disease duration ( p = 0.01), and H&Y score of 2 or higher ( p < 0.01). Clinical features that associated with higher IOIT score were freezing of gait (FOG) ( p < 0.001) and camptocormia ( p < 0.05). Conclusions In our cohort, IOIT scores showed a positive correlation with axial motor signs, but not with non-motor symptoms. IOIT may be a useful tool not only for supporting PD diagnosis but also for providing prognostic information about motor function.

INTRODUCTION:Diagnostic criteria for Parkinson's disease (PD) rely on clinical, mainly motor, features, implying that pre-motor phase cannot be accurately identified. To achieve a reliable early diagnosis, similar to what has been done for Alzheimer's disease (AD), a shift from clinical to biological identification of PD is being pursued. This shift has taken great advantage from the research on cerebrospinal fluid (CSF) biomarkers as they mirror the ongoing molecular pathogenic mechanisms taking place in PD, thus intercepting the disease timely with respect to clinical manifestations. AREAS COVERED:CSF α-synuclein seed amplification assay (αS-SAA) has emerged as the most promising biomarker of α-synucleinopathy. CSF biomarkers reflecting AD-pathology and axonal damage (neurofilament light chain) and a novel marker of dopaminergic dysfunction (DOPA decarboxylase) add valuable diagnostic and prognostic information in the neurochemical characterization of PD. EXPERT OPINION:A biological classification system of PD, encompassing pathophysiological and staging biomarkers, might ensure both early identification and prognostic characterization of the patients. This approach could allow for the best setting for disease-modifying treatments which are currently under investigation.

Freezing of gait is a frequent phenomenon and can be one of the most debilitating motor impairments in Parkinson’s disease, especially in the advanced stages. It is currently defined as a brief episodic absence or any marked reduction in the forward progression of the feet, despite the intention to walk. Greater severity of freezing of gait has been associated with more frequent falls, postural instability, and executive dysfunction. However, botulinum neurotoxin is one of the most widely administered therapies for motor and non-motor symptoms, including freezing of gait, in parkinsonism. To date, the literature has had conflicting results on the use of botulinum toxin in the treatment of freezing of gait in Parkinson’s disease patients. In light of this, we reviewed the findings of past studies that specifically investigated the effects of botulinum toxin on freezing of gait in Parkinson’s disease in order to better understand this issue.

Although the discovery of the critical role of α-synuclein (α-syn) in the pathogenesis of Parkinson's disease (PD) is now twenty-five years old, it still represents a milestone in PD research. Abnormal forms of α-syn trigger selective and progressive neuronal death through mitochondrial impairment, lysosomal dysfunction, and alteration of calcium homeostasis not only in PD but also in other α-syn-related neurodegenerative disorders such as dementia with Lewy bodies, multiple system atrophy, pure autonomic failure, and REM sleep behavior disorder. Furthermore, α-syn-dependent early synaptic and plastic alterations and the underlying mechanisms preceding overt neurodegeneration have attracted great interest. In particular, the presence of early inflammation in experimental models and PD patients, occurring before deposition and spreading of α-syn, suggests a mechanistic link between inflammation and synaptic dysfunction. The knowledge of these early mechanisms is of seminal importance to support the research on reliable biomarkers to precociously identify the disease and possible disease-modifying therapies targeting α-syn. In this review, we will discuss these critical issues, providing a state of the art of the role of this protein in early PD and other synucleinopathies.

Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant neurodegenerative disorder caused by gene ataxin7 mutation with a polymorphic CAG repeat tract that falls in first axon. The gene which encodes ataxin7 normally contains a ten CAG repeat tract starting a codon 30, in affected patients the CAG repeat tract expands from 37 to 250 triplets, decreasing the transcription of an antisense non-coding RNA. Clinically SCA7 is characterized by progressive cerebellar ataxia, slow saccadic eye movements and progressive blindness. SCA7 neurotoxicity can be showed by the cone-rod dystrophy which follows in the generations the CAG repeats expansions in the affected patients. As retinal disease progresses in SCA7, the photoreceptors cells do become involved, and then loss of central visual acuity proceeds to complete blindness. The presence in the long run of the altered cone function, allows SCA7 to be classified as a cone dystrophy type of retinal degeneration [1]. Considering the X-linked inheritance of color vision deficiency, fixed sampling of only males, that compensation’s phenomenon in the heterozygous females [2], which can hid a real acquired color vision deficiency. The acquired color vision deficiency is real in the males where the anomaly has not hidden, and due to this reason we suggest sampling only male patients when color vision has studied both in neurological and metabolic diseases [3].

The differential diagnosis of rest tremor (RT) disorders is challenging, and often requires single photon emission computed tomography with 123I-ioflupane (DaTscan). We investigated the performance of several tremor electrophysiological features in distinguishing RT patients with and without striatal dopaminergic deficit.

The R2 component of blink reflex recovery cycle (R2BRrc) is a simple neurophysiological tool to detect the brainstem hyperexcitability commonly occurring in several neurological diseases such as Parkinson’s disease and atypical parkinsonisms. In our study, we investigated for the first time the usefulness of R2BRrc to assess brainstem excitability in patients with idiopathic Normal Pressure Hydrocephalus (iNPH) in comparison with healthy subjects. Eighteen iNPH patients and 25 age-matched control subjects were enrolled. R2BRrc was bilaterally evaluated at interstimulus intervals (ISIs) of 100, 150, 200, 300, 400, 500 and 750 ms in all participants. We investigated the diagnostic performance of R2BRrc in differentiating iNPH patients from control subjects using ROC analysis. Midbrain area and Magnetic Resonance Hydrocephalic Index (MRHI), an MRI biomarker for the diagnosis of iNPH, were measured on T1-weighted MR images, and correlations between R2BRrc values and MRI measurements were investigated. Fourteen (78%) of 18 iNPH patients showed an enhanced R2BRrc at ISIs 100–150–200 ms, while no control subjects had abnormal R2BRrc. The mean amplitude of bilateral R2BRrc at the shortest ISIs (100–150–200 ms) showed high accuracy in differentiating iNPH patients from controls (AUC = 0.89). R2BRrc values significantly correlated with midbrain area and MRHI values. This study represents the first evidence of brainstem hyperexcitability in iNPH patients. Given its low cost and wide availability, R2BRrc could be a useful tool for selecting elderly subjects with mild gait and urinary dysfunction who should undergo an extensive diagnostic workup for the diagnosis of NPH.

BACKGROUND:The differentiation of functional dystonia from idiopathic dystonia may be clinically challenging.OBJECTIVE:To identify clinical features suggestive of functional dystonia to guide physicians to distinguish functional dystonia from idiopathic dystonia.METHODS:Patient data were extracted from the Italian Registry of Functional Motor Disorders and the Italian Registry of Adult Dystonia. Patients with functional and idiopathic dystonia were followed up at the same clinical sites, and they were similar in age and sex.RESULTS:We identified 113 patients with functional dystonia and 125 with idiopathic dystonia. Sudden onset of dystonia, evidence of fixed dystonia, and acute peripheral trauma before dystonia onset were more frequent in the functional dystonia group. No study variable alone achieved satisfactory sensitivity and specificity, whereas a combination of variables yielded 85% sensitivity and 98% specificity. A diagnostic algorithm was developed to reduce the risk of misclassifying functional dystonia.CONCLUSION:Our findings extend the current diagnostic approach to functional dystonia by showing that clinical information about symptom onset, fixed dystonia, and history of peripheral trauma may provide key clues in the diagnosis of functional dystonia.

Progressive supranuclear palsy (PSP) patients can show ventricular enlargement mimicking normal pressure hydrocephalus (NPH). The aim of this study was to distinguish PSP patients with marked ventricular dilatation (PSP-vd) from those with normal ventricular system and to evaluate the coexistence of NPH in PSP-vd patients. One hundred three probable PSP patients, 18 definite NPH patients, and 41 control subjects were enrolled in the study. Evans index (EI) > 0.32 associated with callosal angle (CA) < 100° was used to identify PSP-vd patients. Automated ventricular volumetry (AVV) and Magnetic Resonance Hydrocephalic Index (MRHI) were performed on T1-weighted MR images to evaluate the presence of NPH in PSP-vd patients. Twelve (11.6%) out of 103 PSP patients had both abnormal EI and CA values (PSP-vd). In two of these 12 patients, AVV and MRHI values suggested PSP + NPH. In the remaining 10 PSP-vd patients, AVV and MRHI values were higher than PSP patients with normal ventricular system and controls, but lower than PSP + NPH and NPH patients, suggesting a non-hydrocephalic ventricular enlargement. Our study provides evidence that the combination of EI and CA biomarkers allowed to identify PSP patients with marked ventricular dilatation mimicking NPH. Only a few of these patients had PSP + NPH. Recognition of these PSP patients with enlarged ventricles can positively impact the care of this disease, helping clinicians to identify patients with PSP + NPH who could benefit from shunt procedure and avoid surgery in those with enlarged ventricles without NPH.

Deep grey nuclei of the human brain accumulate minerals both in aging and in several neurodegenerative diseases. Mineral deposition produces a shortening of the transverse relaxation time which causes hypointensity on magnetic resonance (MR) imaging. The physician often has difficulties in determining whether the incidental hypointensity of grey nuclei seen on MR images is related to aging or neurodegenerative pathology. We investigated the hypointensity patterns in globus pallidus, putamen, caudate nucleus, thalamus and dentate nucleus of 217 healthy subjects (ages, 20-79 years; men/women, 104/113) using 3T MR imaging. Hypointensity was detected more frequently in globus pallidus (35.5%) than in dentate nucleus (32.7%) and putamen (7.8%). A consistent effect of aging on hypointensity (p < 0.001) of these grey nuclei was evident. Putaminal hypointensity appeared only in elderly subjects whereas we did not find hypointensity in the caudate nucleus and thalamus of any subject. In conclusion, the evidence of hypointensity in the caudate nucleus and thalamus at any age or hypointensity in the putamen seen in young subjects should prompt the clinician to consider a neurodegenerative disease.

Rest tremor (RT) is typical of Parkinson's disease (PD) but can occur in other tremulous disorders, such as essential tremor (ET) plus dystonic tremor, drug-induced tremor, ET-PD syndrome, and scans without evidence of dopaminergic deficit (SWEDD).1 Differentiating RT disorders clinically may be challenging and often requires DaTscan (123I-ioflupane),2, 3 an expensive and time-consuming procedure not widely available and rarely used in routine diagnosis of tremulous disorders. Thus, there is an urgent need for new reliable and cost-effective biomarkers to reveal striatal dopaminergic deficit in tremulous patients in the absence of DaTscan. A few studies investigated the electrophysiological features of RT, suggesting the possible usefulness of tremor pattern for differentiating PD from other tremulous disorders.4-7 These studies, however, were conducted in small patient series and focused on differentiation between the diseases rather than on the association between tremor pattern and DaTscan. In our study, we enrolled 205 consecutive patients with RT and assessed the performance of tremor features (pattern, frequency, amplitude, burst duration, coherence) in differentiating patients with abnormal DaTscan (DaT+) from those with normal DaTscan (DaT−) (see Methods in Supporting Information Appendix S1). A total of 123 patients with RT had DaT+, while 82 patients had DaT−. Clinical characteristics of these patients with RT are shown in Supporting Information Table S1. The pattern (alternating or synchronous, Fig. 1A) was the RT feature that performed the best in distinguishing patients with striatal dopaminergic deficit from those with integrity of striatal dopaminergic neurons (Fig. 1B,C; Supporting Information Table S2). Random Forest feature selection and multivariate logistic regression model did not significantly improve the classification of DaT+ and DaT− patients compared with using RT pattern alone (Fig. 1D), suggesting that this tremor feature, which balances simplicity and accuracy, may represent the best option in clinical practice. RT pattern and DaTscan were strongly associated with each other, supporting the usefulness of pattern for predicting DaTscan result (odds pattern DaT−/synchronous, 3.74; odds pattern DaT+/alternating, 9.45; odds ratio, 34.3; confidence interval, 14.9–86.1). In our cohort, the large majority (104/115, 90.4%) of alternating patients were DaT+, while 71/90 (78.9%) synchronous patients were DaT−. Eighty-five of 104 (81.7%) alternating DaT+ patients had parkinsonian tremor, while all DaT− synchronous patients were affected by non-parkinsonian RT disorders (Supporting Information Table S3). Our study has several strengths. First, we demonstrated the stability of RT pattern both in the short- and long-term periods (Supporting Information Results), which is necessary to use this biomarker in the diagnosis of tremulous syndromes. Second, patients were prospectively followed for 2 years to confirm clinical diagnosis. Third, the use of RT pattern for predicting DaTscan result can translate into economic advantages by reducing the need for expensive procedures for correct tremor diagnosis. A limitation to this study is that it was performed in a large cohort from a single center, and further validation in an independent international cohort is warranted. The alternating pattern of RT is a powerful, low-cost, and widely available biomarker of striatal dopaminergic deficit in tremulous patients. The evaluation of tremor pattern could help clinicians distinguish parkinsonian RT associated with dopaminergic deficit from non-parkinsonian RT with intact dopaminergic neurons and guide the decision making in clinical practice. 1. Research project: A. Conception, B. Organization, C. Execution; 2. Statistical analysis: A. Design, B. Execution, C. Review and Critique; 3. Manuscript: A. Writing of the first draft, B. Review and Critique. Andrea Quattrone: 1A, 1B, 1C, 3A, 3B Rita Nisticò: 1B, 1C Maurizio Morelli: 1B, 1C Gennarina Arabia: 1B, 1C Marianna Crasà: 1B, 1C Basilio Vescio: 2A, 2B, 2C Alessandro Mechelli: 1B, 1C Giuseppe L. Cascini: 1B, 1C Aldo Quattrone: 1A, 1B, 3B The authors received no funding from any institution, including personal relationships, interests, grants, employment, affiliations, patents, inventions, honoraria, consultancies, royalties, stock options/ownership, or expert testimony for the last 12 months. The data that support the findings of this study are available from the corresponding author upon reasonable request. Table S1. Demographic, clinical, electrophysiological and imaging data of patients with rest tremor Table S2. Diagnostic performance of tremor electrophysiological features in distinguishing rest tremor patients with striatal dopaminergic deficit from those with normal DaTscan. Table S3. Clinical diagnoses of patients with alternating or synchronous rest tremor pattern at the two-year follow-up. Appendix S1. Supporting Information Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

There is increasing evidence that isolated rapid eye movement sleep behavior disorder (iRBD) is a critical prodromal stage of α-synucleinopathies, occurring years to decades before the evolution to Parkinson’s disease (PD) and dementia with Lewy bodies (DLBs). As up to 75%–90% of iRBD patients may develop DLB disorders after long follow-up, these patients represent a unique opportunity for potentially neuroprotective interventions. Iranzo and colleagues provided evidence that most isolated RBD patients had misfolded α-synuclein in the cerebrospinal fluid (CSF) and that α-synuclein positivity was associated with a higher risk of developing PD or DLB within the following 10 years. In this longitudinal observational study, 52 patients with polysomnographic-confirmed iRBD and 40 healthy controls underwent lumbar puncture to obtain CSF samples; iRBD patients were clinically followed up for a mean of 7.1 years and healthy controls for 7.7 years in. Real-time quakinginduced conversion (RT-QuIC) detected misfolded α-synuclein in the CSF aliquots of 47 of 52 (90%) iRBD patients and only in 4 of 40 (10%) control subjects, resulting in a very high sensitivity and specificity. A major finding of the study was that 31 of 47 (66%) patients with iRBD who were α-synuclein positive at baseline developed either PD or LBD during follow-up after a mean time interval of 3.2 years (range 0.4–9.1 years), whereas only 1 of 5 iRBD patients with negative α-synuclein assay phenoconverted to PD. None of the healthy controls developed α-synucleinopathy during the follow-up. This RT-QuIC assay showed 96.9% sensitivity and 20.0% specificity in predicting conversion to either PD or DLB in iRBD patients. The suboptimal specificity is due to the presence of some α-synuclein-positive iRBD patients who did not develop PD or LBD at the end of the study. A key question is whether these patients may convert in the future to PD or DLB, and a longer follow-up in these nonconverter iRBD patients is warranted. The main limitation to this study is the relatively small sample of iRBD patients from a single center. These results thus need validation in larger independent cohorts to ensure generalizability of this RT-QuIC assay in different settings. Overall, Iranzo’s study demonstrates that the detection of α-synuclein in CSF of iRBD patients may be a biomarker of prodromal PD and DLB. The clinical relevance of this finding relies on the identification of individuals in the prodromal stage of α-synucleinopathies who may represent a target population for future neuroprotective trials, especially with agents that interfere with brain deposition and propagation of misfolded α-synuclein.

Idiopathic normal pressure hydrocephalus (iNPH) shares clinical and radiological features with progressive supranuclear palsy (PSP) and Alzheimer’s disease (AD). Corpus callosum (CC) involvement in these disorders is well established on structural MRI and diffusion tensor imaging (DTI), but alterations overlap and lack specificity to underlying tissue changes. We propose a semi-automated approach to assess CC integrity in iNPH based on the spatial distribution of DTI-derived principal diffusion direction orientation (V1). We processed DTI data from 121 subjects (Site1: iNPH = 23, PSP = 27, controls = 14; ADNI: AD = 35, controls = 22) to obtain V1, fractional anisotropy (FA) and mean diffusivity (MD) maps. To increase the estimation accuracy of DTI metrics, analyses were restricted to the midsagittal CC portion (± 6 slices from midsagittal plane). Group-wise comparison of normalized altered voxel count in midsagittal CC was performed using Kruskal–Wallis tests, followed by post hoc comparisons (Bonferroni-corrected p < 0.05). ROC analysis was used to evaluate the diagnostic power of DTI alterations compared to callosal volume. We found specific changes of V1 distribution in CC splenium of iNPH compared to AD and PSP, while MD and FA showed patterns of alterations common to all disorders. ROC curves showed that, compared to splenial volume, V1 represented the most accurate marker of iNPH diagnosis versus AD and PSP. Our results provide evidence that V1 is a powerful biomarker for distinguishing patients with iNPH from patients with AD or PSP. Indeed, our findings also provide more specific insight into the pathophysiological mechanisms that underlie tissue damage across iNPH and its mimics.

BACKGROUND:Microstructural alterations of corticospinal tract (CST) have been found in idiopathic normal pressure hydrocephalus (iNPH). No study, however, investigated the effect of ventricular dilatation on CST in Progressive Supranuclear Palsy (PSP).OBJECTIVE:The aim of this study was to investigate CST diffusion profile in a large cohort of PSP patients with and without ventricular dilatation.METHODS:Twenty-three iNPH patients, 87 PSP patients and 26 controls were enrolled. Evans index (EI) and ventricular volume (VV) were measured in all patients. CST tractography was performed to calculate FA, MD, AxD and RD in six different anatomical regions: medulla oblungata (MO), pons (P), cerebral peduncle (CP), posterior limb of internal capsule (PLIC), corona radiata (CR), subcortical white matter (SWM). ANCOVA was used for comparing CST diffusion profiles between the groups and association between CST microstructural metrics and measures of ventricular dilatation (EI and VV) was assessed.RESULTS:Thirty-three PSP patients had ventricular dilatation (EI > 0.30, PSP-vd) while 54 PSP patients had normal ventricular system (EI ≤ 0.30, PSP-wvd). iNPH patients had the most marked FA and AxD increase in PLIC and CR of CST followed by PSP-vd, PSP-wvd and controls; RD was altered only in iNPH. A strong correlation was found between CST diffusion metrics and EI or VV.CONCLUSIONS:Our findings confirm the microstructural changes of CST in iNPH patients and demonstrate for the first time similar alterations in PSP-vd patients, suggesting a crucial role of ventricular dilatation in the mechanical compression of CST.

Neurological manifestations of COVID-19 have been described. We report a case of seropositive NMOSD and acute myositis following SARS-CoV-2 infection. A previous healthy 35-years old man was admitted for NORB, a month after paucisymptomatic SARS-CoV-2 infection. Nasopharyngeal tests for SARS-CoV-2 was negative and serological IgG and IgM were positive. The neurological examination showed left eye blindness and myalgia. Blood examination showed elevated CK (>1000 UI/l), positive ANA (1:640) and anti-TPO (>1300 U/ml). Brain MRI showed T2/FLAIR left optic nerve hyperintensity with contrast enhancement. The EMG revealed signs of acute myogenic damage. He received intravenous methylprednisolone with poor recovery on vison but full recovery on muscle symptoms. Four months later he present NORB in contralateral eye; MRI showed optic chiasm hyperintensity, serum anti-AQP-4-antibodies were positive, EMG and CK were normalized. The patient received intravenous steroids and Immunoglobulins and started rituximab. Nevertheless, three months later he developed the area postrema syndrome, he was retreated with intravenous steroids and immunoglobulins and achieved a complete recovery. In March 2021, he underwent the second course of rituximab with clinical and radiological stability. The patient was diagnosed with seropositive NMOSD, presented with recurrent NORB and area postrema syndrome, associated to acute myositis and autoimmune tiroiditis after SARS-CoV-2 infection. We supposed that SARS-CoV-2 may cause a post-infectious autoimmune response directed against AQP4 and other target (the muscle, the tiroid gland). Post-infectious autoimmunity is a potential mechanism in a subset of patients with COVID-19-related neurologic disease. Further research is needed to clarify this association.

The aim of this study was to investigate sex differences in hemodynamic response of the cortical motor system after levodopa intake, in patients affected by Parkinson's disease (PD) with levodopa-induced dyskinesias (LID), by means of functional near-infrared spectroscopy (fNIRS).