Structural and microstructural predictors of cognitive decline in deep brain stimulation of subthalamic nucleus in Parkinson's disease.

BACKGROUND AND OBJECTIVES: The intricate relationship between deep brain stimulation (DBS) in Parkinson's disease (PD) and cognitive impairment has lately garnered substantial attention. The presented study evaluated pre-DBS structural and microstructural cerebral patterns as possible predictors of future cognitive decline in PD DBS patients. METHODS: Pre-DBS MRI data in 72 PD patients were combined with neuropsychological examinations and follow-up for an average of 2.3 years after DBS implantation procedure using a screening cognitive test validated for diagnosis of mild cognitive impairment in PD in a Czech population - Dementia Rating Scale 2. RESULTS: PD patients who would exhibit post-DBS cognitive decline were found to have, already at the pre-DBS stage, significantly lower cortical thickness and lower microstructural complexity than cognitively stable PD patients. Differences in the regions directly related to cognition as bilateral parietal, insular and cingulate cortices, but also occipital and sensorimotor cortex were detected. Furthermore, hippocampi, putamina, cerebellum and upper brainstem were implicated as well, all despite the absence of pre-DBS differences in cognitive performance and in the position of DBS leads or stimulation parameters between the two groups. CONCLUSIONS: Our findings indicate that the cognitive decline in the presented PD cohort was not attributable primarily to DBS of the subthalamic nucleus but was associated with a clinically silent structural and microstructural predisposition to future cognitive deterioration present already before the DBS system implantation.

Whole brain pattern of iron accumulation in REM sleep behavior disorder.

Isolated REM sleep behavior disorder (iRBD) is an early stage of synucleinopathy with most patients progressing to Parkinson's disease (PD) or related conditions. Quantitative susceptibility mapping (QSM) in PD has identified pathological iron accumulation in the substantia nigra (SN) and variably also in basal ganglia and cortex. Analyzing whole-brain QSM across iRBD, PD, and healthy controls (HC) may help to ascertain the extent of neurodegeneration in prodromal synucleinopathy. 70 de novo PD patients, 70 iRBD patients, and 60 HCs underwent 3 T MRI. T1 and susceptibility-weighted images were acquired and processed to space standardized QSM. Voxel-based analyses of grey matter magnetic susceptibility differences comparing all groups were performed on the whole brain and upper brainstem levels with the statistical threshold set at family-wise error-corrected p-values <.05. Whole-brain analysis showed increased susceptibility in the bilateral fronto-parietal cortex of iRBD patients compared to both PD and HC. This was not associated with cortical thinning according to the cortical thickness analysis. Compared to iRBD, PD patients had increased susceptibility in the left amygdala and hippocampal region. Upper brainstem analysis revealed increased susceptibility within the bilateral SN for both PD and iRBD compared to HC; changes were located predominantly in nigrosome 1 in the former and nigrosome 2 in the latter group. In the iRBD group, abnormal dopamine transporter SPECT was associated with increased susceptibility in nigrosome 1. iRBD patients display greater fronto-parietal cortex involvement than incidental early-stage PD cohort indicating more widespread subclinical neuropathology. Dopaminergic degeneration in the substantia nigra is paralleled by susceptibility increase, mainly in nigrosome 1.

Ultrasound-Navigated Multiple Hippocampal Transections: An Anatomical Study.

BACKGROUND: Multiple hippocampal transection (MHT) is a surgical technique used for the treatment of drug-resistant mesial temporal lobe epilepsy in situations where standard procedures would pose a high risk for memory deterioration. During MHT, the longitudinal fibers of the hippocampus, implicated in epilepsy spreading, are interrupted, while the transverse memory circuits are spared. The extent of MHT is governed by intraoperative electrocorticography; abolition of epileptic discharges serves as an end point to terminate the transection. In other words, the aim of MHT is not the anatomical completeness of hippocampal transection. In contrast, we hypothesize that only the complete transection of hippocampal cross-section is needed to durably terminate epilepsy, avoiding possible postoperative reorganization of longitudinal pathways. Here, we report an anatomical study designed to evaluate the feasibility of complete transection of hippocampus with the aid of ultrasound neuronavigation and we propose new instruments to reach this goal. METHODS: Five cadaveric brains were analyzed in this study. MHT was performed on both sides of each brain either with or without ultrasound neuronavigation. The percentage of transected cross-section of the hippocampus was measured using magnetic resonance imaging (MRI) and both sides were compared. RESULTS: The ultrasound-guided MHTs were more likely to achieve complete hippocampal transection compared with the nonnavigated MHT transection (73 vs 58%; p < 0.01). Our study also allowed us to propose specialized transectors to minimize invasivity of this procedure. CONCLUSION: Completeness of MHT can be better reached with the aid of an ultrasound neuronavigation system; modified instruments for this procedure were also designed.

Cortical and subcortical morphometric changes and their relation to cognitive impairment in isolated REM sleep behavior disorder.

OBJECTIVE: To date, very few studies have focused on structural changes and their association with cognitive performance in isolated REM sleep behaviour disorder (iRBD). Moreover, the results of these studies are inconclusive. This study aims to evaluate differences in the associations between brain morphology and cognitive tests in iRBD and healthy controls. METHODS: Sixty-three patients with iRBD and thirty-six controls underwent MRI with a 3 T scanner. The cognitive performance was assessed by a comprehensive neuropsychological battery. Based on performance, the iRBD group was divided into two subgroups with (iRBD-MCI) and without mild cognitive impairment (iRBD-NC). The high-resolution T1-weighted images were analysed using an automated atlas segmentation tool, voxel-based (VBM) and deformation-based (DBM) morphometry to identify between-group differences and correlations with cognitive performance. RESULTS: VBM, DBM and the comparison of ROI volumes yielded no significant differences between iRBD and controls. In the iRBD group, significant correlations in VBM were found between several cortical and subcortical structures primarily located in the temporal, parietal, occipital lobe, cerebellum, and basal ganglia and three cognitive tests assessing psychomotor speed and one memory test. Between-group analysis of cognition revealed a significant difference between iRBD-MCI and iRBD-NC in tests including a processing speed component. CONCLUSIONS: iRBD shows deficits in several cognitive tests that correlate with morphological changes, the most prominent of which is in psychomotor speed and visual attention as measured by the TMT-A and associated with the volume of striatum, insula, cerebellum, temporal lobe, pallidum and amygdala.

Magnetic susceptibility changes in the brainstem reflect REM sleep without atonia severity in isolated REM sleep behavior disorder.

REM sleep without atonia (RWA) is the hallmark of isolated REM sleep behavior disorder (iRBD) and is caused by neurodegeneration of brainstem structures. Previously, quantitative susceptibility mapping (QSM) was shown to detect microstructural tissue changes in neurodegenerative diseases. The goal of the study was to compare brainstem magnetic susceptibility (MS) in iRBD and controls using the voxel-based QSM approach and to examine the association between brainstem MS and severity of RWA in iRBD. Sixty iRBD patients and 41 healthy controls were included in the study. Phasic, tonic, mixed RWA and SINBAR score was quantified. QSM maps were reconstructed with QSMbox software from a multi-gradient-echo sequence acquired at 3T MRI system and normalized using a custom T1 template. Voxel-based analysis with age and gender as covariates was performed using a two-sample t-test model for between-group comparison and using a linear regression model for association with the RWA parameters. Statistical maps were generated using threshold free cluster enhancement with p-value p < 0.05, corrected for family wise error. Compared to controls, the iRBD group had higher MS in bilateral substantia nigra (SN), red nucleus and the ventral tegmental area. MS positively correlated with iRBD duration in the right pedunculotegmental nucleus and white matter of caudal mesencephalic and pontine tegmentum and with phasic RWA in bilateral SN. QSM was able to detect MS abnormalities in several brainstem structures in iRBD. Association of MS levels in the brainstem with the intensity of RWA suggests that increased iron content in SN is related to RWA severity.

Comorbid Neurodegeneration in Primary Progressive Aphasia: Clinicopathological Correlations in a Single-Center Study.

Introduction: Primary progressive aphasia (PPA) is a clinically variable syndrome manifesting as slow progressive loss of speech and language with multiple underlying neurodegenerative pathologies. Materials and Methods: We included data from nine PPA patients with available autopsies. We then retrospectively reviewed all available medical records, neuropsychology, and MRI results to confirm the corresponding subtypes of PPA and compared them with postmortem neuropathological results. Results: Clinical presentations corresponded to the nonfluent/agrammatic variant in six cases, the semantic variant in one case, the logopenic variant in one case, and the mixed variant (concomitant nonfluent/agrammatic plus semantic variant) in one case. Patients with a broader clinical presentation, i.e., combining manifestations of one PPA subtype and symptoms of another PPA variant, had autopsy comorbidities showing multiple neurodegenerative disorders. Of the nine subjects enrolled in the study, Alzheimer's disease (AD) was found in eight cases; however, in only one case, AD was detected as an isolated neuropathological substrate of PPA. In eight brain samples, different comorbid neuropathologies were detected: three cases with comorbid AD and dementia with Lewy bodies, two cases with comorbid AD and TDP-43 pathology, one case with comorbid AD and complex tauopathies, and one case with comorbid AD with both tau and TDP-43 deposits. Finally, one case had comorbid tau and TDP-43 pathology but without comorbid AD pathology. Conclusions: Our observation suggests that PPA cases could be more heterogeneous in their etiology than previously thought and underlying neurodegenerative comorbidities should be considered in routine practice, especially if the clinical presentation of PPA is atypical.

Influence of Hyperglycaemia and CRP on the Need for Mechanical Ventilation in Guillain-Barré Syndrome.

Objectives: Elevated blood glucose and CRP (C-reactive protein) are usually related to a worsened clinical outcome in neurological diseases. This association in Guillain-Barré syndrome (GBS) has been studied rarely. We tried to analyse if hyperglycaemia and CRP at admission may influence the outcome of GBS, including mechanically ventilated (MV) patients. Methods: We retrospectively studied 66 patients (40 males, 19-93 years, average 56 years) without diabetes mellitus and free of corticoid treatment, who fulfilled the clinical criteria for diagnosis of GBS. Hyperglycaemia (the level of fasting plasma glucose, FPG) was defined as blood glucose level >5.59 mmol/L according to our laboratory. CRP >5 mg/L was considered as an abnormally elevated value. Results: At admission, 32 GBS patients (48%) had hyperglycaemia according to FPG level. A severe form of GBS (>4 according to Hughes GBS scale) was observed in 17 patients (26%); and 8 of them (47%) had hyperglycaemia. Fourteen patients (21%) were MV, and in 10 of them (71%) hyperglycaemia was present. CRP was significantly increased in MV patients. The linear model revealed a significant relationship between CRP and glycemia (p = 0.007) in subjects without MV (p = 0.049). In subjects with MV the relationship was not significant (p = 0.2162, NS). Conclusion: In the acute phase of GBS at admission, hyperglycaemia and higher CRP occur relatively frequently, and may be a risk factor for the severity of GBS. Stress hyperglycaemia due to impaired glucose homeostasis could be one explanation for this condition.

Modulation of Motor Cortex Activity After Intrathecal Baclofen Delivery in Chronic Thoracic Spinal Cord Injury.

Objectives: Intrathecal baclofen (ITB) is commonly used for reduction of spasticity in chronic spinal cord injury (SCI). Its clinical effect is well-known; however, exact mechanisms of long-term effect of continuous ITB administration (cITBa) on modulation of cortical processes have not been elucidated. The aim of this study was to evaluate changes in motor cortex activation for healthy upper limbs in comparison to impaired lower limbs by functional magnetic resonance imaging (fMRI). Methods: Ten subjects (eight males, 20-69 years) with thoracic SCI presenting no voluntary movements of lower limbs (except one) were enrolled in the fMRI study. fMRI at 1.5T with a finger tapping paradigm and mental movement simulating foot flexion on the dominant side were performed before, 3 months, and 1 year after start of cITBa. fMRI data processing was carried out using FMRI Expert Analysis Tool (FEAT), part of FSL. A second-level analysis was carried out using FLAME stages 1 and 2. The level of spasticity was assessed with the Modified Ashworth scale (MAS). Results: Continuous ITB significantly decreased limb spasticity in all the subjects (group MAS spasticity dropped from 3 to 0.3). The second-level analysis (Z > 1.6, cluster significance threshold p =0.05) revealed increased activation of the primary sensorimotor cortex of the foot between baseline and 3 months, and 3 months and 1 year. Conclusion: Increased sensorimotor cortex activation with spasticity reduction after cITBa may reflect distant functional reorganization because of long-term mediated neuroplastic changes in the sensorimotor cortex. Better understanding of modulation of brain function in SCI after cITBa may influence the field of neurorehabilitation.

Biomarkers Analysis and Clinical Manifestations in Comorbid Creutzfeldt-Jakob Disease: A Retrospective Study in 215 Autopsy Cases.

Creutzfeldt-Jakob disease (CJD), the most common human prion disorder, may occur as "pure" neurodegeneration with isolated prion deposits in the brain tissue; however, comorbid cases with different concomitant neurodegenerative diseases have been reported. This retrospective study examined correlations of clinical, neuropathological, molecular-genetic, immunological, and neuroimaging biomarkers in pure and comorbid CJD. A total of 215 patients have been diagnosed with CJD during the last ten years by the Czech National Center for Prion Disorder Surveillance. Data were collected from all patients with respect to diagnostic criteria for probable CJD, including clinical description, EEG, MRI, and CSF findings. A detailed neuropathological analysis uncovered that only 11.16% were "pure" CJD, while 62.79% had comorbid tauopathy, 20.47% had Alzheimer's disease, 3.26% had frontotemporal lobar degeneration, and 2.33% had synucleinopathy. The comorbid subgroup analysis revealed that tauopathy was linked to putaminal hyperintensity on MRIs, and AD mainly impacted the age of onset, hippocampal atrophy on MRIs, and beta-amyloid levels in the CSF. The retrospective data analysis found a surprisingly high proportion of comorbid neuropathologies; only 11% of cases were verified as "pure" CJD, i.e., lacking hallmarks of other neurodegenerations. Comorbid neuropathologies can impact disease manifestation and can complicate the clinical diagnosis of CJD.

Corpus callosum hypersignals and focal atrophy: Neuroimaging findings in globular glial tauopathy type I.

BACKGROUND AND PURPOSE: Globular glial tauopathies (GGTs) have heterogeneous presentations; little evidence regarding typical clinical and magnetic resonance imaging (MRI) presentations are available. METHODS: We retrospectively assessed MRIs from three postmortem-confirmed GGT cases, in two patients with atypical progressive aphasia and one with corticobasal syndrome. RESULTS: We suggest that four principal concomitant MRI findings characterize GGT type I: a sagittal callosal hyperintense band, marked focal callosal atrophy suggesting white matter degeneration originating in cortical areas responsible for symptoms (anterior atrophy in predominantly language manifestations and posterior atrophy in predominantly apraxia), periventricular white matter lesions, and mild-to-moderate brain stem atrophy. CONCLUSIONS: We observed four concomitant MRI abnormalities in patients with atypical dementia, parkinsonism, and late incomplete supranuclear gaze palsy. Two patients had atypical progressive aphasia and one had corticobasal syndrome.

Quantification of artifacts during cardiac magnetic resonance in patients with leadless Micra pacemakers.

INTRODUCTION: When cardiac magnetic resonance (MR) is performed after previous leadless transcatheter pacemaker implantation, an image distortion has to be expected in the heart region and evaluation of myocardial tissue can be affected. In this clinical prospective study, we aim to assess the extent and impact of this artifact on individual ventricular segments and compare it to conventional pacing devices. METHODS: Total of 20 patients with leadless pacemaker placed in the right ventricle underwent cardiac MR imaging in a 1.5 Tesla scanner. A multiplanar segmentation was used to demarcate the left and right ventricular myocardium as well as the pacemaker-caused image artifact in systolic and diastolic time frames. Artifact size and its relative influence on myocardial segments were quantitatively assessed and expressed in AHA-17 model. RESULTS: Implanted leadless pacemaker caused an image artifact with a volume of 48 ± 5 ml. Most distorted were the apical septal (53 ± 23%), apical inferior (30 ± 18%), and midventricular inferoseptal (30 ± 20%) segments. The artifact intersection with basal and lateral segments was none or negligible (up to 2%). The portion of left ventricular (LV) myocardium affected by the artifact was significantly higher in systole (8 ± 4%) compared to diastole (10 ± 3%; p < .001). CONCLUSION: Implantation of leadless pacemaker represents no obstacle for cardiac MR imaging but causes an image artifact located mostly in septal, inferoseptal, and anteroseptal segments of apical and midventricular LV myocardium. With the exception of the apex, diastolic timing reduces the image distortion of all segments and improves global ventricular assessment.

Improvement of Memory Functions in Chronic Spinal Cord Injury After Long-Term Intrathecal Baclofen Delivery for Spasticity Relief.

BACKGROUND: Intrathecal baclofen (ITB) pump delivery systems are safe and effective in the treatment of generalized spasticity in chronic spinal cord injury (SCI). Despite its widespread use, few and discrepant data are available in animal studies on the effects of ITB on cognitive functions, such as memory. The effects of chronic administration of baclofen on humans have not been investigated to date. The aim of this study is to find out, whether a long-term administration of ITB has any effects on cognitive functions in SCI subjects. MATERIALS AND METHODS: In 11 out of 22 subjects with chronic SCI, we performed comprehensive neuropsychological assessment carried out using specialized tests focused on memory and other higher cognitive domains and emotional state. RESULTS: All patients receiving ITB treatment for spasticity relief improved significantly in RAVLT Trials 1-5 (p = 0.049), Logical memory-immediate recall (p = 0.019) and Logical memory-delayed recall (p = 0.008). Visual memory, long-term semantic memory, attention, executive, perceptual and spatial functions, and mood status remained stable. CONCLUSION: No significant decline in memory functions were detected following one year of ITB delivery, creating an opportunity for careful prescription of this treatment in chronic SCI. Moreover, we have detected a significant increase in short-term auditory-verbal memory and logical memory performance.

Virtual reality-based treatment for regaining upper extremity function induces cortex grey matter changes in persons with acquired brain injury.

BACKGROUND: Individuals with acquired brain injuries (ABI) are in need of neurorehabilitation and neurorepair. Virtual anatomical interactivity (VAI) presents a digital game-like format in which ABI survivors with upper limb paresis use an unaffected limb to control a standard input device and a commonplace computer mouse to control virtual limb movements and tasks in a virtual world. METHODS: In a prospective cohort study, 35 ambulatory survivors of ABI (25/71% stroke, 10/29% traumatic brain injury) were enrolled. The subjects were divided into three groups: group A received VAI therapy only, group B received VAI and physical/occupational therapy (P/OT), and group C received P/OT only. Motor skills were evaluated by muscle strength (hand key pinch strength, grasp, and three-jaw chuck pinch) and active range of motion (AROM) of the shoulder, elbow, and wrist. Changes were analyzed by ANOVA, ANCOVA, and one-tailed Pearson correlation analysis. MRI data was acquired for group A, and volumetric changes in grey matter were analyzed using voxel-based morphometry (VBM) and correlated with quantified motor skills. RESULTS: AROM of the shoulder, elbow, and wrist improved in all three groups. VBM revealed grey matter increases in five brain areas: the tail of the hippocampus, the left caudate, the rostral cingulate zone, the depth of the central sulcus, and the visual cortex. A positive correlation between the grey matter volumes in three cortical regions (motor and premotor and supplementary motor areas) and motor test results (power and AROM) was detected. CONCLUSIONS: Our findings suggest that the VAI rehabilitation program significantly improved motor function and skills in the affected upper extremities of subjects with acquired brain injuries. Significant increases in grey matter volume in the motor and premotor regions of affected hemisphere and correlations of motor skills and volume in nonaffected brain regions were present, suggesting marked changes in structural brain plasticity. TRIAL REGISTRATION: The trial "Limitations of motor brain activity - use of virtual reality for simulation of therapeutic interventions" has been registered under reference number ISRCTN11757651 .

Clinical Variability in P102L Gerstmann-Sträussler-Scheinker Syndrome.

Gerstmann-Sträussler-Scheinker syndrome (GSS) with the P102L mutation is a rare genetic prion disease caused by a pathogenic mutation at codon 102 in the prion protein gene. Cluster analysis encompassing data from 7 Czech patients and 87 published cases suggests the existence of 4 clinical phenotypes (typical GSS, GSS with areflexia and paresthesia, pure dementia GSS, and Creutzfeldt-Jakob disease-like GSS); GSS may be more common than previously estimated. In making a clinical diagnosis or progression estimates of GSS, magnetic resonance imaging and real-time quaking-induced conversion may be helpful, but the results should be evaluated with respect to the overall clinical context. ANN NEUROL 2019;86:643-652.

Comparison of Prostate Imaging Reporting and Data System (PI-RADS) version 1 and version 2 and combination with apparent diffusion coefficient as a predictor of biopsy outcome.

PURPOSE: The main aim of the study was to compare the diagnostic performance of Prostate Imaging Reporting and Data System (PI-RADS) versions 1 and 2 for detection of prostate carcinoma (PCa) and clinically significant prostate carcinoma (CSPCa). The second aim was to evaluate the potential benefit of adding the apparent diffusion coefficient (ADC) and prostate specific antigen (PSA) density to the standard evaluation protocol. METHODS: A total of 167 consecutive patients with elevated PSA underwent magnetic resonance imaging. The images were evaluated prospectively using both versions of the PI-RADS and the results compared with 12-core template biopsy and magnetic resonance/transrectal ultrasound fusion biopsy. Receiver-operating characteristic (ROC) curves were compared for each scoring system using DeLong\'s test. The area under the curve (AUC) was calculated for ADC and PSA density for lesions scored 4. RESULTS: PI-RADS V2 had high discriminative ability for PCa prediction with an AUC of 0.824 (95% CI 0.763 to 0.885), compared to an AUC of 0.724 (95% CI 0.654 to 0.794) for PI-RADS V1 (p = 0.0335). ADC demonstrated a higher discriminative ability with an AUC of 0.702 (95% CI 0.548 to 0.856) in CSPCa prediction. Using the obtained ADC threshold of 828x10^-6 mm^2/s improved specificity to 86.73% with a sensitivity of 60.38%. CONCLUSION: PI-RADS version 2 exhibited significantly higher discriminative ability for PCa and CSPCa detection compared to PI-RADS version 1. Using the ADC can improve the tumor predictability of PI-RADS version 2 in lesions scored 4.

Globular Glial Tauopathy Type I Presenting as Atypical Progressive Aphasia, With Comorbid Limbic-Predominant Age-Related TDP-43 Encephalopathy.

Globular glial tauopathies (GGTs) have heterogeneous presentations with little available information regarding typical clinical manifestations. We report on a case of atypical primary progressive aphasia (PPA) due to comorbid GGT and limbic transactive response DNA binding protein of 43 kDa (TDP-43) proteinopathy. The initial clinical phenotype was compatible with the nonfluent-agrammatical variant of PPA and early hippocampal amnesia. Progressively, parkinsonism and supranuclear oculomotor impairment occurred, and finally, late mutism with frontal-type dementia, impaired comprehension, and behavioral manifestations developed. The neuropathology was characteristic of GGT type I with vascular changes and comorbid limbic-predominant age-related TDP-43 encephalopathy (LATE). Our findings expand the clinical spectrum of GGTs to include a complex progressive aphasia syndrome. The extraordinary feature, in this case, was the combination of two progressive aphasia subtypes, that is, the early nonfluent-agrammatical variant and the late semantic variant. Our findings also expand the spectrum of neuropathological comorbidities in GGT.

Prospective memory impairment in idiopathic REM sleep behavior disorder.

OBJECTIVE: The aim of the present study was to investigate if prospective memory (PM) is impaired in idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). RBD is a parasomnia characterized by dream enactment and by REM sleep without muscle atonia. iRBD is considered as the initial stage of neurodegeneration with pathological storage of alpha-synuclein. METHOD: Sixty iRBD patients with polysomnography-confirmed RBD without parkinsonism and dementia and 30 demographically matched normal controls (NC) were enrolled in the present study. Clinical assessment included Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), dopamine transporter single-photon emission computed tomography (DaT-SPECT) for imaging synapses of dopaminergic neurons in the striatum and a neuropsychological battery with embedded time-based and event-based PM measures. RESULTS: iRBD differed significantly from NC in event-based PM, a number of event-based failures to recall intention and total PM performance (all p < .001) but did not differ in time-based PM and recognition. PM did not contribute to impairment of instrumental activities of daily living in iRBD. Despite being preserved in iRBD in comparison to NC, time-based PM correlated significantly with dopaminergic neuronal loss measured by DaT-SPECT. CONCLUSIONS: We show evidence for a differential pattern of PM impairment in iRBD with severe impairment of event-based and concurrent preservation of time-based PM. We theorize that event-based PM impairment in iRBD is caused by severe impairment of retention and recognition mechanisms in episodic memory whereas time-based PM seems to be affected by reduced striatal dopaminergic synapses.

Possibilities of objective identification of meniscoids in joint blocks of the axial system, by MRI and Transfer Vibration through the Spine.

OBJECTIVE: The aim of the study was to identify the meniscoids of the cervical spine using in-vivo MRI imaging and to determine their potential role in the development of functional joint blocks of the axial system (AS). Another objective was to find out how the articular blocks affect the rheological properties of the spine by the Transfer Vibration through the Spine (TVS) method. METHOD: In this study were used methods TVS and MRI. The study was conducted on a research file of 12 subjects and was conceived as a pilot one. RESULTS: It has been shown that the MRI method, in appropriate circumstances, enables the detection of changes in the size and shape of meniscoids in-vivo. On the basis of the investigations carried out, it can be assumed that several mechanisms are involved in the formation of functional joint blocks, and are not primarily caused by the incarceration of meniscoidal tissue. Using the TVS method, it has also been found that a functional articular blockade affects the rheological properties of the axial system, specifically reducing the damping capabilities of the particular spine segment. CONCLUSION: In the follow-up studies, it will be necessary to verify the theoretical interpretations on a larger statistical set.

Genetic Alzheimer Disease and Sporadic Dementia With Lewy Bodies: A Comorbidity Presenting as Primary Progressive Aphasia.

We report a 44-year-old woman, with a family history of early-onset dementia, presenting with primary progressive aphasia. This clinically variable syndrome has multiple underlying pathologies, and correlations between clinical manifestations and postmortem neuropathologic findings are controversial. Our patient suffered worsening language impairment with major word-finding difficulties but preserved comprehension. She also developed episodic memory impairment. Her condition progressed to dementia with behavioral changes. Magnetic resonance imaging showed early left perisylvian and bitemporal atrophy. The patient died shortly afterward from colon cancer. Neuropathologic examination revealed advanced early-onset Alzheimer and Lewy body disease, plus a clinically nonrelevant metastasis of her colon cancer in her left parietal lobe. Genetic examination revealed a p.Glu184Asp mutation in the presenilin1 gene. Our findings confirm the importance of a thorough appreciation for the clinical and neuropathologic correlations in patients with atypical neurodegenerative dementias.