@misc{KellerGorgesAhoOezhanetal., author = {Keller, J{\"u}rgen and Gorges, Martin and Aho-{\"O}zhan, Helena Eira Anneli and Carmona, S. and Schneider, Erich}, title = {Eye-tracking control to assess cognitive functions in patients with amyotrophic lateral sclerosis}, series = {JoVE}, volume = {116}, journal = {JoVE}, issn = {1940-087X}, doi = {10.3791/54634}, pages = {e54634}, language = {en} } @misc{DonaldTanChakrapanietal., author = {Donald, Aimee and Tan, Chong Y. and Chakrapani, Anupam and Hughes, Derralyn A. and Sharma, Reena and Cole, Duncan and Bardins, Stanislav and Gorges, Martin and Jones, Simon A. and Schneider, Erich}, title = {Eye movement biomarkers allow for the definition of phenotypes in Gaucher Disease}, series = {Orphanet journal of rare diseases : OJRD}, volume = {15}, journal = {Orphanet journal of rare diseases : OJRD}, issn = {1750-1172}, doi = {10.1186/s13023-020-01637-9}, pages = {12}, abstract = {Background: Neurological forms of Gaucher disease, the inherited disorder of β-Glucosylceramidase caused by bi-allelic variants in GBA1, is a progressive disorder which lacks a disease-modifying therapy. Systemic manifestations of disease are effectively treated with enzyme replacement therapy, however, molecules which cross the blood-brain barrier are still under investigation. Clinical trials of such therapeutics require robust, reproducible clinical endpoints to demonstrate efficacy and clear phenotypic definitions to identify suitable patients for inclusion in trials. The single consistent clinical feature in all patients with neuronopathic disease is the presence of a supranuclear saccadic gaze palsy, in the presence of Gaucher disease this finding serves as diagnostic of 'type 3' Gaucher disease.}, language = {en} } @misc{NanningBrauneUttneretal., author = {Nanning, Felix and Braune, Katharina and Uttner, Ingo and Ludolph, Albert Christian and Gorges, Martin and Lul{\´e}, Doroth{\´e}e}, title = {Altered Gaze Control During Emotional Face Exploration in Patients With Amyotrophic Lateral Sclerosis}, series = {Neurology}, volume = {101}, journal = {Neurology}, number = {6}, issn = {0028-3878}, doi = {10.1212/WNL.0000000000207214}, pages = {264 -- 269}, abstract = {Objectives Up to 50\% of patients with amyotrophic lateral sclerosis (ALS) present with cognitive problems and behavioral dysfunctions including recognition of human faces presenting different emotions. We investigated whether impaired processing of emotional faces is associated with abnormal scan paths during visual exploration. Methods Cognitively unimpaired patients with ALS (n = 45) and matched healthy controls (n = 37) underwent neuropsychological assessment and video-based eye tracking. Eye movements were recorded while participants visually explored faces expressing different emotions (neutral, disgusted, happy, fearful, and sad) and houses mimicking faces. Results Compared with controls, patients with ALS fixated significantly longer to regions which are not relevant for emotional information when faces expressed fear (p = 0.007) and disgust (p = 0.006), whereas the eyes received less attention in faces expressing disgust (p = 0.041). Fixation duration in any area of interest was not significantly associated with the cognitive state or clinical symptoms of disease severity. Discussion In cognitively unimpaired patients with ALS, altered gaze patterns while visually exploring faces expressing different emotions might derive from impaired top-down attentional control with possible involvement of subliminal frontotemporal areas. This may account for indistinctness in emotion recognition reported in previous studies because nonsalient features retrieve more attention compared with salient areas. Current findings may indicate distinct emotion processing dysfunction of ALS pathology, which may be different from, for example, executive dysfunction.}, language = {en} } @misc{CharisseErusPomponioetal., author = {Chariss{\´e}, Daniel and Erus, Guray and Pomponio, Raymond and Gorges, Martin and Schmidt, Nele and Schneider, Christine and Liepelt-Scarfone, Inga and Riedel, Oliver and Reetz, Kathrin and Schulz, J{\"o}rg B. and Berg, Daniela and Storch, Alexander and Witt, Karsten and Dodel, Richard and Kalbe, Elke and Kassubek, Jan and Hilker-Roggendorf, R{\"u}diger and Baudrexel, Simon}, title = {Brain age and Alzheimer's-like atrophy are domain-specific predictors of cognitive impairment in Parkinson's disease}, series = {Neurobiology of Aging}, volume = {109}, journal = {Neurobiology of Aging}, issn = {0197-4580}, doi = {10.1016/j.neurobiolaging.2021.08.020}, pages = {31 -- 42}, abstract = {Recently, it was shown that patients with Parkinson's disease (PD) who exhibit an "Alzheimer's disease (AD)-like" pattern of brain atrophy are at greater risk for future cognitive decline. This study aimed to investigate whether this association is domain-specific and whether atrophy associated with brain aging also relates to cognitive impairment in PD. SPARE-AD, an MRI index capturing AD-like atrophy, and atrophy-based estimates of brain age were computed from longitudinal structural imaging data of 178 PD patients and 84 healthy subjects from the LANDSCAPE cohort. All patients underwent an extensive neuropsychological test battery. Patients diagnosed with mild cognitive impairment or dementia were found to have higher SPARE-AD scores as compared to patients with normal cognition and healthy controls. All patient groups showed increased brain age. SPARE-AD predicted impairment in memory, language and executive functions, whereas advanced brain age was associated with deficits in attention and working memory. Data suggest that SPARE-AD and brain age are differentially related to domain-specific cognitive decline in PD. The underlying pathomechanisms remain to be determined.}, language = {en} } @misc{RamaioliSteinmetzerBrietzkeetal., author = {Ramaioli, Cecilia and Steinmetzer, Tobias and Brietzke, Adrian and Meyer, Paul and Pham Xuan, Rebecca and Schneider, Erich and Gorges, Martin}, title = {Assessment of vestibulo-ocular reflex and its adaptation during stop-and-go car rides in motion sickness susceptible passengers}, series = {Experimental Brain Research}, volume = {241}, journal = {Experimental Brain Research}, number = {6}, issn = {1432-1106}, doi = {10.1007/s00221-023-06619-4}, pages = {1523 -- 1531}, abstract = {Motion sickness is a physiological condition that negatively impacts a person's comfort and will be an emerging condition in autonomous vehicles without proper countermeasures. The vestibular system plays a key role in the origin of motion sickness. Understanding the susceptibility and (mal) adaptive mechanisms of the highly integrated vestibular system is a prerequisite for the development of countermeasures. We hypothesize a differential association between motion sickness and vestibular function in healthy individuals with and without susceptibility for motion sickness. We quantified vestibular function by measuring the high-frequency vestibulo-ocular reflex (VOR) using video head impulse testing (vHIT) in 17 healthy volunteers before and after a 11 min motion sickness-inducing naturalistic stop-and-go car ride on a test track (Dekra Test Oval, Klettwitz, Germany). The cohort was classified as motion sickness susceptible (n = 11) and non-susceptible (n = 6). Six (out of 11) susceptible participants developed nausea symptoms, while a total of nine participants were free of these symptoms. The VOR gain (1) did not differ significantly between participant groups with (n = 8) and without motion sickness symptoms (n = 9), (2) did not differ significantly in the factor time before and after the car ride, and showed no interaction between symptom groups and time, as indicated by a repeated measures ANOVA (F(1,15) = 2.19, p = 0.16. Bayesian inference confirmed that there was "anecdotal evidence" for equality of gain rather than difference across groups and time (BF10 < 0.77). Our results suggest that individual differences in VOR measures or adaptation to motion sickness provocative stimuli during naturalistic stop-and-go driving cannot predict motion sickness susceptibility or the likelihood of developing motion sickness.}, language = {en} }