Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 88
Filter
1.
Curr Neurol Neurosci Rep ; 23(5): 213-224, 2023 05.
Article in English | MEDLINE | ID: covidwho-2320410

ABSTRACT

PURPOSE OF REVIEW: This article reviews hypopituitarism after TBI, the importance of pituitary hormones, and related controversies, concluding with a suggested patient approach. RECENT FINDINGS: While earlier studies focused on increased pituitary deficiencies after moderate-severe TBI, recent studies have focused on deficiencies after mild TBI. There has been increasing focus on the role of growth hormone after injury; growth hormone is the most frequent reported deficiency at 1 year post-TBI, and an area with unresolved questions. While more research is needed to quantify the risk of deficiencies in special populations, and establish the natural history, increasing data indicate an increase in hypopituitarism after other acquired brain injuries; the potential role of pituitary hormone deficiencies after stroke and after COVID-19 infection is an area of active inquiry. Given the negative health effects of untreated hypopituitarism and the opportunity to intervene via hormone replacement, it is important to recognize the role of pituitary hormone deficiencies after TBI.


Subject(s)
Brain Injuries , COVID-19 , Human Growth Hormone , Hypopituitarism , Humans , COVID-19/complications , Hypopituitarism/epidemiology , Hypopituitarism/etiology , Growth Hormone
2.
Front Immunol ; 14: 1157179, 2023.
Article in English | MEDLINE | ID: covidwho-2296687

ABSTRACT

Introduction: Although many studies have demonstrated the existing neurological symptoms in COVID-19 patients, the mechanisms are not clear until now. This study aimed to figure out the critical molecular and immune infiltration situations in the brain of elderly COVID-19 patients. Methods: GSE188847 was used for the differential analysis, WGCNA, and immune infiltration analysis. We also performed GO, KEGG, GSEA, and GSVA for the enrich analysis. Results: 266 DEGs, obtained from the brain samples of COVID-19 and non-COVID-19 patients whose ages were over 70 years old, were identified. GO and KEGG analysis revealed the enrichment in synapse and neuroactive ligand-receptor interaction in COVID-19 patients. Further analysis found that asthma and immune system signal pathways were significant changes based on GSEA and GSVA. Immune infiltration analysis demonstrated the imbalance of CD8+ T cells, neutrophils, and HLA. The MEpurple module genes were the most significantly different relative to COVID-19. Finally, RPS29, S100A10, and TIMP1 were the critical genes attributed to the progress of brain damage. Conclusion: RPS29, S100A10, and TIMP1 were the critical genes in the brain pathology of COVID-19 in elderly patients. Our research has revealed a new mechanism and a potential therapeutic target.


Subject(s)
Asthma , Brain Injuries , COVID-19 , Aged , Humans , COVID-19/genetics , Brain , Genes, Regulator
3.
Pediatrics ; 151(5)2023 05 01.
Article in English | MEDLINE | ID: covidwho-2251851

ABSTRACT

Long-term neurodevelopmental sequelae are a potential concern in neonates following in utero exposure to severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2). We report 2 neonates born to SARS-CoV-2 positive mothers, who displayed early-onset (day 1) seizures, acquired microcephaly, and significant developmental delay over time. Sequential MRI showed severe parenchymal atrophy and cystic encephalomalacia. At birth, neither infant was SARS-CoV-2 positive (nasopharyngeal swab, reverse transcription polymerase chain reaction), but both had detectable SARS-CoV-2 antibodies and increased blood inflammatory markers. Placentas from both mothers showed SARS-CoV-2-nucleocapsid protein and spike glycoprotein 1 in the syncytiotrophoblast, fetal vascular malperfusion, and significantly increased inflammatory and oxidative stress markers pyrin domain containing 1 protein, macrophage inflammatory protein 1 ßη, stromal cell-derived factor 1, interleukin 13, and interleukin 10, whereas human chorionic gonadotropin was markedly decreased. One infant (case 1) experienced sudden unexpected infant death at 13 months of age. The deceased infant's brain showed evidence of SARS-CoV-2 by immunofluorescence, with colocalization of the nucleocapsid protein and spike glycoprotein around the nucleus as well as within the cytoplasm. The constellation of clinical findings, placental pathology, and immunohistochemical changes strongly suggests that second-trimester maternal SARS-CoV-2 infection with placentitis triggered an inflammatory response and oxidative stress injury to the fetoplacental unit that affected the fetal brain. The demonstration of SARS-CoV-2 in the deceased infant's brain also raises the possibility that SARS-CoV-2 infection of the fetal brain directly contributed to ongoing brain injury. In both infants, the neurologic findings at birth mimicked the presentation of hypoxic-ischemic encephalopathy of newborn and neurologic sequelae progressed well beyond the neonatal period.


Subject(s)
Brain Injuries , COVID-19 , Pregnancy Complications, Infectious , Infant, Newborn , Pregnancy , Female , Humans , SARS-CoV-2 , Placenta/pathology , Nucleocapsid Proteins , Glycoproteins , Infectious Disease Transmission, Vertical
5.
Ann Ist Super Sanita ; 58(4): 236-243, 2022.
Article in English | MEDLINE | ID: covidwho-2164050

ABSTRACT

INTRODUCTION: During the COVID-19 pandemic, several restrictions were imposed to limit the circulation of the infection within communities. Hospitals denied access to the family and friends of inpatients, and thus to caregivers. This observational study evaluated the impact of the physical absence of caregivers during the lockdown period due to the COVID-19 emergency on the rehabilitation of inpatients with severe acquired brain injury (sABI). METHODS: The functional outcome at discharge was measured in 25 inpatients with sABI through the Disability Rating Scale (DRS), Glasgow Outcome Scale (GOS), and Levels of Cognitive Functioning scale (LCF) after neuropsychological rehabilitation in an Adult Inpatient Neurorehabilitation Unit for Patients with sABI. Fourteen patients were directly assisted by their informal caregivers physically present in the neurorehabilitation ward. Eleven patients were indirectly supported via remote connection because during the lockdown period (from March to July 2020) caregivers could not be admitted to the rehabilitation hospital. The Caregiving Impact on Neuro-Rehabilitation Scale (CINRS) was also used to evaluate both the change since the admission and the impact of the caregiver from the perspective of the cognitive therapist. Demographic characteristics, time since injury, injury severity (duration of impaired consciousness measured by the time to follow commands), level of functioning at the beginning of the rehabilitation, and duration of the rehabilitation treatment were comparable between the groups. RESULTS: Both groups improved after the treatment; however, the improvement was consistently greater in the group directly assisted by the caregivers. The results showed that although the caregivers ensured their virtual presence at distance, their physical absence played a role in hindering the functional outcome of the patients. CONCLUSIONS: The role of the caregiver of patients with sABI is underlined in being not only a person handing out generic aid, cares, and affection, but also an integral part of the rehabilitation process.


Subject(s)
Brain Injuries , COVID-19 , Adult , Humans , Pandemics , Brain Injuries/rehabilitation , Treatment Outcome , Communicable Disease Control
6.
J Head Trauma Rehabil ; 37(6): E502-E608, 2022.
Article in English | MEDLINE | ID: covidwho-2161222

Subject(s)
Brain Injuries , Humans , Brain , Head
7.
Dev Neurosci ; 44(4-5): 175-176, 2022.
Article in English | MEDLINE | ID: covidwho-2138284

Subject(s)
Brain Injuries , Brain , Humans
8.
psyarxiv; 2022.
Preprint in English | PREPRINT-PSYARXIV | ID: ppzbmed-10.31234.osf.io.qjx25

ABSTRACT

Intolerance of uncertainty (IU) is a risk factor for poor mental health. Acquired brain injury (ABI; e.g., stroke, traumatic brain injury), often brings considerable uncertainty and increased mood disorder vulnerability. The Intolerance of Uncertainty Scale-12 (IUS-12) is a brief, well-validated measure of IU argued to comprise two subscales, Prospective Anxiety and Inhibitory Anxiety. Here, for the first time, we investigated its reliability and validity (N = 118), and factor structure (N = 176), in ABI. Both subscales had high test-retest reliability (ICCs of 0.75 and 0.86) and were significantly associated with mood disorder symptoms. The two-factor model was superior to a one-factor IU model fit. IUS-12 scores were stable despite great uncertainties of COVID-19, consistent with its conceptualisation as a trait. Consistent with recent debates about the factor structure of IUS-12 and, in exploratory analyses, we found indications of improved fits that warrant further investigation in independent ABI samples.


Subject(s)
Stroke , COVID-19 , Brain Diseases , Anxiety Disorders , Brain Injuries , Mood Disorders
9.
J Clin Neurosci ; 106: 135-140, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-2069369

ABSTRACT

To investigate the pandemic's impact on critically ill patients with neurological emergencies, we compared care metrics and outcomes of patients with severe acute brain injury (SABI) before and during the initial COVID-19 surge at our institution. We included adult patients with SABI during two separate three-month time periods: 'pre-COVID vs COVID'. We further stratified the COVID cohort to characterize outcomes in patients requiring COVID-19 precautions (Patient Under Investigation, 'PUI'). The primary endpoint was in-hospital mortality; secondary endpoints included length of stay (LOS), diagnostic studies performed, time to emergent decompressive craniectomies (DCHC), ventilator management, and end-of-life care. We included 394 patients and found the overall number of admissions for SABI declined by 29 % during COVID (pre-COVID n = 231 vs COVID, n = 163). Our primary outcome of mortality and most secondary outcomes were similar between study periods. There were more frequent extubation attempts (72.1 % vs 76 %) and the mean time to extubation was shorter during COVID (55.5 h vs 38.2 h). The ICU LOS (6.10 days vs 4.69 days) and hospital LOS (15.32 days vs 11.74 days) was shorter during COVID. More PUIs died than non-PUIs (51.7 % vs 11.2 %), but when adjusted for markers of illness severity, this was not significant. We demonstrate the ability to maintain a consistent care delivery for patients with SABI during the pandemic at our institution. PUIs represent a population with higher illness severity at risk for delays in care. Multicenter, longitudinal studies are needed to explore the impact of the pandemic on patients with acute neurological emergencies.


Subject(s)
Brain Injuries , COVID-19 , Adult , Humans , COVID-19/epidemiology , Emergencies , Pandemics , Critical Illness , Intensive Care Units , Retrospective Studies
10.
Brain ; 145(11): 3738-3740, 2022 11 21.
Article in English | MEDLINE | ID: covidwho-2051321
11.
psyarxiv; 2022.
Preprint in English | PREPRINT-PSYARXIV | ID: ppzbmed-10.31234.osf.io.bgrc7

ABSTRACT

Intolerance of uncertainty (IU) is a risk factor for poor mental health. Acquired brain injury (ABI), such as stroke or traumatic brain injury, often brings considerable uncertainty. This is the first of a two-part investigation of the psychometric properties of the Intolerance of Uncertainty Scale-12 (IUS-12) in ABI. Here, we evaluate its internal consistency and factor structure in 176 adults with ABI. A two-factor structure (Prospective Anxiety and Inhibitory Anxiety) was superior to a one-factor model. However, some fit statistics were unacceptable. In an exploratory factor analysis, a new two-factor model emerged with a superior fit. A bifactor model provided even better fit, though the sample size precluded exhaustive evaluation. For now, retaining the original Prospective Anxiety and Inhibitory Anxiety subscales is recommended for ABI. IUS-12 scores did not differ pre- or during COVID-19 assessment, suggesting the IUS-12 is measuring individual differences regardless of uncertainty levels.


Subject(s)
Stroke , COVID-19 , Brain Diseases , Brain Injuries , Anxiety Disorders
12.
Cardiovasc Hematol Agents Med Chem ; 20(3): 178-188, 2022.
Article in English | MEDLINE | ID: covidwho-2039581

ABSTRACT

The post-COVID neurological syndrome has been coined, which describes the functional and structural sequelae of coronavirus infection disease-19 (COVID-19) in the brain. Mild/severe manifestations of the post-COVID neurological syndrome have been identified in approximately 33.00% of COVID-19 survivors. The presence of neurological complications after COVID allowed neuropathologists to investigate in-depth the role of viral infection in neurons. The pathophysiology of the post-COVID neurological syndrome involved the development of a systematic response, including coagulopathy characterized by the formation of microthrombi. Coagulopathy, an old term for a new disease, describes the discrepancy between pro-coagulant and anticoagulant systems due to overexpression of pro-coagulant substances and or their receptors in addition to suppression of the anticoagulant molecules and or their receptors. Vascular endothelial cells and hepatocytes play a central role in the regulation of hemostasis that is disrupted during the acute phase response (APR) of coronavirus-19 (COVID-19). Currently, coagulopathy and inflammation are termed together since both form a complementary system, indicated by the elevation of inflammatory biomarkers (APR) and fibrinolysis biomarkers (D-dimer/fibrin). The later events of the post-COVID neurological syndrome are primarily induced by coagulopathy and direct viral tropism. Therefore, the paper introduces the hypothesis of coagulopathy induced post-COVID neurological syndrome.


Subject(s)
Blood Coagulation Disorders , Brain Injuries , COVID-19 , Anticoagulants , Biomarkers , Blood Coagulation Disorders/etiology , Brain Injuries/complications , COVID-19/complications , Endothelial Cells , Humans , SARS-CoV-2 , Post-Acute COVID-19 Syndrome
13.
Brain ; 145(11): 4097-4107, 2022 11 21.
Article in English | MEDLINE | ID: covidwho-2017743

ABSTRACT

COVID-19 is associated with neurological complications including stroke, delirium and encephalitis. Furthermore, a post-viral syndrome dominated by neuropsychiatric symptoms is common, and is seemingly unrelated to COVID-19 severity. The true frequency and underlying mechanisms of neurological injury are unknown, but exaggerated host inflammatory responses appear to be a key driver of COVID-19 severity. We investigated the dynamics of, and relationship between, serum markers of brain injury [neurofilament light (NfL), glial fibrillary acidic protein (GFAP) and total tau] and markers of dysregulated host response (autoantibody production and cytokine profiles) in 175 patients admitted with COVID-19 and 45 patients with influenza. During hospitalization, sera from patients with COVID-19 demonstrated elevations of NfL and GFAP in a severity-dependent manner, with evidence of ongoing active brain injury at follow-up 4 months later. These biomarkers were associated with elevations of pro-inflammatory cytokines and the presence of autoantibodies to a large number of different antigens. Autoantibodies were commonly seen against lung surfactant proteins but also brain proteins such as myelin associated glycoprotein. Commensurate findings were seen in the influenza cohort. A distinct process characterized by elevation of serum total tau was seen in patients at follow-up, which appeared to be independent of initial disease severity and was not associated with dysregulated immune responses unlike NfL and GFAP. These results demonstrate that brain injury is a common consequence of both COVID-19 and influenza, and is therefore likely to be a feature of severe viral infection more broadly. The brain injury occurs in the context of dysregulation of both innate and adaptive immune responses, with no single pathogenic mechanism clearly responsible.


Subject(s)
Brain Injuries , COVID-19 , Influenza, Human , Humans , Neurofilament Proteins , COVID-19/complications , Biomarkers , Autoantibodies , Immunity
14.
Eur J Med Res ; 27(1): 150, 2022 Aug 13.
Article in English | MEDLINE | ID: covidwho-2002233

ABSTRACT

A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury.


Subject(s)
Acute Lung Injury , Brain Injuries , Respiratory Distress Syndrome , Acute Lung Injury/etiology , Brain , Brain Injuries/complications , Humans , Lung , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , Tidal Volume
15.
J Head Trauma Rehabil ; 37(3): 131-133, 2022.
Article in English | MEDLINE | ID: covidwho-1967918
16.
Int J Psychophysiol ; 172: 17-23, 2022 02.
Article in English | MEDLINE | ID: covidwho-1956176

ABSTRACT

Cognitive deficits in infants born preterm and infants at term with risk factors for brain damage are a common outcome. Attention deficits in preterm infants are related to the development of attention-deficit/hyperactivity disorder (ADHD), and therefore, there is a need for earlier evaluations and treatment procedures that are implemented before the presence of signs of ADHD. METHODS: We studied preterm (74%) and term infants with the Infant Scale of Selective Attention (ISSA, Escala de Evaluación de la Atención Selectiva (EEAS), in Spanish). This scale evaluates both visual- and auditory-orienting attention. Two groups participated, one with attention deficits (n = 26) and another with regular performance (n = 36). An early attention-stimulation program (EASP) was implemented in the infant group with attention deficits from three to eight months of age. All infants underwent magnetic resonance imaging (MRI), and visual and auditory evoked responses were assessed. RESULTS: All infants had prenatal and perinatal risk factors for brain damage and abnormal MRI findings, and the majority had abnormalities compatible with white matter injury. However, there were four infants with porencephalic cysts; 3 of them were in the treated group. At the beginning of the treatment, ISSA values showed differences between groups. These differences persisted for five months in the visual test and up to the sixth month in the auditory evaluation. Afterward, there were no significant differences, indicating that infants with attention deficits had satisfactorily responded to the treatment. CONCLUSIONS: The ISSA is helpful for the early evaluation of visual and auditory attention. Infants with attention deficits react well enough after six months of EASP.


Subject(s)
Attention Deficit Disorder with Hyperactivity , Brain Injuries , Attention Deficit Disorder with Hyperactivity/diagnosis , Attention Deficit Disorder with Hyperactivity/pathology , Attention Deficit Disorder with Hyperactivity/therapy , Brain/diagnostic imaging , Brain/pathology , Brain Injuries/pathology , Humans , Infant , Infant, Newborn , Infant, Premature/physiology , Magnetic Resonance Imaging/methods , Risk Factors
17.
Sci Transl Med ; 14(652): eabj4310, 2022 07 06.
Article in English | MEDLINE | ID: covidwho-1949948

ABSTRACT

Inflammatory processes induced by brain injury are important for recovery; however, when uncontrolled, inflammation can be deleterious, likely explaining why most anti-inflammatory treatments have failed to improve neurological outcomes after brain injury in clinical trials. In the thalamus, chronic activation of glial cells, a proxy of inflammation, has been suggested as an indicator of increased seizure risk and cognitive deficits that develop after cortical injury. Furthermore, lesions in the thalamus, more than other brain regions, have been reported in patients with viral infections associated with neurological deficits, such as SARS-CoV-2. However, the extent to which thalamic inflammation is a driver or by-product of neurological deficits remains unknown. Here, we found that thalamic inflammation in mice was sufficient to phenocopy the cellular and circuit hyperexcitability, enhanced seizure risk, and disruptions in cortical rhythms that develop after cortical injury. In our model, down-regulation of the GABA transporter GAT-3 in thalamic astrocytes mediated this neurological dysfunction. In addition, GAT-3 was decreased in regions of thalamic reactive astrocytes in mouse models of cortical injury. Enhancing GAT-3 in thalamic astrocytes prevented seizure risk, restored cortical states, and was protective against severe chemoconvulsant-induced seizures and mortality in a mouse model of traumatic brain injury, emphasizing the potential of therapeutically targeting this pathway. Together, our results identified a potential therapeutic target for reducing negative outcomes after brain injury.


Subject(s)
Brain Injuries , COVID-19 , Animals , Astrocytes/metabolism , Disease Models, Animal , GABA Plasma Membrane Transport Proteins/metabolism , Inflammation/pathology , Mice , Polymers , Rodentia/metabolism , SARS-CoV-2 , Seizures , Thalamus/metabolism , Thalamus/pathology
18.
J Neurol Sci ; 439: 120324, 2022 08 15.
Article in English | MEDLINE | ID: covidwho-1895239

ABSTRACT

OBJECTIVE: Neurological symptoms (NS) were often reported in COVID-19 infection. We examined the plasma levels of glial fibrillary acidic protein (GFAP) and S100B together, as brain injury biomarkers, in relation to persistent NS in a cohort of patients with COVID-19 during the acute phase of the disease. METHODS: A total of 20 healthy controls and 58 patients with confirmed COVID-19 were enrolled in this prospective study. Serum GFAP and S100B levels were measured by using enzymle linked immunoassay method from blood samples. RESULTS: Serum GFAP levels were found to be significantly higher in the severe group than in the controls (p = 0.007). However, serum S100B levels were similar between control and disease groups (p > 0.05). No significant results for GFAP and S100B were obtained between the disease groups depending on whether the sampling time was below or above 5 days (p > 0.05). We did not find a correlation between serum GFAP and S100B levels and the presence of NS (p > 0.05). However, serum S100B levels were slightly higher in patients with multiple NS than in those with a single symptom (p = 0.044). CONCLUSIONS: Elevated GFAP was associated with disease severity but not with NS in COVID-19 patients. Whereas, high serum S100B was associated with the multipl NS in these patients. Our data suggest that GFAP and S100B may be of limited value currently in order to represent the neuronal damage, though serving a basis for the future work.


Subject(s)
Brain Injuries , COVID-19 , Biomarkers , COVID-19/complications , Glial Fibrillary Acidic Protein/metabolism , Humans , Prospective Studies , S100 Calcium Binding Protein beta Subunit
19.
Childs Nerv Syst ; 38(9): 1727-1734, 2022 09.
Article in English | MEDLINE | ID: covidwho-1888856

ABSTRACT

PURPOSE: To evaluate change in the severity of hypoxic-ischemic encephalopathy (HIE) and associated morbidities between pre- and during COVID-19 pandemic periods in Canada. METHODS: We conducted a retrospective cohort study extracting the data from level-3 NICUs participating in Canadian Neonatal Network (CNN). The primary outcome was a composite of death in the first week after birth and/or stage 3 HIE (Sarnat and Sarnat). Secondary outcomes included rate and severity of HIE among admitted neonates, overall mortality, brain injury on magnetic resonance imaging (MRI), neonates requiring resuscitation, organ dysfunction, and therapeutic hypothermia (TH) usage. We included 1591 neonates with gestational age ≥ 36 weeks with HIE during the specified periods: pandemic cohort from April 1st to December 31st of 2020; pre-pandemic cohort between April 1st and December 31st of 2017, 2018, and 2019. We calculated the odds ratio (OR) and confidence intervals (CI). RESULTS: We observed no significant difference in the primary outcome (15% vs. 16%; OR 1.08; 95%CI 0.78-1.48), mortality in the first week after birth (6% vs. 6%; OR 1.10, 95%CI 0.69-1.75), neonates requiring resuscitation, organ dysfunction, TH usage, or rate of brain injury. In the ad hoc analysis, per 1000 live births, there was an increase in the rate of infants with HIE and TH use. CONCLUSIONS: Severity of HIE, associated morbidities, and mortality were not significantly different during the pandemic lockdown compared to a pre-pandemic period in Canada. Anticipated risks and difficulties in accessing healthcare have not increased the mortality and morbidities in neonates with HIE in Canada.


Subject(s)
Brain Injuries , COVID-19 , Hypothermia, Induced , Hypoxia-Ischemia, Brain , Brain Injuries/complications , Canada/epidemiology , Cohort Studies , Communicable Disease Control , Humans , Hypoxia-Ischemia, Brain/epidemiology , Hypoxia-Ischemia, Brain/pathology , Hypoxia-Ischemia, Brain/therapy , Infant , Infant, Newborn , Multiple Organ Failure/complications , Multiple Organ Failure/therapy , Pandemics , Retrospective Studies
20.
researchsquare; 2022.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-1749644.v1

ABSTRACT

Background: The relearning of movements after brain injury can be optimized by providing intensive, meaningful, and motivating training using virtual reality (VR). However, most current solutions use two-dimensional (2D) screens, where patients interact via symbolic representations of their limbs (e.g., a cursor). These 2D screens lack depth cues, potentially deteriorating movement quality and increasing cognitive load. Head-mounted displays (HMDs) have great potential to provide naturalistic movement visualization by incorporating improved depth cues, reduce visuospatial transformations by rendering movements in the space where they are performed, and preserve eye-hand coordination by showing an avatar – with immersive VR (IVR) – or the user’s real body – with augmented reality (AR). However, elderly populations might not find these novel technologies usable, hampering potential motor and cognitive benefits. Methods: : We compared movement quality, cognitive load, motivation and system usability in twenty elderly participants (>59 y.o.) while performing a dual motor-cognitive task with different visualization technologies: IVR HMD, AR HMD, and a 2D screen. We evaluated participants’ self-reported cognitive load, motivation, and usability using questionnaires. We also conducted a pilot study with five brain-injured patients comparing the visualization technologies while using an assistive device. Results: : Elderly participants performed straighter, shorter duration, and smoother movements when the task was visualized with the HMDs than screen. The IVR HMD led to shorter duration movements than AR, and both HMDs were associated with shorter movement duration than the screen. Movement onsets were shorter with IVR than AR, and shorter for both HMDs than the screen, potentially indicating facilitated reaction times due to reduced cognitive load. No differences were found in the questionnaires regarding cognitive load, motivation, or usability between technologies in elderly participants. Both HMDs proved high usability in our small sample of patients. Conclusions: : HMDs are a promising technology to be incorporated into neurorehabilitation, as their more naturalistic movement visualization improves movement quality compared to conventional screens. HMDs demonstrate high usability, without decreasing participants’ motivation, and might potentially lower cognitive load. Our preliminary clinical results suggest that brain-injured patients may especially benefit from more immersive technologies. However, larger patient samples are needed to draw stronger conclusions.


Subject(s)
Brain Injuries , Movement Disorders
SELECTION OF CITATIONS
SEARCH DETAIL