Syfte: Att beskriva arbetsterapeutiska interventioner och deras effekter för vuxna personer med kognitiva nedsättningar efter stroke. Metod: Författarna använde en graderande sammanställning av kvantitativ forskning som metod, vilket resulterade i tio studier. Datainsamling utfördes genom systematisk sökning i databaserna CINAHL med full text och PubMed. Data analyserades, interventionerna beskrevs och kategoriserades i fyra underrubriker baserade på Occupational Therapy Intervention Process Model´s (OTIPM) interventionsmodeller; modell för kompensation, modell för utbildning och undervisning, modell för att förvärva färdigheter i aktivitet, samt återställsmodell för förbättring av kroppsfunktioner och andra klientkomponenter. Vidare beskrevs effekten av de olika interventionerna. Resultat: Åtta av de inkluderade studierna hade statistiskt signifikant effekt på olika kognitiva funktioner. Resultatet visar att det bland annat används datorbaserade interventioner, dual-task training, The Cognitive Orientation to Daily Occupational Performance och kombinerade interventioner vid kognitiv nedsättning efter stroke. Interventioner inom återställsmodell för förbättring av kroppsfunktioner och andra klientkomponenter var mest förekommande. Efterföljande var modell för att förvärva färdigheter i aktivitet och modell för kompensation. Majoriteten av interventionerna utgick från ett bottom-up förhållningssätt. Interventioner utfördes inom öppen vård samt i sjukhusmiljö, både under akut, subakut och kronisk fas efter stroke. Slutsats: Det finns flera olika typer av arbetsterapeutiska interventioner för personer med kognitiva nedsättningar efter stroke. Resultatet visar att interventionerna har god effekt för olika kognitiva funktioner och aktivitetsutförande. Återställning och förbättring av kroppsfunktioner eller andra klientkomponenter är oftast det huvudsakliga syftet med interventionen. Behov av vidare forskning finns, både nationellt och internationellt, för att säkerställa effekten av arbetsterapeutiska interventioner för personer med kognitiva nedsättningar efter stroke. / Aim: To describe occupational therapy interventions and their effects for adults with cognitive impairments post-stroke. Method: The authors used a graded compilation of quantitative research as a method, resulting in ten studies. Data was collected through a systematic search of the databases CINAHL with full text and PubMed. Data were analyzed, the interventions were described and categorized into four subheadings based on the Occupational Therapy Intervention Process Model´s (OTIPM) intervention models; compensatory model, education and teaching model, acquisitional model for occupational skills training and restorative model for enhancing body functions and other client elements. Furthermore, the effects of the various interventions were described. Result: Eight of the included studies had a statistically significant effect on various cognitive functions. The result shows that computer-based interventions, dual-task training, The Cognitive Orientation to Daily Occupational Performance and combined interventions are often used in cognitive impairment post-stroke. Interventions within the restorative model for enhancing body functions and other client elements, were most prevalent. Following was the acquisitional model for occupational skills training and compensatory model. The majority of interventions were based on a bottom-up approach. Interventions were carried out in outpatient care, as well as  hospital environment, both during the acute, subacute and chronic phase post-stroke. Conclusion: There are several different types of occupational therapy interventions for people with cognitive impairments post-stroke. The result showed effects for various cognitive functions and occupational performance. Restoring and developing body functions or other client elements is usually the main purpose. There is a need for further research, both nationally and internationally to ensure the effects of occupational therapy interventions for persons with cognitive impairments post-stroke.

Introdução: Muitos pacientes acometidos por acidente vascular cerebral (AVC) sofrem sequelas motoras e cognitivas permanentes, as quais promovem maior risco de quedas que constitui a complicação mais frequente nesse grupo de pacientes. Dessa forma, a identificação dos fatores que predispõem a quedas em pacientes após AVC se faz necessária para a elaboração de estratégias de prevenção dos fatores modificáveis a fim de evitar suas consequências, melhorar prognóstico funcional, expectativa e qualidade de vida desta enorme população. Objetivos: O objetivo primário deste estudo foi analisar os fatores preditivos de quedas em uma amostra de pacientes acometidos por AVC atendidos em um hospital de referência de Ribeirão Preto e incluídos no Registro de AVC de Ribeirão Preto (REAVER), no período de seis meses após o AVC. Os objetivos secundários foram analisar a frequência relativa de quedas nos 6 primeiro meses após o AVC; analisar as características da ocorrência de quedas ocorridas nos 6 primeiros meses após o AVC; analisar as características clínicas, funcionais e processos de reabilitação em pacientes caidores e não-caidores da amostra estudada. Metodologia: Foram incluídos todos os pacientes com diagnóstico de AVC isquêmico ou hemorrágico internados na Unidade de Emergência do HCFMRP-USP no período de setembro de 2015 a março de 2016 com Escala de Rankin modificado prévia menor que 1. De forma retrospectiva, foram coletadas variáveis do REAVER referentes aos dados pessoais, doenças associadas, déficits neurológicos, funcionalidade, estado cognitivo e reabilitação. De forma prospectiva após 6 meses do AVC, coletamos por meio de contato telefônico informações sobre uso de medicações que afetam o sistema nervoso central, presença de parkinsonismo, demência após AVC, sintomas de tontura e desequilíbrio, déficit visual, além da ocorrência, número, local e circunstâncias em que as quedas ocorreram neste período. Resultados: Foram investigados 304 e incluídos 129 pacientes no estudo, com uma prevalência de 31 quedas que ocorreram em 24% da amostra. Os locais mais frequentes de queda foram nas proximidades do quarto do paciente no período de maior atividade (manhã e tarde). A maior parte das quedas ocorreram entre 3 a 6 meses após o evento. As principais atividades envolvidas foram a deambulação e transferências. Encontramos associação positiva entre ocorrência de quedas e os seguintes fatores: déficit visual antes do AVC (p=0,02), síndrome demencial após AVC (p=0,01), uso de inibidores da acetilcolinesterase (p=0,01), parkinsonismo (p =0,01), sintomas de tontura e desequilíbrio após o AVC (p<0,001) e Escala Modificada de Rankin em 3 meses após o AVC (p=0,007). A análise de regressão logística evidenciou que a presença de desequilíbrio postural ou tonturas são fatores preditivos independentes para quedas na amostra estudada. Conclusões: As quedas são um problema frequente em pacientes que sofreram AVC e sua ocorrência é maior nos períodos de atividade do paciente e em atividades simples como deambulação e transferências. Alterações do equilíbrio postural consolida-se como fator preditivo independente de quedas após o AVC / Introduction: Many patients affected by stroke suffer from permanent motor and cognitive deficits, which lead to greater risk of falls that constitutes the most frequent complication in this group of patients. Thus, the identification of the factors that predict falls in patients after stroke is necessary for the elaboration of prevention strategies to avoid falls\' consequences, increasing functional prognosis, expectancy and quality of life in this huge population. Objectives: The primary goal of the study was to analyze the fall predictor factors in a sample of stroke patients included in the Stroke Register of Ribeirão Preto (REAVER) in a period of six months after stroke. The secondary goals were to analyze the relative frequency of falls in the first six months after stroke; to analyze the characteristics of fall occurrence in the first six months after stroke; to investigate the rehabilitation processes, clinical and functional characteristics in faller and non-faller patients in this sample. Methodology: We included all stroke patients with ischemic and hemorrhagic strokes admitted to the Emergency U nit of the HCFMRP-USP, between 2015 September and 2016 March, with previous Modified Rankin Scale (mRS) less than 1. We did a retrospective collection of data from REAVER related to personal data, concomitant diseases, neurologic deficits, functionality, cognitive assessment, and rehabilitation. After six months of the stroke ictus, we did a prospective investigation by phone regarding the use of medications that affect central nervous system, parkinsonism and dementia before stroke, vertigo, imbalance, and visual deficit after stroke, in addition to the occurrence, number, location and circumstances of falls in six months period after stroke. Results: We investigated 304 patients and 129 were included in the study, with a prevalence of 31 falls that occurred in 24% of the study sample. The most frequent locations of falls were next to the patient\'s bedroom and in the period of more activity (morning and afternoon). Most of the falls occurred between 3 to 6 months after the stroke. The main activities related to the falls were gait and transfer. We found positive association between the occurrence of falls and the following factors: visual deficits before stroke (p=0,02), dementia after stroke (p=0,01), use of acetylcholinesterase inhibitors (p=0,01), parkinsonism (p=0,01), vertigo and imbalance after stroke (p<0,001) and mRS 3 months after stroke (p=0,007). The logistic regression analysis showed that vertigo and imbalance are independent predictive factors for falls in this study. Conclusions: Falls are frequent after stroke. Their occurrence is greater in the periods of more activity and in simple activities like gait and transfer. Disturbance of postural balance is consolidated as an independent risk factor for falls

One of the most common risk factors for stroke is diabetes. Diabetics are 2 to 4 times more likely to have a stroke and are also significantly more likely to show poor functional recovery. In order to determine why diabetes is associated with poor stroke recovery, we tested the hypotheses that diabetes either exacerbates initial stroke damage, or inhibits neuronal circuit plasticity in surviving brain regions that is crucial for successful recovery. Type 1 diabetes was chemically induced in mice four weeks before receiving a targeted photothrombotic stroke in the right forelimb somatosensory cortex to model a chronic diabetic condition. Following stroke, a subset of diabetic mice were treated with insulin to determine if controlling blood glucose levels could improve stroke recovery. Consistent with previous studies, one behavioural test revealed a progressive improvement in sensory function of the forepaw in non-diabetic mice after stroke. By contrast, diabetic mice treated with and without insulin showed persistent deficits in sensori-motor forepaw function. To determine whether these different patterns of stroke recovery correlated with changes in functional brain activation, forepaw evoked responses in the somatosensory cortex were imaged using voltage sensitive dyes at 1 and 14 weeks after stroke. In both diabetic and non-diabetic mice that did not have a stroke, brief mechanical stimulation of the forepaw evoked a robust and near simultaneous depolarization in the primary (FLS1) and secondary somatosensory (FLS2) cortex. One week after stroke, forepaw-evoked responses had not been remapped in the peri-infarct cortex in both diabetic and non-diabetic mice. Fourteen weeks after stroke, forepaw evoked responses in non-diabetic mice re-emerged in the peri-infarct cortex whereas diabetic mice showed very little activation, reminiscent of the 1 week recovery group. Moreover, controlling hyperglycemia using insulin therapy failed to restore sensory evoked responses in the peri-infarct cortex. In addition to these differences in peri-infarct responsiveness, we discovered that stroke was associated with increased responsiveness in FLS2 of non-diabetic, but not diabetic or insulin treated mice. To determine the importance of FLS2 in stroke recovery, we silenced the FLS2 cortex and found that it re-instated behavioural impairments in stroke recovered mice, significantly more so than naïve mice that still had a functioning FLS1. Collectively, these results indicate that both diabetes and the secondary somatosensory cortex play an important role in determining the extent of functional recovery after ischemic cortical stroke. Furthermore, the fact that insulin therapy after stroke did not normalize functional recovery, suggests that prolonged hyperglycemia (before stroke) may induce pathological changes in the brain’s circulation or nervous system that cannot be easily reversed. / Graduate

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / In ischemic stroke, damage to the brain is caused by a reduction or complete blockage of blood flow to parts of the brain, resulting in glucose and oxygen deficiency. It is a leading cause of mortality and disability particularly in the elderly. The majority of strokes are not fatal and survivors are at a high risk of subsequent vascular complications and new vascular accidents. Hypertension is the most important risk factor in strokes, being that it is present in 70% of all cases. Oxidative stress is believed to be one of the mechanisms taking part in neuronal damage in stroke. The key role the cholinergic system plays in normal brain functions and in memory disturbances of several pathological processes, such as in cerebral blood flow regulation, has been well documented. This study investigated the oxidative status and acetylcholinesterase (AChE) activity in whole blood in patients diagnosed with the acute and chronic stage of ischemia, as well as with hypertension. We determined the catalase activity in the blood, reduced glutathione (GSH) in erythrocytes, and TBARS and protein carbonyl content from serum samples. The oxidative profile of lipids and proteins represented by MDA levels and protein carbonylation content, respectively, showed increased levels both in the acute ischemic group and in the hypertensive group, when compared to the control. Catalase activity and GSH levels in the acute group also were higher than in the hypertensive and control groups. No difference was found between the catalase activity of the chronic ischemic group and the hypertensive group (p< 0.05). The activity of AChE in acute ischemic patients was significantly higher than that presented by the control, hypertensive and chronic ischemic patients (p<0.05). No significant difference was observed between the chronic and control groups. The hypertensive group presented AChE activity significantly lower than the other groups. The results suggest increased antioxidant defense as a compensatory mechanism in consequence of the overproduction of reactive oxygen species (ROS) after acute stroke. This sudy also demonstrated that hypertension, in and of itself, acts as a prevalent risk factor of stroke, contributing to oxidative cellular damage. Futhermore, the results revealed that ischemia exerted a modulator effect on AChE activity in erythrocytes, in an attempt to maintain adequate levels of the neurotransmitter acetylcholine (ACh), as a response to the differents phases following neurological injury caused by ischemia. The ischemic event, in spite of having a defined location, results in a systemic disorder that induces changes, which can be detect by mesuring the peripheral markers of oxidative stress and AChE activity in erytrocytes. / No acidente vascular isquêmico, o dano ao encéfalo é causado por uma redução ou um bloqueio completo do fluxo sangüíneo resultando em liberação deficiente de glicose e oxigênio. É uma das principais causas de mortalidade e incapacitação entre os idosos. Em sua maioria não são fatais e os sobreviventes têm alto risco de complicações vasculares subseqüentes. A hipertensão é o mais importante fator de risco para o acidente vascular cerebral, presente em 70% de todos os casos. Acredita-se que o estresse oxidativo é um dos mecanismos associados ao dano neuronal após o evento isquêmico. O papel chave que o sistema colinérgico desempenha nas funções normais do encéfalo e distúrbios de memória de vários processos patológicos assim como no controle do fluxo sanguíneo cerebral vem sendo bem documentado. Este trabalho investigou o perfil oxidativo e a atividade da enzima acetilcolinesterase sangüínea em pacientes com diagnóstico de acidente vascular cerebral isquêmico, na fase aguda e crônica assim como a influência da hipertensão em tal patologia. Determinou-se a atividade da catalase em sangue total, os níveis de glutationa reduzida em eritrócitos, TBARS e o conteúdo de proteína carbonil em amostras de soro da população estudada. O perfil oxidativo de lipídeos e proteínas, representado pelos níveis de MDA e conteúdo de proteína carbonil mostrou-se aumentado na fase aguda do evento isquêmico e no grupo hipertenso quando comparado com o controle. A atividade da catalase e os níveis de glutationa reduzida nos pacientes pertencentes ao estágio agudo encontraram-se aumentadas em relação aos grupos hipertenso e controle. Nenhuma diferença na atividade da catalase foi encontrada entre pacientes do estágio crônico da isquemia carebral e aqueles do grupo hipertenso (p<0,05). A atividade da AChE sangüínea durante a fase aguda do acidente vascular isquêmico foi aumentada em relação àquela apresentada pelos grupos controle, hipertenso e crônico (p< 0,05). Também, nenhuma diferença foi observada entre o grupo crônico e o controle. O grupo hipertenso apresentou atividade da AChE significativamente menor que os outros grupos. Os resultados sugerem que o aumento da defesa antioxidante age como um mecanismo compensatório como consequência da superprodução de espécies reativas de oxigênio (EROs) após o evento isquêmico agudo. Este estudo também demonstrou que a hipertensão atua como um fator de risco prevalente para o acidente vascular isquêmico, contribuindo para o dano oxidativo celular. Os resultados também revelaram que a isquemia exerce efeito modulador na atividade da AChE em eritrócitos, a fim de manter adequados níveis do neurotransmissor acetilcolina (ACh) em resposta as diferentes fases da injúria neurológica causada pela isquemia. Conclui-se então que o evento isquêmico, apesar de ter localização definida, resulta em uma desordem sistêmica, induzindo mudanças, as quais podem ser detectadas pela medida de marcadores periféricos do estresse oxidativo e atividade da AChE sangüínea.

Background: Recent studies showed that the safety and benefit of early intravenous (IV) thrombolysis on favourable outcomes in acute ischemic stroke are also seen in the elderly. Furthermore, it has shown that age increases times for pre- and in-hospital procedures. We aimed to assess the applicability of these findings to telestroke. Methods: We retrospectively analysed 542 of 1659 screened consecutive stroke patients treated with IV thrombolysis in our telestroke network in East-Saxony, Germany from 2007 to 2012. Outcome data were symptomatic intracranial hemorrhage (sICH) by ECASS-2-criteria, survival at discharge and favourable outcome, defined as a modified Rankin scale (mRS) of 0–2 at discharge. Results: Thirty-three percent of patients were older than 80 years (elderly). Being elderly was associated with higher risk of sICH (p¼0.003), less favourable outcomes (p¼0.02) and higher mortality (p¼0.01). Using logistic regression analysis, earlier onsetto-treatment time was associated with favourable outcomes in not elderly patients (adjusted odds ratio (OR) 1.18; 95% CI 1.03–1.34; p¼0.01), and tended to be associated with favourable outcomes (adjusted OR 1.13; 95% CI 0.92–1.38; p¼0.25) and less sICH (adjusted OR 0.88; 95% CI 0.76–1.03; p¼0.11) in elderly patients. Age caused no significant differences in onset-to-doortime (p¼0.25), door-to-treatment-time (p¼0.06) or onset-to-treatment-time (p¼0.29). Conclusion: Treatment time seems to be critical for favourable outcome after acute ischemic stroke in the elderly. Age is not associated with longer delivery times for thrombolysis in telestroke.

In a stroke-certified 500-bed acute care hospital, the 30-day readmission rates for patients discharged to rehabilitation centers or skilled nursing facilities were higher than the rates for patients discharged to home. A review of data by the stroke team showed 44 patients readmitted within 30 days of initial stroke discharge between October 2016 and January 2017. The rate of re-admission for those discharged home was 41% (18 patients), whereas the rate for those discharged to acute inpatient rehabilitation, long-term acute care, or skilled nursing facilities was 59% (26 patients). The practice-focused question for this project assessed whether using a re-admission risk-assessment tool and implementing interventions during the initial acute-care admission, would help to identify and improve risk for 30-day re-admissions for patients diagnosed with stroke. The goal of this research project was to adopt, test, and recommend the implementation of a readmission risk assessment tool to enable discharge planners to identify stroke patients at risk for readmission and implement interventions to help reduce this risk. Lewin’s theory of change was used to inform the project. A stroke re-admission risk-assessment tool in use at a similar hospital was adopted and tested for 1 week on the hospital’s 28-bed stroke unit by nurse case managers. The test was conducted among 5 patients with confirmed diagnosis of stroke. A re-admission data review was performed 30 days after their discharge, which showed no readmissions for the 5 patients involved in the trial. The tool helped to improve case manager awareness of increased risk for readmissions, guide interventions, and improve patient transition and outcomes. The implications of this project for positive change include the potential to improve risk for patients with stroke in the acute-care facility.

Background: While intravenous thrombolysis (IVT) in ischemic stroke can be safely applied in telestroke networks within 3 h from symptom onset, there is a lack of evidence for safety in the expanded 3- to 4. 5-h time window. We assessed the safety and short-term efficacy of IVT in acute ischemic stroke (AIS) in the expanded time window delivered through a hub-and-spoke telestroke network. Methods: Observational study of patients with AIS who received IVT at the Stroke Eastern Saxony Telemedical Network between 01/2014 and 12/2015. We compared safety data including symptomatic intracerebral hemorrhage (sICH; according to European Cooperative Acute Stroke Study II definition) and any intracerebral hemorrhage (ICH) between patients admitted to telestroke spoke sites and patients directly admitted to a tertiary stroke center representing the hub of the network. We also assessed short-term efficacy data including favorable functional outcome (i.e., modified Rankin Scale ≤ 2) and National Institutes of Health Stroke Scale (NIHSS) at discharge, hospital discharge disposition, and in-hospital mortality. Results: In total, 152 patients with AIS were treated with IVT in the expanded time window [spoke sites, n = 104 (26.9%); hub site, n = 48 (25.9%)]. Patients treated at spoke sites had less frequently a large vessel occlusion [8/104 (7.7) vs. 20/48 (41.7%); p < 0.0001], a determined stroke etiology (p < 0.0001) and had slightly shorter onset-to-treatment times [210 (45) vs. 228 (58) min; p = 0.02] than patients who presented to the hub site. Both cohorts did not display any further differences in demographics, vascular risk factors, median baseline NIHSS scores, or median baseline Alberta stroke program early CT score (p > 0.05). There was no difference in the frequency of sICH (4.9 vs. 6.3%; p = 0.71) or any ICH (8.7 vs. 16.7%; p = 0.15). Neither there was a difference regarding favorable functional outcome (44.1 vs. 39.6%; p = 0.6) nor median NIHSS [3 (5.5) vs. 2.5 (5.75); p = 0.92] at discharge, hospital discharge disposition (p = 0.28), or in-hospital mortality (9.6 vs. 8.3%; p = 1.0). Multivariable modeling did not reveal an association between telestroke and sICH or favorable functional outcome (p > 0.05). Conclusions: Delivery of IVT in the expanded 3- to 4.5-h time window through a telestroke network appears to be safe with equivalent short-term functional outcomes for spoke-and-hub center admissions.

Sickle cell disease is a genetic disorder that affects 100,000 Americans and millions more worldwide. Although the sickle mutation affects one protein, which is only expressed in a single cell type, it has profound detrimental effects on nearly every organ system in the body. Young children with sickle cell disease have an 11\% chance of suffering a major stroke event by the age of 16, and a 35\% chance of developing ÒsilentÓ strokes that often result in significant learning and mental disabilities. Clinical investigations suggest that stroke development in people with sickle cell disease results from luminal narrowing of the carotid and cerebral arteries due to excess matrix deposition and fragmentation of the elastic lamina; however, the underlying cellular mechanisms that initiate arterial remodeling in sickle cell disease remain relatively unknown. Cathepsins K and V are members of the cysteine family of proteases and represent two of the most potent elastases yet identified in humans. Furthermore, the role of Cathepsins has been well established in other cardiovascular remodeling diseases, such as atherosclerosis. Due to the compelling histological similarities between vasculopathy in sickle cell disease and atherosclerosis, we tested the hypothesis that the unique inflammatory milieu, in conjunction with the biomechanical vascular environment of sickle cell disease upregulates cathepsin K and V activity in large artery endothelial cells, ultimately leading to arterial remodeling and stroke. Currently, there are few therapeutic options for the prevention of stroke in sickle cell disease; those that do exist carry significant health risks and side effects. Together, this body of work has generated a more mechanistic understanding of how the sickle milieu stimulates the endothelium to initiate arterial remodeling, which has enabled us to identify important pathways (JNK, NF$\kappa$B) downstream of inflammatory and biomechanical stimuli and validate new therapeutic targets within the JNK pathway to establish preclinical proof of efficacy for the prevention of arterial remodeling in sickle cell disease.

BACKGROUND:There is an association between cryptogenic stroke and patent foramen ovale (PFO). The optimal treatment strategy for secondary prevention remains unclear. The purpose of this study was to analyze aggregate data examining the safety and efficacy of transcatheter device closure versus standard medical therapy in patients with PFO and cryptogenic stroke.METHODS:A search of published data identified 3 randomized clinical trials for inclusion. The primary outcome was a composite end-point of death, stroke and transient-ischemic attack (TIA). Pre-defined subgroup analysis was performed with respect to baseline characteristics including age, sex, atrial septal aneurysm and shunt size. Data was synthesized using a random effects model and results presented as hazard ratios (HRs) with 95% confidence intervals (CIs).RESULTS:A cohort of 2,303 patients with a history of cryptogenic stroke and PFO were randomized to device closure (n=1150) and medical therapy (n=1153). Mean follow-up was 2.5years. Transcatheter closure was not superior to medical therapy in the secondary prevention of stroke or TIA in intention-to-treat analysis (HR: 0.66, 95% CI: 0.43 to 1.01 / p=0.056). However, the results were statistically significant using per-protocol analysis (HR: 0.64, 95% CI: 0.41 to 0.98 / p=0.043). Males had significant benefit with device closure (HR: 0.48, 95% CI: 0.24 to 0.96 / p=0.038).CONCLUSIONS:In this meta-analysis, using intention-to-treat analysis, transcatheter device closure of PFO was not superior to standard medical therapy in the secondary prevention of cryptogenic stroke. Transcatheter closure was superior using per-protocol analysis.

Hemianopia is a disorder where a patient loses vision in one half of their visual field, following damage to the post-chiasmal visual pathway. If the hemianopia does not spontaneously resolve within the first few months, the prognosis for recovery is poor, with very few patients recovering vision in the affected area of the visual field. The reasons for this are unclear, although it is likely that both degeneration and plasticity in the visual system have an impact on patient outcome. The goal of this research is to investigate the changes that occur in hemianopia, and how these differ for lesions at different locations in the visual pathway and with differing underlying pathologies. Patients with hemianopia arising from different causes were recruited, including 17 with a hemianopia acquired in adulthood, 9 with congenital hemianopia, and 6 patients with hemianopia due to posterior cortical atrophy (PCA). Structural, functional, and diffusion-weighted MRI data were acquired for each patient, in order to examine changes in the structural and function of the visual pathways. Analyses focused on either atrophy, or plasticity and residual function. Atrophy was assessed in acquired and congenital hemianopia by quantifying transneuronal degeneration in the optic tract, which was present in all patients with long-term lesions. Degeneration was also assessed more generally in PCA, who have substantial loss of white and grey matter in posterior brain regions. Investigation of plasticity and residual function focused on the motion processing area (MT), quantifying the level of functional activity in MT, and assessing whether subcortical pathways from the pulvinar to MT exist in hemianopia. A wide degree of variation existed between patients in the extent to which motion processing was preserved, which had no clear link to lesion location, however was related to the size of the lesion.