Why am I overwhelmed by bright lights? The behavioural mechanisms of post-stroke visual hypersensitivity.

After stroke, patients can experience visual hypersensitivity, an increase in their sensitivity for visual stimuli as compared to their state prior to the stroke. Candidate behavioural mechanisms for these subjective symptoms are atypical bottom-up sensory processing and impaired selective attention, but empirical evidence is currently lacking. In the current study, we aimed to investigate the relationship between post-stroke visual hypersensitivity and sensory thresholds, sensory processing speed, and selective attention using computational modelling of behavioural data. During a whole/partial report task, participants (51 stroke patients, 76 orthopedic patients, and 77 neurotypical adults) had to correctly identify a single target letter that was presented alone (for 17-100 ms) or along a distractor (for 83ms). Performance on this task was used to estimate the sensory threshold, sensory processing speed, and selective attention abilities of each participant. In the stroke population, both on a group and individual level, there was evidence for impaired selective attention and -to a lesser extent- lower sensory thresholds in patients with post-stroke visual hypersensitivity as compared to neurotypical adults, orthopedic patients, or stroke patients without post-stroke sensory hypersensitivity. These results provide a significant advancement in our comprehension of post-stroke visual hypersensitivity and can serve as a catalyst for further investigations into the underlying mechanisms of sensory hypersensitivity after other types of acquired brain injury as well as post-injury hypersensitivity for other sensory modalities.

Sensory hypersensitivity after acquired brain injury: the patient perspective.

PURPOSE: Sensory hypersensitivity is a frequently reported complaint after acquired brain injury (ABI). This study explores patients' perceptions of sensory hypersensitivity following ABI and its impact on everyday life. MATERIALS AND METHODS: Semi-structured interviews were conducted with 18 patients with ABI (stroke, brain tumour, TBI) who reported complaints of sensory hypersensitivity. Interview data were analysed using qualitative thematic analysis. RESULTS: Six themes emerged from the data: (1) definition of sensory hypersensitivity, relating to individual perceptions of sensory hypersensitivity; (2) type of sensory stimuli, relating to the variety of stimuli that patients may be sensitive to; (3) course, relating to changes in sensory hypersensitivity following ABI; (4) fatigue, relating to its association with sensory hypersensitivity; (5) consequences of sensory hypersensitivity, relating to the physical, social and emotional impact of sensory hypersensitivity on patients' lives; and (6) coping strategies, relating to behaviours used to cope with sensory hypersensitivity. CONCLUSIONS: Sensory hypersensitivity can have a major impact on patients' physical well-being, return to work and (social) participation after ABI. Characteristics of sensory hypersensitivity vary between patients with ABI. To develop treatments for sensory hypersensitivity, future studies should focus on cognitive (e.g., filtering information) and psychological factors (e.g., coping) in relation to sensory hypersensitivity.

Sensory hypersensitivity occurs in all types of acquired brain injury (ABI).It is important to ask an ABI patient how sensory hypersensitivity is experienced.It is recommended to investigate the physical (e.g., headache) and emotional (e.g., irritability, anger, frustration) consequences of sensory hypersensitivity and its impact on return to work and social participation.When the patient mentions sensory hypersensitivity, also map cognition (with a focus on attention), fatigue, stress, and coping.

The impact of etiology in lesion-symptom mapping - A direct comparison between tumor and stroke.

INTRODUCTION: Lesion-symptom mapping is a key tool in understanding the relationship between brain structures and behavior. However, the behavioral consequences of lesions from different etiologies may vary because of how they affect brain tissue and how they are distributed. The inclusion of different etiologies would increase the statistical power but has been critically debated. Meanwhile, findings from lesion studies are a valuable resource for clinicians and used across different etiologies. Therefore, the main objective of the present study was to directly compare lesion-symptom maps for memory and language functions from two populations, a tumor versus a stroke population. METHODS: Data from two different studies were combined. Both the brain tumor (N = 196) and stroke (N = 147) patient populations underwent neuropsychological testing and an MRI, pre-operatively for the tumor population and within three months after stroke. For this study, we selected two internationally widely used standardized cognitive tasks, the Rey Auditory Verbal Learning Test and the Verbal Fluency Test. We used a state-of-the-art machine learning-based, multivariate voxel-wise approach to produce lesion-symptom maps for these cognitive tasks for both populations separately and combined. RESULTS: Our lesion-symptom mapping results for the separate patient populations largely followed the expected neuroanatomical pattern based on previous literature. Substantial differences in lesion distribution hindered direct comparison. Still, in brain areas with adequate coverage in both groups, considerable LSM differences between the two populations were present for both memory and fluency tasks. Post-hoc analyses of these locations confirmed that the cognitive consequences of focal brain damage varied between etiologies. CONCLUSION: The differences in the lesion-symptom maps between the stroke and tumor population could partly be explained by differences in lesion volume and topography. Despite these methodological limitations, both the lesion-symptom mapping results and the post-hoc analyses confirmed that etiology matters when investigating the cognitive consequences of lesions with lesion-symptom mapping. Therefore, caution is advised with generalizing lesion-symptom results across etiologies.

The relationship between ischaemic brain lesions and cognitive outcome after aneurysmal subarachnoid haemorrhage.

BACKGROUND: Cerebral ischaemia is thought to be an important determinant of cognitive outcome after aneurysmal subarachnoid haemorrhage (aSAH), but the exact relationship is unclear. We studied the effect of ischaemic brain lesions during clinical course on cognitive outcome 2 months after aSAH. METHODS: We studied 74 consecutive patients admitted to the University Medical Center Utrecht who had MRI post-coiling (3-21 days post-aSAH) and neuropsychological examination at 2 months. An ischaemic lesion was defined as hyperintensity on T2-FLAIR and DWI images. We measured both cognitive complaints (subjective) and cognitive functioning (objective). The relationship between ischaemic brain lesions and cognitive outcome was analysed by logistic regression analyses. RESULTS: In 40 of 74 patients (54%), 152 ischaemic lesions were found. The median number of lesions per patient was 2 (1-37) and the median total lesion volume was 0.2 (0-17.4) mL. No difference was found between the group with and the group without ischaemic lesions with respect to the frequency of cognitive complaints. In the group with ischaemic lesions, significantly more patients (55%) showed poor cognitive functioning compared to the group without ischaemic lesions (26%) (OR 3.4, 95% CI 1.3-9.1). We found no relationship between the number and volume of the ischaemic lesions and cognitive functioning. CONCLUSIONS: Ischaemic brain lesions detected on MRI during clinical course after aSAH is a marker for poor cognitive functioning 2 months after aSAH, irrespective of the number or volume of the ischaemic lesions. Network or connectivity studies are needed to better understand the relationship between location of the ischaemic brain lesions and cognitive functioning.

Effect of magnesium on cognition after aneurysmal subarachnoid haemorrhage in a randomized trial.

BACKGROUND AND PURPOSE: In randomized trials magnesium supplementation did not improve clinical outcome after aneurysmal subarachnoid haemorrhage (aSAH) on handicap scales. After aSAH, many patients have cognitive problems that may not translate into handicap. The effect of magnesium on cognitive outcome after aSAH was studied. METHODS: In total, 209 patients who had been included in the Magnesium for Aneurysmal Subarachnoid Haemorrhage (MASH-2) trial in the University Medical Centre of Utrecht were studied. Patients had been randomized to 64 mmol magnesium sulfate daily or placebo during hospitalization. Three months after aSAH patients underwent a neuropsychological examination (NPE) consisting of six neuropsychological tests or a brief cognitive assessment. Poisson and linear regression analyses were used to analyse the effect of magnesium on cognition. RESULTS: In the magnesium group 53 (49.5%) of the 107 patients and in the placebo group 51 (50.0%) of the 102 patients scored lower than the median cognitive score [relative risk 0.99, 95% confidence interval (CI) 0.76-1.30]. Linear regression analyses showed no significant relationship between intervention and cognition (B = 0.05, 95% CI -0.15 to 0.33). CONCLUSIONS: Treatment with magnesium has no effect on cognitive outcome after aSAH.