Peripheral and bimanual reaching in a stroke survivor with left visual neglect and extinction.

Whether attentional deficits are accompanied by visuomotor impairments following posterior parietal lesions has been debated for quite some time. This single-case study investigated reaching in a stroke survivor (E.B.) with left visual neglect and visual extinction following right temporo-parietal-frontal strokes. Unlike most neglect patients, E.B. did not present left hemiparesis, homonymous hemianopia nor show evidence of motor neglect or extinction allowing us to examine, for the first time, if lateralised attentional deficits co-occur with deficits in peripheral and bimanual reaching. First, we found a classic optic ataxia field effect: E.B.'s accuracy was impaired when reaching to peripheral targets in her neglected left visual field (regardless of the hand used). Second, we found a larger bimanual cost for movement time in E.B. than controls when both hands reached to incongruent locations. E.B.'s visuomotor profile is similar to the one of patients with optic ataxia showing that attentional deficits are accompanied by visuomotor deficits in the affected field.

Assessment and recovery of visually guided reaching deficits following cerebellar stroke.

The cerebellum is known to play an important role in the coordination and timing of limb movements. The present study focused on how reach kinematics are affected by cerebellar lesions to quantify both the presence of motor impairment, and recovery of motor function over time. In the current study, 12 patients with isolated cerebellar stroke completed clinical measures of cognitive and motor function, as well as a visually guided reaching (VGR) task using the Kinarm exoskeleton at baseline (∼2 weeks), as well as 6, 12, and 24-weeks post-stroke. During the VGR task, patients made unassisted reaches with visual feedback from a central 'start' position to one of eight targets arranged in a circle. At baseline, 6/12 patients were impaired across several parameters of the VGR task compared to a Kinarm normative sample (n = 307), revealing deficits in both feed-forward and feedback control. The only clinical measures that consistently demonstrated impairment were the Purdue Pegboard Task (PPT; 9/12 patients) and the Montreal Cognitive Assessment (6/11 patients). Overall, patients who were impaired at baseline showed significant recovery by the 24-week follow-up for both VGR and the PPT. A lesion overlap analysis indicated that the regions most commonly damaged in 5/12 patients (42% overlap) were lobule IX and Crus II of the right cerebellum. A lesion subtraction analysis comparing patients who were impaired (n = 6) vs. unimpaired (n = 6) on the VGR task at baseline showed that the region most commonly damaged in impaired patients was lobule VIII of the right cerebellum (40% overlap). Our results lend further support to the notion that the cerebellum is involved in both feedforward and feedback control during reaching, and that cerebellar patients tend to recover relatively quickly overall. In addition, we argue that future research should study the effects of cerebellar damage on visuomotor control from a perception-action theoretical framework to better understand how the cerebellum works with the dorsal stream to control visually guided action.

[Clinical examination of spatial neglect and other disorders of spatial cognition]. / Klinische Untersuchung des unilateralen Neglects und weiterer Störungen der Raumkognition.

Neglect occurring after stroke, neoplasms or degenerative processes can lead to considerable disability in everyday life as can other disorders of spatial orientation. Therefore, a dedicated examination and early diagnostic classification are obligatory. Behavioral tests are helpful in this respect, enabling the clinician to obtain an initial overview of the existing deficits even at the patient's bedside. The clinical (bedside) examination of spatial neglect as well as the corresponding differential diagnostic procedure for the clarification of (possibly additionally or exclusively existing) hemianopia and extinction, as well as the examination of disorders of visuospatial perception, visuoconstructive disorders, topographic disorders, Bálint's syndrome, simultanagnosia, and optic ataxia are presented. The presentation is based on the newly revised (year 2023) guidelines of the Association of the Scientific Medical Societies in Germany (AWMF) on this subject area.

Spatial bias in anti-saccade endpoints following bilateral dorsal posterior parietal lesions.

Anti-saccades are eye movements in which the saccade is executed in the opposite direction of a visual target and are often hypometric. Because the visual target and saccade goal are decoupled, it has been suggested that competition between the two locations occurs and needs to be resolved. It has been hypothesized that the hypometria of anti-saccades reflects this spatial competition by revealing a bias towards the visual target. To confirm that this hypometria is not simply due to reduced gain, we tested 10 healthy subjects on three different anti-saccade spatial configuration tasks: 90° away across hemifields, 90° away within the same hemifield and 180° away (classic, diagonally opposite). Specifically, we examined whether saccade endpoints showed evidence for the visual target location's interference with anti-saccade programming and execution processes. Among other neural substrates involved in anti-saccades production, the dorsal posterior parietal cortex (PPC) has been implicated in the spatial inhibition of contralateral visual target. To gain insight into the neural processes involved in spatial competition during anti-saccades, we also tested one patient with a bilateral dorsal PPC lesion. In all spatial configurations, we observed that anti-saccade endpoints demonstrated a spatial bias towards the visual target for all participants, likely due to an incomplete inhibition of the visual target location. This spatial bias was exacerbated in our patient, which suggests that the dorsal PPC contributes to the amalgamation of the two competing spatial representations.

White matter tract disconnection in Gerstmann's syndrome: Insights from a single case study.

It has been suggested that Gerstmann's syndrome is the result of subcortical disconnection rather than emerging from damage of a multifunctional brain region within the parietal lobe. However, patterns of white matter tract disconnection following parietal damage have been barely investigated. This single case study allows characterising Gerstmann's syndrome in terms of disconnected networks. We report the case of a left parietal patient affected by Gerstmann's tetrad: agraphia, acalculia, left/right orientation problems, and finger agnosia. Lesion mapping, atlas-based estimation of probability of disconnection, and DTI-based tractography revealed that the lesion was mainly located in the superior parietal lobule, and it caused disruption of both intraparietal tracts passing through the inferior parietal lobule (e.g., tracts connecting the angular, supramarginal, postcentral gyri, and the superior parietal lobule) and fronto-parietal long tracts (e.g., the superior longitudinal fasciculus). The lesion site appears to be located more superiorly as compared to the cerebral regions shown active by other studies during tasks impaired in the syndrome, and it reached the subcortical area potentially critical in the emergence of the syndrome, as hypothesised in previous studies. Importantly, the reconstruction of tracts connecting regions within the parietal lobe indicates that this critical subcortical area is mainly crossed by white matter tracts connecting the angular gyrus and the superior parietal lobule. Taken together, these findings suggest that this case study might be considered as empirical evidence of Gerstmann's tetrad caused by disconnection of intraparietal white matter tracts.

Peripheral reaching in Alzheimer's disease and mild cognitive impairment.

Recent evidence has implicated areas within the posterior parietal cortex (PPC) as among the first to show pathophysiological changes in Alzheimer's disease (AD). Focal brain damage to the PPC can cause optic ataxia, a specific deficit in reaching to peripheral targets. The present study describes a novel investigation of peripheral reaching ability in AD and mild cognitive impairment (MCI), to assess whether this deficit is common among these patient groups. Individuals with a diagnosis of mild-to-moderate AD, or MCI, and healthy older adult controls were required to reach to targets presented in central vision or in peripheral vision using two reaching tasks; one in the lateral plane and another presented in radial depth. Pre-registered case-control comparisons identified 1/10 MCI and 3/17 AD patients with significant peripheral reaching deficits at the individual level, but group-level comparisons did not find significantly higher peripheral reaching error in either AD or MCI by comparison to controls. Exploratory analyses showed significantly increased reach duration in both AD and MCI groups relative to controls, accounted for by an extended Deceleration Time of the reach movement. These findings suggest that peripheral reaching deficits like those observed in optic ataxia are not a common feature of AD. However, we show that cognitive decline is associated with a generalised slowing of movement which may indicate a visuomotor deficit in reach planning or online guidance.

Integrating visual search, eye movement training and reversing prism exposure in the treatment of Balint-Holmes syndrome: a single case report.

OBJECTIVE: For the first time, we administered reversing prism exposure to treat optic ataxia in a single patient with Balint-Holmes Syndrome (BHS), who also underwent specific trainings for simultanagnosia and ocular apraxia. METHOD AND RESULTS: By an introduction and withdrawal experimental design, we observed that the active treatment periods improved patient's visuospatial defects and functional autonomy. CONCLUSIONS: We thus provided a proof of principle supporting the use of reversing prism exposure in optic ataxia within an integrated and personalized rehabilitative approach for BHS.

Partial Balint's syndrome and left homonymous hemianopsia presenting after resection of a right occipito-parietal glioblastoma.

A 66-year-old left-handed male was admitted to our acute inpatient rehabilitation (AIR) unit following a resection of the right occipito-parietal glioblastoma. He presented with symptoms of horizontal oculomotor apraxia, contralateral optic ataxia and left homonymous hemianopsia. We diagnosed this patient with partial Bálint's syndrome (BS)- oculomotor apraxia, optic ataxia but not simultanagnosia. BS is typically caused by bilateral posterior parietal lesions, but we here describe a unique case due toresection of a right intracranial tumor. A short AIR stay allowed our patient to learn how to compensate for visuomotor and visuospatial deficits, and improved his quality of life significantly.

Impaired Spatial Inhibition Processes for Interhemispheric Anti-saccades following Dorsal Posterior Parietal Lesions.

Anti-saccades are eye movements that require inhibition to stop the automatic saccade to the visual target and to perform instead a saccade in the opposite direction. The inhibitory processes underlying anti-saccades have been primarily associated with frontal cortex areas for their role in executive control. Impaired performance in anti-saccades has also been associated with the parietal cortex, but its role in inhibitory processes remains unclear. Here, we tested the assumption that the dorsal parietal cortex contributes to spatial inhibition processes of contralateral visual target. We measured anti-saccade performance in 2 unilateral optic ataxia patients and 15 age-matched controls. Participants performed 90 degree (across and within visual fields) and 180 degree inversion anti-saccades, as well as pro-saccades. The main result was that our patients took longer to inhibit visually guided saccades when the visual target was presented in the ataxic hemifield and the task required a saccade across hemifields. This was observed through anti-saccades latencies and error rates. These deficits show the crucial role of the dorsal posterior parietal cortex in spatial inhibition of contralateral visual target representations to plan an accurate anti-saccade toward the ipsilesional side.

Bálint syndrome.

This chapter starts by reviewing the various interpretations of Bálint syndrome over time. We then develop a novel integrative view in which we propose that the various symptoms, historically reported and labeled by various authors, result from a core mislocalization deficit. This idea is in accordance with our previous proposal that the core deficit of Bálint syndrome is attentional (Pisella et al., 2009, 2013, 2017) since covert attention improves spatial resolution in visual periphery (Yeshurun and Carrasco, 1998); a deficit of covert attention would thus increase spatial uncertainty and thereby impair both visual object identification and visuomotor accuracy. In peripheral vision, we perceive the intrinsic characteristics of the perceptual elements surrounding us, but not their precise localization (Rosenholtz et al., 2012a,b), such that without covert attention we cannot organize them to their respective and recognizable objects; this explains why perceptual symptoms (simultanagnosia, neglect) could result from visual mislocalization. The visuomotor symptoms (optic ataxia) can be accounted for by both visual and proprioceptive mislocalizations in an oculocentric reference frame, leading to field and hand effects, respectively. This new pathophysiological account is presented along with a model of posterior parietal cortex organization in which the superior part is devoted to covert attention, while the right inferior part is involved in visual remapping. When the right inferior parietal cortex is damaged, additional representational mislocalizations across saccades worsen the clinical picture of peripheral mislocalizations due to an impairment of covert attention.

Attention attracts action in healthy participants: An insight into optic ataxia?

Patients with optic ataxia following lesions to superior parts of the posterior parietal cortex make large errors when reaching to targets in the peripheral visual field. These errors are characterised by a contraction, or attraction, towards the point of fixation. These patients also have a reduced ability to allocate visual attention away from the point of fixation, but it is unclear whether the core symptom of misreaching is related to these attentional problems. In neurologically-intact adults, we tested the effect of an attention-demanding dual-task performed at fixation upon visually-guided reaching to peripheral targets. The dual task was associated with delayed movement initiation, and a shortened deceleration phase of movement suggesting a reduced ability to benefit from online control. It also induced a small but consistent shift of reaching endpoints towards the side of fixation. Our experimental restriction of visual attention thus impaired both the programming and control of reaching, and induced a spatial pattern of errors that was qualitatively reminiscent of optic ataxia, albeit much less severe. These findings are consistent with a close functional link between attention and action in the healthy brain, and suggest that attentional disturbances could be a core component of optic ataxia following parietal lesions.

Unusual cortical symptoms of dural arteriovenous fistula mimicking transient ischemic attack.

The clinical presentation of dural arteriovenous fistula (DAVF) can vary. A 47-year-old man complained of transient difficulty playing badminton and speech disturbance for 10 minutes. His symptoms were suspected to be visuomotor coordination deficit similar to optic ataxia and anomic aphasia. Magnetic resonance imaging and angiography revealed vasogenic edema and perfusion delay in the left temporo-occipital area and an abnormal connection between the left occipital artery and transverse sinus. Transverse sinus DAVF was diagnosed by conventional cerebral angiography. We believe that this is the unique case of DAVF manifested as visuomotor coordination deficit suspected optic ataxia and anomic aphasia.

Effect of object substitution, spontaneous compensation and repetitive training on reaching movements in a patient with optic ataxia.

We report the case of M.B. who demonstrated severe optic ataxia with the right hand following stroke in the left hemisphere. The clinical picture may shed light on both the pathological characteristics of reaching and grasping actions, and potential rehabilitation strategies for optic ataxia. First, M.B. demonstrated a dissociation between severely impaired reaching and relatively spared grasping and tool use skills and knowledge, which confirms that grasping may be more intermingled with non-motoric cognitive mechanisms than reaching. Besides, M.B.'s reaching performance was sensitive to movement repetition. We observed a substitution effect: Reaching time decreased if M.B. repeatedly reached toward the same object but increased when object identity changed. This may imply that not only object localization but also object identity, is integrated into movement programming in reach-to-grasp tasks. Second, studying M.B.'s spontaneous compensation strategies ascertained that the mere repetition of reaching movements had a positive effect, to the point M.B. almost recovered to normal level after an intensive one-day repetitive training session. This case study seems to provide one of the first examples of optic ataxia rehabilitation. Reaching skills can be trained by repetitive training even two years post-stroke and despite the presence of visuo-imitative apraxia.

Impairments in action and perception after right intraparietal damage.

We examined visually-guided reaching and perception in an individual who underwent resection of a small tumor in right intraparietal sulcus (pIPS). In the first experiment, she reached to targets presented on a touch screen. Vision was occluded from reach onset on half of the trials, whereas on the other half she had vision during the entire reach. For visually-guided reaching, she demonstrated significantly more reach errors for targets left of fixation versus right of fixation. However, there were no hemispatial differences when reaching without vision. Furthermore, her performance was consistent for reaches with either hand, providing evidence that pIPS encodes location based on an eye-centered reference frame. Second, previous studies reported that optic ataxics are more accurate when reaching to remembered versus visible target locations. We repeated the first experiment, adding a five second delay between stimulus presentation and reach initiation. In contrast to prior reports, she was less accurate in delayed versus immediate reaching. Finally, we examined whether a small pIPS resection would disrupt visuospatial processing in a simple perceptual task. We presented two small circles in succession in either the same location or offset at varying distances, and asked whether the two circles were presented in the same or different position. She was significantly more impaired left of fixation compared to right of fixation, providing evidence for a perceptual deficit after a dorsal stream lesion.

Bimanual visually guided movements are more than the sum of their parts: Evidence from optic ataxia.

Many reaching actions involve both hands. An open question is whether two-handed reaching involves two simultaneous, independent unimanual reaches, or recruits additional or different processes than those mediating one-handed reaching. We tested optic ataxic patient MDK on a set of unimanual and bimanual reaching tasks. Although MDK was impaired in both types of reaching task, his bimanual reaching was considerably better than his unimanual reaching. These results imply that bimanual reaching involves different or additional processes relative to unimanual reaching. We suggest that bimanual reaching may involve monitoring of the distance between the two hands relative to the distance between the two targets.

Optic ataxia: beyond the dorsal stream cliché.

This chapter reviews clinical and scientific approaches to optic ataxia. This double historic track allows us to address important issues such as the link between Bálint syndrome and optic ataxia, the alleged double dissociation between optic ataxia and visual agnosia, and the use of optic ataxia to argue for a specific vision-for-action occipitoposterior parietal stream. Clinical cases are described and reveal that perceptual deficits have been long shown to accompany ataxia. Importantly, the term ataxia appears to be misleading as patients exhibit a combination of visual and nonvisual perceptual, attentional, and visuomotor guidance deficits, which are confirmed by experimental approaches. Three major features of optic ataxia are described. The first is a spatial feature whereby the deficits exhibited by patients appear to be specific to peripheral vision, akin to the field effect. Visuomotor field examination allows us to quantify this deficit and reveals that it consists of a highly reliable retinocentric hypometria. The third is a temporal feature whereby these deficits are exacerbated under temporal constraints, i.e., when attending to dynamic stimuli. These two aspects combine in a situation where patients have to quickly respond to a target presented in peripheral vision that is experimentally displaced upon movement onset. In addition to the field effect, a hand effect can be described in conditions where the hand is not visible. Spatial and temporal aspects as well as field and hand effects may rely on several posterior parietal modules that remain to be precisely identified both anatomically and functionally. It is concluded that optic ataxia is not a visuomotor deficit and there is no dissociation between perception and action capacities in optic ataxia, hence a fortiori no double dissociation between optic ataxia and visual agnosia. Future directions for understanding the basic pathophysiology of optic ataxia are proposed.

Bilateral parietal dysfunctions and disconnections in simultanagnosia and Bálint syndrome.

In 1909 Rezsö Bálint published an extraordinary case study of a man with complex visuospatial deficits resulting from bilateral parietal lesions. Despite some controversies over the nature of reported symptoms, in 1954 Hecaen and Ajuriaguerra conceived the term "Bálint syndrome," not only to honor Bálint's influential work but to firmly conceptualize this striking neurologic disorder. Nowadays it is largely agreed that, while Bálint syndrome may result from multiple etiologies, it is principally diagnosed based on the presence of three symptoms: simultanagnosia, optic ataxia, and ocular apraxia. One of the most striking characteristics of Bálint syndrome, perfectly capturing the nature of this remarkable disorder, is that affected patients cannot perceive more than one object at a time or comprehend multiobject visual scenes due to a lack of ability to detect several objects concurrently and to grasp the spatial relationships between them. This chapter gives an overview of the cognitive mechanisms and neuroanatomy underlying Bálint syndrome, which provides key insights into our understanding of the role of parietal cortex in human attention, visual perception, and visuomotor control. This chapter also pays homage to Glyn Humphreys (1954-2016), who pioneered contributions to the knowledge about complexity of visual and spatial deficits associated with Bálint syndrome.

Asymmetric oculomotor apraxia, optic ataxia, and simultanagnosia with right hemispatial neglect from a predominantly left-sided lesion of the parieto-occipital area.

INTRODUCTION: Bálint's syndrome involves bilateral damage to the parieto-occipital area. The extent of the effect of unilateral damage on the Bálint's triad (oculomotor apraxia, optic ataxia, and simultanagnosia) remains unknown. METHODS: We examined a 63-year-old, right-handed woman who developed right hemianopia, oculomotor apraxia, optic ataxia, simultanagnosia, and hemispatial neglect (HSN) for the right after a cerebral infarction, with detailed neuropsychological tests, magnetic resonance imaging, and single photon emission computed tomography (SPECT). RESULTS: Neuropsychological examination showed that oculomotor apraxia, optic ataxia, and simultanagnosia were more pronounced in the right hemi-space, probably due to the limited eye movement in the right visual field, whereas HSN was restricted to the right hemi-space. Diffusion-weighted MR images revealed hyperintensity in the left parieto-temporo-occipital region, and several spotty areas of the bilateral frontal and parietal subcortical regions. SPECT revealed hypoperfusion in the left parieto-occipital region and frontal operculum and small areas of the right superior parietal lobule. CONCLUSIONS: The case suggests that asymmetric (more pronounced in the right hemi-space) oculomotor apraxia, optic ataxia, and simultanagnosia occur in an extensive lesion of the left parieto-occipital cortices. Although HSN is not a prerequisite for simultanagnosia, the coexistence of HSN aggravates simultanagnosia in the hemi-space opposite the lesion.