David P. Crewther

Fish Oil Diet Associated with Acute Reperfusion Related Hemorrhage, and with Reduced Stroke-Related Sickness Behaviors and Motor Impairment

Ischemic stroke is associated with motor impairment and increased incidence of affective disorders such as anxiety/clinical depression. In non-stroke populations, successful management of such disorders and symptoms has been reported following diet supplementation with long chain omega-3-polyunsaturated-fatty-acids (PUFAs). However, the potential protective effects of PUFA supplementation on affective behaviors after experimentally induced stroke and sham surgery have not been examined previously. This study investigated the behavioral effects of PUFA supplementation over a 6-week period following either middle cerebral artery occlusion or sham surgery in the hooded-Wistar rat. The PUFA diet supplied during the acclimation period prior to surgery was found to be associated with an increased risk of acute hemorrhage following the reperfusion component of the surgery. In surviving animals, PUFA supplementation did not influence infarct size as determined 6 weeks after surgery, but did decrease omega-6-fatty-acid levels, moderate sickness behaviors, acute motor impairment, and longer-term locomotor hyperactivity and depression/anxiety-like behavior.

Magnocellular visual evoked potential delay with high autism spectrum quotient yields a neural mechanism for altered perception

Everyone has autistic characteristics to a greater or lesser degree, encapsulated in the Autism Spectrum Quotient, a scale that measures the degree to which an adult of normal intelligence displays traits associated with autism spectrum disorders. Recent psychophysical analyses of autism spectrum disorders point to superior local processing, and impaired or ignored global and contextual processing. The aim of this study was to test whether low- and high-scoring individuals on the Autism Spectrum Quotient differ on a measure of local and global processing, motion processing and visual pathway integrity. Fifteen low-scoring individuals and 14 high-scoring individuals derived from a normal population participated in the study. The results indicate that the initial cortical response to the magnocellular afferents is weaker at low contrast in the high autistic tendency group and that a second-order response, reflecting magnocellular activity, demonstrated a delay for high versus low scorers when the parvocellular pathway was also active in response to a high contrast stimulus. High-scoring individuals also demonstrated difficulty in identifying the global components of locally salient hierarchical Navon figures. Furthermore, cross-validated discriminant analysis, using four physiologically and three psychophysically derived parameters, correctly classified 83% of individuals who scored either high or low on the Autism Spectrum Quotient. These findings in the group scoring high on the Autism Spectrum Quotient indicate that a delay in primary visual/prestriate cortical processing of magnocellular input diminishes the advantage of its early arrival to primary visual cortex. This appears to be associated with impaired global visual perception, predicting with high accuracy behavioural tendencies associated with autism spectrum disorders. It has been proposed that perceptual impairment in autism may be attributed to a dysfunction of horizontal connections within early visual areas, presumably parvocellular in nature. However, the timing of such form processing aberrations is much later than the timing of abnormal magnocellular visual processing measured directly here. Thus it is proposed that a magnocellular processing delay decreases the ability of autistic individuals to benefit perceptually from feedback normally associated with the magnocellular advantage.

Separate magnocellular and parvocellular contributions from temporal analysis of the multifocal VEP.

Temporal analysis of the multifocal cortical visual evoked potential (VEP) was studied using pseudo-random (m-sequence) achromatic stimulation. The effects of variation of luminance contrast on the first-order response were complex. At low to mid contrasts (< 60%), a wave doublet (P100-N115) predominated. A second wave complex (N100-P120-N160) dominated at high contrasts. The second-order responses, however, showed an extremely simple variation with luminance contrast. Intrinsic differences in the adaptation time of the generators of these two components caused a distinct separation in the slices of the second-order response. A rapidly adapting nonlinearity saturating at low contrasts was only observable when measuring the responses from two consecutive flashes. Its latency coincided with the contrast saturating first-order response component. By comparison, the nonlinearity derived from the responses to the stimuli with longer interstimulus intervals (second and third slices) yielded a much more linear contrast response function with lower contrast gain and latencies, which clearly corresponded to the longer latency component of the first-order response. Thus, the second-order responses show a first slice which is predominantly driven by neural elements that have a latency and contrast function that mimic those of the magnocellular neurons of the primate LGN and a second slice which is dominated by a generator whose properties resemble primate parvocellular function. This division into magno and parvocellular contribution to the VEP is based on function (interaction time) as distinct from other currently available analyses, with potential for neural analysis of visual disease.

Disease-associated visual image degradation and spherical refractive errors in children

ABSTRACT Retrospective clinical data from 496 eyes of 256 children attending a low vision clinic were analyzed to determine the relation between disease states which involve visual image degradation and refractive error. Refractive data from 1023 normal vision children were used as a control. The low vision children were grouped according to their disease classification and the acknowledged age‐of‐onset of their visual disability. It was found that there was an overall inability to emmetropize and a trend towards myopia. It was also observed that the diseases which led to myopia were associated with a peripheral or peripheral plus central impairment of vision and that those conditions in which foveal vision was primarily impaired showed a mild hypermetropic trend. Eyes in which the visual impairment was not congenital but occurred before the age of 3 years tended to develop hypermetropia. The deviation from emmetropia decreased with increasing age‐of‐onset of the visual impairment, as did the variation about the mean refraction. The plastic period for emmetropization is estimated to end at 8 to 9 years of age.

Neural site of strabismic amblyopia in cats: spatial frequency deficit in primary cortical neurons

SummaryThe acuities of cells in the primary visual cortex of five tenotomized strabismic cats were measured. Previous behavioural studies have shown such animals to possess a severe amblyopia of approximately 1.5 octaves of spatial frequency, yet the acuities of both retinal ganglion and lateral geniculate X-cells are normal. The receptive fields of the cortical cells sampled were within 5° of the area centralis projection. On average, the acuities of cortical cells driven by the amblyopic eye were nearly 1 octave less than those for the non-deviating eye. However, the best cell acuities for each eye were nearly the same. The relationship between ocular dominance and cell acuity was found to be different for the two eyes despite a symmetrical ocular dominance distribution. The acuity deficit for cells driven through the amblyopic eye was present at all depths along the electrode tracks. We conclude that in this model amblyopia, the initial spatial processing deficit lies in the visual cortex, and most probably in the cells of layer IV. Further-more, the presence of a few cells driven by the amblyopic eye which can perform nearly as well as those from the fellow eye in processing high spatial frequencies gives new insight into the way in which strabismic and deprivation amblyopias differ.

Referral rates for a functional vision screening among a large cosmopolitan sample of Australian children

The aim of this study was to investigate the incidence of functional vision problems in a large unselected cosmopolitan population of primary school‐age children and to investigate whether constant clinical criteria for functional vision problems would be implemented by the practitioners involved in the screening. Refractive errors, near point of convergence, stereopsis, strabismus, heterophoria and accommodative facility were assessed for 2697 children (3–12 years) of varying racial backgrounds living in Australia. The spherical component of the refractive error ranged from −7.75 to +9.50 D (mean +0.54 D, ±0.79) with a distribution skewed towards hypermetropia; astigmatism ranged from 0 to 4.25 D (mean −0.16 D, ±0.35). There was a trend towards less hypermetropia and slightly more astigmatism with age. Mean near point of convergence was 5.4 ± 2.9 cm, heterophoria at far and near was 0.12 ± 1.58Δ exophoria and 1.05 ± 2.53Δ exophoria, respectively, 0.55% of children exhibited vertical phoria at near >0.5Δ, accommodative facility ranged from 0 to 24 cycles per minute (cpm) (mean 11.2 cpm, ±3.7), stereopsis varied from 20 to 800 s (′′) of arc with 50% of children having 40′′ or better. The prevalence of strabismus was particularly low (0.3%).

The role of photoreceptors in the control of refractive state

The current state of research into experimentally induced refractive errors is reviewed. The area is analysed in three components-the transduction of defocus or deprivation, the vector for transmitting the error message from the retina to the outer tunics of the eye, and the identity of the effector for causing growth modulation in the sclera. Anatomical, pharmacological, electrophysiological and optical factors are considered in terms of which elements of the retina are necessary to support a refractive response to deprivation or defocus. Two of the current models are discussed-one emphasizing the role of the choroid in effecting ocular and refractive change, while the second model approaches the problem from the aspect of scleral changes that are associated with growth adaptation without emphasis on the error detection mechanism. A third model is proposed in which the error signal for deprivation or defocus is detected in the outer retina and where error is translated through separate signals for stimulus brightening and darkening into a net signal for fluid flow across and under the active control of the retinal pigment epithelium with the fluid communication between the vitreous chamber and the choroidal lymphatics. The directions of research both fundamental and clinical which are needed to create pharmaceutical or environmental solutions to refractive control are discussed.

Common and distinct brain activation to viewing dynamic sequences of face and hand movements

The superior temporal sulcus (STS) and surrounding lateral temporal and inferior parietal cortices are an important part of a network involved in the processing of biological movement. It is unclear whether the STS responds to the movement of different body parts uniformly, or if the response depends on the body part that is moving. Here we examined brain activity to recognizing sequences of face and hand movements as well as radial grating motion, controlling for differences in movement dynamics between stimuli. A region of the right posterior STS (pSTS) showed common activation to both face and hand motion, relative to radial grating motion, with no significant difference between responses to face and hand motion in this region. Distinct responses to face motion relative to hand motion were observed in the right mid-STS, while the right posterior inferior temporal sulcus (pITS) and inferior parietal lobule (IPL) showed greater responses to hand motion relative to face motion. These findings indicate that while there may be distinct processing of different body part motion in lateral temporal and inferior parietal cortices, the response of the pSTS is not body part specific. This region may provide input to other parts of a network involved with processing human actions with a high-level visual description of biological motion.

A role for choroidal lymphatics during recovery from form deprivation myopia

BACKGROUND The choroid of the chick swells markedly during recovery from experimentally induced myopia. It has been demonstrated previously that the lymphatic sinusoids of the choroid contribute most to the expansion. This raises important questions about the particular ultrastructural changes occurring in choroidal lymphatics as a means of understanding the role these vessels might play in emmetropization. METHODS Thirteen hatchling chicks were monocularly occluded for 2 weeks to induce myopia and then allowed normal visual experiences during recovery for periods of 0 to 72 h before sacrifice. RESULTS Electron microscopic analysis detailed the temporal progression of vascular changes and provides qualitative evidence for edema in the extravascular space. Quantitative analysis showed that the frequency of open junctions between lymphatic endothelial cells (an indicator of passive fluid transfer) increased over the 3 days of recovery. Lymphatic fenestrations (an indicator of active fluid transfer) were rare in both nondeprived eyes and in form-deprived eyes at the time of occluder removal, but increased in density significantly over the first 24 h of recovery before returning to control levels by 72 h. The number of lymphatic endothelial caveolae did not change significantly during recovery, nor did the number of fenestrations along the walls of choriocapillaris vessels. CONCLUSIONS The walls of the lymphatics of the chick choroid open to allow greater fluid transfer during re-emmetropization than normal; the lymphatics may play an important role in the maintenance of chorioretinal fluid balance and homeostasis.

Inflammation and depression: why poststroke depression may be the norm and not the exception

Ischaemic stroke often precedes the appearance of clinical depression. Poststroke depression in turn influences the prognostic outcome. In the interest of advancing our understanding of the biological mechanisms underlying the development of poststroke depression, this systematic review explores the immunological processes driving the development of inflammation-related cell death in mood-related brain regions. Particular attention has been paid to cytokine-driven intrinsic apoptosis factors, including intracellular calcium, glutamate excitotoxicity and free radicals that appear in the brain following ischaemic damage and whose presence significantly increases the likelihood of clinically defined depression.