Greater magnocellular saccadic suppression in high versus low autistic tendency suggests a causal path to local perceptual style.

Saccadic suppression-the reduction of visual sensitivity during rapid eye movements-has previously been proposed to reflect a specific suppression of the magnocellular visual system, with the initial neural site of that suppression at or prior to afferent visual information reaching striate cortex. Dysfunction in the magnocellular visual pathway has also been associated with perceptual and physiological anomalies in individuals with autism spectrum disorder or high autistic tendency, leading us to question whether saccadic suppression is altered in the broader autism phenotype. Here we show that individuals with high autistic tendency show greater saccadic suppression of low versus high spatial frequency gratings while those with low autistic tendency do not. In addition, those with high but not low autism spectrum quotient (AQ) demonstrated pre-cortical (35-45 ms) evoked potential differences (saccade versus fixation) to a large, low contrast, pseudo-randomly flashing bar. Both AQ groups showed similar differential visual evoked potential effects in later epochs (80-160 ms) at high contrast. Thus, the magnocellular theory of saccadic suppression appears untenable as a general description for the typically developing population. Our results also suggest that the bias towards local perceptual style reported in autism may be due to selective suppression of low spatial frequency information accompanying every saccadic eye movement

Fish oil supplementation associated with decreased cellular degeneration and increased cellular proliferation 6 weeks after middle cerebral artery occlusion in the rat

Anti-inflammatory long-chain omega-3 polyunsaturated fatty acids (n-3-LC-PUFAs) are both neuroprotective and have antidepressive effects. However the influence of dietary supplemented n-3-LC-PUFAs on inflammation-related cell death and proliferation after middle cerebral artery occlusion (MCAo)-induced stroke is unknown. We have previously demonstrated that anxiety-like and hyperactive locomotor behaviors are reduced in n-3-LC-PUFA-fed MCAo animals. Thus in the present study, male hooded Wistar rats were exposed to MCAo or sham surgeries and examined behaviorally 6 weeks later, prior to euthanasia and examination of lesion size, cell death and proliferation in the dentate gyrus, cornu ammonis region of the hippocampus of the ipsilesional hemispheres, and the thalamus of the ipsilesional and contralesional hemispheres. Markers of cell genesis and cell degeneration in the hippocampus or thalamus of the ipsilesional hemisphere did not differ between surgery and diet groups 6 weeks post MCAo. Dietary supplementation with n-3-LC-PUFA decreased cell degeneration and increased cell proliferation in the thalamic region of the contralesional hemisphere. MCAo–associated cell degeneration in the hippocampus and thalamus positively correlated with anxiety-like and hyperactive locomotor behaviors previously reported in these animals. These results suggest that anti-inflammatory n-3-LC-PUFA supplementation appears to have cellular protective effects after MCAo in the rat, which may affect behavioral outcomes

Parietal function in good and poor readers

BACKGROUND: While there are many psychophysical reports of impaired magnocellular pathway function in developmental dyslexia (DD), few have investigated parietal function, the major projection of this pathway, in good and poor readers closely matched for nonverbal intelligence. In view of new feedforward-feedback theories of visual processing, impaired magnocellular function raises the question of whether all visually-driven functions or only those associated with parietal cortex functions are equally impaired and if so, whether parietal performance is more closely related to general ability levels than reading ability. METHODS: Reading accuracy and performance on psychophysical tasks purported to selectively activate parietal cortex such as motion sensitivity, attentional tracking, and spatial localization was compared in 17 children with DD, 16 younger reading-age matched (RA) control children, and 46 good readers of similar chronological-age (CA) divided into CA-HighIQ and a CA-LowIQ matched to DD group nonverbal IQ. RESULTS: In the age-matched groups no significant differences were found between DD and CA controls on any of the tasks relating to parietal function, although performance of the DD group and their nonverbal IQ scores was always lower. As expected, CA and RA group comparisons indicated purported parietal functioning improves with age. No difference in performance was seen on any of the parietally driven tasks between the DD and age-nonverbal IQ matched groups, whereas performance differentiated the DD group from the age-matched, higher nonverbal IQ group on several such tasks. An unexpected statistical difference in performance between lower reading age (DD and RA children) and all higher reading age (CA) children was seen on a test of chromatic sensitivity, whereas when high and low nonverbal IQ normal readers were compared performance was not different CONCLUSION: The results indicate that performance on purported parietal functions improves with age and may be more associated with nonverbal mentation than reading accuracy. Performance on a cognitively demanding task, traditionally considered to rely on ventral stream functions, was more related to reading accuracy

Flicker fusion thresholds as a clinical identifier of a magnocellular-deficit dyslexic subgroup.

The magnocellular-dorsal system is well isolated by high temporal frequency. However, temporal processing thresholds have seldom been explored in developmental dyslexia nor its subtypes. Hence, performances on two, four-alternative forced-choice achromatic flicker fusion threshold tasks modulated at low (5%) and high (75%) temporal contrast were compared in dyslexic and neurotypical children individually matched for age and intelligence (8-12 years, n = 54 per group). As expected, the higher modulation resulted in higher flicker fusion thresholds in both groups. Compared to neurotypicals, the dyslexic group displayed significantly lower ability to detect flicker at high temporal frequencies, both at low and high temporal contrast. Yet, discriminant analysis did not adequately distinguish the dyslexics from neurotypicals, on the basis of flicker thresholds alone. Rather, two distinct dyslexic subgroups were identified by cluster analysis - one characterised by significantly lower temporal frequency thresholds than neurotypicals (referred to as 'Magnocellular-Deficit' dyslexics; 53.7%), while the other group ('Magnocellular-Typical' dyslexics; 46.3%) had comparable thresholds to neurotypicals. The two dyslexic subgroups were not differentially associated with phonological or naming speed subtypes and showed comparable mean reading rate impairments. However, correlations between low modulation flicker fusion threshold and reading rate for the two subgroups were significantly different (p = .0009). Flicker fusion threshold performances also showed strong classification accuracy (79.3%) in dissociating the Magnocellular-Deficit dyslexics and neurotypicals. We propose that temporal visual processing impairments characterize a previously unidentified subgroup of dyslexia and suggest that measurement of flicker fusion thresholds could be used clinically to assist early diagnosis and appropriate treatment recommendations for dyslexia

Efficiency in Magnocellular Processing: A Common Deficit in Neurodevelopmental Disorders

Several neurodevelopmental disorders (NDDs) including Developmental Dyslexia (DD), Autism Spectrum Disorder (ASD), but not Attention Deficit Hyperactive Disorder (ADHD), are reported to show deficits in global motion processing. Such behavioral deficits have been linked to a temporal processing deficiency. However, to date, there have been few studies assessing the temporal processing efficiency of the Magnocellular M pathways through temporal modulation. Hence, we measured achromatic flicker fusion thresholds at high and low contrast in nonselective samples of NDDs and neurotypicals (mean age 10, range 7–12 years, n = 71) individually, and group matched, for both chronological age and nonverbal intelligence. Autistic tendencies were also measured using the Autism-Spectrum Quotient questionnaire as high AQ scores have previously been associated with the greater physiological amplitude of M-generated nonlinearities. The NDD participants presented with singular or comorbid combinations of DD, ASD, and ADHD. The results showed that ASD and DD, including those with comorbid ADHD, demonstrated significantly lower flicker fusion thresholds (FFTs) than their matched controls. Participants with a singular diagnosis of ADHD did not differ from controls in the FFTs. Overall, the entire NDD plus control populations showed a significant negative correlation between FFT and AQ scores (r = −0.269, p < 0.02 n = 71). In conclusion, this study presents evidence showing that a temporally inefficient M pathway could be the unifying network at fault across the NDDs and particularly in ASD and DD diagnoses, but not in singular diagnosis of ADHD

Flicker fusion thresholds as a clinical identifier of a magnocellular-deficit dyslexic subgroup.

The magnocellular-dorsal system is well isolated by high temporal frequency. However, temporal processing thresholds have seldom been explored in developmental dyslexia nor its subtypes. Hence, performances on two, four-alternative forced-choice achromatic flicker fusion threshold tasks modulated at low (5%) and high (75%) temporal contrast were compared in dyslexic and neurotypical children individually matched for age and intelligence (8-12 years, n = 54 per group). As expected, the higher modulation resulted in higher flicker fusion thresholds in both groups. Compared to neurotypicals, the dyslexic group displayed significantly lower ability to detect flicker at high temporal frequencies, both at low and high temporal contrast. Yet, discriminant analysis did not adequately distinguish the dyslexics from neurotypicals, on the basis of flicker thresholds alone. Rather, two distinct dyslexic subgroups were identified by cluster analysis - one characterised by significantly lower temporal frequency thresholds than neurotypicals (referred to as 'Magnocellular-Deficit' dyslexics; 53.7%), while the other group ('Magnocellular-Typical' dyslexics; 46.3%) had comparable thresholds to neurotypicals. The two dyslexic subgroups were not differentially associated with phonological or naming speed subtypes and showed comparable mean reading rate impairments. However, correlations between low modulation flicker fusion threshold and reading rate for the two subgroups were significantly different (p = .0009). Flicker fusion threshold performances also showed strong classification accuracy (79.3%) in dissociating the Magnocellular-Deficit dyslexics and neurotypicals. We propose that temporal visual processing impairments characterize a previously unidentified subgroup of dyslexia and suggest that measurement of flicker fusion thresholds could be used clinically to assist early diagnosis and appropriate treatment recommendations for dyslexia

Age Related Decline in Cortical Multifocal Flash VEP: Latency Increases Shown to Be Predominately Magnocellular

As the visual system ages, flicker sensitivity decreases and the latencies of cortical visual evoked potentials (VEP) increase. However, the extent to which these effects reflect age-related changes in the magnocellular (M) and or parvocellular (P) pathways remain unclear. Here, we investigated the relation between flicker fusion frequencies and VEP non-linearities induced by rapid stimulation, as a function of age over 6 decades. The approach, using Wiener kernel analysis of multifocal flash (mf)VEP, allows the extraction of signatures of both M and P processing and hence establishing a neural basis of the known decline in flicker fusion threshold. We predicted that, in a sample of 86 participants, age would be associated with a latency increase in early mfVEP response components and that flicker fusion thresholds, for both low and high contrast stimuli, would relate to the temporal efficiency of the M-generated VEP component amplitudes. As expected, flicker fusion frequency reduced with age, while latencies of early second order peaks of the mfVEP increased with age, but M temporal efficiency (amplitude ratio of first to second order peaks) was not strongly age-related. The steepest increases in latency were associated with the M dominated K2.1 (second order first slice) N70 components recorded at low and high contrast (6.7 and 5.9 ms/decade, respectively). Interestingly, significant age-related latency shifts were not observed in the first order responses. Significant decreases in amplitude were found in multiple first and second order components up to 30 years of age, after which they remained relatively constant. Thus, aging and decline in visual function appears to be most closely related to the response latencies of non-linearities generated by the M pathway

Homocysteine as a potential biochemical marker for depression in elderly stroke survivors

Background: Elderly stroke survivors have been reported to be at risk of malnutrition and depression. Vitamin B-related metabolites such as methylmalonic acid and homocysteine have been implicated in depression. Objective: We conducted a study exploring the relationship between homocysteine and post-stroke depression. Design: Three methodologies were used: Observational cohort study of elderly Swedish patients (n=149) 1.5 years post-stroke, assessed using Diagnostic and Statistical Manual of Mental Disorders, Montgomery &#x00C5;sberg Depression Rating Scale and serum blood levels of methylmalonic acid and homocysteine. Results: Homocysteine significantly correlated with depressive symptomatology in stroke survivors (&#x03B2;&#x200A;=&#x200A;0.18*). Individuals with abnormal levels of methylmalonic acid and homocysteine were almost twice more likely to show depressive symptomatology than those with normal levels (depressive symptoms 22%; no depressive symptoms 12%). Comparison of methylmalonic acid and homocysteine levels with literature data showed fewer stroke survivors had vitamin deficiency than did reference individuals (normal range 66%; elevated 34%). Conclusions: Homocysteine is significantly associated with depressive symptomatology in elderly Swedish stroke survivors