Rapid Auditory Processing Deficits Research Articles

Associations between rapid auditory processing of speech sounds and specific verbal communication skills in autism.

The ability to rapidly process speech sounds is integral not only for processing other's speech, but also for auditory processing of one's own speech, which allows for maintenance of speech accuracy. Deficits in rapid auditory processing have been demonstrated in autistic individuals, particularly those with language impairment. We examined rapid auditory processing for speech sounds in relation to performance on a battery of verbal communication measures to determine which aspects of verbal communication were associated with cortical auditory processing in a sample of individuals with autism. Participants were 57 children and adolescents (40 male and 17 female) ages 5-18 who were diagnosed with an Autism Spectrum Disorder (ASD). Rapid auditory processing of speech sounds was measured via a magnetoencephalographic (MEG) index of the quality of the auditory evoked response to the second of two differing speech sounds ("Ga" / "Da") presented in rapid succession. Verbal communication abilities were assessed on standardized clinical measures of overall expressive and receptive language, vocabulary, articulation, and phonological processing. Associations between cortical measures of left- and right-hemisphere rapid auditory processing and verbal communication measures were examined. Rapid auditory processing of speech sounds was significantly associated with speech articulation bilaterally (r = 0.463, p = 0.001 for left hemisphere and r = 0.328, p = 0.020 for right hemisphere). In addition, rapid auditory processing in the left hemisphere was significantly associated with overall expressive language abilities (r = 0.354, p = 0.013); expressive (r = 0.384, p = 0.005) vocabulary; and phonological memory (r = 0.325, p = 0.024). Phonological memory was found to mediate the relationship between rapid cortical processing and receptive language. These results demonstrate that impaired rapid auditory processing for speech sounds is associated with dysfunction in verbal communication in ASD. The data also indicate that intact rapid auditory processing may be necessary for even basic communication skills that support speech production, such as phonological memory and articulatory control.

Rapid auditory processing of puretones is associated with basic components of language in individuals with autism spectrum disorders

The goal of this study was to identify the specific domains of language that may be affected by deficits in rapid auditory processing in individuals with ASD. Auditory evoked fields were collected from 63 children diagnosed with ASD in order to evaluate processing of puretone sounds presented in rapid succession. Measures of language and its components were assessed via standardized clinical tools to quantify expressive and receptive language, vocabulary, articulation, and phonological processing abilities. Rapid processing was significantly and bilaterally associated with phonological awareness, vocabulary, and articulation. Phonological processing was found to mediate the relationship between rapid processing and language. M100 response latency was not significantly associated with any language measures. Results suggest that rapid processing deficits may impact the basic components of language such as phonological processing, and the downstream effect of this impact may in turn impact overall language development.

Mutation of Dcdc2 in mice leads to impairments in auditory processing and memory ability.

Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain-containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short-term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre-pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2(del2/del2) mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability.

Age, dyslexia subtype and comorbidity modulate rapid auditory processing in developmental dyslexia.

The nature of Rapid Auditory Processing (RAP) deficits in dyslexia remains debated, together with the specificity of the problem to certain types of stimuli and/or restricted subgroups of individuals. Following the hypothesis that the heterogeneity of the dyslexic population may have led to contrasting results, the aim of the study was to define the effect of age, dyslexia subtype and comorbidity on the discrimination and reproduction of non-verbal tone sequences. Participants were 46 children aged 8–14 (26 with dyslexia, subdivided according to age, presence of a previous language delay, and type of dyslexia). Experimental tasks were a Temporal Order Judgment (TOJ) (manipulating tone length, ISI and sequence length), and a Pattern Discrimination Task. Dyslexic children showed general RAP deficits. Tone length and ISI influenced dyslexic and control children's performance in a similar way, but dyslexic children were more affected by an increase from 2 to 5 sounds. As to age, older dyslexic children's difficulty in reproducing sequences of 4 and 5 tones was similar to that of normally reading younger (but not older) children. In the analysis of subgroup profiles, the crucial variable appears to be the advantage, or lack thereof, in processing long vs. short sounds. Dyslexic children with a previous language delay obtained the lowest scores in RAP measures, but they performed worse with shorter stimuli, similar to control children, while dyslexic-only children showed no advantage for longer stimuli. As to dyslexia subtype, only surface dyslexics improved their performance with longer stimuli, while phonological dyslexics did not. Differential scores for short vs. long tones and for long vs. short ISIs predict non-word and word reading, respectively, and the former correlate with phonemic awareness. In conclusion, the relationship between non-verbal RAP, phonemic skills and reading abilities appears to be characterized by complex interactions with subgroup characteristics.

Cell size anomalies in the auditory thalamus of rats with hypoxic-ischemic injury on postnatal day 3 or 7

Children born prematurely (<37 weeks gestational age) or at very low birth weight (VLBW; <1500g) are at increased risk for hypoxic ischemic (HI) brain injuries. Term infants can also suffer HI from birth complications. In both groups, blood/oxygen delivery to the brain is compromised, often resulting in brain damage and later cognitive delays (e.g., language deficits). Literature suggests that language delays in a variety of developmentally impaired populations (including specific language impairment (SLI), dyslexia, and early HI-injury) may be associated with underlying deficits in rapid auditory processing (RAP; the ability to process and discriminate brief acoustic cues). Data supporting a relationship between RAP deficits and poor language outcomes is consistent with the “magnocellular theory,” which purports that damage to or loss of large (magnocellular) cells in thalamic nuclei could underlie disruptions in temporal processing of sensory input, possibly including auditory (medial geniculate nucleus; MGN) information This theory could be applied to neonatal HI populations that show subsequent RAP deficits. In animal models of neonatal HI, persistent RAP deficits are seen in postnatal (P)7 HI injured rats (who exhibit neuropathology comparable to term birth injury), but not in P1-3 HI injured rodents (who exhibit neuropathology comparable to human pre-term injury). The current study sought to investigate the mean cell size, cell number, and cumulative probability of cell size in the MGN of P3 HI and P7 HI injured male rats that had previously demonstrated behavioral RAP deficits. Pilot data from our lab (Alexander, 2011) previously revealed cell size abnormalities (a shift toward smaller cells) in P7 but not P1 HI injured animals when compared to shams. Our current finding support this result, with evidence of a significant shift to smaller cells in the experimental MGN of P7 HI but not P3 HI subjects. P7 HI animals also showed significantly fewer cells in the affected (right) MGN as compared P3 HI and shams animals. Moreover, cell number in the right hemisphere was found to correlate with gap detection (fewer cells=worse performance) in P7 HI injured subjects. These findings could be applied to clinical populations, providing an anatomic marker that may index potential long-term language disabilities in HI injured infants and possibly other at-risk populations.

Effects of test experience and neocortical microgyria on spatial and non-spatial learning in rats

Neocortical neuronal migration anomalies such as microgyria and heterotopia have been associated with developmental language learning impairments in humans, and rapid auditory processing deficits in rodent models. Similar processing impairments have been suggested to play a causal role in human language impairment. Recent data from our group has shown spatial working memory deficits associated with neocortical microgyria in rats. Similar deficits have also been identified in humans with language learning impairments. To further explore the extent of learning deficits associated with cortical neuronal migration anomalies, we evaluated the effects of neocortical microgyria and test order experience using spatial (Morris water maze) and non-spatial water maze learning paradigms. Two independent groups were employed (G1 or G2) incorporating both microgyria and sham conditions. G1 received spatial testing for five days followed by non-spatial testing, while the reverse order was followed for G2. Initial analysis, including both test groups and both maze conditions, revealed a main effect of treatment, with microgyric rats performing significantly worse than shams. Overall analysis also revealed a task by order interaction, indicating that each group performed better on the second task as compared to the first, regardless of which task was presented first. Independent analyses of each task revealed a significant effect of treatment (microgyria worse than sham) only for the spatial water maze condition. Results indicate that prior maze experience (regardless of task type) leads to better subsequent performance. Results suggest that behavioral abnormalities associated with microgyria extend beyond auditory and working memory deficits seen in previous studies, to include spatial but not non-spatial learning impairments and that non-specific test experience may improve behavioral performance.

Neocortical disruption and behavioral impairments in rats following in utero RNAi of candidate dyslexia risk gene Kiaa0319

Within the last decade several genes have been identified as candidate risk genes for developmental dyslexia. Recent research using animal models and embryonic RNA interference (RNAi) has shown that a subset of the candidate dyslexia risk genes—DYX1C1, ROBO1, DCDC2, KIAA0319—regulate critical parameters of neocortical development, such as neuronal migration. For example, embryonic disruption of the rodent homolog of DYX1C1 disrupts neuronal migration and produces deficits in rapid auditory processing (RAP) and working memory—phenotypes that have been reported to be associated with developmental dyslexia. In the current study we used a modified prepulse inhibition paradigm to assess acoustic discrimination abilities of male Wistar rats following in utero RNA interference targeting Kiaa0319. We also assessed spatial learning and working memory using a Morris water maze (MWM) and a radial arm water maze. We found that embryonic interference with this gene resulted in disrupted migration of neocortical neurons leading to formation of heterotopia in white matter, and to formation of hippocampal dysplasia in a subset of animals. These animals displayed deficits in processing complex acoustic stimuli, and those with hippocampal malformations exhibited impaired spatial learning abilities. No significant impairment in working memory was detected in the Kiaa0319 RNAi treated animals. Taken together, these results suggest that Kiaa0319 plays a role in neuronal migration during embryonic development, and that early interference with this gene results in an array of behavioral deficits including impairments in rapid auditory processing and simple spatial learning.

Reprint of “Early testosterone modulated sex differences in behavioral outcome following neonatal hypoxia ischemia in rats”

Hypoxia ischemia (HI; reduced blood oxygenation and/or flow to the brain) represents one of the most common injuries for both term and preterm/very low birth weight (VLBW) infants. These children experience elevated incidence of cognitive and/or sensory processing disabilities, including language based learning disabilities. Clinical data also indicate more substantial long-term deficits for HI injured male babies as compared to HI injured females. Previously, we reported significant deficits in rapid auditory processing and spatial learning in male rats with postnatal day 1 (P1), P7, or P10 HI injury. We also showed sex differences in HI injured animals, with more severe deficits in males as compared to females. Given these findings, combined with extant clinical data, the current study sought to assess a putative role for perinatal testosterone in modulating behavioral outcome following early hypoxic-ischemic injury in rats. Male, female, and testosterone-propionate (TP) treated females were subjected to P7 HI or sham surgery, and subsequently (P30+) underwent a battery of auditory testing and water maze assessment. Results confirm previous reports of sex differences following HI, and add new findings of significantly worse performance in TP-treated HI females compared to vehicle treated HI females. Post mortem anatomic analyses showed consistent effects, with significant brain weight decreases seen in HI male and TP-treated HI females but not female HI or sham groups. Further neuromorphometric analysis of brain structures showed that HI male animals exhibited increased pathology relative to HI females as reflected in ventricular enlargement. Findings suggest that neonatal testosterone may act to enhance the deleterious consequences of early HI brain injury, as measured by both neuropathology and behavior.

Early testosterone modulated sex differences in behavioral outcome following neonatal hypoxia ischemia in rats

Hypoxia ischemia (HI; reduced blood oxygenation and/or flow to the brain) represents one of the most common injuries for both term and preterm/very low birth weight (VLBW) infants. These children experience elevated incidence of cognitive and/or sensory processing disabilities, including language based learning disabilities. Clinical data also indicate more substantial long-term deficits for HI injured male babies as compared to HI injured females. Previously, we reported significant deficits in rapid auditory processing and spatial learning in male rats with postnatal day 1 (P1), P7, or P10 HI injury. We also showed sex differences in HI injured animals, with more severe deficits in males as compared to females. Given these findings, combined with extant clinical data, the current study sought to assess a putative role for perinatal testosterone in modulating behavioral outcome following early hypoxic-ischemic injury in rats. Male, female, and testosterone-propionate (TP) treated females were subjected to P7 HI or sham surgery, and subsequently (P30+) underwent a battery of auditory testing and water maze assessment. Results confirm previous reports of sex differences following HI, and add new findings of significantly worse performance in TP-treated HI females compared to vehicle treated HI females. Post mortem anatomic analyses showed consistent effects, with significant brain weight decreases seen in HI male and TP-treated HI females but not female HI or sham groups. Further neuromorphometric analysis of brain structures showed that HI male animals exhibited increased pathology relative to HI females as reflected in ventricular enlargement. Findings suggest that neonatal testosterone may act to enhance the deleterious consequences of early HI brain injury, as measured by both neuropathology and behavior.

Developmental learning impairments in a rodent model of nodular heterotopia

Developmental malformations of neocortex—including microgyria, ectopias, and periventricular nodular heterotopia (PNH)—have been associated with language learning impairments in humans. Studies also show that developmental language impairments are frequently associated with deficits in processing rapid acoustic stimuli, and rodent models have linked cortical developmental disruption (microgyria, ectopia) with rapid auditory processing deficits. We sought to extend this neurodevelopmental model to evaluate the effects of embryonic (E) day 15 exposure to the anti-mitotic teratogen methylazoxymethanol acetate (MAM) on auditory processing and maze learning in rats. Extensive cortical anomalies were confirmed in MAM-treated rats post mortem. These included evidence of laminar disruption, PNH, and hippocampal dysplasia. Juvenile auditory testing (P21–42) revealed comparable silent gap detection performance for MAM-treated and control subjects, indicating normal hearing and basic auditory temporal processing in MAM subjects. Juvenile testing on a more complex two-tone oddball task, however, revealed a significant impairment in MAM-treated as compared to control subjects. Post hoc analysis also revealed a significant effect of PNH severity for MAM subjects, with more severe disruption associated with greater processing impairments. In adulthood (P60–100), only MAM subjects with the most severe PNH condition showed deficits in oddball two-tone processing as compared to controls. However, when presented with a more complex and novel FM sweep detection task, all MAM subjects showed significant processing deficits as compared to controls. Moreover, post hoc analysis revealed a significant effect of PNH severity on FM sweep processing. Water Maze testing results also showed a significant impairment for spatial but not non-spatial learning in MAM rats as compared to controls. Results lend further support to the notions that: (1) generalized cortical developmental disruption (stemming from injury, genetic or teratogenic insults) leads to auditory processing deficits, which in turn have been suggested to play a causal role in language impairment; (2) severity of cortical disruption is related to the severity of processing impairments; (3) juvenile auditory processing deficits appear to ameliorate with maturation, but can still be elicited in adulthood using increasingly complex acoustic stimuli; and (4) malformations induced with MAM are also associated with generalized spatial learning deficits. These cumulative findings contribute to our understanding of the behavioral consequences of cortical developmental pathology, which may in turn elucidate mechanisms contributing to developmental language learning impairment in humans.

Event-related potentials to pitch and rise time change in children with reading disabilities and typically reading children

Objective The purpose of the present study was to investigate whether children with reading disabilities (RD) process rise time and pitch changes differently to control children as a function of the interval between two tones. Methods Children participated in passive oddball event-related potential (ERP) measurements using paired stimuli. Mismatch negativity (MMN), P3a and late discriminative negativity (LDN) responses to rise time and pitch changes were examined. Results Control children produced larger responses than children with RD to pitch change in the P3a component but only when the sounds in the pair were close to each other. Compared to children with RD, MMN was smaller and LDN larger in control children in response to rise time change when the sounds in the pair were further apart. The non-overlap in ERP measures between the groups was 40–50%. Conclusions Problems in rapid processing of pitch change were reflected in a component associated with attention switching while amplitude envelope processing problems were reflected in components associated with stimulus detection or discrimination. Significance Children with RD process both rise time and pitch changes differently from control children thus providing evidence for the nature of amplitude envelope processing and rapid auditory processing deficits in dyslexia.

Age at developmental cortical injury differentially Alters corpus callosum volume in the rat

BackgroundFreezing lesions to developing rat cortex induced between postnatal day (P) one and three (P1 – 3) lead to malformations similar to human microgyria, and further correspond to reductions in brain weight and cortical volume. In contrast, comparable lesions on P5 do not produce microgyric malformations, nor the changes in brain weight seen with microgyria. However, injury occurring at all three ages does lead to rapid auditory processing deficits as measured in the juvenile period. Interestingly, these deficits persist into adulthood only in the P1 lesion case [1]. Given prior evidence that early focal cortical lesions induce abnormalities in cortical morphology and connectivity [1-4], we hypothesized that the differential behavioral effects of focal cortical lesions on P1, P3 or P5 may be associated with underlying neuroanatomical changes that are sensitive to timing of injury. Clinical studies indicate that humans with perinatal brain injury often show regional reductions in corpus callosum size and abnormal symmetry, which frequently correspond to learning impairments [5-7]. Therefore, in the current study the brains of P1, 3 or 5 lesion rats, previously evaluated for brain weight, and cortical volume changes and auditory processing impairments (P21-90), were further analyzed for changes in corpus callosum volume.ResultsResults showed a significant main effect of Treatment on corpus callosum volume [F (1,57) = 10.2, P < .01], with lesion subjects showing significantly smaller callosal volumes as compared to shams. An Age at Treatment × Treatment interaction [F(2,57) = 3.2, P < .05], indicated that corpus callosum size decreased as the age of injury decreased from P5 to P1. Simple effects analysis showed significant differences between P1 and P3 [F(1,28) = 8.7, P < .01], and P1 and P5 [F(1,28) = 15.1, P < .001], subjects. Rats with P1 injury resulting in microgyria had the greatest reduction in corpus callosum volume (22% reduction), followed by the P3 group (11% reduction), which showed a significant reduction in corpus callosum volume compared to shams [F(1,31) = 5.9, P < .05]. Finally, the P5 lesion group did not significantly differ from the sham subjects in callosal volume.ConclusionDecrements in corpus callosum volume in the P1 and 3 lesion groups are consistent with the reductions in brain weight and cortical volume previously reported for microgyric rats [1,8]. Current results suggest that disruption to the cortical plate during early postnatal development may lead to more widely dispersed neurovolumetric anomalies and subsequent behavioral impairments [1], compared with injury that occurs later in development. Further, these results suggest that in a human clinical setting decreased corpus callosum volume may represent an additional marker for long-term behavioral outcome.

Developmental disruptions and behavioral impairments in rats following in utero RNAi of Dyx1c1

Developmental malformations of cortex have been shown to co-occur with language, learning, and other cognitive deficits in humans. Rodent models have repeatedly shown that animals with such developmental malformations have deficits related to auditory processing and learning. More specifically, freeze-lesion induced microgyria as well as molecular layer ectopias have been found to impair rapid auditory processing ability in rats and mice. In humans, deficits in rapid auditory processing appear to relate to later impairments of language. Recently, genetic variants of four different genes involved in early brain development have been proposed to associate with an elevated incidence of developmental dyslexia in humans. Three of these, DYX1C1, DCDC2, and KIAA0319, have been shown by in utero RNAi to play a role in neuronal migration in developing neocortex. The present study assessed the effects of in utero RNAi of Dyx1c1 on auditory processing and spatial learning in rats. Results indicate that RNAi of Dyx1c1 is associated with cortical heterotopia and is suggestive of an overall processing deficit of complex auditory stimuli in both juvenile and adult periods ( p = .051, one-tail). In contrast, adult data alone reveal a significant processing impairment among RNAi treated subjects compared to shams, indicating an inability for RNAi treated subjects to improve detection of complex auditory stimuli over time ( p = .022, one-tail). Further, a subset of RNAi treated rats exhibited hippocampal heterotopia centered in CA1 (in addition to cortical malformations). Malformations of hippocampus were associated with robust spatial learning impairment in this sub-group ( p < .01, two-tail). In conclusion, in utero RNAi of Dyx1c1 results in heterogeneous malformations that correspond to distinct behavioral impairments in auditory processing, and spatial learning.

Developmental timeframes for induction of microgyria and rapid auditory processing deficits in the rat

Induction of a focal freeze lesion to the skullcap of a 1-day-old rat pup leads to the formation of microgyria similar to those identified postmortem in human dyslexics. Rats with microgyria exhibit rapid auditory processing deficits similar to those seen in language-impaired (LI) children, and infants at risk for LI and these effects are particularly marked in juvenile as compared to adult subjects. In the current study, a startle response paradigm was used to investigate gap detection in juvenile and adult rats that received bilateral freezing lesions or sham surgery on postnatal day (P) 1, 3 or 5. Microgyria were confirmed in P1 and 3 lesion rats, but not in the P5 lesion group. We found a significant reduction in brain weight and neocortical volume in P1 and 3 lesioned brains relative to shams. Juvenile (P27–39) behavioral data indicated significant rapid auditory processing deficits in all three lesion groups as compared to sham subjects, while adult (P60+) data revealed a persistent disparity only between P1-lesioned rats and shams. Combined results suggest that generalized pathology affecting neocortical development is responsible for the presence of rapid auditory processing deficits, rather than factors specific to the formation of microgyria per se. Finally, results show that the window for the induction of rapid auditory processing deficits through disruption of neurodevelopment appears to extend beyond the endpoint for cortical neuronal migration, although, the persistent deficits exhibited by P1 lesion subjects suggest a secondary neurodevelopmental window at the time of cortical neuromigration representing a peak period of vulnerability.

Rapid auditory processing and learning deficits in rats with P1 versus P7 neonatal hypoxic-ischemic injury

Hypoxia-ischemia (HI) is associated with premature birth, and injury during term birth. Many infants experiencing HI later show disruptions of language, with research suggesting that rapid auditory processing (RAP) deficits (i.e., impairment in the ability to discriminate rapidly changing acoustic signals), play a causal role in language problems. We recently bridged these lines of research by showing RAP deficits in rats with unilateral-HI injury induced on postnatal days 1, 7, or 10 (P1, P7, or P10 [McClure MM, Peiffer AM, Rosen GD, Fitch RH. Auditory processing deficits in rats with neonatal hypoxic-ischemic injury. Int J Dev Neurosci, 2005;23:351–362]). While robust RAP deficits were found in HI animals, it was suggested that our within-age sample size did not provide sufficient power to detect age-at-injury differences within the pooled HI group. The current study sought to examine differences in neuropathology and behavior following unilateral-HI injury on P1 versus P7 in rats. Ages chosen for HI induction reflect differential stages of neurodevelopmental maturity, and subsequent regional differences in vulnerability to reduced blood flow/oxygen (modeling age-related differences in premature/term HI injury). Results showed that during the juvenile period, both P1 and P7 HI groups exhibited significant RAP deficits, but deficits in the P1 HI group resolved with repeated testing (compared to shams), while P7 HI animals showed lasting deficits in RAP and spatial learning/memory through adulthood. The current findings are in accord with evidence that HI injury during different stages of developmental maturity (age-at-injury) leads to differential neuropathologies, and provide the novel observation that in rats, P1 versus P7 induced pathologies are associated with different patterns of auditory processing and learning/memory deficits across the lifespan.

The effects of erythropoietin on auditory processing following neonatal hypoxic–ischemic injury

Neonatal hypoxia–ischemia (HI) is a common cause of brain damage and subsequent behavioral deficits in premature/term infants. Rapid auditory processing deficits have been suggested to play a role in later language impairments in this population. We have previously shown auditory deficits in rats with neonatal HI injury and now report novel effects of behavioral sparing and neuroprotection following treatment with a low dose of Erythropoietin using this HI injury model.

What is the Role of Audition in Literacy?

What is the Role of Audition in Literacy?

Auditory processing deficits in unilaterally and bilaterally injured hypoxic–ischemic rats

Hypoxic-ischemic represents a common cause of damage to the prenatal brain and can co-occur with prematurity. Prematurity is associated with emergent language impairments, and it has been suggested that rapid auditory processing deficits play a causal role in language difficulties. We previously demonstrated rapid auditory processing deficits in juvenile rats receiving neonatal unilateral hypoxic-ischemic injury, but these deficits appeared to resolve by adulthood. The current study compared unilaterally and bilaterally injured hypoxic-ischemic rats on auditory tasks, to assess whether rapid auditory processing recovery in adulthood is related to this aspect of injury. Current results indicate that while neonatal unilateral and bilateral hypoxic-ischemic injury both lead to rapid auditory processing deficits in the juvenile period, only rats with bilateral hypoxic-ischemic injury exhibit deficits that persist into adulthood.

Sex differences in rapid auditory processing deficits in microgyric rats

Early neocortical injury has been associated with rate-specific auditory processing deficits using rodent models. In the few cases where females were studied, they appeared less vulnerable than males to the behavioral consequences of early neocortical injury. In the current study, male rats with neocortical microgyria were found to exhibit significant impairments in detecting tone sequences at short but not long inter-stimulus intervals (ISI) as compared to sham-operated male littermates. Microgyric females, however, performed similarly to sham-operated female littermates on this task at all durations. Current findings support an association between focal cortical malformations and impaired rapid auditory processing in males, and less vulnerability in females to the behavioral consequences of these malformations on a task eliminating confounds of motivation, experience, and estrus.

Rapid auditory processing deficits in dyslexia: a commentary on two differing views

Rapid auditory processing deficits in dyslexia: a commentary on two differing views