Research Report

Vibrotactile adaptatioadults with autism

M. Tommerdahla,, V. TannanaDepartment of Biomedical Engineering, UnivebDepartment of Allied Health Sciences, UnivercDepartment of Cellular and Molecular PhysiodNeurodevelopmental Disorders Research Cen

performance is improved following adaptation because adaptation is accompanied by an

(SI) tomechanical skin stimulationan effect identified in previous imaging studies of SI cortex

experiments described in this report, a paradigm identical to that employed previously by

Spatial localization

Adaptation

B R A I N R E S E A R C H 1 1 5 4 ( 2 0 0 7 ) 1 1 6 1 2 3

ava i l ab l e a t www.sc i enced i rec t . comTannanet al. [Tannan,V., Tommerdahl,M.,Whitsel, B.L., 2006.Vibrotactile adaptationenhancesspatial localization. Brain Res. 1102(1), 109116 (Aug 2)] was used to study adults with autism.The results demonstrate that although cutaneous localization performance of adults withautism is significantly better than the performance of control subjects when the period ofadapting stimulation is short (i.e., 0.5 s), tactile spatial discriminative capacity remained un-altered in the same subjects when the duration of adapting stimulation was increased (to 5 s).in anesthetized non-human primates [e.g., Simons, S.B., Tannan, V., Chiu, J., Favorov, O.V.,Whitsel, B.L., Tommerdahl, M, 2005. Amplitude-dependency of response of SI cortex to flutterstimulation. BMCNeurosci. 6(1), 43 (Jun 21) ; Tommerdahl, M., Favorov, O.V., Whitsel, B.L., 2002.Optical imaging of intrinsic signals in somatosensory cortex. Behav. Brain Res. 135, 8391;Whitsel, B.L., Favorov, O.V., Tommerdahl, M., Diamond, M., Juliano, S., Kelly, D., 1989. Dynamicprocessesgovern the somatosensorycortical response tonatural stimulation. In: Lund, J.S., (Ed.),Sensory Processing in the Mammalian Brain. Oxford Univ. Press, New York, 79107]. In the

TactileVibrotactile Corresponding author.E-mail address: Mark_Tommerdahl@med

0006-8993/$ see front matter 2007 Elsevidoi:10.1016/j.brainres.2007.04.032increase in the spatial contrast in the response of contralateral primary somatosensory cortexKeywords:SomatosensoryAutismn fails to enhance spatial localization in

a, C.J. Casciod, G.T. Baranekb, B.L. Whitsela,c

rsity of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USAsity of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USAlogy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USAter, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA

A B S T R A C T

A recent study [Tannan, V., Tommerdahl, M., Whitsel, B.L., 2006. Vibrotactile adaptationenhances spatial localization. Brain Res. 1102(1), 109116 (Aug 2)] showed that pre-exposure of askin region to a 5 s 25 Hz flutter stimulus (adaptation) results in an approximately 2-foldimprovement in the ability of neurologically healthy human adults to localize mechanicalstimulation delivered to the same skin region that received the adapting stimulation. Tannan etal. [Tannan, V., Tommerdahl, M., Whitsel, B.L., 2006. Vibrotactile adaptation enhances spatiallocalization. Brain Res. 1102(1), 109116 (Aug 2)] proposed that tactile spatial discriminative

www.e l sev i e r. com/ loca te /b ra in resA R T I C L E I N F O

Article history:Accepted 4 April 2007Available online 19 April 2007Both the failure of prior history of tactile stimulation to alter tactile spatial localization in adultswith autism, and the better-than-normal tactile localization performance of adults withautismwhen the period of adaptation is short are concluded to be attributable to the deficientcerebral cortical GABAergic inhibitory neurotransmission characteristic of this disorder.

2007 Elsevier B.V. All rights reserved.

.unc.edu (M. Tommerdahl).

er B.V. All rights reserved.

1. Introduction

In a recent paper in this Journal (Tannan et al., 2006), wereported that in healthy adult subjects spatial localization of a25 Hz flutter stimulus on the skin of the hand improvessubstantially following adaptation. In that study we deliveredan adapting stimulus (0.5 or 5 s) to a randomly selectedlocation on the skin, and in 2 subsequent temporal intervalseither the standard or a test skin flutter stimulus (the 25 Hzstandard and test stimuli were equal in amplitude) wasdelivered either at the locus of the adapting stimulus, or atanother randomly located skin site. Subjects then werequeried as to which interval contained the standard stimulus.The observations revealed that long-duration (5 s) adaptationimproved spatial acuity by nearly 2-fold relative to performanceunder the short-duration (0.5 s) adaptation condition. This

considerable improvement in performance was hypothesizedto be due to adaptation-induced pericolumnar lateral inhibi-tory interactions which lead to a more focused (spatiallyfunneled) primary somatosensory cortical response to me-chanical skin stimulation (Simons et al., 2005; Tommerdahlet al., 2002; Whitsel et al., 1989; Juliano et al., 1989).

The above-described human psychophysical findings ap-pear fully consistent with published theoretical accounts ofthe effects of repetitive skin stimulation on the SI corticalresponse to stimulation. More specifically, observationsobtained in the pioneering neurophysiological recordingstudies led Mountcastle and colleagues to advance theproposal (Mountcastle and Darian-Smith, 1968; LaMotte andMountcastle, 1975; LaMotte and Mountcastle, 1979) that asubjects ability to localize a mechanical stimulus on the skindepends on stimulus-evoked dynamic (time-dependent) peri-columnar lateral inhibitory interactions which increase the

ofon

117B R A I N R E S E A R C H 1 1 5 4 ( 2 0 0 7 ) 1 1 6 1 2 3Fig. 1 Spatial localization tracking plots, under 2 conditionssubjects. Top panel: Tracking data for two subjects from the c

et al., 2006). Note that spatial localization performance is distinccondition. Bottom panel: Tracking plots for each of the 4 subjectsadapting stimulus duration, were averaged for individualtrol group, obtained in a previously reported study (Tannan

tly better in the 5.0 s vs. 0.5 s duration adapting stimuluswith autism.

spatial contrast between regions of SI cortex activateddifferentially by stimulus-evoked afferent drive. The ideathat a subjects ability to accurately perceive the spatiallocus of a mechanical skin stimulus depends on the spatialcontrast of the activity profile that a stimulus evokes in theresponding region of contralateral SI cortex has received wideacceptance, but the continuing absence of direct experimentalsupport for this concept motivated us to re-evaluate thephenomenon using optical intrinsic signal imaging methods(OIS imaging; Tommerdahl et al., 2002; Simons et al., 2005;Simons et al., 2006) to investigate the effect of differentdurations of repetitive mechanical stimulation of a skin siteon the spatial profile of SI activation. Briefly summarized, wefound that exposure of a skin site to a temporally extended(N0.5 s) 25 Hz vibrotactile stimulus is consistently accompa-nied by a dramatic but stereotypical sequence of changes inthe global SI activity patternwhile activation in SI initially

has been suggested to be a common feature of the autistic brain(Hussman, 2001). For example, parietal cortex in subjects withautism exhibits a ~50% reduction in protein levels of theenzymes that synthesize GABA, glutamic acid decarboxylase(GAD) 65 and 67 (Fatemi et al., 2002). Both of these observationsappear to be fully consistent with the frequently reportedhypersensitivity (Cascio et al., in press; Blakemore et al., 2006)and abnormally widespread (Belmonte et al., 2004) cerebralcortical response to skin stimulation in autism. If parietalcortical pericolumnar lateral inhibitory interactions are, in fact,deficient in subjects with autism, and if adaptation-inducedspatial funneling of the primary somatosensory cortical re-sponse to repetitive skin stimulation is achieved via GABA-mediated postsynaptic inhibitory mechanisms intrinsic toprimary somatosensory cortex, subjects with autism shouldnot beexpected toexhibit theadaptation-induced improvementof tactile spatial localization capacity that occurs reliably in

the four individual subjects with autism in Fig. 1. Note that in

muortrva

118 B R A I N R E S E A R C H 1 1 5 4 ( 2 0 0 7 ) 1 1 6 1 2 3occurred in much of the extensive region that receives inputfrom the stimulated skin site, with continuing stimulation notonly did the activated region shrink in size, but the survivingregion of activation came to be bounded by one or moreregions where activity was reduced to significantly below-background values (Tommerdahl et al., 2002; Simons et al.,2005; Simons et al., 2006). In addition, evidence obtained in invivo and in vitro imaging studies indicates unambiguously thatGABA-mediated cortical inhibitory processes are responsiblefor the time-dependent spatial contraction of the SI activationpattern that accompanies the delivery of repetitive thalamo-cortical afferent drive (e.g., as can be achieved using tempo-rally extended vibrotactile stimulation (Juliano et al., 1989), orrepetitive electrical stimulation of thalamocortical afferents(Kohn et al., 2000).

Experimental evidence provided by others led the authors toconsider the possibility that individuals diagnosed with autismwould not exhibit the adaptation-induced enhancement oftactile spatial localization characteristic of neurologically nor-mal subjects. First, Casanova and colleagues have reported thatneocorticalminicolumnar size inautism issignificantly reducedin ways that could reduce within-network communication(Casanovaetal., 2006). Second, suppressedGABAergic inhibition

Fig. 2 Spatial localization under 2 conditions of adapting stidisplayed from the control subjects (left panel; previously repdisplayed in themiddle panel which were obtained from obse

although they clearly outperformed the controls in the 0.5 s adapcondition. Panel at far right summarizes the findings with averaeach of the data sets from the control subjects, there was amarked improvement in spatial localization tracking perfor-mance that occurred when the task was preceded by a 5 sduration adapting stimulus. In contrast, the plots of the data

lus duration for adults with and without autism. Dataed, Tannan et al., 2006), contrast markedly from the datations of subjects with autism. Note that subjects with autism,neurologically normal subjects. The goal of the present studywas to obtain evidence bearing on this possibility using thesame human psychophysical procedures and instrumentationdescribed by Tannan et al. (2006).

2. Results

A two-interval forced-choice (2IFC) tracking protocol (2 up1down; 2 correct answers are followed by a decrease of thedistance between the standard and test stimuli; the distance isincreased following an incorrect answer) was used to deter-mine spatial localization threshold under two different dura-tions of adapting stimulation (0.5 s vs. 5.0 s) for subjects withautism. Five sessions (two runs in each session) wereconducted for eachof the four subjectswith autism. Exemplaryindividual averaged plots for two control subjects (previouslypublished in Tannan et al., 2006) are compared with data fromting condition, did not improve with the 5.0 s adaptingges of the last 5 trials.

the localization distance values for the controls in the right

1 1 5panel of Fig. 2: 10.2830.280 for the short-duration adaptor,and 6.9830.366 for the long-duration adaptor.

ANOVA testing was performed on the data averaged acrossall subjects with autism; the null hypothesis evaluated wasthat mean tactile localization performance is not significantlydifferent when the duration of adapting stimulation is 0.5 or5.0 s. The results (F=0.21416; pN0.05) confirmed that tactilelocalizationperformanceof subjectswith autismdoesnot altersignificantly when the duration of adapting stimulation isincreased from 0.5 to 5.0 s. In addition, the analysis revealedthat at eitherdurationof adapting stimulation (for 5.0 s adapta-tion F=96.17924, pb0.01; for 0.5 sec adaptation F=15.23406,pb0.01) mean tactile localization performance for controlsubjects is significantly different than that of the subjectswith autism.

3. Discussion

The present study evaluated the effects of adaptation onspatial localization of a 25 Hz flutter stimulus on the dorsalsurface of the attended hand in adults with autism. Tactilelocalization performance did not change (i.e., spatial acuitywas the same) when the duration of adapting stimulation waschanged from 5.0 to 0.5 s. Thus, although in normal subjectslonger duration (5.0 s) adaptation results in a nearly 2-foldimprovement in spatial acuity relative to that measured underthe short-duration (0.5 s) adaptation condition (Tannan et al.,2006), duration of exposure to adapting stimulation fails tomodify spatial acuity in subjects with autism. Also notablewas the finding that when the duration of adaptation wasshort (0.5 s), subjects with autism actually outperformed sub-jects without autism. This superior performance not onlydemonstrates that the subjects with autism could clearlyunderstand and perform the tracking task, but it points out amajor difference between subjects with autism and thecontrol population: i.e., the subjects with autism exhibit noobtained from the individuals with autism show that there isno discernable difference between the results generated by thetwo different adapting stimulus conditions.

To determine across-subject consistency, the tracking datacollected under each condition for the subjectswith autism (20sessions in total) were averaged. As seen in the middle panelof Fig. 2, the localization distance of these subjects tracked to89 mm for both the 0.5 s and 5 s durations of adaptingstimulation. To summarize, in subjects with autism, thelocalization of tactile skin flutter stimulation did not changewith a 5 s adaptor compared to that with a 0.5 s adaptor. Inorder tomore directly compare the responsesmeasured undereach of the stimulus conditions, the tracking values obtainedfrom the last five trials across all subjects with autism wereaveraged, shown in the right panel of Fig. 2. These values were8.9830.534 mm for the short-duration adaptor and 9.1330.511 mm for the long-duration adaptor (meanSD error).Averaged spatial localization tracking performance obtainedfrom control subjects in the previous study (Tannan et al.,2006) is shown in the left panel of Fig. 2 for comparison, as are

B R A I N R E S E A R C Himprovement in tactile localization performance when theduration of adapting stimulation is increased.The observed improvement in tactile spatial localizationperformance that in control subjects accompanies increasingstimulus duration is presumed to reflect the spatial separationof the responses of primary somatosensory cortex to dual-siteskin stimulation. If this widely held presumption is correct,the findings obtained in the present study raise the possibilitythat local corticocortical functional connectivity in subjectswith autism may be substantially abnormal. While a numberof findings have demonstrated that long-range functionalconnectivity in subjects with autism is very different from thatpresent in the general population (for review, see Polleux andLauder, 2004; Herbert, 2005), it is unlikely that the differentobservations obtained from subjects with autism and controlsubjects reported in this study are attributable to differencesin long-range corticocortical connections. Instead, the im-proved tactile spatial localization that accompanies an in-crease in duration of adapting stimulation most likely wouldoccur as a result of local dynamic corticocortical interactionsthat operate to improve the contrast of the primary somato-sensory cortical response to a repetitive stimulus throughlateral inhibition. Based on this perspective, the measuresof tactile localization performance described in this paperappear to reflect the deficit in short-range parietal corticocor-tical connectivity identified in subjects with autism by Casa-nova and colleagues (Casanova et al., 2002, 2004, 2006). Suchchanges in connectivity could lead to the imbalance in exci-tation and inhibition that others have predicted to underliethe neocortical hyperexcitability and unstable activity in cor-tical networks characteristic of autism (Polleux and Lauder,2004; Rubenstein and Merzenich, 2003).

There is substantial evidence that in autism, cerebralcortical information processing not only is abnormal in thehigh-order neocortical areas that underlie language andsocial interaction skills, but also is deficient in the lower-order areas which receive and carry out the initial processingof the thalamocortical afferent activity evoked by sensorystimulation. Abnormalities of the stimulus-evoked responseof primary sensory cortex in subjects with autism have beendemonstrated using psychophysical testing procedures andneurophysiological recording methods. For example, somesubjects with autism exhibit hyper-arousal to natural sensoryinput, and a decreased ability to select among competingsensory inputs (Belmonte and Yurgelun-Todd, 2003; Gomotet al., 2002; Kootz et al., 1981; Plaisted et al., 2003). Further-more, regions of cortex devoted to stimulus-driven sensoryprocessing display excessive responsivity in subjects withautism, and exhibit little-to-no specificity in response to eitherthe location or modality of sensory stimulation (Belmonteet al., 2004; Baron-Cohen and Belmonte, 2005). Althoughmanyreports acknowledge a widespread neocortical dysfunction inautism, it is less widely recognized that the dysfunction isnon-uniforme.g., the excessive responsivity of primarysensory cortex to peripheral stimulation is accompanied (inthe same subject) by abnormally low activation/responsivityin cortical regions devoted to higher-order information pro-cessing (Belmonte et al., 2004; Belmonte and Yurgelun-Todd,2003).

Consideration of the above-described observations, togeth-

1194 ( 2 0 0 7 ) 1 1 6 1 2 3er with the relatively recent demonstration that autism isassociated with mutation in regions centered around the

that was attached to a free-standing, rigid platform (fabricated

1 1 5GABAA-3 receptor subunit gene, led some researchers (Bel-monte et al., 2004; Polleux and Lauder, 2004) to suggest that theneocortical dysfunction in this disorder may be attributable toa deficiency during early development in GABA-mediatedsynaptic neurotransmission. According to this view, theexcessive excitatory neurotransmission within low-orderneocortical processing areas that accompanies insufficientGABA-mediatedneocortical inhibition leads to the experience-driven abnormalities in neocortical functional connectivitycharacteristic of autism. More specifically, in subjects thatdevelop autism, abnormal neocortical information processingstrategies attributable to excess excitation in the early-developing low-order processing areas are viewed to directthe formation (via activity-dependent neuroplasticity) of along range inter-areal connectivity incapable of supporting thebetween-area communication and neuronal synchronizationessential for normal social interaction and language proces-sing skills (Belmonte et al., 2004; Just et al., 2004). Consistentwith this perspective are: (i) the recommendation that drugsthat promote GABAergic CNS synaptic neurotransmission beconsidered for early intervention and as potential therapeuticagents for autism (Belmonte et al., 2004; Bethea and Sikich,2007); and (ii) the neuromechanistic proposal that an increasedratio of excitation to inhibition in CNS information processingsystems accounts for the principal features of autism (Ruben-stein and Merzenich, 2003).

The results described in this paper used an approach(Tannan et al., 2006) that enables convenient and rapidacquisition of quantitative measures of somatosensory tactilespatial localization capacitya somatosensory perceptualcapacity that animal functional neuroimaging evidencestrongly reflects the status of GABA-mediated inhibitoryneurotransmission in primary somatosensory cortex (Simonset al., 2005; Tommerdahl et al., 2002; Whitsel et al., 1989;Juliano et al., 1989). Additionally, the findings reveal statisti-cally highly significant differences between the tactile local-ization performance of normal subjects and those withautism. The deficient tactile spatial localization performanceof subjects with autism demonstrated in the present studyappears consistent with the proposal that somatosensorycortical GABAergic inhibitory neurotransmission is deficientin autism. In addition, the inability of adapting stimulation toimprove tactile localization performance in subjects withautism (presumably because of the failure of such stimulationto dynamically recruit GABA-mediated local lateral inhibitoryinteractions in the responding region of primary somatosen-sory cortex) provides a potential explanation for the widelyknown, but poorly understood tendency for subjects withautism to perform poorly (relative to control subjects) onmorecomplex tasks requiring spatial and/or temporal integration,but better-than-normal when the task emphasizes apprecia-tion of local detail (for review, see Mottron et al., 2006). Theseconsiderations lead the authors to regard it as feasible that thebetter-than-normal performance of subjects with autism ontasks emphasizing appreciation of local detail may be due tothe complete absence in these individuals of adaptation inprimary somatosensory cortex. Critical to this view is the factthat the local GABA-mediated lateral inhibitory interactions

120 B R A I N R E S E A R C Hwepresume to underlie tactile adaptationmanifest a non-zerolevel of activity in a normal subject, and, accordingly, even inlocally) which enables convenient adjustment and mainte-nance of stimulus position. Spatial discrimination tasks gen-erate similar psychometric functions at the fingertip and thehand dorsum, differing essentially only by an order of mag-nitude (Schlereth et al., 2001; Mahns et al., 2006). A transver-sallyoriented lineararray (20mmin length)on thehanddorsumwas selected to receive the stimulation because: (1) innervationdensity across this skin region remains relatively constant, (2)the surface is easily accessible and permits convenient stimu-lator placement, (3) the surface is relatively flat, reducing con-founds of skin curvature present at other potential sites ofstimulation, and (4) it permits positioning of the subject's armthe absence of recent skin stimulation normal primarysomatosensory cortex is assumed to exhibit partial/incom-plete adaptation.

To our knowledge, this study has provided the firstobjective metric that clearly defines a difference between thecentrally mediated somatosensory discriminative capacitiesof the general population and a sample of individuals withautism. We consider it likely that further studies of this typewill provide valuable insights not only about the nature of theneocortical information processing defects that underlieautism, but other neurological disorders as well.

4. Experimental procedures

The subjectswere four Caucasianmales between the ages of 21and 42 years, clinically diagnosed with autism (i.e., AutisticDisorder or Asperger Disorder; DSM-IV-TR; APA, 2000), andnaive both to the study design and issue under investigation.They were recruited from the University of North CarolinaNeurodevelopmental Disorders Research Center Subject Reg-istry. All four individuals had been previously tested with theAutismDiagnostic Interview Revised (ADI-R; LeCouteur et al.,2003), the Autism Diagnostic Observation Schedule - Module 4(ADOS; Lord et al., 1999), as well as the Wechsler AbbreviatedScale of Intelligence (WASI; Wechsler, 1999). All four subjectsmet diagnostic criteria for autism on the ADI-R, and had aver-age to above average intelligence (WASI Full Scale IQs rangedfrom 87 to 129). Education levels were as follows: one subjectcompleted the 8th grade, two subjects completed high school,and one subject received a bachelors degree. Participantswerescreened for comorbid psychiatric diagnoses, peripheral in-jury, and other conditions that would affect somatosensation.The subjects gave informed consent and were paid $20/h fortheir time. All procedures were reviewed and approved in ad-vance by an institutional review board.

Sinusoidal vertical skin displacement stimuli were deliv-ered to the dorsum of the hand using a vertical displacementstimulator (CantekMetatronCorp., Canonsburg, PA) fittedwithaTwo-Point Stimulator (TPS). TheTPS and its use are describedin detail in two separate reports (Tannan et al., 2005a; Tannanet al., 2005b). A single probe tip (2 mm diameter) is positionedalong a linear axis 20 mm long at incremental steps of 1 mm(steperror of approximately 1%). The stimulator apparatuswasmountedonanadjustablemechanical armwith lockable joints

4 ( 2 0 0 7 ) 1 1 6 1 2 3and hand in a comfortable and stable position for the fullduration of an experimental session.

The subject was seated in a chair with the right arm placedresting on anX-ray bag filledwith glass beads. The investigatormolded the bag to fit the contours of the subjects arm, andwhen the subject was comfortable and the arm positioned toallow unimpeded access of the stimulator to the center of thedorsal surface of the right hand, the bag was made rigid byevacuating it of air (achievedbyconnecting thebag toa vacuumline). The subject was unable to see either the experimenter orthe stimulator and stimulus-control instrumentation. Whitenoise presented via headphones eliminated potential auditorycues. A micrometer permitted the stimulator transducer andprobe assembly to be lowered towards the predefined skin site.The micrometer position at which the digital display on thestimulator controllers registered a 0.l0.2 g change in resistiveforce was interpreted as the point at which the stimulatorprobe made initial contact with the skin.

A two-interval forced-choice (2IFC) tracking protocol wasused to evaluate spatial localization. The subject was in-structed to attend to the percept evoked by 25 Hz (100 mpeak-to-peak amplitude) vibrotactile stimulus to the righthand. Each trial consisted of three stimuli: (1) an adaptingstimulus (either 5 or 0.5 s in duration), (2) a standard sti-mulus (0.5 s) delivered at the same site as the adaptingstimulus, and (3) a test stimulus (0.5 s) delivered to a skin sitedifferent from the standard stimulus. Duration of the inter-stimulus (ISI) and inter-trial (ITI) intervals was held constantfor all runs at 2 and 30 s, respectively. All stimuli weresuperimposed on a pedestal of skin indentation (500 m),and following each stimulus the probe was retracted to aposition 500 m above the skin surface. Timing and stimulusposition diagrams of the experimental protocol, shown in Fig.3, are reported in a recent study (Tannan et al., 2006). The

l pof ang

121B R A I N R E S E A R C H 1 1 5 4 ( 2 0 0 7 ) 1 1 6 1 2 3Fig. 3 Stimulus position and timing diagram of experimentasubjects spatial localization threshold under two conditionssubject was instructed to report which of the two post-adapti

correct/incorrect response resulted in a decrease/increase in the d2006).rotocol. (A) A 2IFC tracking protocol was used to determine adapting stimulus duration (0.5 or 5 s). (B) In each trial, thestimuli was in the same place as the adapting stimulus. A

istance by 1mm. Each run consisted of 20 trials (Tannan et al.,

for a minimum of 20 trials in an attempt to identify the mini-

Acknowledgments

1 1 5This work was supported, in part by NIH R01 grant NS043375(M. Tommerdahl, P.I.), and NIH R01 grant HD042168 (G. Bara-nek, P.I.). VT received salary support fromNIH grant NS045685.CC was supported by NRSA T32 5T32HD040127-04. BLW wassupported, in part, by NIH RO1 grant NS037501.

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Vibrotactile adaptation fails to enhance spatial localization in adults with autismIntroductionResultsDiscussionExperimental proceduresAcknowledgmentsReferences