Overview about CAPD

INTRODUCTION

Auditory processing refers to processes that occur in the auditory system in response to acoustic stimuli. Auditory processing disorder is defined as a deficit in the processing of information that is specific to the auditory modality, that may be exacerbated in unfavorable acoustic environments and that may be associated with difficulties in listening, speech understanding, language development and learning (Jerger & Musiek, 2000). The concept of auditory processing disorder is not novel. Though the term auditory processing disorder was not used, Myklebust (1954) had defined this deficit. However, over these fifty years, audiologist's understanding of neurophysiology of the auditory system, assessment of auditory processing disorder and management of auditory processing disorder has expanded rapidly.

It is known that every structure in the auditory system, from external ear to temporal lobe, contribute to hearing but the role of certain structures are more important than others in understanding speech. The central auditory nervous system is a complex system in which parallel as well as sequential processes take place (Musiek & Oxholm, 2000). Contributions to anatomy and physiology of the central auditory nervous system have been and continue to be made from careful study of patients with lesions of the auditory system. Such studies have now been enhanced with the use of PET and fMRI studies as they provide insight about the locus and degree of function in normal and abnormal states. These techniques have the advantage of making it possible to study the processing of complex stimuli such as speech in humans. Continued research has thrown light on functioning of not only afferent system but also efferent system, especially the role of olivocochlear bundle in hearing in noise.

Understanding of auditory plasticity i.e. plasticity in the auditory nervous system has helped in reviving the management strategies. It has been now proved that though the brain is more plastic in early stages of development through adolescence, even the adult brain is plastic (Musiek, 2002). Functional imaging, magneto encephalography and auditory evoked potentials have emerged as non-invasive tools for studying auditory plasticity in humans. It has been observed that there can be alteration in the central auditory nervous system due to acoustic stimulation or lack of stimulation. Types of neural changes that are noted include neurochemical, physiological and structural changes (Musiek & Berge, 1998). Recent investigations have shown training related changes in cortical potentials (Trembley et al., 2001; Trembley & Kraus, 2002).

Intrinsic CANS redundancy is based on the multiplicity of neural pathways, centers, and decussarions; interrelated ness of these pathways, centers, and decussations; and bi­lateral representation of the auditory system. Extrinsic re­dundancy stems from aspects of the auditory signal such as the frequency range, sound duration, context in which the message is given, rhythm, and the individual's familiarity with the semantic, syntactic, and phonologic rules of lan­guage. Extrinsic redundancy is inherent in the speech mes­sage and enables the message to be perceived even when parts of the message are degraded or absent. Intrinsic re­dundancy is reduced by CANS lesions but the effect of this reduction on performance on conventional speech-recognition tests is not apparent unless the lesion affects a significant proportion of the neurons and nuclei in the CANS. Extrinsic redundancy of speech can be reduced by various means of degradation such as filtering, time altera­tion, or noise. Since pure-tone signals have fewer parame­ters than speech signals, the extrinsic redundancy of pure-tones is more difficult to reduce than that of speech.

The principles of "subtlety" and "bottleneck" also apply when investigating central auditory function (Jetger, 1960a). The former principle states that the subtlety of the auditory signs of central auditory dysfunction increases as the level of the lesion becomes more rostral. Thus, at pe­ripheral levels, a lesion may be detected by simple tests such as the audiogram. At central levels, however, the lesion can be detected only by more complex tests such as distorted speech tests. According to the bottleneck principle, a com­plex signal such as speech encounters neural congestion at the junction of the eighth nerve and brainstem; lesions at these sites have a very deleterious effect on speech-recognition scores whereas lesions more peripheral or central to these sites have less deleterious effects on speech-recognition scores.

Incidence and Prevalence of Auditory Processing Disorder

There is dearth for information on the incidence and prevalence of auditory processing disorder. Chermak (2001) estimated that auditory processing disorder occurs in 2 to 3 % of children, with a 2:1 ratio between boys and girls. The prevalence rate in older adults varies from 20 % (Cooper & Gates, 1991) to 70 % (Stach et al. Cited in Chermak, 2001). Some of the population in whom auditory processing may be affected include children learning disorder (Chermak, 1997; Radhika, 1997; Guruprasad, 2000; Srividya, 2002), specific language impairment (Korpilahti & Lang, 1995; Kaur, 2003), aphasics (Divenyi & Robinson, 1989 cited in Chermak, & Musiek, 1997; Gupta, 2003) and children with history of otitis media (Bellis, 1996; Tyagi, 2002; James, 2003).

BEHAVIOR CHARACTERISTICS OF THE CHILD WITH CENTRAL AUDITORY PROCESSING DISORDERS (CAPD)

Children with central auditory processing disorders often have the following hearing difficulties,and behavior characteristics.

HEARING DIFFICULTIES

1.   Inability to follow verbal commands of instructions, particularly if they are long and complex.

2.   Gives inappropriate response to questions.

3.   Inconsistent response to auditor)' stimulation (sometimes responds appropriately, sometimes not) or inconsistent auditory awareness (one-to-one conversation is bet­ter than in a group).

4.   Repeatedly asks for repetition. Poor auditory discrimination skills—misunder­stands what is said.

5.   Poor listener: Ignores sound totally (ignoring because he or she cannot process)— difficulty attending to class work..

6.   Difficulty with auditory localization skills.

7.   Says what/huh: Is buying time to process or figure out what is being said.

8.   Sometimes responds too quickly (before instructions are complete])' given ] to avoid fear of failure, although this impulsive behavior actually may increase his or her failure. By this over-hasty responding, child is not aware of the rest of the incoming message.

9.   Discrepancy in performance on verbal versus written instruction.

10.   Frightened or upset by loud noise.

11.   Uses a loud voice.

12.   Withdraws in a group or when there is excessive noise.   May have poor "social skills" and be immature for age.

BEHAVIOR CHARACTERISTICS

Academic Performance

1. Having academic problems (especially in reading, spelling and writing) nonachievers, academic failures, performing below expected academic levels.

2. No correlation between I.Q. and CAPD, but there is often a discrepancy between IQ. and achievement.

3. Difficulty completing class assignments.

4.   Short attention span, fatigued easily by a long or complex activity.

5.   Easily distracted by auditory or visual stimuli.

6.   Not able to remember long or short term information. (Is the difficulty in storin° or did he get the information auditorally in the first place?)

Behavior

1.   Hyperactive—high activity levels. Acting out in class with classroom behavior

problems,

2.   Hypoactive—passive, reserved, lethargic. Trouble beginning task, seldom com­pletes a task. Very fatigued after school (goes home and goes to sleep).

3.   Loners—may play with younger children or adults rather than with peers (.can better control conversation with younger children or adults).

4.   Poor self-concept fin older group there is a high drop-out rate).

5.   Reluctance to try new tasks for fear of failure—"I can't do it."

6.   "Don't care" attitude.

7.   Emotional and social overlays-—inadequacy, rejection, unacceptability, depression

in the older child (may result in delinquency).

Other

1.   Uncoordinated.

2.   Difficulty with time concepts.

3.   Speech and language problems (obvious or subtle).

Diagnostic Problem (Jerger & Musiek, 2000)

􀂄 Other types of childhood disorders may exhibit similar behaviors, e.g., attention deficit hyperactivity disorder (ADHD), language impairment, reading disability, autistic spectrum disorders

􀂄 Some audiological test battery may fail to distinguish CAPD from children with other problems

􀂄 Other confounding factors, e.g., lack of motivation, attention, cooperation and

Understanding

Differentiation Between CAPD & ADHD

􀂄 Only 2 (i.e., inattention & distractibility) of the 11 most frequently cited behaviors reported as common to both condition

Assessment of Auditory Processing Disorder

The history of the assessment of the auditory processing disorder dates back to 1954, when Bocca and colleagues developed the low pass filtered speech test to assess central auditory nervous system. Over the years a number of tests were developed using degraded acoustic stimuli such as time compressed speech, speech with ipsilateral or contralateral competing message, dichotic stimuli. Earlier, tests were available for only assessment of the afferent system but now there are tests for assessment of efferent system as well. Initially audiologists attempted to localize the site of dysfunction based on the results of various tests. However, the redundancy in the central auditory nervous system makes it difficult to assess any structure independently and makes it difficult to localize the site of dysfunction. In the recent years the emphasis is more on assessing various processes that are involved in auditory processing rather than different anatomical loci. The processes that are normally assessed include temporal processing, binaural interaction, binaural integration, binaural separation and auditory closure.

No single test can assess the variety of functions required by the central auditory nervous system in different listening situations; therefore it is necessary to use a test-battery approach. On the other hand of the spectrum, some believe that the difficulties experienced in everyday life situations involve various cognitive processes that are intimately intertwined with auditory processes and include tests to assess memory, attention and decoding (Medwrsky, 2002)

The assessment recommended by the American Speech-Language-Hearing Association (1995) includes the following:

•    History

•    Observation of auditory behaviors

•   Audiological test procedures: pure tones, speech recognition, immittance, temporal processes, localization & liberalization, low redundancy monaural speech, dichotic stimuli, binaural interaction procedures

•    Speech-language pathology measures:

The test used can be behavioral or electrophysiological, linguistic or non-linguistic. Both screening and diagnostic test procedures are available to assess these functions. Though the processes that need to be assessed are defined, there is no consensus among audiologists about the specific tests that need to be included in the test battery. The test battery is chosen based on a number of factors, which include subject-related factors such as age, complaints, language level, intelligence and the tests/ facilities available in the clinic.

Minimum requirements required for carrying out a majority of the behavioral tests are a calibrated audiometer, a CD player and a CD of the test material. Advancement in technology has made it easier to develop the tests for auditory processing disorder and store it in a CD. Thus tests for auditory processing disorders are not far from the reach of the audiologists even in India. Some of the tests available in India with norms on Indian population include Dichotic CV test (Yathiraj, 1999), Dichotic Digit test (Shivashankar&Herlekar, 1991; Regishia, 2003), Pitch Pattern test (Tiwari & Vanaja, 2003), Duration Pattern test (Tamane, 2003), Gap Detection test (Shivaprakash & Manjula, 2003), Screening Test for Auditory Processing (Yathiraj & Mascarenhas, 2003).

Though the results of behavioral tests are affected by a number of factors other than auditory processing disorder, behavioral tests are more useful in assessment of auditory processing when compared to electrophysiological tests. Electrophysiological tests are administered when it is not feasible to administer behavioral tests or to supplement the results of behavioral tests. Electrophysiological tests are the choice of tests in identifying central auditory problems in children, who do not have sufficient speech and language (Ajith kumar & Vanaja, 2002) and those who have poor speech identification scores in even in quiet (Vanaja & Manjula, 2002).

Classification and Etiology:

Although no CAPD subtypes have been universally accepted, investigators have attempted to document the heterogeneous nature of CAPD by describing the characteristics in terms of commonalities (Bellis and Ferre, 1999; Katz, 1992; Musiek and Gollegly, 1988). For example, Musiek and Gollegly (1988) reported three causes of CAPD in children with learning disabilities: one based on neuro-maturational delay, a second resulting from a neuromorphologic disorder, and a third arising from neurologic disease or insult. Recent research suggests inefficient interhemispheric transfer of auditory information and/or lack of appropriate hemispheric lateralization, and atypical hemispheric asymmetries. A much less frequent etiology of CAPD is a neurologic disorder, insult or abnormality in children (Jerger and Musiek, 2000; Kraus et al, 1996; Musiek, Baran and Pinheiro, 1994). In   adults, CAPD may result from accumulated damage or deterioration to the central auditory nervous system due to neurologic/neurodegenerative diseases, disorders or insults, and the aging process itself, which leads to poorer neural synchrony, slower refractory periods, decreased central inhibition, and interhemispheric transfer asymmetry/deficits (Bellis, Nicol and Kraus, 2000; Bellis and Wilber, 2001; Jerger, Greenwald, Wambacq, Seipel and Moncrieff, 2000; Pichora-Fuller and Souza, 2003; Tremblay, Piskosz and Souza, 2003; Williot, 1996; Woods and Clayworth, 1986).

Categories of APD

Four major categories have been suggested (Katz and Smith, 1991; Katz, 1992). The categories are not mutually exclusive and their characteristics may range from borderline to severe and may be noted from SSW and other central tests.

Decoding type: abnormal performance in the right competing and left non competing conditions as well as order effect low/high and ear effect high/low Response biases are associated with poor phonemic decoding skills. They are likely to have all or some of the following: poor phonic skills (reading and spelling) as well as receptive language and articulation difficulties in early years.

Tolerance-Fading Memory type:  abnormal left competing and the order high/low and ear low/high are signs of one or both of the following:  

 (a) difficulty in blocking out background sounds, and (b) short term memory problem. They are not as educationally handicapped as poor decoders, but their classroom behavior is generally more noticeable (inattentive, hyperactive). They may have reading comprehension problems and expressive difficulties in speaking or writing and poor handwriting.

Integration type: sharp left competing peak of errors, very long delays in responding on the SSW or when questioned. There are 2 subtypes:

(a)   severe auditory-visual integration difficulties and severe reading and spelling dysfunction, poor in phonics (dyslexic).

(b)  Less severe in its learning problems, performing much like TFM subjects, peculiar behaviors, poor responders on pure tone tests.

Organization type: significant number of reversals on SSW. It may manifest as sloppiness, poor spelling, and difficulty in keeping things in order, visual reversals (b/d).

Comorbid Conditions

Many patients with CAPD will also present with one or more comorbid conditions. These include speech and language disorders, learning disability, attention deficit disorders with or without hyperactivity, frank neurological involvement of the CANS, peripheral hearing loss, psychological disorders and emotional disorders (Baran and Musiek, 1999; Chermak and Musiek). Causal relationships have been difficult to establish (Baran, 2002). Relationships are complex, interconnected and most likely not unidirectional. In some individuals the two conditions simply coexist and they are not directly linked to one underlying cause. For example, a person who has a peripheral hearing loss and then acquires a CAPD as a result of a neurological insult. It is important, that a comprehensive, and preferably multidisciplinary, assessment of the individual’s auditory, linguistic, cognitive, academic and vocational functioning be undertaken. The degree of neural synchronization and connectivity among brain regions is reduced, leading to the frequently observed range of comorbid conditions (e.g: CAPD and attention deficit disorder, language impairment, learning disability).

Disorders associated with Auditory Processing Disorders

For many years APD has been associated with learning disabilities (LD), especially reading problems (Monroe, 1932; Orton, 1964; Sawyer, 1981). Difficulty with phonics and limitations in reading comprehension are both associated with AP dysfunction (Border, 1973; Fried et al, 1981; Shankweiler and Liberman, 1989). In addition, spelling (Bannatyne and Wichiarajote, 1969) and foreign language skills (Sparks et al, 1991) are often depressed in those with APD.

Those with poor communicative skills such as articulation problems (Mange, 1960; Stovall et al, 1977) as well as both receptive and expressive language disorders (Tallal, 1976; Burns and Canter, 1977; Lubert, 1981; Lasky and Cox, 1983; Sloan, 1986) are also at risk for APD. Research is also being done in terms of APD in schizophrenia (Yozawitz et al, 1979), attention deficit disorder (ADD) (Ludlow et al, 1983; Keller, 1992), prison populations (Katz, Singer and Faming, 1988) and Alzheimer’s Disease (Grimes at al, 1985).

Audiological Findings:

In isolated brain stem lesion, acoustic reflexes are absent (either ipsilaterally, contralaterally, or both, depending on the size and site of the lesion), OAEs and CM are recordable, ABR waves I and II are recordable, absent/delayed waves III AND V, and abnormal psychoacoustic tests. Rapin and Gravel (2003) classified these results as representing a central auditory disorder.

Behavioral tests

Pure Tone Audiometry

PTA thresholds for patients with CAPD are, by definition, normal, although individuals with CAPD can also present comorbid hearing impairment, particularly among older adults (Stach, Spretnjak and Jerger, 1990). However, on the aerage, PTA thresholds are normal and do not fluctuate.

Speech Audiometry

Many patients with CAPD present the auditory complaint of difficulty hearing in background noise (Bellis, 2003). Jerger and Musiek (2002) stated: “One important dimension in the differential diagnosis of APD is to differentiate APD from speech understanding problems due to malfunction at either the auditory periphery or the low brainstem level.”

Electroacoustic Assessment

Immittance

Tympanometry is generally normal in patients with CAPD, although children with CAPD may experience otitis media and resulting abnormal Tympanometry (Willeford and Burleigh, 1985). Generally, acoustic reflexes are present at normal levels in patients with CAPD, unless there is a lower brainstem lesion. In some patients with CAPD who had a positive history of otitis media, however, acoustic reflexes may be slightly elevated or absent due to the middle ear effect of the otitis media (Willeford and Burleigh, 1985).

Thomas, McMurry and Pillsbury (1985) described ipsilateral and contralateral acoustic reflex findings in a rather heterogeneous series of 62 children with normal pure-tone hearing thresholds and Tympanometry and referred for suspected delays in development of language, learning disabilities or disorders of auditory processing. Remarkably 32% of the subjects showed acoustic reflex abnormalities in both the ipsilateral and contralateral signal conditions.

Expected abnormalities in acoustic reflex findings are elevated thresholds, reduced amplitudes, or total absence of the acoustic reflex. At the other extreme of the spectrum of abnormalities, Downs and Crum (1980) described in four children with APD, “hyperactive” acoustic reflexes, characterized by unusually low (better than expected) thresholds. The authors considered the pattern of findings as evidence of “decreased central inhibition of the peripheral auditory system” in some children with APD.

Jerger, Jerger and Loiselle (1988) reported a third category for acoustic reflex findings, namely normal acoustic reflex findings in a series of young children (3-8 years) who had evidence of APD on dichotic listening tasks.

For children diagnosed with APD on the basis of speech perception measures most sensitive to cortical and interhemispheric (corpus callosum) auditory dysfunction, abnormalities in the lower brainstem pathways involved in the acoustic reflex arc would be unlikely. On the other hand, an unselected group of children with suspected APD would by chance include some patients with dysfunction within more caudal regions of the central auditory nervous system, including abnormalities in excitatory (afferent) pathways (elevated, diminished or absent acoustic reflexes) or, at the other end of the abnormality spectrum, unusually brisk reflexes with less intense stimuli.

OAE

Individuals with CAPD are expected to have normal OAEs. The obvious exceptions are the patients who have histories of protracted otitis media, resulting in absent or abnormal OAEs, which reflects a mild impairment of sound transmission through the middle ear (Rappaport and Provencal, 2002).

Musiek and Chermak analyzed Audiological records for a series of 65 children (5-20 years) referred for assessment of APD. Approximately one-in-five (21%) of the 65 children had anabnormal finding on PTA, as defined by a threshold at or exceeding 20 dBHL for one or more of the test frequencies. Among this subset of children, 78.5% had average hearing thresholds meeting common criteria for hearing impairment (>20dBHL) within the speech frequency region. More than one-third of the series of children (35.5%) showed OAE abnormalities. Clearly, the proportion of children with DPOAE abnormalities exceeded the proportion with abnormal audiogram findings.

In a study of what is referred to as King Kopetsky syndrome or, mostly in the United Kingdom “obscure auditory dysfunction”, Stephens and Zhao (2000) reported “notches” in DPOAEs and also abnormalities in TEOAEs even though pure-tone audiometry was normal. Muchnik and colleagues (2004) studied contralateral suppression of TEOAEs in 13 children from 8-13 years who were diagnosed with APD. In comparison to a control group, the children with APD showed significantly less suppression of TEOAE activity. According to the authors, their results imply that some children with APD present low activity of the MOCB system, which may indicate a reduced auditory inhibition function and affect their ability to hear in the presence of noise.

Electrophysiological Assessment

As shown in the figure, acoustic reflex and auditory evoked response abnormalities are not uncommon in an unselected series of children evaluated clinically for APD (Hall and Baer, 1992; Hall and Mueller, 1997). The proportion of abnormalities is higher as expected, for cortical auditory evoked responses (AMLR, ALR and P300) than for ABR.

Cochlear Microphonic

In CAPD, the CM is expected to be of normal amplitude. To ensure accurate interpretation, clinicians are encouraged to obtain CM recordings using both rarefaction and condensation clicks, which allows ABR waves to be separated from the CM response (Berlin et al, 1998).

Auditory Brainstem Response

Most investigators report normal ABRs in children with CAPD (Hurley, 2004; Mason and Mellor, 1984; Roush and Tait, 1984). However, reports of compromised ABR in patients with CANS dysfunction demonstrate the importance of this potential in the central auditory processing battery (Musiek, Charette, Morse and Baran, 2004). ABR is a valuable tool in CAPD assessment as it will provide objective evidence of CANS involvement, especially in patients with protracted histories of otitis media or hyperbilirubinemia (Dublin, 1985).

Mason and Mellor (1984) compared AER findings for eight children with severe language disorders and six with severe motor speech disorders. Data also were collected for an age-matched normal control group. ABR latency was equivalent among groups, although amplitude was smaller in the children with speech and language disorders for all wave components. AMLR and ALR latency values also were comparable among groups. Grillon, Courchesne and Akshoomoff (1989) recorded ABR and AMLR from 8 subjects (mean of 16 years) with “receptive developmental language disorder”. There was no significant difference between an RDLD group and an age-matched control group for ABR and AMLR.

Auditory Middle Latency Response

The AMLR recording is also a valuable tool in assessing maturity of the central auditory pathway with a multiple electrode montage being recommended in CAPD assessment (Chermak and Musiek, 1997). The multi-site amplitude measures are compared over hemispheres to determine if there is an electrode effect (Musiek, Baran, and Pinheiro, 1994) or ear effect (Musiek et al, 1999).

Some studies (Grillon et al, 1989; Mason and Mellor, 1984) reported no significant difference in the detection, or the latency and amplitude values, of the Pa component in children with learning disabilities (LD) or language impairment.

A typical finding for AMLR in children with APD is latency prolongation and, particularly, amplitude reduction for the Na and Pa components with an electrode over one or both cerebral hemispheres. Among auditory evoked responses, the AMLR and the P300 response are abnormal in approximately 40% of patients referred for an APD assessment (Hall and Mueller, 1997).

Schochat, Musiek, Alonso and Ogata (2006) have demonstrated the ability of the AMLR to differentiate children behaviorally diagnosed with APD from matched controls. The difference was seen primarily in the amplitude of the AMLR. Diagnostically, it has been shown that the MLR is sensitive and specific to involvement of the central auditory system (Kileny, Paccioretti and Wilson, 1987; Musiek, Charette, Kelly, Lee and Musiek, 1999).

Auditory Long Latency Response

Jirsa and Clontz (1990) reported prolonged P300 latencies in a group of children with APD. Non auditory factors may affect the P300 recording (Knight, 1990); thus, an absent or abnormal ALR and P300 recording does not warrant a diagnosis for CAPD.

The N1 and P2 have been shown to be either reduced in amplitude and/or delayed in latency for children with APD and language disorders (Jirsa and Clontz, 1990; Tonnquist, 1996). Davies (2002) included ALR components in an investigation of cortical auditory evoked responses in children with learning disabilities, including APD, and a control group of children with no history of learning or auditory problems. The P2 component was not consistently recorded, and was typically small in amplitude. There were also significant group differences for the ALR P1 (shorter latency in the APD group) and the N1 component (smaller amplitude in the APD group).

Purdy, Kelly and Davies (2002) conducted an investigation of multiple AERs (ABR, AMLR, ALR and P300) in a small group (n=10) of children (7-11 years) with the rather general diagnosis of learning disabilities. Purdy et al (2002) failed to record a Pb component. They did report AMLR differences for the LD versus control group, including delayed Na latency and smaller amplitude (less negativity) for the Nb component. Pa latency prolongation were not statistically significant.

P300

Most papers describe P300 response findings in children with other disorders that sometimes include auditory dysfunction, for example, autism, language impairment, and learning disabilities (Purdy et al, 2002). There is evidence that lesions in the auditory regions of the cortex compromise the P300 in both latency and amplitude (Knight, Scabini, Woods and Clayworth, 1989; Musiek, Baran and Pinheiro, 1992).

MMN

Case reports and group studies on the clinical use of MMN in the diagnosis of APD date back to the early 1990s. Among them are studies of the MMN response in dyslexia, an auditory-based reading disorder. Leppanen and  Lyyinen (1997) found differences in the MMN response for infants with a family history of delayed speech acquisition and dyslexia versus a control group. Baldeweg et al (1999) reported abnormal MMN responses in persons with dyslexia using pure tone standard and deviant stimuli. Baldeweg et al (1999) reported a correlation between the MMN findings and behavioral performance in processing the stimuli. The very early detection with the MMN response of children at risk for such common and academically critical disorders as dyslexia helps in early intervention and preventive management.

New Directions

In APD assessment, measurement and analysis of the AMLR Pb wave would be useful because the Pb wave represents contributions from regions of the auditory cortex not tapped by the Pa wave, presumably secondary auditory regions within the superior temporal gyrus of the temporal lobe. It appears that the AMLR Pb wave is the same as the P1 wave of the ALR. Nelson, Hall and Jacobson (1997) showed that the AMLR Pb wave is recorded consistently, even in children , with modification of the test protocol.

With one test protocol, the AMLR Pb component is evoked with a pair of stimuli, a measurement approach sometimes referred to as the “double click paradigm” (Rosburg et al, 2004).

The waveforms in the top of the figure depict an AMLR recorded with a conventional stimulus paradigm in which the response is averaged for a series of identical stimuli presented at a consistent rate (eg: 1/sec) and the patient is not attending to the stimuli. In the simplest version of the sensory-gating stimulus paradigm (middle waveform) the two identical stimuli (eg: both clicks or both tone bursts at same frequency) are presented as a pair. The first stimulus (S1) is followed relatively soon after (eg: <500ms) by the second stimulus (S2), and then a longer interval (eg:8 to 10 seconds) separates the stimulus pair from the subsequent signal pair. Some authors refer to the first and second stimulus as the “conditioning” and “test” stimuli respectively (Ambrosini et al, 2001; Kisley et al, 2003). The amplitude change from the first to the second stimulus is calculated as a ratio (S2/S1) or simple mathematical difference (S2-S1), with lower ratios and larger differences consistent with more inhibition or “gating out” of irrelevant sensory input. If the second stimulus is different from the first or novel stimulus, then larger ratios and smaller differences is consistent with “gating in” or a preattentive response the brain indicating the ability to identify novel or potentially significant stimuli (Boutros and Belger, 1999; Rosburg et al, 2004). This novel approach for eliciting, recording and analyzing the Pb of the AMLR seems to be well suited for clinical application in children with APD.