EEG Assessment and Treatment of Seizure activity in Autism Spectrum Disorder
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EEG Assessment and Treatment of Seizure activity in Autism Spectrum Disorder
Robert Coben, PhD Presented at Autism One 2009 Chicago, Illinois May 24, 2009
Seizures in ASD
• Prevalence of at least 20% (Canitano, 2007) • As high as 46% (Hughes & Melyn, 2005) • Average prevalence of 36% • Associated with increasing cognitive/intellectual disability • May be more likely • Paroxysmal discharges occur at even higher rates in ASD • Spikes appear to reflect underlying intracranial foci, morphological brain abnormalities, and/or metabolic disturbances
Regression in ASD
• 20 – 30% of all autistic children have a regression in speech or behavior early in life (Canitano, 2007) • More severe symptomatology, speech and behavior • The EEG is abnormal in a greater proportion of autistic children that regress • Is regression associated with seizure disorders in ASD? • Mixed findings: some show seizures to be related to regression and others do not • No other factor has been found to be related to regression • EEG’s are recommended in the evaluation of autistic disorders
Case 1
• 6 year old boy diagnosed with PDDnos • Didn’t speak until 3, with poor expression and understanding • G/C free diet, multiple supplements, multisensory intervention all without significant improvements • Presented with poor communication, social skills, repetitive interests, low muscle tone and academic delays
• ADOS = 12 (AS = 8; A = 12) • ADI-R: > cutoff all 4 scales • PDDBI Autism = 46 (> 40) • WISC-IV FSIQ = 59 • Severe visualperceptual impairments (< 1st %ile) • Expressive and
Case 2
• 7 year old by diagnosed with PDD at the age of 5 • Born 36 weeks gestation due to gestational diabetes with high liver enzymes • Walked at 2 years and spoke in utternaces by 3 years • Difficulties with focusing, sitting still, temper outbursts, socialization, head • FSIQ = 80; Verbal IQ 75; Performance IQ = 90 • Impairments in receptive language, motor sequencing, visual-perceptual analysis. • Unable to read or identify letters
Case 3
• 8 year old boy diagnosed with PDD/Asperger’s (???) • Epilepsy (complex partial) since the age of 4 ½ taking Trileptol • Spoke in sentences at 2 years of age but with poor initiation and reciprocity • Difficulties with attention, transitions, social boundaries, eye • ADOS = 7 (AS = 7) • ADI-R: all 4 scales above cutoff/Recip Social Inter = 21 (10) • PDDBI Autism = 46 (40) • WISC-IV FSIQ = 99 • NP impairments in affect recognition, theory of mind, visual-perceptual integration, math and writing • SRS Total t-score =
What is Neurofeedback?
Human EEG biofeedback was first attempted in the 1960s by Joe Kamiya at the University of Chicago. Early investigations focused on operant conditioning of alpha brain waves primarily to facilitate deep relaxation and meditation. SMR/beta biofeedback developed from operant conditioning of cats' EEG. Barry Sterman of UCLA serendipitiously discovered that when cats were exposed to toxic chemicals that usually induce epileptic seizures, those who had been trained in the middle to high frequency range (12-20 Hz) from a previous unrelated experiment had greater latency to seizure onset, and a higher threshold for seizure onset, than untrained cats. These results were replicated in monkeys and humans. The results with humans were subsequently replicated in some twelve research centers, comprising some twenty studies. After several years of treating patients with intractable seizures with SMR biofeedback, it was noted that the hyperactive children not only had decreased seizure activity, but their behavior improved as well. In the mid 70's, Joel Lubar at the University of Tennessee examined the effect of neurofeedback on hyperactivity absent
EEG-trained cats
Coben, R. (2009). Efficacy of Connectivity Guided Neurofeedback for Autistic Spectrum Disorder: Controlled Analysis of 75 cases with a 1-2 year follow-up. Journal of Neurotherapy, 13 (1), 81.
• N = 110; 85 (expt), 25 (wlc) • Age = 5 – 22 (mean = 9.72) • IQ = 50 – 130 (mean = 92) • ATEC = 35 – 105 (mean = 55) • Sessions = 30 – 170 (mean = 74 / 8 months) • Matched for age, meds, IQ, ATEC,
55 %
52 % 48 %
57 %
67 %
56 %
48 %
47 % 43 %
ANOVA atectotalchangepercentout Sum of Squares Between Groups 726.906 Within Groups 19437.809 Total 20164.715 df 2 57 59 Mean Square 363.453 341.014 F 1.066 Sig. .351 atectotalchangepercentout Sum of Squares Between Groups 144.584 Within Groups 27543.146 Total 27687.730
ANOVA
df 2 62 64
Mean Square 72.292 444.244
F .163
Sig. .850
• Groups divided into quartiles based on IQ and ATEC. • IQ 50 – 83 / 84 – 103 / 104 – 130 • ATEC 35 – 50 / 51 – 64 / 65 – 105 • Compared this estimates of level of functioning to ATEC change scores. • No significant differences.
QEEG changes I: Frontal hyperconnectivity
QEEG changes II: Right posterior hypoconnectivity
EEG biofeedback – Case 1 (case 2)
• 7 year old by diagnosed with PDD at the age of 5 • Born 36 weeks gestation due to gestational diabetes with high liver enzymes • Walked at 2 years and spoke in utternaces by 3 years • Difficulties with focusing, sitting still, temper outbursts, socialization, head • FSIQ = 80; Verbal IQ 75; Performance IQ = 90 • Impairments in receptive language, motor sequencing, visual-perceptual analysis. • Unable to read or identify letters
EEG biofeedback – Case 1 (case 2)
EEG biofeedback – Case 1 (case 2)
EEG biofeedback – Case 1 (case 2)
Neuropsychological measures all within normal limits, except receptive language rated as mildly impaired. Went from being alexic
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2 (20 sessions)
EEG Assessment and Treatment of Seizure activity in Autism Spectrum Disorder
Robert Coben, PhD Presented at Autism One 2009 Chicago, Illinois May 24, 2009
Seizures in ASD
• Prevalence of at least 20% (Canitano, 2007) • As high as 46% (Hughes & Melyn, 2005) • Average prevalence of 36% • Associated with increasing cognitive/intellectual disability • May be more likely • Paroxysmal discharges occur at even higher rates in ASD • Spikes appear to reflect underlying intracranial foci, morphological brain abnormalities, and/or metabolic disturbances
Regression in ASD
• 20 – 30% of all autistic children have a regression in speech or behavior early in life (Canitano, 2007) • More severe symptomatology, speech and behavior • The EEG is abnormal in a greater proportion of autistic children that regress • Is regression associated with seizure disorders in ASD? • Mixed findings: some show seizures to be related to regression and others do not • No other factor has been found to be related to regression • EEG’s are recommended in the evaluation of autistic disorders
Case 1
• 6 year old boy diagnosed with PDDnos • Didn’t speak until 3, with poor expression and understanding • G/C free diet, multiple supplements, multisensory intervention all without significant improvements • Presented with poor communication, social skills, repetitive interests, low muscle tone and academic delays
• ADOS = 12 (AS = 8; A = 12) • ADI-R: > cutoff all 4 scales • PDDBI Autism = 46 (> 40) • WISC-IV FSIQ = 59 • Severe visualperceptual impairments (< 1st %ile) • Expressive and
Case 2
• 7 year old by diagnosed with PDD at the age of 5 • Born 36 weeks gestation due to gestational diabetes with high liver enzymes • Walked at 2 years and spoke in utternaces by 3 years • Difficulties with focusing, sitting still, temper outbursts, socialization, head • FSIQ = 80; Verbal IQ 75; Performance IQ = 90 • Impairments in receptive language, motor sequencing, visual-perceptual analysis. • Unable to read or identify letters
Case 3
• 8 year old boy diagnosed with PDD/Asperger’s (???) • Epilepsy (complex partial) since the age of 4 ½ taking Trileptol • Spoke in sentences at 2 years of age but with poor initiation and reciprocity • Difficulties with attention, transitions, social boundaries, eye • ADOS = 7 (AS = 7) • ADI-R: all 4 scales above cutoff/Recip Social Inter = 21 (10) • PDDBI Autism = 46 (40) • WISC-IV FSIQ = 99 • NP impairments in affect recognition, theory of mind, visual-perceptual integration, math and writing • SRS Total t-score =
What is Neurofeedback?
Human EEG biofeedback was first attempted in the 1960s by Joe Kamiya at the University of Chicago. Early investigations focused on operant conditioning of alpha brain waves primarily to facilitate deep relaxation and meditation. SMR/beta biofeedback developed from operant conditioning of cats' EEG. Barry Sterman of UCLA serendipitiously discovered that when cats were exposed to toxic chemicals that usually induce epileptic seizures, those who had been trained in the middle to high frequency range (12-20 Hz) from a previous unrelated experiment had greater latency to seizure onset, and a higher threshold for seizure onset, than untrained cats. These results were replicated in monkeys and humans. The results with humans were subsequently replicated in some twelve research centers, comprising some twenty studies. After several years of treating patients with intractable seizures with SMR biofeedback, it was noted that the hyperactive children not only had decreased seizure activity, but their behavior improved as well. In the mid 70's, Joel Lubar at the University of Tennessee examined the effect of neurofeedback on hyperactivity absent
EEG-trained cats
Coben, R. (2009). Efficacy of Connectivity Guided Neurofeedback for Autistic Spectrum Disorder: Controlled Analysis of 75 cases with a 1-2 year follow-up. Journal of Neurotherapy, 13 (1), 81.
• N = 110; 85 (expt), 25 (wlc) • Age = 5 – 22 (mean = 9.72) • IQ = 50 – 130 (mean = 92) • ATEC = 35 – 105 (mean = 55) • Sessions = 30 – 170 (mean = 74 / 8 months) • Matched for age, meds, IQ, ATEC,
55 %
52 % 48 %
57 %
67 %
56 %
48 %
47 % 43 %
ANOVA atectotalchangepercentout Sum of Squares Between Groups 726.906 Within Groups 19437.809 Total 20164.715 df 2 57 59 Mean Square 363.453 341.014 F 1.066 Sig. .351 atectotalchangepercentout Sum of Squares Between Groups 144.584 Within Groups 27543.146 Total 27687.730
ANOVA
df 2 62 64
Mean Square 72.292 444.244
F .163
Sig. .850
• Groups divided into quartiles based on IQ and ATEC. • IQ 50 – 83 / 84 – 103 / 104 – 130 • ATEC 35 – 50 / 51 – 64 / 65 – 105 • Compared this estimates of level of functioning to ATEC change scores. • No significant differences.
QEEG changes I: Frontal hyperconnectivity
QEEG changes II: Right posterior hypoconnectivity
EEG biofeedback – Case 1 (case 2)
• 7 year old by diagnosed with PDD at the age of 5 • Born 36 weeks gestation due to gestational diabetes with high liver enzymes • Walked at 2 years and spoke in utternaces by 3 years • Difficulties with focusing, sitting still, temper outbursts, socialization, head • FSIQ = 80; Verbal IQ 75; Performance IQ = 90 • Impairments in receptive language, motor sequencing, visual-perceptual analysis. • Unable to read or identify letters
EEG biofeedback – Case 1 (case 2)
EEG biofeedback – Case 1 (case 2)
EEG biofeedback – Case 1 (case 2)
Neuropsychological measures all within normal limits, except receptive language rated as mildly impaired. Went from being alexic
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2
EEG Biofeedback – Case 2 (20 sessions)
