8/23/2016. Optimizing Patient Outcome: Integrating EEG

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1 Optimizing Patient Outcome: Integrating EEG Raising qeeg to a Medical Standard Ron J. Swatzyna, Ph.D., LCSW Board Certified in Neurofeedback, Associate Fellow Board Certified in Biofeedback, Associate Fellow Director of Neurotherapy Director of Electro-Neurophysiology Research Board of Directors: Rice University/Texas Medical Center Chapter Sigma Xi: The Scientific Research Society Optimizing Patient Outcome Having performed thousands of EEGs and qeegs, we placed all the client data in a deidentifiedarchive andare nowresearching on the findings. We are in the process of publishing our research (see references) This webinar will bring you current on our findings 2 Clinical Research Since 2005 we have done over 1800 EEGs Each EEG was interpreted by a board certified electroencephalographer Each qeeg was done by a service 3 1

2 Clinical Research Since 2008 The Basic Application of Pharmaco-EEG in a Clinical Setting ISNR Conference (2008) 46 peer-reviewed presentations/publications on brain abnormalities presented nationally and internationally 2 research assistants 2 Rice University research interns NO FUNDING 4 IRB Approved Data Archive N = 735 Ages variables each plus 296 Likertscaled answers to questions over 42 neurodiagnosticcategories 5 Questions Our Outcome Data Answers What are the common EEG findings predicting treatment failure? How can we transfer data with HIPAA compliance? What is the incidence of IED in ASD and ADHD? If IEDs are empirically treated, what is the outcome? What has the cost/benefit been of having the EEG/qEEG medically interpreted? 6 2

3 National Institute of Mental Health Dr. Thomas Insel: The DSM is an invalid instrument (2012). Their goal is to move away from symptombased treatment and to instead develop evidence-based diagnosis Research Domain Criteria project (RDoC) 7 QEEGs Last resort? Many who come to get qeegshave often tried many other treatments prior including: Individual and group therapy Medication Behavioral therapy Nutrition Hyperbaric oxygen 8 Treatment Failure? Why did prior treatments fail? Why did they have such an atypical response to medications? If we could use the EEG data we collect for more than just brain maps why wouldn t we? 9 3

4 QEEG Brain Mapping (qeeg) Individual brain function is compared to a database of normal subjects 10 EEGs reveal transient abnormal brain activity Is a recording of electrical brain activity 11 EEG Interpretation Service Commercial EEG services With board certified electroencephalographers licensed in each state Upload the EEG data and download the report. Note: Reporting of EEG findings by non-certified clinicians is practicing medicine without a license 12 4

5 Prevalence of Abnormal EEGs Abnormal EEGs are common especially in those who have: Failed multiple medication trials Failed to respond to treatment (including NFB) Had a sudden change in mental status Have an abnormal physical presentation Whose mother s gut instinct tell her we are missing something EEG Abnormalities and EEG Presentation Encephalopathies Congenital abnormalities Cerebrovascular issues Epileptiform activity 15 5

6 Encephalopathy Disease, Damage, or Malfunction of the Brain Need to identify etiology Most common causes identified in the past 11 years: - Metabolic - Toxic - Electrolytic - Anoxic - Traumatic Psychotropic medication needs metabolic support to work Treat by identifying and rectifying the cause of the problem 16 Metabolic/Toxic Encephalopathy The patient's EEG showed an extreme "low voltage slow" (LVS) pattern. LVS is highly correlated with either a toxic or metabolic issues. In essence, the brain is not getting enough energy to function cognitively. 17 Eyes Open background EEG rhythms 9 y/o M Scale: 50 mcv/cm Note: muscle artifacts at: Fp1 18 6

7 Metabolic Encephalopathy Thyroid issues Case examples Hashimoto s thyroiditis Radiation exposure 19 Toxic Encephalopathy Toxic exposure (delayed response) Case examples: Insecticide Ingestion of insecticide at 3 y/o Enuresis started age 5 bedwetting and soiling himself during the day 20 Toxic Encephalopathy 9 y/o Male 21 7

8 Metabolic Encephalopathy 24 y/o Male 22 Anoxic Encephalopathy Chronic sleep apnea Case example Prevents normal brain aging Made worse with stimulants 23 Anoxic Encephalopathy 22 y/o male Sleep Walker 24 8

9 Anoxic Encephalopathy The appearance of generalized encephalopathy in the most recent EEG lead me to believe that his extended history of sleep apnea may have substantially affected his brain. Hypoxia has been linked to encephalopathy. Three months following removal of his tonsils and adenoids brain stabilized and sleep walking was no longer an issue. 25 Iron, salt, potassium Case example Addison s disease Electrolyte Imbalance 26 Addison s Disease EEG abnormalities: High voltage bursts of 3 to 6 seconds Diffuse slowing, 1-to 3-second bursts of slow activity Paroxysmal sharp and slow wave discharges Neuropsychiatric symptoms are progressive Cognitive impairment Mental status change Stroke-like-symptoms Psychosis possible 27 9

10 Traumatic Encephalopathy Multiple concussions or blast injuries Case examples Sport injuries Combat injuries 28 Structural Defects Agenesis of the Corpus Coliseum Case example of total agenesis Tumor Case example 29 Complete Agenesis of the Corpus Coliseum 34 y/o Male Dx: ASD 30 10

11 Subcortical Tumor 17 y/o Male ODD/LD 31 Case Series Study EEG/qEEG 1 November y/o male: ADHD CNS underarousal, Mu rhythm, EEG has transients and paroxysmal discharges This patient s EEG is moderately slow for age in occipital leads bilaterally and must be considered mildly and nonspecifically abnormal on this basis. There are no focal or lateralizing features. 32 EEG

12 QEEG 1 34 EEG/qEEG 2 August 2014 This patient s EEG shows evidence of right posterior hemisphere abnormality: during the eyes-open state there was a focus of slow activity in the right occipital region; during the eyes-closed state there was alpha asymmetry with right occipital alpha activity appearing higher in voltage on the right side, and right occipital spike activity. Findings are most consistent with the presence of a subacuteor chronic lesion in the right posterior hemisphere. 35 EEG

13 QEEG 2 Absolute Power 37 MRI Study: MR MRI Brain w/wo Impression: 1. Normal appearance of the brain without signal abnormality or structural irregularity. 2. Extensive paranasal sinus inflammatory mucosal disease with moderate-seized fluid levels seen in the maxillary sinuses. 38 EEG/qEEG 3 November 2014 Dx: Sinus disease Tx: Antibotics This patient s EEG has improved when compared with his most recent study of 8/7/14 in that the right occipital abnormalities noted at that time are no longer seen. The present study is intermittently slow in anterior leads but otherwise approaches normal character for age

14 EEG 3 40 QEEG 3 41 Temporal Mild Slow and Sharp Activity Cardiovascular (pump) issues Case example Cerebrovascular(vessel) issues Case Example 42 14

15 Cardiovascular 61 y/o Male Memory Failing EEG report: This patient s EEG shows some independent slow activity in the left and right temporal regions. Such findings may occur in asymptomatic individuals in this age group but are believed to have some association with cerebrovascular insufficiency. MD Recommendations: Evaluation of cardiac and carotid sufficiency is suggested along with neuroimaging to evaluate these areas. 43 History of Cardiovascular Issues 44 EO Scale: 50 mcv/cm 45 15

16 55 y/o Female Sudden onset of symptoms: word finding difficulties, could no longer sing, loss of hand coordination MRI unremarkable Dx: Conversion disorder ordered neurophychological testing Report Findings: Temporal sharp-slow changes on the left may be seen with early vascular changes and various forms of ischemia. 46 Temporal Mile Sharp & Slow Activity 55 y/o Female

17 49 50 Treatment Femoral artery procedure Two stints and three coils Symptoms resolved over the next two years 51 17

18 Epileptiform Activity Isolated epileptiform discharges cannot be identified in a qeeg Absence seizures Temporal lobe epilepsy Multi foci poly-spike wave complexes 52 Absence Seizure Case 6 y/o Male 53 Treatment Referred to pediatric neurologist who recommended ethosuximide Mother refused because she did not see any symptoms Six months later he had his first unprovoked seizure 54 18

19 Temporal Lobe Epilepsy Case 21 y/o male with no history of mental health issues prior to 2 years ago Patient started experiencing syncope episodes (drop seizures) Forced to withdrawal from school Inpatient treatment at mental health facility and then hospitalized 55 Symptoms & Diagnosis 21 y/o Male Sx: Visual and auditory hallucinations, sleep onset issues, memory issues, syncope episodes Dx: Conversion disorder; GAD, Mood disorder, OCD, Psychosis Zyprexa 10mg QPM; Lexipro 20mg; Clonipin Past Medications tried: benzodiazepines; Depakote, Rexulti; Lamictal 56 Findings EEG: This patient s EEG shows a focus of spike activity in the left posterior temporal region, suggesting the presence of an irritative and epileptogenic lesion in this area. There are transient semirhythmicsharp waves seen temporally, with spikes identified in the visual EEG analysis and with the temporal semirhythmic spikes reported commonly in temporal lobe epilepsy. The automatic spike detector failed to identify any spikes

20 EEG Segment EO 58 Treatment & Prognosis Referred to a neurologist who prescribed Trileptal Symptoms abated Started neurofeedback August 2016 Prognosis: if improvement continues, patient should be able to return to school January No pathology MRI unremarkable 24 y/o Female Abnormal EEG 60 20

21 EEG shows sharp wave activity in the left and right occipitotemporal regions, suggesting the presence of irritative and potentially epileptogenic lesions or disturbances in these areas. 61 Conclusions Our industry sees very complicated cases What is our ethical responsibility? The costs of the report is small The costs if something is missed can be EEG studies can be of benefit to prescribing physicians and treating clinicians 62 Questions? 63 21

22 References Swatzyna, RJ, Tarnow, JD, Turner, RP, Roark, AJ, MacInerney, EK, and Kozlowski, GP (submitted). Integration of EEG into Psychiatric Practice: A Step Toward Precision Medicine. Journal of Clinical Neurophysiology.(submitted August 16, 2016).. Swatzyna, R.J., Tarnow, J.D., Roark, A., & Mardick, J. (2016). The Utility of EEG in Attention Deficit Hyperactivity Disorder: A Replication Study. Clinical EEG and Neuroscience. DOI Swatzyna, R.J., Kozlowski, G.P. & Tarnow, J.D. (2015). Pharmaco-EEG: A Study of Individualized Medicine in Clinical Practice. Clinical EEG and Neuroscience. Vol. 46(3) : DOI: / Arns, M., Swatzyna, R.J., Gunkelman, J., & Olbrich, S. (2015). Sleep maintenance, spindling excessive beta and regulatory systems approach? Neuropsychiatric Electrophysiology electronically published June References Swatzyna, R.J., Tarnow, J.D., Tannous, J., Schieszler, C., Pillai, V.J. & Kozlowski, G.P. (2014). EEG/QEEG Technology Identifies NeurobiomarkersCritical to Medication Selection and Treatment: A Preliminary Study. Journal of Psychology and Clinical Psychiatry. Swatzyna, R.J. (2014). EEG & qeeg Technology Identifies Neurobiomarkers Critical to Medication Selection and Treatment for Children and Adolescents with ADHD. NeuroConnections Spring 2014: Anglin, RE, Rosebush, PI, & Mazurek, ME (2006). The neuropsychitric profile of Addison s Disease: Revisiting a forgotten phenomenon. Journal of Neuropsychiatry and Clinical Neurosciences; 18: