Optimizing Patient Outcome: Integrating...
Transcript of Optimizing Patient Outcome: Integrating...
8/23/2016
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Optimizing Patient Outcome:
Integrating EEG
Raising qEEG to a Medical Standard
Ron J. Swatzyna, Ph.D., LCSWBoard 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 de-
identified archive and are now researching on
the findings.
• We are in the process of publishing our
research (see references)
• This webinar will bring you current on our
findings
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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
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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
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IRB Approved Data Archive
• N = 735
• Ages 4 – 72
• 87 variables each plus
• 296 Likert scaled answers to questions over 42
neurodiagnostic categories
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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
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National Institute of Mental Health
• Dr. Thomas Insel: The DSM is an invalid
instrument (2012).
• Their goal is to move away from symptom-
based treatment and to instead develop
evidence-based diagnosis
• Research Domain Criteria project (RDoC)
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QEEGs
Last resort?
• Many who come to get qEEGs have often tried
many other treatments prior including:
– Individual and group therapy
– Medication
– Behavioral therapy
– Nutrition
– Hyperbaric oxygen
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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?
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QEEG Brain Mapping
• (qEEG) Individual brain function is compared
to a database of “normal” subjects
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EEGs reveal transient
abnormal brain activity
• Is a recording of electrical brain activity
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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
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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
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EEG Abnormalities and EEG Presentation
• Encephalopathies
• Congenital abnormalities
• Cerebrovascular issues
• Epileptiform activity
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EncephalopathyDisease, 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
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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.
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Eyes Open – background EEG rhythms 9 y/o M
Scale: 50 mcV/cm Note: muscle artifacts at: Fp1
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Metabolic Encephalopathy
• Thyroid issues
• Case examples
– Hashimoto’s thyroiditis
– Radiation exposure
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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
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Toxic Encephalopathy
9 y/o Male
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Metabolic Encephalopathy
24 y/o Male
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Anoxic Encephalopathy
• Chronic sleep apnea
• Case example
– Prevents normal brain aging
– Made worse with stimulants
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Anoxic Encephalopathy
22 y/o male Sleep Walker
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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.
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Electrolyte Imbalance
• Iron, salt, potassium
• Case example
– Addison’s disease
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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
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Traumatic Encephalopathy
• Multiple concussions or blast injuries
• Case examples
– Sport injuries
– Combat injuries
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Structural Defects
• Agenesis of the Corpus Coliseum
– Case example of total agenesis
• Tumor
– Case example
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Complete Agenesis of the Corpus Coliseum34 y/o Male Dx: ASD
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Subcortical Tumor17 y/o Male ODD/LD
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Case Series Study EEG/qEEG 1 November 2012
• 8 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.
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EEG 1
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QEEG 1
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EEG/qEEG 2August 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 subacute or chronic lesion in the right posterior
hemisphere.
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EEG 2
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QEEG 2 Absolute Power
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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.
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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.
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EEG 3
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QEEG 3
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Temporal Mild Slow and Sharp Activity
• Cardiovascular (pump) issues
– Case example
• Cerebrovascular (vessel) issues
– Case Example
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Cardiovascular61 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 neuro-
imaging to evaluate these areas.
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History of Cardiovascular Issues
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EO
Scale: 50 mcV/cm
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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
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Treatment
• Femoral artery procedure
• Two stints and three coils
• Symptoms resolved over the next two years
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Epileptiform Activity
• Isolated epileptiform discharges cannot be
identified in a qEEG
• Absence seizures
• Temporal lobe epilepsy
• Multi foci poly-spike wave complexes
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Absence Seizure Case
6 y/o Male
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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
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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
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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
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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 semirhythmic sharp waves
seen temporally, with spikes identified in the
visual EEG analysis and with the temporal semi-
rhythmic spikes reported commonly in temporal
lobe epilepsy. The automatic spike detector failed
to identify any spikes.57
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EEG Segment EO
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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
2017
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24 y/o Female
Abnormal EEG
• No pathology
• MRI unremarkable
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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.
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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
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Questions?
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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 10.1177-1550059416640441.
• 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) 192-196: DOI: 10.1177/15500594|4556|20
• Arns, M., Swatzyna, R.J., Gunkelman, J., & Olbrich, S. (2015). Sleep
maintenance, spindling excessive beta and regulatory systems approach?
Neuropsychiatric Electrophysiology electronically published June 2015.
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References
• Swatzyna, R.J., Tarnow, J.D., Tannous, J., Schieszler, C., Pillai, V.J. & Kozlowski,
G.P. (2014). EEG/QEEG Technology Identifies Neurobiomarkers Critical 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: 66-71.
• Anglin, RE, Rosebush, PI, & Mazurek, ME (2006). The neuropsychitric profile
of Addison’s Disease: Revisiting a forgotten phenomenon. Journal of
Neuropsychiatry and Clinical Neurosciences; 18:450-459.
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