The High Prevelance of EEG Cerebral Dysrhythmic Abnormalities in Psychiatric Populations: The Phychopharmacological & Neurofeedback

Treatment Implications

Biofeedback Society of Texas 37th Annual Conference

Dallas, TXOctober 15, 2011

Ronald J. Swatzyna, Ph.D., L.C.S.W.BCB, BCN, CBIST, CCFC, CART

Board Certified in Biofeedback

Board Certified in Neurotherapy

Certified Brain Injury Specialist Trainer

Clinically Certified Forensic Counselor

Certified Anger Resolution Therapist

The Tarnow Center for Self Management

Director of Neurotherapy

Introduction

• Cerebral dysrhythmic abnormalities are normal variants however

• When the location of the dysrhythmias correlate with presenting pathology, they are important in regard to• Further testing• Medication selection• Neurofeedback treatment

Cerebral DysrhythmiasCerebral Dysrhythmias

• Paroxysmal EEGs have transients with a sudden Paroxysmal EEGs have transients with a sudden increase in voltage, generally 50% above a increase in voltage, generally 50% above a baseline level, with a sudden onset and sudden baseline level, with a sudden onset and sudden cessation.cessation.

Clinico-Electroencephalographic Associations of Anomalous EEG Patterns

• Rhythmic Mid-Temporal Discharges

• Wicket Spikes/Mu Rhythm

• 14 & 6 Hz Positive Spikes

• Benign Epileptiform Transients of Sleep

• 6 Hz Spike & Slow Wave Complex

• Mid temporal sharp slow transientsid temporal sharp slow transients

Electroencephalographic Cerebral Dysrhythmic Abnormalities Electroencephalographic Cerebral Dysrhythmic Abnormalities in the Trinity of Nonepileptic General Population, in the Trinity of Nonepileptic General Population, Neuropsychiatric, and Neurobehavioral DisordersNeuropsychiatric, and Neurobehavioral Disorders

• Bhaskara P. Shelley, M.B., B.S., M.D., D.M.Bhaskara P. Shelley, M.B., B.S., M.D., D.M.• Michael R. Trimble, M.D., F.R.C.P., FRCPsychMichael R. Trimble, M.D., F.R.C.P., FRCPsych• Nash N. Boutros, M.D.Nash N. Boutros, M.D.

• (The Journal of Neuropsychiatry and Clinical(The Journal of Neuropsychiatry and Clinical• Neurosciences 2008; 20:7–22)Neurosciences 2008; 20:7–22)

Schizophrenia• Hill, 1950; Abrahams & Taylor, 1979; Stevens et al., 1979; Small,

1993; Ellingson, 1954; Small et al., 1984; Inui et al., 1998

• Non-paroxysmal dysrhythmias

• Left-sided temporal EEG abnormalities

• Temporal EEG abnormalities

• Left-sided slow-wave asymmetries, slow bursts, SSS; left anterior temporal region

• Phantom spike and wave, positive spikes, SSS

Mood DisordersEllingson, 1954; Small et al., 1993; Cook et al., 1986; McElroy et

al., 1998; Taylor, Abrams, 1881; Small et al., 1975; Struve et al., 1977; Hughes, 1984; Levy et al., 1988; Inui et al., 1998; Inui et al., 2001; Ikeda et al., 2002; Motomura et al., 2002

• SSS, 6/sec spike & wave, phantom spike wave, RMTD, 14 & 6 Hz positive spikes and B-mitten pattern

• 6/sec spike & wave, SSS, 14 & 6 Hz Positive spikes

• 6/sec spike & wave complexes

• Paroxysmal bi-temporal EDs

• 6 Hz phantom spike & wave, 14 & 6 Hz positive spike, SSS

• (TLID, TMSSA, BORTT)

• EDs

• EEG temporal slow waves

Anxiety, Panic, OCD

• Jenike & Brotman, 1984; Ito et al., 1993; Small, 1993

• Temporal non-specific EEG abnormalities

• Fronto-temporal EEG abnormalities

• EEG abnormalities

Panic • Lepola et al., 1990; Abraham, Duffy, 1991;

Jabourian et al. 1992; Hughes, 1996; Weilburg et al., 1995

• Slow-wave dysrhythmia

• EEG abnormalities

• EEG temporal paroxysmal activity

• Focal paroxysmal temporal abnormalities

Eating Disorders

• Gibbs & Gibbs, 1964; Chrisp et al., 1968; Davis et al., 1974; Wermuth et al., 1978; Rau et al., 1979; Neil et al., 1980; Struve, 1987

• Slow and generalized spike & wave; B-mitten pattern; diffuse slow paroxysmal discharges

• Abnormalities bilateral 4-6/sec spike-wave complexes• Bilateral anterio-mesial temporal spikes; 6/sec spike-wave

complexes• SSS; diffused spike & wave; bitemporal slowing• 14 & 6 positive spikes, B-mitten patterns, SSS, paroxysmal

slowing, focal slow, minimal generalized slow, focal and diffused spiking, generalized fast, 6/sec spike & wave and slow with spiking; paroxysmal finding of the EEG dysrhythmia

• Generalized slow; paroxysmal slow; focal spike or sharp-wave transients; generalized spikes; B-mitten patterns; extreme spindles

• EEG dysrhythmia

EEG Cerebral Dysrhythmia in Pediatric Neurobehavioral Disorders

Autism• Small et al., 1977; Tuchman et al., 1991; Rossi et al., 1995; Villalobos et

al., 1996; Beaumanoir et al., 1995; Tuchman et al., 1997; Tuchman, Rapin, 1997; Gabis et al., 2005; Hughes, Melyn, 2005; Canitano et al., 2005; Kim et al., 2006; Chez et al., 2006

• EEG abnormalities

• EEG (subclinical) epileptiform dysrhythmia

• Benign rolandic epilepsy

• Paroxysmal EEG dysrhythmia

• Subclinical EDs

• EDs

• Paroxysmal EEG dysrhythmia

• EDs; focal sharp waves, multifocal sharp wave, generalized spike-wave complexes, and generalized paroxysmal fast activity/polyspikes

• EDs right temporal localization

Tourette’s Syndrome

• Bergen et al., 1982; Krumholz et al., 1983; Lees et al., 1984; Verma et al., 1986; Neufeld et al., 1990; Semerci et al., 2000 • Dysrhythmia• Dysrhythmia: central spikes, generalized and

paroxysmal slow activity, and background slowing

• Dysrhythmia• Dysrhythmia; EDs• Dysrhythmia

ADHD• Small et al., 1978; Boutros et al., 1998; Hughes et al., 2000; Hemmer et al., 2001; Richer

et al., 2002; Holtmann et al., 2003; Millichap, Millichap & Stack, 2011

• Diffuse generalized and/or intermittent slow wave dysrhythmia• 14/second and 6/second positive spike patterns; EDs; slow wave dysrhythmia• Abnormal EEGs; focal EDs- occipital/frontal; generalised spike-wave EDs;

controversial 6–7/ second and 14/second positive spike patterns; abnormal frontal/temporal slow waves; Frontal arousal rhythm; extreme spindles

• EDs; rolandic spikes; focal abnormalities• EDs; generalized 3 Hz spike slow wave; generalized spike/multispike-slow wave;

midtemporal spikes, rolandic spikes; bilateral midtemporal and/or rolandic spikes, occipital spikes (19%)

• Rolandic spikes in nonepileptic ADHD (prevalence 5.6%); right sided lateralization (51%) and bilateral localization

• Epileptiform discharges

Study

• EEG/QEEG June 1, 2009 to August 30, 2011

• All patients referred for EEG/QEEG (N=145)

• Of the 145 cases, 15 were excluded: non-clinical or 2nd EEG/QEEGs

• N=130

Demographics Female Male Total

EEG/QEEGs

June 2009 –

September 2011

(N=130)

Child 19 (1 Hisp, 1 Asian)

46(4 Hisp)

65

Adult 22 (2 Hisp, 2 Blk)

43 (3 Hisp, 1Blk)

65

Total 41 89 130

Note: Adults >= 18 y/o

Dysrhythmic

Group38.6%

(N=50)

Child 3 17 (2 Hisp)

20

Adult 11 (1 Blk)

19 30

Total 14 36 50

Dysrhythmic Group Findings

• 40% of total males• 37% child males• 44% adult males

• 34% of total females• 16% child females• 50% adult total females (highest rate)

TBI History

• Of the 130 patients in the study:

• 61.5% had at least one substantial concussion

• Of the 50 in the dysrhythmic group:

• 78.0% were found to have at least one substantial concussion

Case 1

• 16 y/o female• CC: continuous tension headaches with chronic

migraine episodes 4/wk• Duration: 3 years• Migraines preceded by bouts of vertigo and often

include nausea, vomiting and “floaters”

Symptoms

• Three year duration• Vertigo precedes migraine onset (3-4/wk)• Constant tension headaches• Atypical sleep pattern• Neurological treatment failure• Referred by neurologist for biofeedback

Physiological Evaluation & Treatment

• Psychophysiological Assessment• Heart Rate Variability Biofeedback • Cognitive Behavior Therapy• Hypnosis• Results: no significant change in tension

headaches and no reduction in migraine activity or intensity

• EEG/QEEG

EEG & QEEG

• Interpretation: This patient's EEG is intermittently slow on anterior leads, but the findings are otherwise within the range of normal variation. There was no EEG evidence of a focal cerebral lesion and no definitely epileptic findings.

• Conclusion: The alpha is widespread with eyes closed, including the frontal areas and right temporally, suggesting a lateralized disturbance in cerebro-cortical function. Though not pathognomonic, the temporal alpha and slower content temporally may be seen with migraine ischemia. The temporal changes may be related to migraine ischemia, which can cause a sharp and slow change in the EEG… sometimes minor, and sometimes more dramatic… Niedermeyer mentions ischemia as one of the etiologies even of the minor variant of this pattern.

Eyes Closed

Spectra (EEG power vs. EEG frequency) Eyes Closed condition

Neurofeedback Treatment

• The patient saw the TMSSA and said she was able to feel it in her head when these transient patterns appeared on the monitor.

• Within 2 sessions the patient’s migraines stopped (5 sessions total were done).

• However, tension headaches continued.

Case 2

• A 55 year-old female:• deterioration of language function. Visser et al. (1987)

found that slight left-sided anterior temporal abnormalities are an early subclinical sign of temporal lobe pathology expressed in deteriorating language functioning.

• MRI was negative• EEG/QEEG identifies TMSSA centered left temporal

lobe

EEG & QEEG

• Conclusions: The background alpha is seen at 9-11 Hz posteriorly, with excessive slower alpha content at 7-9 Hz seen left temporally. The slower alpha on the left suggests an idling of the local cortex, such as seen in older gray matter lesions. The temporal sharp-slow changes on the left may be seen with early vascular changes and various forms of ischemia.

MRA Identified Aneurysm

• MRA identified a 9 mm aneurysm on her left interior carotid artery (paraclinoid area).

• An endovascular stent and coil procedure stopped the progression of the aneurysm.

Eyes Open

Spectra (EEG power vs. EEG frequency) Eyes Open condition

Spectra differences: patient-norms Relative EEG power

Maps for relative power spectra deviations from normality

Eyes Closed

Spectra (EEG power vs. EEG frequency) Eyes Closed condition

Maps for relative power spectra deviations from normality

Case 3

• 20 y/o female with history of delusions and failure of multiple pharmacological intervention.

• Paroxysmal discharges centered in the medial temporal area (T3) with accompanied phase inversions noted during her EEG

• Gunkelman defined these discharges to be likely due to an irritative process in the left insula area

• Paroxysmal discharges in the left insula have been linked to psychotic symptoms

Kaplan, P.W., Fisher, R.S., editors (2005) (Imitators of Epilepsy. 2nd addition. New York: Demos Medical Publishing)

• "The term ictal psychosis describes the occurrence of psychotic symptoms in association with epileptiform activity on EEG; it is an example of NCSE…

• Critical features included the episodic nature of the symptoms and the consistency of symptoms in each patient over time."

Eyes Open

Spectra (EEG power vs. EEG frequency) Eyes Open condition

Treatment

• Ictal hallucinations are best treated by controlling the ictus, and thus by antiepileptic drugs.

• A trial of Lamictal would be of clinical interest, however high dosing is not recommended.

• Results: Low dose Lamictal proved to be very effective in reducing psychosis and stabilization. • Elliott, B., Joyce, E. & Shorvon, S. (2008) (Epilepsy

Research 85, 172-186)

Case 4

• 16 y/o male on Remeron and Lithium

• Decompensating past 6 months

• Departing for home in Guatemala next day

EEG & QEEG

• Interpretation

• EEG shows a focus of sharp wave activity in the right parietal region, suggesting the presence of an irritative and potentially epileptogenic lesion or disturbance in this area.

• Conclusions

• There is irregular slower content seen at the midline and right temporal-parietally. The right temporal alpha and irregular slower content is noted…These findings correspond well with the location of the spikes seen in the raw EEG right parietally (T6).

Eyes Open

Spectra (EEG power vs. EEG frequency) Eyes Open

Treatment

• Stop Remeron and Lithium

• Start anticonvulsant

• Patient stabilized and continued to improve

Case 5

• 17 y/o male home schooled past 2 years due to anxiety and learning issues

• 3 concussions (3-4 years ago): football hit, impact from rock and a fall (T5) a week later

EEG & QEEG

• Interpretation: This patient's EEG is generally slow and shows a focus of slow activity in the left occipital region, suggesting a lesion in this area.

• Conclusion: The background alpha is poorly organized with rhythmic slower content seen left frontally and temporally with dominant left posterior temporally with eyes closed. The rhythmic slow focus suggests a localized white matter lesion, and though no frankly epileptiform content is seen, the rhythmic slower content is suggestive of a lesion.

Eyes Closed

Spectra (EEG power vs. EEG frequency) Eyes Closed

Spectra differences: patient-norms Absolute EEG power.

Spectra differences: patient-norms Relative EEG power

Relative power spectra deviations from normality in 1 Hs windows

Case 6

• 23 y/o female• Concussion 1 month prior fall from a horse and another at

age of 12 when fell from horse and it stepped on her head• History of learning issues thought to be from ADD• Multiple unsuccessful interventions

EEG & QEEG

• Interpretation: This patient’s EEG shows a generalized mixed fast and slow pattern suggestive of a moderate metabolic encephalopathy but the findings are otherwise within the range of normal variation.

• Conclusions: The background alpha is seen temporally with irregular slower content seen frontally at the midline. There are transient bursts in the EEG, both during eyes open and eyes closed. These local changes and the bursts may both be related to head injury, though the findings may be considered pathognomonic. The faster alpha suggests a mild CNS over-arousal.

Treatment

• Medication Indications: In light of the instability associated with transient bursts, an empirical trial on an anticonvulsant may be of clinical interest.

• Treatment Plan: Anticonvulsant trial to reduce the transient bursts. Neurotherapy would be a non-invasive stimulation method to return the patient's brain to a more functional state. Add low dose Riddlin once transient burst are regulated.

Eyes Closed

Spectra (EEG power vs. EEG frequency) Eyes Closed

Finding 1

• EEG/QEEG are highly indicated for those who have:• Multiple medication failure • Unexplained onset/worsening of pathology• Unexplained somatic symptoms• TBI Hx with/or wo substance abuse issues• Neurological soft signs• Treatment resistant:

• Logic and reasoning issues• Language & learning issues• Headaches and/or Migraines

Finding 2

• A diagnostic team greatly increases the likelihood of identifying dysrhythmic EEGs without using sleep deprivation

Finding 3

• In a clinical population nearly 4 out of every 10 referred for EEG/QEEG will have dysrhythmias

Finding 4

• In a clinical population, one out of every two adult females referred EEG/QEEG are likely to have a dysrhythmias

Finding 5

• TBI and cerebral dysrhythmias are highly correlated

Finding 6

• Failure to identify and report can have dire consequences & information is critically important for:• Medication selection and management• Further testing• Accurate diagnosis• Treatment planning• Prognosis

Limitations of Study

• Skewed population not reflective of general population• 38.6% in study group• 1% to 3% prevalence rate general population• Higher socio-economic class private pay

• Sleep deprivation was not used in study

Implications

• An EEG/QEEG team has the ability to identify scientifically grounded evidence-based links to unexplained pathology

• Help referring physicians with: • Medication selection• Diagnosis • Selection of further testing• Treatment planning• Prognosis

• Reducing “trial & error” intervention and prolonged suffering

• In essence, “personalized medicine” is born

Conclusion

• Subclinical EEG abnormalities require an examination of associated findings (Daly & Pedley, 1997).

• If the location of the paroxysmal EEG discharges correlates with observed symptomology, it is highly likely that discharges are responsible.

• Therefore, when the team agrees, a diagnostic leap can be proposed and efficacious treatment designed.