The High Prevelance of EEG Cerebral Dysrhythmic
Abnormalities in Psychiatric Populations: The
Phychopharmacological & Neurofeedback
Treatment Implications
Biofeedback Society of Texas
37th Annual Conference
Dallas, TX
October 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 Dysrhythmias
• Paroxysmal EEGs have transients with a sudden
increase in voltage, generally 50% above a
baseline level, with a sudden onset and sudden
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 transients
Electroencephalographic Cerebral Dysrhythmic Abnormalities
in the Trinity of Nonepileptic General Population,
Neuropsychiatric, and Neurobehavioral Disorders
•
•
•
Bhaskara P. Shelley, M.B., B.S., M.D., D.M.
Michael R. Trimble, M.D., F.R.C.P., FRCPsych
Nash N. Boutros, M.D.
•
•
(The Journal of Neuropsychiatry and Clinical
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 Disorders
Ellingson, 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 spikewave 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
Child
EEG/QEEGs
Adult
June 2009 –
September 2011
Total
Male
Total
19
46
65
(1 Hisp, 1 Asian)
(4 Hisp)
22
43
(2 Hisp, 2 Blk)
(3 Hisp, 1Blk)
41
89
130
17
20
65
(N=130)
Note: Adults >= 18 y/o
Child
Dysrhythmic
Group
(2 Hisp)
Adult
11
19
30
36
50
(1 Blk)
38.6%
Total
(N=50)
3
14
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.