AKUH Presentation 15.01.15
Neurological Manifestations of
Psychological Problems
Dilraj S. Sokhi
Outline
 TLOC
 PNES
 MUS
 CBT
 Q&A
TLOC (“Blackouts”)
Blackouts
Problem with blood circulation
(Syncope)
Primary disturbance
of brain function
Epilepsy
Idiopathic generalised
epilepsy
Focal epilepsyUnclassifiable
epilepsy
Non-cardiacCardiac
 Seizure: transient signs and/or symptoms due to abnormal excessive synchronous neuronal activity
in the brain.
 Epilepsy: enduring predisposition to generate epileptic seizures
 Kenya:
1-1.2% of 40 million people
National Epilepsy Guidelines
www.epilepsykenya.org
Epilepsy
TLOC (“Blackouts”)
Blackouts
Problem with blood circulation
(Syncope)
Primary disturbance
of brain function
Epilepsy
Idiopathic generalised
epilepsy
Focal epilepsyUnclassifiable
epilepsy
Non-cardiacCardiac
TLOC (“Blackouts”)
Blackouts
Problem with blood circulation
(Syncope)
Primary disturbance
of brain function
Epilepsy Non-epileptic
attacks
Idiopathic generalised
epilepsy
Focal epilepsyUnclassifiable
epilepsy
Non-cardiacCardiac
Videos
Abversek et al, 2011
PNES vs Epilepsy – Features?
Duncan et al, 2008
PNES & Phenotypes
Transient alteration in behaviour which looks like a seizure,
but without associated abnormal neuronal discharges
“GTCS-like”:
Loss of responsiveness
sinusoidal tremor (not clonic)
high frequency low amplitude or vice versa
 “Faint-like”:
Unresponsive with eyes closed, no tremor
 “Absence-like”
Why should PNES look like epilepsy?
 50% of PNES patients have had some type of past or present contact with
epilepsy  "behavioural modelling"
Bautista et al., 2008
 In those with no previous knowledge of epilepsy:
Ataque de Nervios - people in a medically undeveloped society have
events that look like PNES which are recognized straightforwardly by
those around them as manifestations of stress or distress
Lewis-Fernandez et al., 2002
Maybe PNES are a medicalised form of a naturally behavioural
reaction in humans
PNES - Diagnosis
 Video EEG is gold standard
 Otherwise, use history and EEG:
 Possible
 Probable
 Clinically established
LaFrance et al, 2013
PNES in the Clinic
Conversational Analysis for PNES
Feature Epilepsy PNES
Seizure symptoms Volunteered
Detailed
Negation explained
Interviewer-initiated
No detail
“Focussing resistanee“
Formulation work Extensive Little; Head-turn sign
Gaps in consciousness Exact description ‘I don‘t know‘
Metaphors Consistent image of
independently acting
external opponent
Seizure as place or space
person goes to
Catastrophising
 Always directly ask about symptoms of hyperventilation
Reuber et al, 2009
 Functional neurological symptoms:
 Weakness
 Sensory
 Movement disorder
 Cognitive
 Visual
 Others
Predisposing factors for both are similar
Stone, 2009; Duncan et al, 2011
“MUS” Can Precede PNES
 Hoover’s Test
 Entrainment of tremor  https://
www.youtube.com/watch?v=1ONUxovuWoU
Assessment of Functional Neuro
 Early life trauma
Usually childhood sexual abuse (cf. case study at the end)
Analysis of 34 studies on CSA showed OR 2.9
Sharpe & Faye 2006
 Other traumatic experiences e.g. bullying
 Personality disorder
 Learning difficulties
Sets the stage to develop an insecure adult attachment style with avoidant
tendencies and emotional dysregulation
(Alexithymia) Edwards 2009, Duncan and Oto 2008
Predisposing Factors for PNES
There are biological correlates
Bakvis et al, 2009
Neurology Outpatients:
50% have functional symptom/somatoform problem
– not necessarily the main problem
30% of new patients are ‘‘somewhat not all explained’’
20% of referrals to ‘‘seizure ’’ clinics are PNES
15% have unexplained pain and fatigue
Functional Symptoms are Common
 Usually a physically stressful life event
- Those with LD – usually situational
 10% of people with epilepsy have PNES
 epilepsy a predisposing factor
 1 in 3 don’t have pre-disposing factors
Especially in functional movement
disorders
Why now? Precipitating factors
A 48-year woman presented with acute onset attacks. Her past medical history
was unremarkable. Sh had suffered a severe upper respiratory tract infection and
had to take sick leave from her busy job managing a gym, and was bedridden
for 3 weeks. On attempting to go back to work, she developed "blackouts"
which rapidly evolved into “fits"and were ascribed to her viral illness.
She presented 2 weeks after her attempt to go back to work , and was then
having two or three events per day. The first event she said occurred in the
toilet, just after she got out of bed, and the description clearly indicated
posturally triggered vasovagal syncope, with dizziness, typical visual
prodrome, short period of unconsciousness, and rapid recov-ery.
Case Study 1
Following this, however, the events were not posturally
triggered, lost their prodrome and became longer. An eyewitness
account described loss of responsiveness, generalized tremor
building up, lasting as long as 15 minutes, with rapid respiration
throughout and then gradual recovery.
Events were readily recorded using short video-EEG and were
confirmed as typical by the eyewitness.
Case Study 1 (cont.)
During psychological evaluation it emerged that she had been in the habit of working twelve-
hour days at her gym, and coming in on weekends, which she was not obliged to do. She had
always also checked in on her younger brother who has learning difficulties and who lived 40
miles away. However he had recently been found to have a brain tumour, and over several
months she had been commuting daily to look after him.
She had always been a "coper“ and was the one to take responsibility when there was a crisis
or difficulty in the family. She had been intolerably stressed by her situation, and the "push"
provided by the URTI had been enough for her to "fall off the wall," unable to get back up.
Case Study 1 (cont.)
A 68-year-old man presented with new events over 4 months. He had a recent past
medical history of treated bladder cancer and coronary artery bypass grafting.
The events were described as beginning with dizziness and anxiety, then shaking
movements of the left hand and arm, gradually building up over 20 minutes and then
there was a gap in the patient's memory. After the event, the movements gradually
settled down and he would be left feeling tired and washed out. On direct questioning,
he admitted to tingling of the mouth and face after the attacks, but denied visual
symptoms or any problem with his breathing. He was asked about stressful events
around the time of onset of these attacks, but denied them.
Case Study 2
A typical event was readily induced using hyperventi-lation, and was confirmed
clinically and with EEG to be PNES. The sensory symptoms were reproduced during
the attack. The patient continued to spontaneously hyperven-tilate long after the test
had been completed and despite being reassured and asked to breathe slowly.
The diagnosis was communicated to the patient, and the connection with
psychological trauma and stress explained. The patient then revealed that his wife,
who had a previous mild stroke, had suffered a transi-ent ischemic attack just before
the onset of his symp-toms. During psychological assessment he admitted to anxiety
regarding his own and his wife's health, with a pervasive fear of disability and death.
Case Study 2 (cont.)
Reuber et al, 2002 and 2003 and 2004
Importance of correct diagnosis
Age (years)Age (years)
N=313N=313
PNES is
underdiagnosed
These patients
have lower QOL
to begin with
Mean delay:
7.2 years
Can be fatal...
Communicate diagnosis well…
Aspect Example Hall-Patch et al, 2010
Genuine symptoms Real attacks, can be frightening or disabling
Label Give a name, give other names patients may
hear, reassure is common, recognised. Not mad
Causes and
maintaining factors
Not epilepsy – GIVE THE MODEL:
predisposing factors (difficult – don‘t dig...)
precipitating factors (stress/emotions)
perpetuating factors cycle
worry  stress  attacks  worry
Treatment AEDs useless – can be withdrawn safely
Psychological treatment can help, can refer?
Expectations Can resolve, can expect improvement
…use a leaflet and the website…
www,nonepilepticattacks.info
How I do it…
…as it improves outcome
Explanation of the condition alone can stop up to 50% of
attacks in a good majority (40% or so) of people
 stop attending casualty, GP, etc…
 even if PNES have not stopped
McKenzie et al, 2010 Duncan et al, 2011
In up to 25% attacks stop altogether if involve psycho-
education of the patient over 6 months
N=45, median duration of PNES 4 yrs, 6 attacks/month
Decline in GP visits, estimated annual savings £245pp
Mayor et al, 2012 and 2013
Specialist Psychotherapy
 RCT evidence-based treatment for specialist psychotherapy
 Standard medical care vs combined with CBT in 66 patients
Goldstein et al, 2010
Case Study 3
A 38-year-old woman presented with events going back to
when she was 24, when she had acquired a diagnosis of epilepsy
attributed to a minor head injury. She arrives to the specialist
epilepsy/PNES clinic wearing a protective leather helmet, and in a
wheelchair with a full-time care- giver. She gave a history of
convulsive events that occurred many times a day which had led to
nultiple presentations to casualty.
She had one event during the consultation, consistent with a
PNES. After further evaluation, the diagnosis was confirmed and
communicated to the patient.
Case Study 3 (cont.)
She reacted with anger, directed mainly at the neurologist. She
agreed, nonetheless to the gradual withdrawal of her AEDs. When she
attended for review 3 months later, she walked into the room, still
with her helmet, but minus wheelchair and caregiver. Her PNES had
markedly reduced in frequency, but she remained angry.
After a further 3 months, she walked into the clinic now minus
the helmet, reporting that she had no further PNES. But she remained
very angry. During this consultation she reported an aggravated and
prolonged sexual assault, for which the perpetrators were now in
prison. Their sentence had taken place a few months before the onset
of her attacks. She recognized the connection between the PNES and
the assault, but re-declined psychological help. She did not attend her
next follow-up but presentations to casualty and her GP ceased.
PNES: Bio-psycho-social model
PNES
Look at the whole patient,
not just the seizures!
What does this mean for Kenya?
 There are few documented reports about PNES in Africa
Pretorius et al, 2013
 PNES has been recognised amongst those working in epilepsy
clinics in Kenya (psychiatrists and neurologists)
Personal comm. Dr. Mutisya (Mathare)
 The Kenyan population have significant psychological co-
morbidity (20% severe depression, 40% mild/moderate)
Ndetei et al, 2009
 There are some psychologists and psychotherapists available
Personal comm. Dr. Mutiso (AMHF)
ILAE PNES TF Global Survey
 We will collect Pan-African, including Kenyan, this year
 Awaiting ethics approval locally
Summary
 3 main causes of TLOC; important to differentiate
 Semiology of PNES vs. epileptic fits
 Functional symptoms and PNES sometimes co-exist
 Bio-psycho-social model
 Communicating the diagnosis to the patient is important
 Importance of recognising PNES, as evidence-based
management and specific therapies exist
Acknowledgements
 Professor Markus Reuber
 Dr. Richard Grünewald
 Dr. Stephen Howell
 AKUH (EA)
Questions?
 References available on request

PNES/functional neurology CME AKUH Nairobi 12th January 2015

  • 1.
    AKUH Presentation 15.01.15 NeurologicalManifestations of Psychological Problems Dilraj S. Sokhi
  • 2.
    Outline  TLOC  PNES MUS  CBT  Q&A
  • 3.
    TLOC (“Blackouts”) Blackouts Problem withblood circulation (Syncope) Primary disturbance of brain function Epilepsy Idiopathic generalised epilepsy Focal epilepsyUnclassifiable epilepsy Non-cardiacCardiac
  • 4.
     Seizure: transientsigns and/or symptoms due to abnormal excessive synchronous neuronal activity in the brain.  Epilepsy: enduring predisposition to generate epileptic seizures  Kenya: 1-1.2% of 40 million people National Epilepsy Guidelines www.epilepsykenya.org Epilepsy
  • 5.
    TLOC (“Blackouts”) Blackouts Problem withblood circulation (Syncope) Primary disturbance of brain function Epilepsy Idiopathic generalised epilepsy Focal epilepsyUnclassifiable epilepsy Non-cardiacCardiac
  • 6.
    TLOC (“Blackouts”) Blackouts Problem withblood circulation (Syncope) Primary disturbance of brain function Epilepsy Non-epileptic attacks Idiopathic generalised epilepsy Focal epilepsyUnclassifiable epilepsy Non-cardiacCardiac
  • 7.
  • 8.
    Abversek et al,2011 PNES vs Epilepsy – Features?
  • 9.
    Duncan et al,2008 PNES & Phenotypes Transient alteration in behaviour which looks like a seizure, but without associated abnormal neuronal discharges “GTCS-like”: Loss of responsiveness sinusoidal tremor (not clonic) high frequency low amplitude or vice versa  “Faint-like”: Unresponsive with eyes closed, no tremor  “Absence-like”
  • 10.
    Why should PNESlook like epilepsy?  50% of PNES patients have had some type of past or present contact with epilepsy  "behavioural modelling" Bautista et al., 2008  In those with no previous knowledge of epilepsy: Ataque de Nervios - people in a medically undeveloped society have events that look like PNES which are recognized straightforwardly by those around them as manifestations of stress or distress Lewis-Fernandez et al., 2002 Maybe PNES are a medicalised form of a naturally behavioural reaction in humans
  • 11.
    PNES - Diagnosis Video EEG is gold standard  Otherwise, use history and EEG:  Possible  Probable  Clinically established LaFrance et al, 2013
  • 12.
  • 13.
    Conversational Analysis forPNES Feature Epilepsy PNES Seizure symptoms Volunteered Detailed Negation explained Interviewer-initiated No detail “Focussing resistanee“ Formulation work Extensive Little; Head-turn sign Gaps in consciousness Exact description ‘I don‘t know‘ Metaphors Consistent image of independently acting external opponent Seizure as place or space person goes to Catastrophising  Always directly ask about symptoms of hyperventilation Reuber et al, 2009
  • 14.
     Functional neurologicalsymptoms:  Weakness  Sensory  Movement disorder  Cognitive  Visual  Others Predisposing factors for both are similar Stone, 2009; Duncan et al, 2011 “MUS” Can Precede PNES
  • 15.
     Hoover’s Test Entrainment of tremor  https:// www.youtube.com/watch?v=1ONUxovuWoU Assessment of Functional Neuro
  • 16.
     Early lifetrauma Usually childhood sexual abuse (cf. case study at the end) Analysis of 34 studies on CSA showed OR 2.9 Sharpe & Faye 2006  Other traumatic experiences e.g. bullying  Personality disorder  Learning difficulties Sets the stage to develop an insecure adult attachment style with avoidant tendencies and emotional dysregulation (Alexithymia) Edwards 2009, Duncan and Oto 2008 Predisposing Factors for PNES
  • 17.
    There are biologicalcorrelates Bakvis et al, 2009
  • 18.
    Neurology Outpatients: 50% havefunctional symptom/somatoform problem – not necessarily the main problem 30% of new patients are ‘‘somewhat not all explained’’ 20% of referrals to ‘‘seizure ’’ clinics are PNES 15% have unexplained pain and fatigue Functional Symptoms are Common
  • 19.
     Usually aphysically stressful life event - Those with LD – usually situational  10% of people with epilepsy have PNES  epilepsy a predisposing factor  1 in 3 don’t have pre-disposing factors Especially in functional movement disorders Why now? Precipitating factors
  • 20.
    A 48-year womanpresented with acute onset attacks. Her past medical history was unremarkable. Sh had suffered a severe upper respiratory tract infection and had to take sick leave from her busy job managing a gym, and was bedridden for 3 weeks. On attempting to go back to work, she developed "blackouts" which rapidly evolved into “fits"and were ascribed to her viral illness. She presented 2 weeks after her attempt to go back to work , and was then having two or three events per day. The first event she said occurred in the toilet, just after she got out of bed, and the description clearly indicated posturally triggered vasovagal syncope, with dizziness, typical visual prodrome, short period of unconsciousness, and rapid recov-ery. Case Study 1
  • 21.
    Following this, however,the events were not posturally triggered, lost their prodrome and became longer. An eyewitness account described loss of responsiveness, generalized tremor building up, lasting as long as 15 minutes, with rapid respiration throughout and then gradual recovery. Events were readily recorded using short video-EEG and were confirmed as typical by the eyewitness. Case Study 1 (cont.)
  • 22.
    During psychological evaluationit emerged that she had been in the habit of working twelve- hour days at her gym, and coming in on weekends, which she was not obliged to do. She had always also checked in on her younger brother who has learning difficulties and who lived 40 miles away. However he had recently been found to have a brain tumour, and over several months she had been commuting daily to look after him. She had always been a "coper“ and was the one to take responsibility when there was a crisis or difficulty in the family. She had been intolerably stressed by her situation, and the "push" provided by the URTI had been enough for her to "fall off the wall," unable to get back up. Case Study 1 (cont.)
  • 23.
    A 68-year-old manpresented with new events over 4 months. He had a recent past medical history of treated bladder cancer and coronary artery bypass grafting. The events were described as beginning with dizziness and anxiety, then shaking movements of the left hand and arm, gradually building up over 20 minutes and then there was a gap in the patient's memory. After the event, the movements gradually settled down and he would be left feeling tired and washed out. On direct questioning, he admitted to tingling of the mouth and face after the attacks, but denied visual symptoms or any problem with his breathing. He was asked about stressful events around the time of onset of these attacks, but denied them. Case Study 2
  • 24.
    A typical eventwas readily induced using hyperventi-lation, and was confirmed clinically and with EEG to be PNES. The sensory symptoms were reproduced during the attack. The patient continued to spontaneously hyperven-tilate long after the test had been completed and despite being reassured and asked to breathe slowly. The diagnosis was communicated to the patient, and the connection with psychological trauma and stress explained. The patient then revealed that his wife, who had a previous mild stroke, had suffered a transi-ent ischemic attack just before the onset of his symp-toms. During psychological assessment he admitted to anxiety regarding his own and his wife's health, with a pervasive fear of disability and death. Case Study 2 (cont.)
  • 25.
    Reuber et al,2002 and 2003 and 2004 Importance of correct diagnosis Age (years)Age (years) N=313N=313 PNES is underdiagnosed These patients have lower QOL to begin with Mean delay: 7.2 years Can be fatal...
  • 26.
    Communicate diagnosis well… AspectExample Hall-Patch et al, 2010 Genuine symptoms Real attacks, can be frightening or disabling Label Give a name, give other names patients may hear, reassure is common, recognised. Not mad Causes and maintaining factors Not epilepsy – GIVE THE MODEL: predisposing factors (difficult – don‘t dig...) precipitating factors (stress/emotions) perpetuating factors cycle worry  stress  attacks  worry Treatment AEDs useless – can be withdrawn safely Psychological treatment can help, can refer? Expectations Can resolve, can expect improvement
  • 27.
    …use a leafletand the website… www,nonepilepticattacks.info How I do it…
  • 28.
    …as it improvesoutcome Explanation of the condition alone can stop up to 50% of attacks in a good majority (40% or so) of people  stop attending casualty, GP, etc…  even if PNES have not stopped McKenzie et al, 2010 Duncan et al, 2011 In up to 25% attacks stop altogether if involve psycho- education of the patient over 6 months N=45, median duration of PNES 4 yrs, 6 attacks/month Decline in GP visits, estimated annual savings £245pp Mayor et al, 2012 and 2013
  • 29.
    Specialist Psychotherapy  RCTevidence-based treatment for specialist psychotherapy  Standard medical care vs combined with CBT in 66 patients Goldstein et al, 2010
  • 30.
    Case Study 3 A38-year-old woman presented with events going back to when she was 24, when she had acquired a diagnosis of epilepsy attributed to a minor head injury. She arrives to the specialist epilepsy/PNES clinic wearing a protective leather helmet, and in a wheelchair with a full-time care- giver. She gave a history of convulsive events that occurred many times a day which had led to nultiple presentations to casualty. She had one event during the consultation, consistent with a PNES. After further evaluation, the diagnosis was confirmed and communicated to the patient.
  • 31.
    Case Study 3(cont.) She reacted with anger, directed mainly at the neurologist. She agreed, nonetheless to the gradual withdrawal of her AEDs. When she attended for review 3 months later, she walked into the room, still with her helmet, but minus wheelchair and caregiver. Her PNES had markedly reduced in frequency, but she remained angry. After a further 3 months, she walked into the clinic now minus the helmet, reporting that she had no further PNES. But she remained very angry. During this consultation she reported an aggravated and prolonged sexual assault, for which the perpetrators were now in prison. Their sentence had taken place a few months before the onset of her attacks. She recognized the connection between the PNES and the assault, but re-declined psychological help. She did not attend her next follow-up but presentations to casualty and her GP ceased.
  • 32.
  • 33.
    Look at thewhole patient, not just the seizures!
  • 34.
    What does thismean for Kenya?  There are few documented reports about PNES in Africa Pretorius et al, 2013  PNES has been recognised amongst those working in epilepsy clinics in Kenya (psychiatrists and neurologists) Personal comm. Dr. Mutisya (Mathare)  The Kenyan population have significant psychological co- morbidity (20% severe depression, 40% mild/moderate) Ndetei et al, 2009  There are some psychologists and psychotherapists available Personal comm. Dr. Mutiso (AMHF)
  • 35.
    ILAE PNES TFGlobal Survey  We will collect Pan-African, including Kenyan, this year  Awaiting ethics approval locally
  • 36.
    Summary  3 maincauses of TLOC; important to differentiate  Semiology of PNES vs. epileptic fits  Functional symptoms and PNES sometimes co-exist  Bio-psycho-social model  Communicating the diagnosis to the patient is important  Importance of recognising PNES, as evidence-based management and specific therapies exist
  • 37.
    Acknowledgements  Professor MarkusReuber  Dr. Richard Grünewald  Dr. Stephen Howell  AKUH (EA)
  • 38.

Editor's Notes

  • #4 Half population will have TLOC Half will be seizures, ¼ syncope, 18% NEAD
  • #6 Half population will have TLOC Half will be seizures, ¼ syncope, 18% NEAD
  • #7 Half population will have TLOC Half will be seizures, ¼ syncope, 18% NEAD