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Update On Neurology And Psychiatry Of Women HARVARD MEDICAL SCHOOL CONTINUING MEDICAL EDUCATION COURSE MARCH 30, 2017 GASTON BASLET, M.D. DEPARTMENT OF PSYCHIATRY BRIGHAM AND WOMEN’S HOSPITAL HARVARD MEDICAL SCHOOL Functional Neurological Symptom Disorder (FNSD) and Dissociative Disorders

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Page 1: Functional Neurological Symptom Disorder (FNSD) and ...womensneuropyschcourse.com/files201/Baslet - FNSD... · ¡A. One or more symptoms of altered voluntary motor or sensory function

Update On Neurology And Psychiatry Of WomenHARVARD MEDICAL SCHOOL

CONTINUING MEDICAL EDUCATION COURSEMARCH 30, 2017

GASTON BASLET, M.D.DEPARTMENT OF PSYCHIATRYBRIGHAM AND WOMEN’S HOSPITALHARVARD MEDICAL SCHOOL

Functional Neurological Symptom Disorder (FNSD) and Dissociative Disorders

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¡ Understand differences and similarities between functional neurological symptom disorder (FNSD) and dissociative disorders.

¡ Formulate a diagnosis delivery protocol that can enhance adherence to treatment.

¡ Acknowledge current state of evidence-based treatment and outcomes for FNSD and dissociative disorders.

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¡ A. One or more symptoms of altered voluntary motor or sensory function.¡ B. Clinical findings provide evidence of incompatibility between the

symptom and recognized neurological or medical conditions.¡ C. The symptom or deficit is not explained by another medical or mental

disorder.¡ D. The symptom or deficit causes clinically significant distress or impairment

in social, occupational, or other important areas of functioning or warrants medical evaluation

¡ Specifier: with weakness or paralysis, with abnormal movement (PMD), with swallowing symptoms, with speech symptom, with attacks or seizures (PNES), with anesthesia or sensory loss, with special sensory symptom, with mixed symptom.

¡ Specifier: acute episode (< 6 months), persistent (> 6 months).¡ Specifier: with psychological stressor, without psychological stressor.

American Psychiatric Association, 2013PNES: Psychogenic Non-Epileptic Seizures; PMD: Psychogenic Movement Disorder.

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Stone and Carson, An Integrated Approach to other Functional Neurological Symptoms and Related Disorders ; in Dworetzky and Baslet (Eds) PNES: Towards the Integration of care, OUP, 2017

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Examples of positive signs in functional neurological symptomsWeaknessHoover’s sign: Hip extension weakness that returns to normal with contralateral hip flexion.Hip abductor sign: Hip abduction weakness that return to normal with contralateral hip abduction against resistance.Other evidence of inconsistency: Weakness of ankle plantar flexion on the bed but patient able to walk on tiptoes.Dragging Gait: A gait in which the forefoot remains in contact with the ground, typically with hip externally or internally rotated.

Movement DisorderTremor entrainment test: Patient with a unilateral tremor is asked to copy a rhythmical movement with their unaffected limb. The tremor in the affected hand either ‘entrains’ to the rhythm of the unaffected hand, stops completely or the patient is unable to copy the simple rhythmical movement.Fixed dystonic posture: A typically fixed dystonic posture, characteristically of the hand (with flexion of fingers, wrist and/or elbow) or ankle (with plantar and dorsiflexion) .Distraction during standing: Patients with an apparently positive Romberg’s test is asked to guess numbers written on their back or carry out a complex motor task (e.g. with a phone). In a functional gait problem, their balance will improve significantly.

Visual SymptomsFogging test: Vision in the unaffected eye is progressively “fogged” using lenses of increasing dioptres while reading an acuity chart. A patient who still has good acuity at the end of the test must be seeing out of their affected eye. Stone, Neurophysiol Clin Neurophysiol, 2014

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Levels of Diagnostic Certainty

History Witnessed event EEG

Possible + By witness or self-report/ description

No epileptiform activity in routine or sleep deprived interictal EEG

Probable + By clinician who reviewed video recording or in person, showing semiologytypical of PNES

No epileptiform activity in routine or sleep deprived interictal EEG

Clinically established

+ By clinician experienced in diagnosis of sz disorders (on video or in person) showing semiology typical of PNES

No epileptiform activity in routine or ambulatory EEG during a typical ictus/ event in which the semiology would make ictal epileptiform EEG expectable during equivalent epileptic sz

Documented + By clinician experienced in diagnosis of sz disorders, showing semiology typical of PNES, on video EEG

No epileptiform activity immediately before, during or after ictus captured on ictal video EEG with typical PNES semiology

La France et al, Epilepsia, 2013PNES: Psychogenic Non-Epileptic Seizures

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Signs that favor PNES Evidence from primary studies

Sensitivity (%) for PNES Specificity (%) for ES

Long durationFluctuating course

Asynchronous movements

Pelvic thrusting

Side-to-side head or body movementsClosed eyes

Ictal crying

Memory recall

GoodGood

Good (FLS excluded)

Good (FLS excluded)

Good (convulsive events only)Good

Good

Good

69 (events)47-88 (patients)44-96 (events)9-56 (patients)1-31 (events)7.4-44 (patients)25-63 (events)15-36 (patients)34-88 (events)52-96 (patients)13-14 (events)3.7-37 (patients)63 (events)77-88 (patients)

9696-10093-9693-10096-10092-10096-10092-10074-100971001009690

Signs that favor ES Evidence from primary studies

Sensitivity for ES Specificity for ES

Occurrence from EEG-confirmed sleepPost-ictal confusion

Stertorous breathing

Good

Good

Good (convulsive events only)

31-59 (events)-61-100 (events)67 (patients)61-91 (events)

100-8884100

Other signs Evidence from primary studies

Gradual onsetNon-stereotyped eventsFlailing or thrashing movementsOpisthotonusTongue bitingUrinary incontinence

InsufficientInsufficientInsufficientInsufficientInsufficientInsufficient La France et al, Epilepsia, 2013

PNES: psychogenic non-epileptic seizuresES: epileptic seizures

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Carson and Lehn, Epidemiology, in FND, in Hallet, Stone and Carson (Eds) , Handbook of Clinical Neurology Vol. 139, Functional Neurological Disorders, 2016

(Table 5.2). Twenty-five percent of these 1144 patientshad a coexisting neurologic disorder (8% of all neurol-ogy cases) and another 25% had headache disorders.Typical FND cases comprised a smaller, but nonethelesssignificant, group of 18% (5.4% of all cases).

Age and sex

There is uniformity in cited studies that FND are morefrequent in women, with estimates tending to be around60–75% female (Monday and Jankovic, 1993; Lang,1995; Williams et al., 1995; Kim et al., 1999; Feinsteinet al., 2001; Thomas et al., 2006; plus studies citedabove). It should be noted, however, that these are gen-erally clinic-based samples andwomen aremore likely topresent to health services in general by a factor of 1.5:1.However, this is not always the case and, in some specificpresentations – late-onset dissociative seizures (Duncanet al., 2006) and functional myoclonus – the frequency isthe same in both genders.

Therewas similar consistencywith regard to age, withonset tending to be 35–50 years old within the studiescited above, but clinicians should note that one messagecoming from reported cases series is that incident casesare reported in both sexes and all ages, from young chil-dren to the elderly.

Geographic and historic epidemiology

Most studies of FND have been conducted in industrial-ized countries. It has generally been accepted inacademic textbooks that rates are higher in nonindustria-lized countries and that the prevalence has dramaticallydecreased in the industrialized nations during the 20thcentury. A number of extravagant anthropologic expla-nations have been provided for this. However, the

theories do seem to have run ahead of the data, whichare notably absent (Stone et al., 2008). There have beena small number of high-quality international studies ofgeneral somatoform disorders and they have concludedvery similar rates internationally (Simon et al., 1996).Also, a recent study from the Middle East showed a sim-ilar prevalence of dissociative seizures seen in the West-ern world (Farghaly et al., 2013).

Historic comparators are equally hard to achieve;however, where available, they are notably in keepingwith modern figures. Sydenham (trans. Latham, 1848),suggested that a third of the patients he was seeing withneurologic symptoms had “the vapours” (the equivalentof functional symptoms), a figure strikingly close tomodern data. Charcot’s assistant, Guinon, reported a fre-quency of 8% for hysteria in 3168 consultations (Guinon,1889), again, a figure very in keeping with current esti-mates. Interpretation of such historic data is fraught withcomplications, but does at least suggest that we should behighly sceptical of historically revisionist claims thathysteria was once frequent and is now rare.

ONSET

There is agreement that it is difficult and unreliable to usehistory alone to differentiate an FND from an “organic”neurologic disorder. Nonetheless, a sudden onset is oftenseen in functional movement disorders, with a frequencyof 54–92% (Factor et al., 1995; Deuschl et al., 1998; Kimet al., 1999; Feinstein et al., 2001; Ertan et al., 2009).However, “sudden” generally means over the course of10minutes to 1 hour (Stone et al., 2013), and not the trulysudden onset of a vascular event. Physical injury or painat onset is particularly typical in sudden-onset cases. Theinjury, as in patients with complex regional pain

Table 5.1

Studies measuring the frequency of symptoms unexplained by disease in neurology outpatient clinics

Study Location n % unexplained by disease

Carson et al. (2000) Edinburgh, UK 300 30% (11% “not at all” and 19% “somewhat” explained by disease)Bateman and Harrison(2000)

Bath, UK 356 26% no neurologic disorder

Nimnuan et al. (2001) London, UK 103 62% had “medically unexplained” symptomsStone and Sharpe (2002) Edinburgh, UK 89 36% (7% “not at all” and 29% “somewhat” explained by disease)Stone et al. (2004) Colchester, UK 100 45% had a “nonneurologic” diagnosisSnijders et al. (2004) Utrecht, Netherlands 208 35% considered to have “medically unexplained” symptomsFink et al. (2005) Vejle, Denmark 198* 61% had “medically unexplained” symptoms, 39% had a

somatoform disorderStone et al. (2010a)Ahmad and Ahmad(2016)

Aberdeen, Dundee,Edinburgh, Glasgow, UK

Sydney, Australia

3781884

30% (12% “not at all” and 18% “somewhat” explained by disease)15% had functional neurologic disorder

*Mixture of inpatients and outpatients.

EPIDEMIOLOGY 51

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Psychogenic Non-Epileptic

Seizures(PNES)

FunctionalMovement

Disorder(FMD)MeanAgeofOnset Mid-twenties Midtolatethirties

F:M 3:1 1.5-3:1

Physicalsymptoms Episodic Continuous

Scoresonphysical

disability,depression/

somatizationscores

Higherthanpopulation Higherthanpopulation– not

clearlydifferentto PNES

AdverseChildhood

Experience

2-3timeshigherthanthe

population

Morecommonthan

populationbutoftenlessthan

PNESrates

Illnessperceptions Notkeenonideaof“stress”

beinginvolvedinsymptoms

Evenlesskeenonideaof

‘stress’than PNESFMD: Functional movement disorder; PNES: Psychogenic non-epileptic seizuresStone and Carson, An Integrated Approach to other Functional Neurological Symptoms and Related Disorders ; in Dworetzky and Baslet (Eds) PNES: Towards the Integration of care, OUP, 2017

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Men Women Odds Ratio

Reported etiologiesEpilepsy predisposing factorsSexual abuse

(%)48.59.5

19.047.0

4.018.43

Psychosocial characteristicsAge of onsetAge of first evaluation

35.7340.98

30.0235.17

Work statusOccupied

(%)20.0 39.1 2.57

Mental Health HistoryHistory of self-harm

(%)2.3

(%)12.8 6.18

SemiologyWeeping

(%)20.9

(%)42.6 2.80

Carer’s acceptance of the diagnosis % 48.3 73.0 0.35

PNES: Psychogenic Non-Epileptic Seizures; n=166; only factors with p<0.05 Oto et al, Seizure, 2005

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¡ Conversion disorder (Freud and Breuer): Intolerable affect converted into somatic symptoms.

¡ Dissociation (Janet, Oakley): “autosuggestive disorder” that may lead to dissociative symptoms that are characteristic of conversion and of hypnotic states. Newer theories of dissociation emphasize compartimentalization and to a lower degree detachment.

¡ Cognitive hierarchic models (Brown): Schemata or representations on motor and/or sensory functions are altered; therefore, altered allocation of attentional function to certain sensory states, resulting in activation of dysfunctional hypotheses about sensory and motor outcome (ie, more response to hypotheses about sensorimotor processes than actual sensory input). These “rogue models” are formed via autosuggestion, via earlier experiences, via previous models of disease.

FND: Functional Neurological DisorderRoelofs and Pasman, Stress, childhood trauma and cognitive function in FND, in Hallet, Stone and Carson (Eds), Handbook of Clinical Neurology Vol. 139, Functional Neurological Disorders, 2016

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VulnerabilityTraits/NeuropsychologicalDeficitsAvoidancetendenciesAlexithymiaEmotionregulationstylesHypervigilance/fearsensitivitySomatizationDissociationandconversionExecutivedysfunctionVariablecognitiveperformance

PREDISPOSINGFACTORS

PRECIPITATINGFACTORS

PERPETUATINGFACTORS

Neuromedical ConditionsEpilepsy,mildTBI,intellectualdisabilities,headaches,chronicpain,cognitivedeficits,multipleallergiesPsychiatricComorbiditiesDepression,anxiety,PTSD,somaticsymptomdisorder,dissociativedisorders,personalitydisorders

AdverseEarlyLifeExperiencesChildhoodabuseChildhoodneglectFamilydysfunction

AdverseLaterLifeExperiencesSignificantloss(bereavement),healthproblems,interpersonaldifficulties,work-relatedproblems

Isolation,chronicstress,sickrole/illnessbehavior,misdiagnosis/mistreatment

FNSD

MultiplefactorsareassociatedtoFNSDincludingvulnerabilitytraits/neuropsychologicaldeficits,adverselifeexperiencesandpsychiatriccomorbidities andneuromedical conditions.Thesefactorsinteractatdifferenttimepointsaspredisposing,precipitatingorperpetuating.AdaptedfromBasletetal,Psychosomatics,2016

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PNES PMD6

Axis I Any Mood DisorderMajor Depressive DisorderAny Anxiety DisorderAnxiety + depressionPTSDAny somatoform disorder

24%4-98%1

44%2-80%1

25%1-51%1

29%3-58%1

22%4-98%1

N=42

43%62%29%

5%

Axis IIAny Personality DisorderCluster ACluster B

BPDCluster C

62%1

4%5-23%4

18%4-33%5

49%1

18%4-33%5

N=3642%

History of Sexual Trauma 32.5%7 25%8

FND: Functional Neurological Disorder; PNES: Psychogenic Non-epileptic seizures; PMD: Psychogenic Movement Disorder.1. Bowman and Markand, Am J Psychiatry, 1996, n=45; 2. Seneviratne et al, JCN, 2011, n=39; 3. Mokleby et al, Epilepsia, 2002, n=23; 4. Kuyket al, Epilepsy and Behavior, 2003, n=60; 5. D’Alessio et al, Seizure, 2006, n=24; 6. Feinstein et al, Neuropsychiatry, Neuropsychology and Beh Neurology, 2001; 7. Duncan and Oto, Neurology, 2008; 8. Czarnecki et al, PRD, 2011

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Type of Trauma FND Controls CommentsTotal (22 studies) 14-100% 9-66% (organic,

psychiatric, healthy)In most studies, statistically higher trauma in FND

Physical abuse (22 studies) 5-79% 0-40% About half of the studies had statistically higherrates in FND(same if only childhood abuse tested)

Sexual abuse (30 studies) 0-74% 0-40% About half of the studies had statistically higherrates in FND(same if only childhood abuse tested)

Emotional abuse or neglect (14 studies)

30-74% 11-63% In most studies, statistically higher emotionalabuse in FND (one study in opposite direction against psychiatric controls) (same if only childhood abuse tested)

Non-traumatic life events (5 studies) – closely preceding onset of symptoms

Statistically higher scores/ rates of life events in FND in all analyzed studies (4)

FND: Functional Neurological Disorder.Roelofs and Pasman, Stress, childhood trauma and cognitive function in FND, in Hallet, Stone and Carson (Eds), Handbook of Clinical Neurology Vol. 139, Functional Neurological Disorders, 2016

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¡ Structural and functional neuroimagingstudies in FNSD have demonstrated alteration in the following:

¡ Motor intention1,2,4

¡ Self-agency3

¡ Connectivity between areas involved in emotion processing and motor preparation5

FNSD: Functional Neurological Symptom Disorder1.Marshall et al; Cognition 1997; 2. DeLange et al, Neuropsychologia, 2007; 3. Voon et al, Neurology, 2010; 4. Labatteet al, Epilepsia, 2012; 5. van der Kruijs et al, JNNP, 2012.

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Van der Kruijs et al, JNNP, 2012

Emotion

Emotion

Control

Control

Motor

Motor

PNES

Healthy

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• N=8 subjects with lateralized paresis of an arm.

• Within-subject design to compare activity during imagined movement during the affected versus unaffected arm.

• Motor imagery of the affected arm recruited activation of ventromedial prefrontal cortex and superior temporal cortex.

DeLange et al, Neuropsychologia, 2007

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Right TPJ• 8 patients w positional psychogenic tremor• fMRI comparison of volitional tremor vs. psychogenic positional tremor

• Reduced right temporo-parietal junction (TPJ) activity during psychogenic vs. volitional tremor

• Reduced functional connectivity between TPJ and motor/somatosensory regions, ventral anterior cingulate cortex (ACC), medial prefrontal cortex (PFC).

• Dysfunction in R TPJ associated with impaired action authorship recognition in patients with psychogenic tremor

vACC

Neurology, 2010

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Perez, Barsky, Daffner & Silbersweig: J Neuropsychiatry Clin Neurosci, 2012

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¡ Disruption and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control and behavior.

¡ “Positive” dissociative symptoms: unbidden intrusions into awareness and behavior, with accompanying losses of continuity in subjective experience (i.e., fragmentation of identity [described as possession in some cultures], depersonalization, derealization).

¡ “Negative” dissociative symptoms: inability to access information or to control mental functions that normally are readily amenable to access or control (i.e., amnesia).

¡ Disorders in DSM-5: dissociative identity disorder; dissociative amnesia (specifier with fugue); depersonalization/ derealization disorder; other specified dissociative disorders (chronic and recurrent mixed dissociative symptoms; identity disturbance due to prolonged and coercive persuasion; acute dissociative reactions to stressful events; dissociative trance; PTSD subtype).

American Psychiatric Association, 2013

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Prevalence of dissociative disorders in the past year at mean age 33

Dissociative Disorder Males (N=309) n (%) Females (N=349) n (%)

Total sample (n=658) n (%)

Depersonalization DisorderDissociative Amnesia

Dissociative Identity Disorder (DID)DDNOS

Any dissociative disorder

2 (0.6%)

3 (1.0%)

5 (1.6%)

21 (6.8%)

30 (9.7%)

3 (0.9%)

9 (2.6%)

5 (1.4%)

15 (4.3%)

30 (8.6%)

5 (0.8%)

12 (1.8%)

10 (1.5%)

36 (5.5%)

60 (9.1%)

Johnson et al, Journal of Psychiatric Research, 2006

DDNOS: Dissociative Disorder Not Otherwise Specified

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Distribution of Dissociative Disorder Diagnoses Among 82 Patients Seen in an Inner-City, Hospital-Based Outpatient Psychiatric Clinic

Diagnosis NTotal= 24

%100

Dissociative AmnesiaDissociative Disorder Not Otherwise SpecifiedDissociative Identity DisorderDepersonalization DisorderDissociative Fugue

87540

109650

In this study, 71% of the dissociative disorder patients reported a history of childhood physical abuse and 75% reported a history of childhood sexual abuse, significantly more common than in patients who did not had a dissociative disorder.Dissociative Disorders Interview Schedule was used to establish diagnosis. Only 4 patients had a diagnosis of dissociative disorder recorded in their chart.

Foote et al, AJP, 2006

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All patients were female. N= 44 (DID), 22 (DDNOS), 13 (PTSD)Average number of Axis I psychiatric comorbidities in females with DID and DDNOS was 5.Rodewall et al, JNMD, 2011

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Right Posterior Parietal Cortex Metabolic Disturbances inDepersonalization Disorder

Simeon et al; Am J of Psychiatry 2000

8 Depersonalization Disorder PatientsVs24 Healthy Subjects Increased metabolism in parietal cortex

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www.thelancet.com/psychiatry Vol 1 August 2014 235

Review

retrograde amnesia creates several challenges.19 Standard tests of memory malingering assess anterograde and not retrograde memory; patients with dissociative amnesia might quickly relearn their past (through the semantic memory system107), which makes it diffi cult to distinguish between relearned (known) and remembered personal information; and diff erentiation of conscious from unconscious motivations with symptom validity tests is very diffi cult. However, the additional use of self-report personality assessment inventories could give hints about the presence of repressive coping styles.19 Two recent studies10,26 of retrograde dissociative amnesia that used functional imaging investigated deceptive or fi ctitious elements; their results open a pathway for the use of combined neuropsychological and functional neuro-imaging methods to diff erentiate between dissociative and simulated amnesia in the future. Furthermore, Bayesian methods can complement existing tests for assessment of malingering, since they can be more resistant to coaching eff ects. Ortega and colleagues108 used a Bayesian latent group analysis approach to detect poor eff ort and performed experiments to compare the accuracy indices (sensitivity and specifi city) of their method with those of a symptom validity test. They also assessed how coaching aff ects the classifi cation accuracy indices in the two conditions. The study showed higher sensitivity for the Bayesian method compared with the symptom validity test. The results also suggested that a Bayesian latent group analysis approach is more resistant to possible eff ects of coaching than is a traditional symptom validity test.

The diagnosis of dissociative amnesia can be strengthened if patients obtain scores indicative for the disorder in dimensional and classifi catory scales (table 5, panel 2). Based on a factorial analysis of 2569 datasets from healthy participants and patients, Dell4 suggested that three amnesia factors might be more useful to frontline clinicians than the DSM categorisation of dissociative amnesia: First, “discovering dissociated action” that is “preceded by the amnesic individual being unaware of having done something”; second, “lapses of recent memory and skills”; and third, “gaps in remote memory.” Panel 3 provides an overview of clinical features indicative of dissociative amnesia.

To assess the nature and severity of the memory impairment, a detailed neuropsychological assessment should be done (table 5 and panel 2).123

In retrograde dissociative amnesia, the memories of personal events are believed to still exist, but their retrieval from the episodic-autobiographical memory system is blocked. According to Tulving’s “serial, parallel, independent” (SPI) model,107 indices of these memories could still be accessed through other memory systems. The SPI model posits that information is encoded serially, stored in parallel in diff erent memory systems, and can be retrieved independently of the system in which encoding occurred. Patients with

retrograde dissociative amnesia might therefore still be able to make familiarity judgments about their past familiar surroundings. Since their priming memory system is intact, they can also react to indices of old information in an implicit way.123 However, changes in heart rate or galvanic skin conductance during the presentation of old, consciously inaccessible information should be interpreted with caution.38 Evidence exists for impaired somatic responses to emotional stimuli in dissociative amnesia, which could account for features of emotional fl attening (“la belle indiff érence”).23,28 Several studies show that heart rate variability is lower in patients with dissociative (conversion) disorders than in healthy participants. This outcome diff ers from hypnosis, in which an increase in heart rate variability occurs without changes in heart rate.23,124

Diff erential diagnosisThe diff erential diagnosis of dissociative amnesia encompasses amnesic disorders caused by general medical conditions or substance misuse-related disorders, other dissociative or trauma-related or stress-related disorders in which dissociative amnesia is a symptom, borderline personality disorder, and mood or anxiety disorders. Pseudodementic presentations should be distinguished from neurodegenerative dementias, especially in elderly people. In this age group, physicians might have a tendency to preponderantly attribute

Figure 5: Relative decreases in regional cerebral glucose metabolism in 14 patients with dissociative amnesia with pronounced retrograde memory impairments compared with 19 healthy participantsThe images show sagittal, frontal, and horizontal views superimposed on MRI sections (MRI template). The blue cross indicates the locus of the only signifi cantly deactivated spot in the right inferolateral prefrontal cortex. The homologous hypometabolic region within the left cortex did not reach signifi cance.Adapted from fi gure 1 in Brand and colleagues,27 by permission of Elsevier.

z scores

5

4

3

2

1

0

Downloaded from ClinicalKey.com at President and Fellows of Harvard College on behalf of Harvard University February 03, 2017.For personal use only. No other uses without permission. Copyright ©2017. Elsevier Inc. All rights reserved.

Brand et al, Psych Res, 2009

14 dissociative amnesia patients versus 19 healthy controls

FDG PET at rest

Right inferolateral prefreontal cortex

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Lanius et al; Am J of Psychiatry 2010

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Study NPrimary Disorder

Instruments used Comorbidity rates

Sar et al, 2004

38 pts with conversion disorder

SCID, SDQ-20, CTQ 48% with a dissociative disorder; abuse and neglect more common in comorbid group

Tezcan et al, 2003

59 pts with conversion disorder

DES, DDIS, SCID-D 30.5% with a dissociative disorder (50% DID, 44% DDNOS, 5% dissociative amnesia)

Spitzer et al, 1999

72 conversion disorder patients versus 96 psychiatric controls (neurotic)

DES, SCL-90 DES scores twice as high in the conversion group.No difference in somatization scores.

Espirito-Santo & Pio-Abreu, 2009

26 conversion disorder pts, 38 dissociative disorder pts, 40 somatization disorder pts and 46 psychiatric controls

DES, SDQ-20, BSI Dissociative (DES) and conversion symptoms (SDQ-20) significantly more frequent in conversion and dissociative groups. No difference between these two groups.

1. Sar et al, AJP, 2004; 2. Tezcan et al, Comprehensive Psych, 2003; 3. Spitzer et a, J Psychosom Res, 1999; 4. Espirito-Santo & Pio-Abreu, Aust N Z J Psychiatry, 2009.

DES: Dissociative Experiences Scale; SDQ-20: Somatoform Dissociation Questionnaire-20; CTQ: Childhood Trauma Questionnaire; SCID-D: Structured Clinical Interview for DSM IV Dissociative Disorders; SCL-90: Symptom Check-List-90; BSI: Brief Symptom Inventory

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Symptom Presentation Engagement Acute treatmentPhase

Long-termFollow-up

Baslet et al, Clin EEG Neurosci, 2014

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Covered Topic Communication Points

Negative Diagnosis •What you don’t have (ie, epilepsy)•What you don’t need (ie, treatment with AED’s)

Diagnostic Method •How diagnosis was made (ie, video-EEG captured event)•It is common!

Genuine Symptoms •Symptoms are real, not fabricated

Explanatory Model(Positive Diagnosis)

•Role of accumulating risk factors over time and automatic functional brain patterns

Suggestion •Some patients improve with reassurance

Treatment •There are effective treatments•Psychotherapy works though skills learning, “brain re-training”•No sudden cure, treatment requires training

Some elements extracted from Stone and Edwards, Neurology, 2012 and from Hall-Patch et al, Epilepsia, 2010

FNSD: Functional Neurological Symptom Disorder

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Hall-Patch et al, Epilepsia, 2010; Jirsch et al, Epilepsy & Behavior, 2011Razvi et al, Epilepsy & Behavior, 2012

There is significant decrease of medical utilization at one year post diagnosis.

PNES: Psychogenic Non-Epileptic Seizures

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Time Point Rate of Adherence

1 Immediate follow-up with neurologic team following PNES diagnosis 71-72%1,2

2 Initial referral to behavioral health team 66%3

3 Completion of psychotherapy 31-54%4,5

1-3 Composite Adherence Rate (time points 1-3 considered in series) 15-26%

31

Tolchin and Baslet, Treatment Adherence and Obstacles to Treatment, in Dworetzky and Baslet (Eds)“Psychogenic Non-Epileptic Seizures: Towards the Integration of Care”, OUP, 2017 -- 1. Duncan et al, Epilepsy & Beh, 2014; 2. McKenzie et al, Neurology, 2010; 3. Kanner et al, Neurology, 1999; 4. LaFrance et al, JAMA Psych, 2014; 5. Baslet et al, JNCN, 2013

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Symptom Presentation Engagement Acute treatmentPhase

Long-termFollow-up

Baslet et al, Clin EEG Neurosci, 2014

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Author, Year

N Treatment Design Outcome measures

Goldstein et al, 20101

66 PNES CBT (12 sessions) vs. SMC

Prospective, randomized, OL

Monthly sz frequency, HADS (depression and anxiety), WASAS (work and social adjustment)-Sz reduction in CBT group superior at tx

end

-Mood and employment status showed no change-Both groups w/ decrease in medical

utilization

Sharpe et al, 20112

127 (mixed population)

CBT Guided Self Help (and guidance sessions max four 30-min sessions) vs. SMC

Prospective, randomized, OL.

CGI (change in overall health), change in symptoms, PHQ-13 (symptom burden), HADS (depression and anxiety)Overall health, functional symptoms and

symptom burden improved more in active group at 3 months; functional symptoms and symptom burden improvement maintained at 6 months, plus anxiety and physical function improved at 6 months.

La France et al, 2014

34 PNES 4 arms: CBT-ip, CBT-ip+ sertraline, sertraline, TAU

Prospective, randomized, OL

Within-group analysis showed significant decline in sz count in CBT-ip and CBT-ip + sertraline groups, but not in the other groups.Improvement in most secondary

measures in CBT-ip armsBaseline psychopathology measures

more severe in TAU arm1. Goldstein et al, Neurology, 2010; 2. Sharpe et al, Neurology, 2011; 3. LaFrance et al, JAMA Psychiatry, 2014

Cognitive Behavioral Therapy (CBT) for PNES +

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Situation, relationship, resources and practical problemsGood marriage; husband, mother and father supportive; income currently reduced

SymptomsTremor,

pain in arms and legs, tired all the time

FeelingsDown, confidence

knocked. Annoyed.

Thinking‘People think I’m making

this up’, ‘There’s something seriously

wrong with me’

BehaviorStopped working,

driving and socializing.

Searching the Internet to find out

what’s wrong.

Williams et al, “Overcoming Functional Neurological Symptoms”, Hodder Arnold 2011; Kent and McMillan, Advances in Psych Treatment, 2009

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¡ Usually in the context of PTSD treatment.

¡ Interoceptive exposure proven effective at decreasing symptoms of depersonalization and derealization in panic disorder and PTSD1.

¡ Treatments primarily reported as uncontrolled case series or prospective longitudinal observational studies, with studies showing overall significant effect size overall(0.71) and for dissociation in particular (0.70)2.

¡ Expert consensus guidelines for treatment of dissociative disorders includes3:¡ First stage: Skills development -- emotion regulation, impulse control, interpersonal

effectiveness, grounding and containment of intrusive material.¡ Second stage: Resolution of cognitive distortions, mastery over memories (trauma

processing), exposure/ abreaction techniques (modified to avoid overwhelming dissociative patients).

¡ Third stage: Individualized (reconnecting with oneself, others and current daily life).¡ First manualized treatment for the stabilization phase in DID developed.

1. Weiner and McKay, Behavior Modification, 2013; 2. Brand et al, J Trauma and Dissociation, 2012; 3. Myrick et al, J Trauma and Dissociation, 2015

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FNSD¡ Hypnosis for mixed FNSD (RCT)¡ Brief group psychoeducation for PNES (RCT)¡ Brief augmented psychodynamic interpersonal psychotherapy in PNES¡ Prolonged exposure in dual diagnosis PNES + PTSD¡ Group psychodynamic psychotherapy in PNES¡ Group cognitive-behavioral therapy for PNES (negative trial)¡ Inpatient cognitive-behavioral therapy for PNES¡ Short-term psychodynamic psychotherapy for PMD¡ Physical therapy for conversion paralysis, PMD¡ rTMS over motor cortex for conversion paralysis, PMD¡ SSRI’s (RCT for PNES, PC) (negative trial)/ SNRI’s for PNES and PMD

Dissociative Disorders¡ CBT sessions (not manualized) for depersonalization disorder¡ Inpatient trauma programs for dissociative disorders¡ rTMS for Depersonalization Disorder¡ Lamotrigine in depersonalization disorder (RCT, PC), Fluoxetine in depersonalization

disorder (RCT, PC) (negative trial)¡ Naltrexone in depersonalization disorder

Baslet, Neuropsychiaric Disease and Treatment, 2013; Chen et al, Epilepsia, 2014; Conwill et al, Epilepsy and Behavior, 2014; Ricciardi and Edwards, Neurotherapeutics, 2014; Kompoliti et al, PRD 2014; Pollack et al, JNNP, 2012; Simeon et al, BJP, 2004; Aliyeb and Aliyeb, J Clin Psychopharm, 2011; Myers et al, Epilepsy and Behavior, 2016

FNSD: Functional Neurological Symptom Disorder; PNES: Psychogenic Non-epileptic Seizures; PMD: Psychogenic Movement Disorders.

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MODULE I: UNDERSTANDING YOUR DISEASE AND YOUR TREATMENT¡ Session 1: Understanding Your Illness¡ Session 2: Identifying the function of the symptom¡ Session 3: Identifying values

MODULE II: STRESS MANAGEMENT STRATEGIES¡ Session 4: Understanding the stress cycle¡ Session 5: Mastering a stress management skill

MODULE III: MINDFULNESS¡ Session 6: Introduction to mindfulness¡ Session 7: Incorporating mindfulness into everyday life

MODULE IV: EMOTION MANAGEMENT¡ Session 8: Emotion Recognition¡ Session 9: Emotion Acceptance¡ Session 10: Regulation of emotion-driven behavior

MODULE V: REWORKING COGNITIONS & RELAPSE PREVENTION¡ Session 11: Reworking cognitions¡ Session 12: Relapse Prevention

Baslet et al, Clin EEG Neurosci, 2014

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Baseline 6th session 12th sessionWeeks for 12 sessions

Patient 1 2.5 1.5 0 43Patient 2 8.5 7 5 15Patient 3 2.125 0 0 22Patient 4 0.25 0 0 37Patient 5 70 5 2 20Patient 6 24.5 0 11 21Avg 17.98 2.25 3

Case Series:Mindfulness-Based Protocol

Baslet et al, Clin EEG Neurosci, 2014

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¡ Patient filled postal questionnaire (n=164)¡ 4.1 years post-PNES diagnosis¡ 71% of patients continue to be symptomatic.1

¡ Complaint at doctor’s visit over 6 months (n=167)¡ 5-10 years post-PNES diagnosis¡ 26% of patients continue to complain of seizures.¡ Significant reduction in ED visits and AED prescription, but

not in employment rates.2

¡ Patient inquiry (n=42)¡ 1-7 years post-PMD diagnosis¡ 10% had symptom remission, a third were improved, 24%

was stable and a third “worse”.3

1. Reuber et al, Annals of Neurology, 20032. Duncan et al, JNNP, 20143. Feinstein et al, Neuropsychiatry, Neuropsychology and Beh Neurology,

2001.

PNES: Psychogenic Non-Epileptic SeizuresPMD: Psychogenic Movement DisorderED: Emergency DepartmentAED: Antiepileptic Drug

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¡ FNSD and dissociative disorders share similarities in their underlying psychopathology, but they are not identical disorders.

¡ FNSD are common in neurological practice and dissociative disorders are more common than recognized in psychiatric practice.

¡ For FNSD, presentation of the diagnosis is a very important link to enhance engagement in treatment, and serves a therapeutic purpose.

¡ Evidence-based treatment for either disorder is limited but slowly growing.

¡ Identifying subgroups of patients with different outcomes may help customize treatment protocols for subpopulations and improve overall functional outcomes.

FNSD: Functional Neurological Symptom Disorder