Il paziente "nascosto":

la psicosomatica in medicina

piero.porcelli@unich.it

Piero Porcelli

Dip. Scienze Psicologiche, della Salute e

del Territorio

Università d’Annunzio di Chieti

DSM-IV

Somatization Disorder

Pain Disorder

Undiff.Somatoform Disorder

Somatic Symptom Disorder

DSM-5

Somatoform Disorder NOS Unspecified SSD

Conversion Disorder Conversion Disorder

Body Dysmorphic DisorderBody Dysmorphic Disorder

(OC and Related Dis.)

Illness Anxiety Disorder

Factitious Disorder(separated section)

Factitious Disorder

Imposed on Self/Another

Hypochondriasis

PFAMC(Other Conditions that May Be a

Focus of Clinical Attention)

Psychological Factors Affecting

Other Medical Conditions

Working Group for ICD-11

•Bodily Distress Syndrome

(BSS) for MUS

•Health Anxiety (HA) replacing

Hypochondriasis

•Hypochonadriasis moved to

OC and Related Disorders

Patient 1F, age 32, secretary, separated

(2 yrs ago), one 3-yrs-old son

Patient 2M, age 56, business company

executive, married, 2 adolescent sons

DSM-IVUndiff. somatoform disorder

A) ≥1 somatic symptoms Fatigue, appetite loss, headache,

chronic FAP

Tinnitus, dizziness, frequent episodes

of elevated BP

B) Not explained No medical explanation Autoimmune thyroiditis

C) Exaggerated symptoms Work absenteeism Hard worker

D) Duration ≥6 mo. 12 months 10 years

E) Not accounted by another

mental disorder

Subthreshold depression, grief

reaction, demoralization

Type A behavior, subthreshold bipolar

disorder (mood swing)

F) No simulation No simulation No simulation

DSM-5SSD

A) ≥1 somatic symptoms Fatigue, appetite loss, headache,

chronic FAP

Tinnitus, dizziness, episodes of

elevated BP

B) Health-related worries Frequent medical visits, 2

hospitalizations (last year)

Food avoidance, body checking,

disease phobia

C) Duration ≥6 mo. 12 months 10 years

Failure to represent clinical reality adequately

Rather than

grounding on

symptoms as in DSM

(high reliability, low

validity), RDoC re-

oriented to explore

ways of incorporating

such methods as

genetics, neuro-

imaging, and

cognitive science into

future diagnostic

schemes based upon

behavioral

dimensions and

neural systems.

Caspi et al, Clin Psychol Sci 2014

PSYCHOPATOLOGY COMORBIDITYThe longitudinal Dunedin Health and Development Study

(N = 1037; assessments at age 18-21-26-32-38)

The higher a person scores on p, the worse that person fares on indicators tapping severity, duration of

disorder, extent of sequential comorbidity, adult life impairment, childhood developmental history, family

history of liability to psychiatric illness, and brain function from early life to midlife

3 higher-order

factors with

liabilities for

Antisocial and

Substance-use

Disorders

(Externalizing)

Depression and

Anxiety Disorders

(Internalizing)

Psychotic

Spectrum

Disorders

(Thought

Disorder)

Can = cannabis

CD = Conduct Disorder

Psychiatric research may benefit from approaching

psychopathology as a system rather than as a

category, identifying dynamics of system change

(eg, abrupt vs gradual psychosis onset), and

determining the factors to which these systems are

most sensitive (eg, interpersonal dynamics and

neurochemical change) and the individual variability

in system architecture and change.

A. Change tends to occur gradually in response to

changes or stress (red arrows)

B. System may initially resist change and then

reach a tipping point that involves a sudden and

dramatic shift to an alternative state, maybe

triggered by a massive stress

C. Transitions may be preceded by an increase in

random variance and volatility or, alternatively, a

critical slowing down of activity

DYNAMIC MODELS OF

PSYCHOPATHOLOGY

Nelson et al, JAMA Psychiatry 2017

NETWORK APPROACH TO DIAGNOSIS

Borsboom D, World Psychiatry 2017

Progression from mental health (= stable state of a weakly connected network)

to mental disorder (= alternative stable state of a strongly connected network)

After an asymptomatic phase, in which the network is dormant (Phase 1), an external event (E1) activates some of the symptoms (Phase 2), which in turn activate connected symptoms (Phase 3).

If the network is strongly connected, removal of the external event does not lead to recovery: the network is self-sustaining and is stuck in itsactive state (Phase 4).

CORPO

MENTE

CORPO

MENTE

AFFECT AWARENESS OPERATORY THINKING

Difficulty identifying feelings

Unawareness of feelings. Experience of chronic

dysphoria or show emotional outbursts (rage,

weeping) but inability to link feelings with memory

and fantasies. Inability to distinguish emotions from

feelings

Difficulty describing feelings to

others

Inability to express and communicate emotional

and mental states to others. Difficulty in

understanding emotions in other persons (empathy)

and their perspective (ToM)

Constricted imaginative processes

Marked paucity of fantasies, daydreaming, dream

recalls, wit, playing

External-oriented thinking style

Selective focus on everything is outward, factual,

concrete. Oversimplification and avoidance of

ambiguities or emotional nuances of inner life.

Report of events and actions with no affective

involvement

ALEXITHYMIA

EMOTIONS

• Biological component of affect

• Neurophysiologic and motor-

expressive domain of response

• Genetic programs (hard wired: fear, anger,

sadness, happiness, disgust, surprise)

• Mediated by subcortical and

limbic structures

• Largely based on non-verbal clues

• “play out in the theater of the body”

(A.Damasio, 2003)

• Predominant in right brain hemisphere

FEELINGS

• Psychological component of affect

• Subjective, cognitive-experiential

domain of response

• Individual schemas and developmental

factors

• Mediated by cortical structures

• Largely based on the symbolic function

• “play out in the theater of the mind”

(A.Damasio, 2003)

• Predominant in left brain hemisphere

How do emotions get represented symbolically so that they can be experienced

consciously as feelings that can be named, regulated, and expressed through fantasies?

IMPLICIT

Things we do without monitoring them on a moment-

by-moment basis (eg, bike riding)

EXPLICIT

Situation in which we can put our experiences into

words because we are aware of their occurrence

0

20

40

60

80

100

Classic psychosomatic disorders and

psychoneurotic diordersDisorders of affect regulation

OCD Obsessive-Compulsive Disorder

CAD Coronary Artery Disease

BED Binge Eating Disorder

Sex Multiple Sexual Dysfunction

RA Rheumatoid Arthritis

UC Ulcerative Colitis

SAD Social Anxiety Disorder

NFA Near-Fatal Asthma

TTM Trichotillomania

CFS Chronic Fatigue Syndrome

MDD Major Depression Disorder

CIN Cervical Intraepithelial Neoplasia

SA Suicide Attempters

SLE Systemic Lupus Erythematosus

BN Bulimia Nervosa

TMD Temporomandibolar

HCFU Health Care Frequent Users

CSPG Chronic Severe Pathol Gambling

Dissoc Dissociative Disorder

FGID Functional GI Disorders

AN Anorexia Nervosa

PREVALENCE OF ALEXITHYMIA

ALEXITHYMIA

• Deficit in cognitive processing of emotions

• Trauma and severe physical illness (secondary alexithymia)

• Somatization syndromes (MUS, somatosensory amplification)

• Disorders of affect regulation (hypochondriasis, panic, depression, eating, addiction)

• Insecure attachment patterns

• Decoupling stress hypothesis (higher resting state and physiological hyper-arousal as

salivary cortisol, but low stress perception)

• Sparse findings on immune imbalance of inflammatory markers

• High mortality risk

(Kuopio Ischemic Heart Disease study, 20-year follow-up: RR=1.2, same as HDL-C e

History of CV diseases)

• Deficit of brain inter-emispheric transfer

• Lower dACC and PFC activity/volume and higher AI/SS I-II activity

Defense

I know but can’t tell

Deficit

I don’t know and can’t tell

Overall consensus:

It is not a psychopathology or a category but a

personality dimension

Multidetermined disorders, arising from a composite of factors affecting the gut mucosa and

microflora, the nervous system and its extrinsic neural connections in the gut, and signaling

within the brain and the spinal cord.

These disorders are best understood from a biopsychosocial perspective; as such it would

appear unlikely that any single biomarker – such as mucosal histology, cardiovascular

reactivity, gut permeability, and blood, stool, or genetic markers – can explain the symptoms

and will emerge as a diagnostic tool for these disordersKellow , Am J Gastroenterol 2010

Functional GI Disorders

Psychiatric pts(n = 52)

FGID pts(n = 58)

Anxiety26%

Somatoform26%

Mood24%

Adjustment24%

0%

20%

40%

60%

80%

100%

Comor -

Comor +

Psych w/ GI

FGID w/ psych

0 20 40 60 80

TAS-20

0

5

10

15

20

GSRS SOM OC INT DEP ANX HOS PHOB PAR PSY

SCL-90-R

p < .001

Psychiatric

patients

FGID

patients

Same GI

symptoms

alexithymia

GI medical setting

psychopathology

psychiatric setting

Cognitive, affective, and behavioral response stemming

1) from fear of GI sensations or symptoms, and …

2) the context in which these visceral sensations and symptoms occur.

It is focused specifically on the IBS core features (abdominal pain and bowel

habit) in specific contexts as situations involving food and eating, like

restaurants and parties or locations in which bathroom facilities are not known

or difficult to reach.

Briefly, GSA relates to hypervigilance to, and fear, worry, and avoidance of, GI

sensations and contexts.

Earlier findings showed that GSA was associated to more severe IBS

symptoms, psychological distress, poor quality of life, and mediated the

relationship between general psychological distress and IBS severity.

Gastrointestinal-Specific Anxiety

(GSA)

ALEXITHYMIA TAS-20

GSA Visceral Sensitivity Index (VSI)

Psy distress HADS

Functioning SF-12

IBS symptomsGI Symptom Rating Scale-IBS

(GSRS-IBS)

IBS severityIBS Severity Scoring System

(IBS-SSS)

Mild IBS = score 75–175

Moderate = 175–300

Severe = >300177 IBS patients assessed at

- baseline

- after 6 months of as-needed tx

Block 1: age, GSRS-IBS score, HADS, PCS, MCS

Block 2: VSI

Block 3: TAS-20

The order of forced variables in the 2nd and 3rd blocks was revered in two different models.

The relative contribution of VSI and TAS-20 was very similar, either when

− VSI was forced before TAS-20 (R2 = 0.51, ΔR2 = 0.14, β = 0.307)

− TAS-20 was forced before VSI (R2 = 0.56, ΔR2 = 0.19, β = 0.532).

PREDICTING IBS SEVERITY

Large effect size for

being alexithymic,

higher if also with

higher GSA

PREDICTING TREATMENT OUTCOMEIBS-SSS RCI = D >50

Baseline GSRS-IBS and TAS-20, but not VSI, significantly and independently predicted

the treatment outcome.

In particular, GSRS-IBS significantly explained about 1% of variance while TAS-20 alone

added 10% of explained variance.

The final model accurately predicted 89% of the improved and 61% of the unimproved

patients (OCC rate = 74%).

0

2

4

6

Baseline 3 months Post-therapy Follow-up

Anxiety

Depression

Somatic Symptoms

ALEXITHYMIA AND SOMATIC SYMPTOMS IN HCV+ PATIENTS

DURING IFN THERAPY

N = 111 pts (men 53%, mean age 51, lifetime psychopathology 34%)

0

10

20

30

Baseline 3 months Post-therapy

Follow-up

%

Biological AE

BASELINE• SCID

• TAS-20

• PHQ-15

AT EACH VISIT

• HADS

• Somatic symptoms

• Biological AE

1. Fever

2. Headache

3. Muscle and joint pain

4. Diarrhea

5. Gut discomfort

6. Fatigue

7. Poor appetite

8. Weight loss (>10%)

9. Hair loss

10. Loss of libido

11. Itching

12. Skin rush

13. Dyspnea

14. Cough

15. Eye drying

16. Sleep problems

5-point scale

1 (none) to

5 (most severe)

Main outcome

no. of symptoms

graded as 4-5 (severe

and most severe)

Most common biological Adverse Events:

• Anemia (hemoglobin < 6.5 g/dL)

• Neutropenia (absolute neutrophils count

< 500/mm3)

• Thrombocytopenia (platelets <

25.000/mm3)

Grade 3 (severe) and 4 (disabling) of the

National Cancer Institute criteria

(Common Terminology Criteria for

Adverse Events v3.0, 2006)

MULTIPLE REGRESSION:

partial r

• Baseline: R2 = .80, F = 68.552, p < .001

• 3 months: R2 = .42, F = 77.566, p < .001

• Post-therapy: R2 = .38, F = 70.662, p < .001

• Follow-up: R2 = .77, F = 56.772, p < .001

SOMATIC SYMPTOMS

Gender

Past psychopathology

Alexithymia

Somatization

Anxiety

Depression

SVR

Baseline 3 months End therapy Follow-up

Alexithymiar = .54

Somatizationr = .66

Alexithymiar = .35

Somatizationr = .64

Depressionr = .54

Depressionr = .42

DV = no. of somatic symptoms at each assessment time point

Pre

dic

tors

Porcelli et al, Psychother Psychosom 2014; 83: 310-311

• Paura soverchiante e irrazionale di incontinenza fecale (abbastanza severa

da “mimare” il panico)

• Ruminazioni ideative focalizzate specificamente sull’alvo (dall’umiliazione in

pubblico all’indisponibilità del bagno fuori casa)

• Rituali compulsivi finalizzati a mantenere il controllo corporeo, soprattutto

trascorrere un’enorme quantità di tempo in bagno e limitare l’alimentazione

• Profilo dei sintomi simile al DOC: pensieri ossessivi che innalzano il livello

dell’ansia e rituali compulsivi finalizzati a mitigare l’ansia

• Sintomi sparsi sovrapponibili a disturbo di panico, fobia sociale, fobia

specifica, agorafobia senza panico

Hatch ML, Behav Res Ther 1997

trigger

uscire di casa

(autonomia)

reazione ansiosa

blocco affettivo arousal SNA

pensiero

calmo quando mi

scarico

sintomo

rituale compulsivo

Alexithymia

CONCLUSIONI

• Il paziente "nascosto" o le dimensioni "nascoste" dietro la nosografia

categoriale: evoluzione temporale della sintomatologia, interazione fra

caratteristiche del paziente e circostanze ambientali, fattori latenti unificatori

della sintomatologia, funzioni di personalità (es. alexithymia).

• In gastroenterologia (FGID, IBD, HCV), l'alexithymia può giocare un ruolo

importante nella gestione clinica del paziente nell'influenzare e predire:

• il setting a cui il paziente si rivolge o viene inviato;

• la percezione di gravità e l'esito dell'intervento terapeutico nei disturbi

funzionali del tratto digestivo;

• la presentazione di sintomi fisici in modo inconsueto o anche mascherare

una sindrome psicopatologica (es. ossessivo-compulsiva) come fase di

riacutizzazione di una malattia cronica (es. IBD)

27

piero.porcelli@unich.it