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Pemicu 7

Blok saraf & kejiwaan


Pandu
405140087
• Anxiety symptoms and the resulting disorders are believed to be due
to dysregulation of neuronal activity with the CNS fear circuit.
Physical and emotional manifestations of this dysregulation are the
result of a state of hyperarousal. Several neurotransmitter systems
have been implicated in the genesis of this state.
• The most commonly considered are the serotoninergic and
noradrenergic neurotransmitter systems.
• Very simply, it is believed that an underactivation of the
serotoninergic system and an overactivation of the noradrenergic
system are involved. These systems regulate and are regulated by
other pathways and neuronal circuits in various regions of the brain,
including the locus caeruleus and limbic structures, resulting in
dysregulation of physiologic arousal and the emotional experience
of this arousal. Disruption of the γ-aminobutyric acid (GABA) system
has also been implicated because of the response of many of the
anxiety-spectrum disorders to treatment with benzodiazepines.
• There has also been some interest in the role of corticosteroid
regulation and its relation to symptoms of fear and anxiety.
Corticosteroids might increase or decrease the activity of certain
neural pathways, affecting not only behavior under stress but also
the brain's processing of fear-inducing stimuli

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• The stress response is hardwired into the brain and is most often
triggered when survival of the organism is threatened. The stress
response, however, can be triggered not only by a physical challenge
or threat but also by the mere anticipation (or fear) of threat. As a
result, when humans chronically and erroneously believe that a
threatening event is about to occur, they begin to experience the
physical and psychological symptoms of anxiety and panic.
• Finally, a subcortical neural structure, the amygdala, serves an
important role in coordinating the cognitive, affective,
neuroendocrine, cardiovascular, respiratory, and musculoskeletal
components of fear and anxiety responses (fear expression). It is
central to registering the emotional significance of stressful stimuli
and creating emotional memories. The amygdala receives input from
neurons in the sensory cortex. When activated, the amygdala
stimulates regions of the midbrain and brain stem, causing autonomic
hyperactivity, which can be correlated with the physical symptoms of
anxiety.

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o Teori biologi
• Area otak yg diduga terlibat adalah lobus oksipitalis yg mempunyai
reseptor benzodiasepin tertinggi di otak, basal ganglia, sistem
limbik & korteks frontal jg di hipotesiskan terlibat dlm timbulnya. Pd
pasien jg ditemukan sistem serotonergik yg abnormal.
Neurotransmitter yg berkaitan adalah GABA, serotonin,
nonepinefrin, glutamat, dan kolesistokinin.
• Pemeriksaan PET ditemukan penurunan metabolisme di ganglia
basal & massa putih di otak.

o Teori genetik
• Studi menaptkan bahwa sekitar 25% dari keluarga tingkat pertama
penderita GAD jg menderita ggn yg sama. Sedangkan penderita pd
pasangan kembar di dptkan angka 50% (monozigot) 15% (dizigotik)
• Teori Psikoanalitik
• Menghipotesiskan bahwa ansietas adalah gejala dr konflik bwh
sadar yg tdk terselesaikan. Ansietas dihubungkan dg perpisahan
objek cinta

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
o Teori Psikoanalitik
• Menghipotesiskan bahwa ansietas adalah gejala dr konflik bwh
sadar yg tdk terselesaikan. Pd tingkat yg paling primitif Ansietas
dihubungkan dg perpisahan objek cinta. Pd tingkat yg lebih matang
ansietas dihub dg kehilangan cinta dari objek yg penting, sedangkan
ansietas super ego (ketakutan seorang utk mengecewakan nilai &
pandangan nya sendiri) merupakan ansietas tingkat yg paling
matang.

o Teori kognitif-perilaku
• Penderita GAD berespon salah & tdk tepat terhadap ancaman,
disebabkan olh perhatian yg selektif terhadap hal-hal yg negatif pd
lingkungan, adanya distorsi pd pemrosesan informasi & pandangan
yg sgt negatif terhadap kemampuan diri utk menghadapi ancaman.

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Generalized anxiety disorder (GAD)
Definition
• Generalized anxiety disorder (GAD) is most likely to present in
combination with other psychiatric and medical conditions.
Individuals with GAD commonly present with excessive and
disproportionately high levels of anxiety, fear, or worry for most
days over at least a 6-mo period in a number of areas. The worrying
must be greater than would be expected given the situation, and it
must cause significant interference in functioning. The subjective
anxiety must be accompanied by at least three somatic symptoms
in adults, and one in children (e.g., restlessness, irritability, sleep
disturbance, muscle tension, difficulty concentrating, or fatigue).
GAD cannot be diagnosed if it occurs only in the context of an
active mood disorder, such as depression, or if the anxiety is better
explained by another active anxiety disorder, such as PTSD or panic
disorder.

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Etiology
• Hypotheses include models based on neurotransmitters
(catecholamines, indolamines) and developmental psychology (e.g.,
behavioral inhibition, neuroticism, and harm avoidance).
• Prevalence increased with a family history, increase in stress,
history of physical or emotional trauma, and medical illness.

• Predominant Sex
• Women are more frequently affected (2:1 ratio) but may present
for treatment less often (3:2 female/male).
• Predominant Age
 30% report onset before age 11
 50% have onset before age 18
 Median age of onset: 30 years

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488000567
Physical Findings & Clinical Presentation
• Report of being “anxious” all of their lives.
• Excessive worry, usually regarding family, finances, work, or
health.
• Sleep disturbance, particularly early insomnia.
• Muscle tension (typically in the muscles of neck and
shoulders) or headache.
• Difficulty concentrating.
• Daytime fatigue.
• Physical symptoms are the usual reason for seeking medical
attention.
• Comorbid psychiatric illness (e.g., dysthymia or major
depression) and substance abuse (e.g., alcohol abuse) are
frequent.

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Diagnosis Klinis (PPDGJ-III)
 Penderita harus menunjukkan anxietas sebagai gejala primer yg berlangsung
hampir setiap hari untuk beberapa minggu sampai beberapa bulan, yg tidak
terbatas atau hanya menonjol pada keadaan situasi khusus tertentu saja
('free floating' atau mengambang)
 Gejala tersebut biasanya mencakup unsur-unsur berikut:
a) Kecemasan (kahawatir akan nasib buruk, merasa seperti di ujung taduk, sulit
konsentrasi, dsb)
b) Ketegangan motorik (gelisah, sakit kepala, gemetaran, tidak dapat santai)
c) Overaktivitas otonomik (kepala terasa ringan, berkeringat, jantung berdebar-
debar, sesak nafas, keluhan lambung, pusing kepala, mulut kering,dsb)
 Pada anak-anak sering terlihat adanya kebutuhan berlebihan untuk
ditenangkan (reassurance) serta keluhan somatik berulang yg menonjol
 Adanya gejala lain yg sifatnya sementara (untuk beberapa hari), khususnya
depresi, tidak membatalkan diagnosis utama gangguan anxietas
menyeluruh, selama hal tersebut tidak memenuhi kriteria lengkap dari
episode depresif, gangguan anxietas fobik, gangguan panik, atau gangguan
obsesif-kompulsif
Nonpharmacologic Therapy
• Cognitive-behavioral therapy
• Acceptance and commitment therapy
• Relaxation training
• Biofeedback
• Psychodynamic psychotherapy

Pharmacologic Therapy
• SSRIs and SNRIs (e.g., venlafaxine and duloxetine) are effective typical
first-line treatment. Particularly useful if comorbid depression
present.
• Buspirone can be effective with minimal potential for tolerance or
abuse. May be less effective in patients with previous benzodiazepine
exposure and may require a high-dose titration.
• Benzodiazepines can be effective under close supervision; however,
they have fallen out of favor as a first-line treatment given their
potential for functional impairment, abuse, and dependence.
• Sedating antidepressants, such as mirtazapine, may also be useful for
initial insomnia secondary to anxious ruminations.

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Gangguan campuran anxietas dan Depresi
Pedoman Diagnostic PPDGJ III
• Terdpt gejala2 anxietas maupun depresi, dimana masing2 tdk
menunjukan rangkaian gejala yg cukup berat utk menegakan
diagnosa tersendiri. Utk anxietas bbrp gejala otonomik harus
ditemukan walaupun tdk terus-menerus, disamping rasa cemas
atau kekhawatiran berlebihan.
• Bila ditemukan anxietas berat disertai depresi yg lebih ringan, maka
hrs dipertimbangkan kategori ggn anxietas lainya atau ggn anxietas
fobik.
• Bila ditemukan sindrom depresi & anxietas yg cukup berat utk
menegakan masing2 diagnosis, maka kedua diagnosis tsb harus
dikemukakan satu diagnosis maka ggn depresif harus diutamakan.
• Bila gejala-gejala tsb berkaitan erat dg stress kehidupan yg jelas,
maka harus digunakan kategori F43.2 gangguan penyesuaian.
Phobias
Definition
• Specific phobias are anxiety disorders characterized by an excessive,
persistent fear elicited by a specific object or situation that is then
avoided or tolerated with intense distress. The provoking stimulus may
be a specific object, such as an animal or insect; natural environments,
such as heights or water; or a specific situation, such as the sight of
blood, the receipt of an injection, or being in a tunnel or on a bridge.
• Social anxiety disorder (formerly named social phobia) is a specific,
separately diagnosed disorder characterized by a fear of being
embarrassed, humiliated, or rejected in social or performance situations.
• Agoraphobia also is a separately diagnosed disorder, characterized by an
intense anxiety about being in a place or situation from which they
would not be able to escape in the event of a panic attack or panic-like
symptoms. Such situations include being in enclosed/crowded spaces or
being more than a certain distance from home alone. If agoraphobia is
present in individuals with panic disorder, both diagnoses are given.
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Fobia
Kriteria diagnosis DSM IV
A. Agorafobia :
1. Kecemasan berada dlm situasi atau tempat yg untuknya sulit
meloloskna diri atau sulit utk mendapat pertolongan saat terjadi
serangan panik. Ketakutan agorafobia biasanya pada situasi diluar
rumah sendirian, berada di tempat ramai. Catt : fobia spesifik bila
hanya menghindari bbrp situasi spesifik
2. Situasi dihindari (mis jarang bepergian) atau jika dilakukan akan
menjadi cemas mendapat serangan panik.
3. Kecemasan atau penghindaran fobik tdk lebih baik diterangkan olh
gangguan mental lainya spt fobia sosial, fobia spesifik, gangguan
obsesif-kompulsif, gangguan stress pasca trauma, ggn cemas
perpisahan.

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
2. Fobia spesifik
A. Ketakutan yg jelas & menetap yg berlebihan tanpa alasan,
ditunjukan dg keberadaan atau antisipasi suatu objek yg spesifik
atau situasi tertentu.
B. Paparan terhadap stimulus fobik hampir selalu memprofokasi
respons kecemasan yg segera dlm bentuk serangan panik
situasional atau dipredisposisikan olh situasi.
C. Individu dpt menyadari bahwa ketakutan nya adalah berlebihan &
tanpa alasan
D. Situasi fobik dihindari / dijalani dg kecemasan / distress yg kuat.
E. Penghindaran, antisipasi kecemasan pd situasi yg ditakuti secara
bermakna menganggu kegiatan yg rutin dilakukan
F. Pd individu dibwh 18 thn, durasi berlangsung sekurangnya 6 bln.
G. Ansietas, serangan panik / penghindaran fobia berhub dg objek /
situasi spesifik yg lebih baik tdk diterangkan olh ggn mental lain :
Obsesif-kompulsif, stress pasca trauma, ggn cemas perpisahan,
fobia sosial, ggn panik

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Phobia spesifik
3. Fobia sosial
A. Ketakutan irasional yg jelas & menetap terhadap situasi sosial/
tampil di dpn org2 yg belum dikenal / dgn kemungkinan dinilai olh
org lain yg tdk dikenal. Individu takut bahwa ia akan bertindak dg
cara (atau menunjukan gejala2 kecemasan) yg akan memalukan
B. Pemaparan dg situasi sosial yg ditakuti hampir selalu mencetuskan
kecemasan, yg dpt berupa serangan panik yg berkaitan dg situasi /
dipredisposisikan olh situasi.
C. Orang menyadari bahwa ketakutan adalah berlebihan / tak
beralasan
D. Situasi sosial / tampil di dpn umum yg ditakuti dihindari, atau
dihadapi dg rasa cemas / distress yg berat.
E. Penghindaran, antisipasi kecemasan, atau distress dlm situasi
sosial atau tampil di dpn umum secara bermakna menggangu
rutinitas normal, fungsi sosial, pekerjaan.
F. Pd individu usia dibwh 18 thn durasi sekurang nya adalah 6 bln
G. Ketakutan / penghindaran tdk krn efek suatu zat atau kondisi
medik umum, dan tdk lebih baik diterangkan olh ggn mental lain.
H. Bila terdpt suatu kondisi medis umum / ggn mental lain. Ketakutan
kriteria A tdk berhubungan dgn nya
Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Nonpharmacologic Therapy
• Cognitive-behavioral therapy (CBT) and exposure-based treatments
have been effective for treating specific phobia and social anxiety
disorder in controlled trials and are considered an appropriate first-
line treatment.
• Behavioral treatments sometimes involve relaxation training, often
paired with visualization and progressive desensitization.
• Success rates in treating specific phobias are higher when the
phobia is not complicated by other anxiety disorders.
pharmacologic Therapy
• If the phobic stimulus is rarely encountered, benzodiazepines used
on an as-needed basis can be an appropriate long-term treatment;
however, there is a risk of abuse and dependence that makes them
a less desirable choice for long-term treatment.
• Selective serotonin reuptake inhibitors are the most effective
pharmacologic treatment in reducing symptoms and improving
function for people with social anxiety disorder.
• Monoamine oxidase inhibitors are also effective for treatment of
social anxiety disorder, but are rarely used due to dietary
restrictions and adverse effects.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488005923
Panic Disorder, with or without Agoraphobia
• Panic disorder is diagnosed at least after two uncued panic attacks
have occurred followed by at least 1 mo (or more) of significant
concern about future attacks, worry about their implications, or a
major change in behavior related to these attacks. The criteria for
diagnosis of panic disorder is summarized in Table 1P-8 .
• Agoraphobia is anxiety about, and avoidance of, places or situations
in which the ability to escape is perceived to be limited or
embarrassing or in which help might not be available in the event of
having a panic attack.

https://www.clinicalkey.com/#!/content/3-s2.0-B9780323280488005613?scrollTo=%23t0015
Physical Findings & Clinical Presentation

Panic disorder
 Present either with a panic attack or with fear and anxiety related
to anticipation of a future panic attack or its implications.
 Typical presentation: unexpected, untriggered periods of intense
anxiety and fear with associated physiologic changes (e.g.,
palpitations, sweating, tremulousness, shortness of breath, chest
pain, gastrointestinal distress, faintness, derealization, paresthesia).
This is accompanied by associated fears of dying, heart attack,
stroke, passing out, losing control, or losing one’s mind. Panic
attacks are often described as “the most terrifying” episode an
individual has experienced.
 Emergency or physician visits often occasioned by physical
symptoms such as chest pain, dizziness, or difficulty breathing.

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DSM-V Criteria for Panic Disorder
• Recurrent unexpected panic attacks. A panic attack is an abrupt surge of
intense fear or intense discomfort that reaches a peak within minutes, and
during which time four (or more) of the following symptoms occur:
• Note: The abrupt surge can occur from a calm state or an anxious state.
 Palpitations, pounding heart, or accelerated heart rate
 Sweating
 Trembling or shaking
 Sensations of shortness of breath or smothering
 Feelings of choking
 Chest pain or discomfort
 Nausea or abdominal distress
 Feeling dizzy, light-headed, faint, or unsteady
 Chills or heat sensations
 Parenthesis (numbness or tingling sensations)
 Depersonalization (being detached from oneself) or derealization (feelings
of unreality)
 Fear of “going crazy” or losing control
 Fear of dying

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Kriteria diagnostic PPDGJ III
• Terjadinya bbrp serangan berat ansietas otonomik, yg terjadi
dlm periode kira2 satu bulan.
1. Pada keadaan2 yg sebenarnya secara objektif tdk ada
bahaya.
2. Tidak terbatas hanya pd situasi yg telah diketahui / yg dpt
diduga sebelumnya.
3. Adanya keadaan relatif bebas gejala ansietas dlm periode
antara serangan2 panik.

Maslim R. Diagnosis gangguan jiwa. Bagian ilmu kedokteran jiwa FK-Unika Atmajaya, Jakarta. 2013
• Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache,
uncontrollable screaming or crying) may be seen. Such symptoms should
not count as one of the four required symptoms [to diagnose PD].
• At least one of the attacks has been followed by 1 month (or more) of one
or both of the following:
– Persistent concern or worry about additional panic attacks or their
consequences (e.g., losing control, having a heart attack, “going crazy”)
– A significant maladaptive change in behavior related to the attacks (e.g.,
behaviors designed to avoid having panic attacks, such as avoidance of
exercise or unfamiliar situations)
• The disturbance is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical
condition (e.g., hyperthyroidism, cardiopulmonary disorders)
• The disturbance is not better explained by another mental disorder (e.g.,
the panic attacks do not occur only in response to feared social situations,
as in social anxiety disorder; in response to circumscribed phobic objects or
situations, as in specific phobia; in response to obsessions, as in obsessive-
compulsive disorder; in response to reminders of traumatic events, as in
posttraumatic stress disorder; or in response to separation from
attachment figures, as in separation anxiety disorder)
Agoraphobia:
• Activities usually self-limited by avoiding public situations where
the patient believes he or she might experience a panic attack and
would be unable to exit readily, such as the following:
1. Crowded public areas (stores, public transportation, flying, church)
2. Individual interactions (hairdresser, dentist, neighborhood meetings)
3. Driving (especially if alone, far from home over bridges, through
tunnels, on highways or on isolated roads)
• On exposure to or anticipation of exposure to feared situations,
significant anxiety occurs. Anxiety may generate somatic symptoms
that trigger a full-blown panic attack. Patients believe that escape
from these situations reduces the alarming symptoms, thus
reinforcing future avoidance. In actuality, symptom relief stems
from adrenaline breaking down in the body after approximately 20
minutes.
Treatment
• antidepressants with a significant serotonin reuptake inhibitory
action. Generally start at low dose and titrate upward. Minimum
treatment duration is 6 to 8 mo, but many patients need to take
medications indefinitely.
1. SSRIs: paroxetine (10-60 mg/day), sertraline (50-200 mg/day),
citalopram (20-60 mg/day), escitalopram (5-30 mg/day), and
fluoxetine (5-60 mg/day)
2. Imipramine (100-300 mg/day)
3. Venlafaxine (75-225 mg/day)
• Combination CBT plus SSRI has shown good long-term effects and is
somewhat better than antidepressants or CBT alone. Combination
CBT plus benzodiazepine does not provide any added benefit and
may undermine CBT (interoceptive and in-vivo exposures may be
less effective if the benzodiazepine is completely controlling the
anxiety).
Obsessive-Compulsive Disorder (OCD)

Definition
• Obsessive-compulsive disorder (OCD) is characterized by
obsessions (recurrent and persistent thoughts, urges, or
images experienced as intrusive and unwanted) and/or
compulsions (repetitive behaviors or mental acts performed
in response to obsessions, or according to rules that must be
applied rigidly) that are time-consuming (e.g., >1 hr/day) or
cause marked impairment or distress. The symptoms are
usually perceived as excessive and unreasonable.

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Etiology
• Strong evidence of cortico-striato-thalamo-cortical circuit
dysfunction.
• OCD onset may be temporally associated with infectious illness of
CNS (e.g., Von Economo’s encephalitis, Sydenham’s chorea).
• OCD may follow head trauma or other premorbid neurologic
condition, including birth hypoxia and Tourette’s syndrome.
• Serotonergic, dopaminergic, and glutamatergic systems believed
important in some ritualistic instinctual behaviors, with dysfunction
of these pathways possibly giving rise to OCD.
Genetics
• OCD is a multifactorial familial condition that involves both
polygenic and environmental risk factors.
• Rate of concordance is higher in monozygotic (57%) compared with
dizygotic (27%) twins.
• Rate of disorder is also much higher in first-degree relatives of
individuals with OCD and Tourette’s disorder than in the general
population.
Gambaran klinis ;
1. Adanya ide / impulse yg terus-menerus menekan kedalam kesadaran
individu.
2. Perasaan cemas / takut akan ide / impulse yg aneh.
3. Pasien mengenali obsesi & kompulsi merupakan suatu yg abstrak &
irasional.
4. Individu yg menerima obsesi kompulsi merasa adanya keinginan kuat
utk melawan.

Ada 4 pola gejala utama gangguan obsesi kompulsi yaitu :


o Kontaminasi =
• mencuci / membersihkan / menghindari objek yg dicurigai terkontaminasi
o Sikap ragu-ragu yg patologis
• Sikap ragu2 yg di-ikuti dg perilaku kompulsi mengecek/ memeriksa
o Pikiran yg intrusif
o Simetri =
• kebutuhan utk simetris, ketepatan shg bertindak lamban

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
https://www.clinicalkey.com/#!/content/book/3-s2.0-B9781455750177003974?scrollTo=%23t0055
Kriteria diagnosis DSM – IV
A. Salah satu obsesif atau kompulsif
• Obsesif di definisikan sbb :
1. Pikiran, impuls, atau bayangan yg pernah dialami yg
berulang & menetap yg intrusive & tdk serasi dan yg
menyebabkan ansietas & distress yg ada selama periode
gangguan
2. Pikiran bukan ketakutan pd problem hidup yg nyata.
3. Individu berusaha utk menekan / menetralisir pikiran tsb.
4. Individu menyadari bahwa pikiran yg berulang itu berasal
dari pikiran nya sendiri
• Kompulsi didefinisikan oleh :
1. Perilaku berulang yg individu merasa terdorong melakukan
respon obsesinya.
2. Perilaku / aktivitas mental ditujukan utk mencegah atau
mnurunkan distress.

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
B. Pd waktu tertentu, individu menyadari bahwa obsesi &
kompulsi berlebihan & tdk beralasan.
C. Obsesi & kompulsi menyebabkan distress menghabiskan
waktu ( >1 jam perhari) atau menggangu kebiasaan sosial /
pekerjaan
D. Bila ada gangguan lain pd aksis 1, isi dari obsesi & kompulsi
tdk terkait dg gangguan tsb.
E. Gangguan tdk disebabkan efek langsung dri penggunaan zat
atau kondisi medik umum.

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Nonpharmacologic Therapy
• Treatment will help ∼50% of patients achieve partial remission
within the first 6 mo.
• Cognitive-behavioral therapy (CBT), especially exposure/response
prevention, is successful in up to 70% of patients, but nearly 25%
drop out of treatment because of the initial anxiety the exposures
create. Best results are found for contamination obsessions and
washing compulsions.
pharmacologic Therapy
• Clonazepam may be helpful in patients with extreme anxiety. (2 x
25mg)
• SSRI :
1. Fluoxentin 2x20 mg
2. Sertaline 2x50 mg
3. Esitalopram 2x 10 mg
4. Fluvoxamin 2x 50 mg
Posttraumatic Stress Disorder
Definition
• Posttraumatic stress disorder (PTSD) develops in some people after
witnessing or experiencing a traumatic event that involves actual or
threatened injury to self or others.
• Symptoms continue longer than a month after the event or have
delayed onset and include: intrusive thoughts, nightmares,
flashbacks, avoidance of things associated with the trauma,
hypervigilance, sleep disturbance, and negative changes in mood
and cognition. These symptoms cause distress and a decline in
interpersonal, social, and occupational functioning.
• People with PTSD may feel numb or irritable, may be easily startled
or frightened, and sometimes isolate themselves from others. They
are at risk for comorbid psychiatric illness, substance abuse, and
suicide.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488006229
Etiology
• Common types of trauma: violent personal assault, natural
disaster, military combat, rape, motor vehicle accident,
childhood abuse and neglect, critical illness or
hospitalization in ICU, severe physical injury, diagnosis of
life-threatening illness.
• Risk factors: previous trauma, initial severity of reaction to
event, psychiatric history, childhood abuse or neglect, poor
social support, gender, age.
• Proposed mechanisms include activation of the amygdala,
disruption of prefrontal cortex modulation of the amygdala,
and excessive stress-induced HPA and alpha-1 receptor
activation.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488006229
Physical Findings & Clinical Presentation
• Core symptom clusters include intrusion, avoidance, negative
mood and cognition, hyperarousal, and sometimes dissociative
symptoms. Individuals present with different variations of these
symptoms. Symptoms must occur for >1 month and result in
significant distress and functional impairment.
• Key PTSD symptoms:
1. Distressing memories or dreams of the event. Note: Children
older than 6 may express this symptom in repetitive play.
2. Flashbacks.
3. Intense distress after reminders of the event.
4. Avoidance due to trauma-related thoughts or feelings.
5. Persistent negative trauma-related emotions.
6. Feeling detached.
7. Aggressive or reckless behavior.
8. Hypervigilance.
9. Problems with concentration or sleep.
10. Depersonalization.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488006229
Medications
• There is no definitive cure for PTSD, and individuals have varying
responses to different medications. Sertraline and paroxetine, both
SSRIs, are the only FDA-approved medications for PTSD. Other
medication use is off-label with differing levels of evidence to
support use. Medications are used to target symptoms and the
physiologic changes associated with PTSD.
 SSRIs: sertraline, paroxetine, fluoxetine
 SNRIs: venlafaxine, duloxetine
 Other antidepressants: mirtazapine
 Alpha-adrenergic receptor blockers: Prazosin may decrease
nightmares; guanfacine may be helpful in treating arousal symptoms
 Atypical antipsychotics have had mixed results in clinical trials.
Risperidone been shown to be effective in some studies. Ketamine:
A recent clinical trial of intravenous ketamine infusion at 0.5 mg/kg
showed PTSD symptom reduction at 24 hours
somatic symptom disorder
Definition
• Somatization disorder has been replaced in DSM 5 with the
diagnostic term somatic symptom disorder . In this condition,
one or more somatic symptoms are distressing or disruptive
of daily life. There are often disproportionate thoughts about
the seriousness of one’s symptoms, persistent anxiety about
one’s health, and excessive time and energy devoted to the
symptoms.
• There is often a pattern of recurring multiple somatic
complaints that begin before the age of 30 yr and persist over
several years. Patients complain of multiple symptoms, but
persistent pain is common. DSM 5 drops the term
“unexplained by a medical condition” from the criteria.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488007338
Etiology
• Somatic symptoms may result from a heightened awareness of
certain bodily sensations, combined with a tendency to interpret
these sensations as indicative of a medical illness.
• Believed to be the physical expression of psychologic distress; there
appears to be a biologic predisposition.
• May be more common in individuals without sufficient verbal or
intellectual capacity to communicate psychologic distress,
individuals with alexithymia (inability to describe emotional states),
or individuals from cultural backgrounds that consider emotional
distress as an undesirable quality.
• Some aspects of somatic symptom disorder possibly learned from
somatizing parents.

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323280488007338
Diagnostic Criteria for Somatoform Disorders - DSM V
• Physical symptoms that are misinterpreted or exaggerated, not
accounted for by a diagnosable illness
• Symptoms are not intentionally feigned or produced
• Somatization Disorder
A. Unexplained physical symptoms that are manifested before the
age of 30 years, that last several years, and that result in
treatment being sought with significant impairment in social,
occupational, or other important areas of functioning
B. Presence of the following at any time during the course of the
disorder:
– Four pain symptoms
– Two gastrointestinal tract symptoms
– One sexual symptom
– One pseudoneurologic symptom
• One or more physical symptoms that cause significant distress or
impairment in functioning, lasting at least 6 months

https://www.clinicalkey.com/#!/content/book/3-s2.0-B9781455750177003974?scrollTo=%23t0055
https://www.clinicalkey.com/#!/content/book/3-s2.0-B9781455750177003974?scrollTo=%23t0055
Nonpharmacologic Therapy
• Legitimize patient’s complaints.
• Minimize diagnostic investigation and symptomatic treatment. Only do
invasive testing or procedures when there are clear-cut signs, not just
symptom reports.
• Set attainable treatment goals. Patients may benefit from realizing that
even though they cannot be cured, they will be cared for. This may help
reassure them that they will continue to have a relationship with the
caregiver.
• Treat coexisting psychiatric conditions such as depression and anxiety.

Acute General Rx
• At each visit do a brief physical examination focusing on the area of
complaint.
• Convey empathy with the patient’s suffering and psychosocial difficulties.
• No specific pharmacologic therapy has been clearly proven effective,
although a number of agents, including gabapentin have been useful in
some studies.
Gangguan Konversi
• Adalah ggn pd fs tubuh yg tdk sesuai dg konsep anatomi & fisiologi dari sis
saraf pusat & sis saraf tepi.
• Hal ini terjd scr khas dg adanya stress yg memunculkan disfungsi berat.
Gambaran klinis
• Paling sering muncul adalah paralisis, buta, & mutisme
o Gejala sensorik
• paling sering adalah ansietas 7 parestesi terutama pd ekstremitas. Semua
modalitas sensorik dpt terkena & distribusi ny tdk sesuai dg penyakit saraf
pusat maupun tepi.
• Dpt menimbulkan ketulian, kebutaan & penglihatan terowongan ( tunnel
vision), namun evaluasi neurologis memberikan hasil jaras sensorik yg
intak.
o Gejala motorik
• Terdiri atas : gerak abnormal, ggn gaya berjalan, kelemahan & paralisis
• Refleks2 tetap normal, tdk menunjukan adanya fasikulasi, atrofi otot,
Elektromiografi normal

Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Kriteria diagnosis DSM IV :
A. Defisit fs motorik volunter / sensorik yg diperkirakan suatu
kondisi medik umum.
B. Defisit didahului olh adanya konflik / stresor lain.
C. Gejala / defisit tdk dengan sengaja dibuat / berpura-pura
D. Gejala / defisit stlh dilakukan penelusuran, tdk dpt
dijelaskan sbg kondisi medik umum atau akibat
pengguanaan zat
E. Gejala / defisit menyebabkan penderitaan / hendaya yg
bermakna secara klinis di bidang sosial
F. Gejala / defisit tdk terbatas pd nyeri / disfungsi seksual,
tdk terjadi semata-mata selama perjalanan ggn
somatisasi, dan bkn krn ggn mental lainya.
Elvira SD, Hadisukanto G. Buku Ajar Psikiatri. Edisi ke-2. Badan penerbit Fakultas Kedokteran Universitas
indonesia. 2015
Trichotillomania
• Trichotillomania, also called hair-pulling disorder, is a mental
disorder that involves recurrent, irresistible urges to pull out hair
from your scalp, eyebrows or other areas of your body, despite
trying to stop.
• Hair pulling from the scalp often leaves patchy bald spots, which
causes significant distress and can interfere with social or work
functioning. People with trichotillomania may go to great
lengths to disguise the loss of hair.
• For some people, trichotillomania may be mild and generally
manageable. For others, the compulsive urge to pull hair is
overwhelming. Some treatment options have helped many
people reduce their hair pulling or stop entirely.
Signs and symptoms of trichotillomania often include:
• Repeatedly pulling your hair out, typically from your scalp, eyebrows
or eyelashes, but sometimes from other body areas, and sites may
vary over time
• An increasing sense of tension before pulling, or when you try to
resist pulling
• A sense of pleasure or relief after the hair is pulled
• Noticeable hair loss, such as shortened hair or thinned or bald areas
on the scalp or other areas of your body, including sparse or missing
eyelashes or eyebrows
• Biting, chewing or eating pulled-out hair
• Playing with pulled-out hair or rubbing it across your lips or face
• Repeatedly trying to stop pulling out your hair or trying to do it less
often without success
• Significant distress or problems at work, school or in social situations
related to pulling out your hair

http://www.mayoclinic.org/diseases-conditions/trichotillomania/symptoms-causes/dxc-20268523
• Many people who have trichotillomania also pick their skin, bite
their nails or chew their lips. Sometimes pulling hairs from pets or
dolls or from materials, such as clothes or blankets, may be a sign.
Most people with trichotillomania pull hair in private and generally
try to hide the disorder from others.
• For people with trichotillomania, hair pulling can be:
• Focused. Some people pull their hair intentionally to relieve tension
or distress — for example, pulling hair out to get relief from the
overwhelming urge to pull hair. Some people may develop
elaborate rituals for pulling hair, such as finding just the right hair or
biting pulled hairs.
• Automatic. Some people pull their hair without even realizing
they're doing it, such as when they're bored, reading or watching
TV.
Risk factors
• These factors tend to increase the risk of trichotillomania:
• Family history. Genetics may play a role in the development of
trichotillomania, and the disorder may occur in those who have a
close relative with the disorder.
• Age. Trichotillomania usually develops just before or during the
early teens — most often between the ages of 10 and 13 years —
and it's often a lifelong problem. Infants also can be prone to hair
pulling, but this is usually mild and goes away on its own without
treatment.
• Other disorders. People who have trichotillomania may also have
other disorders, such as depression, anxiety or obsessive-
compulsive disorder (OCD).
• Stress. Severely stressful situations or events may trigger
trichotillomania in some people.
Diagnostic criteria (DSM-5)
• The American Psychiatric Association’s Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM-5),
• places trichotillomania in the category of obsessive-compulsive and related
disorders and notes that it is characterized by recurrent body-focused
repetitive behavior (hair pulling) and repeated attempts to decrease or stop
the behavior. The behavior can occur during both relaxed and stressful times,
but there is often a mounting sense of tension before hair pulling occurs or
when attempts are made to resist the behavior.
• The specific DSM-5 criteria for trichotillomania (hair-pulling disorder) are as
follows:
1. Recurrent pulling out of one’s hair, resulting in hair loss
2. Repeated attempts to decrease or stop the hair-pulling behavior
3. The hair pulling causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning
4. The hair pulling or hair loss cannot be attributed to another medical
condition (eg, a dermatologic condition)
5. The hair pulling cannot be better explained by the symptoms of another
mental disorder (eg, attempts to improve a perceived defect or flaw in
appearance, such as may be observed in body dysmorphic disorder)

http://emedicine.medscape.com/article/1071854-overview

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