BRAIN STIMULATION METHODS IN OBSESSIVE COMPULSIVE DISORDER

1. BRAIN STIMULATION
STRATEGIES IN OCD
Dr. V.L.N.SEKHAR

2. SCHEME OF PRESENTATION
1. Introduction
2. Classification and diagnostic criteria
3. Neurobiology
4. Treatment modalities of OCD
5. Brain stimulation methods
6. Surgical treatment of OCD
7. Conclusion
8. Take home message

3. Introduction
Definition:
 Obsessions are defined by (1 ) and (2):
– 1 . Recurrent and persistent thoughts, urges,
or images that are experienced, at some time
during the disturbance, as intrusive and
unwanted, and that in most individuals cause
marked anxiety or distress.
– 2 . The individual attempts to ignore or
suppress such thoughts, urges, or images, or to
neutralize them with some other thought or
action (i .e., by performing a compulsion).

4.  Compulsions are defined by (1 ) and (2):
– 1 . Repetitive behaviors (e.g., hand washing,
ordering, checking) or mental acts (e.g., praying,
counting, repeating words silently) that the
individual feels driven to perform in response to an
obsession or according to rules that must be applied
rigidly.
– 2 . The behaviors or mental acts are aimed at
preventing or reducing anxiety or distress, or
preventing some dreaded event or situation;
however, these behaviors or mental acts are not
connected in a realistic way with what they are
designed to neutralize or prevent, or are clearly
excessive

5. OCD – CLINICAL DETAILS
OCD the fourth most common psychiatric diagnosis after
phobias, substance-related disorders, and major depressive
disorder.
LIFE TIME PREVALENCE 2-3%
AGE – 10-24 YRS (83%), average 20 yrs; > 35 YEARS (15%)
SEX- WOMEN (52%) > MEN
ADOLESCENT: BOYS (70%) m/c
CO MORBIDITY – DEPRESSION (67%)
TIC DISORDER (5-10%)
SP PHOBIAS (25%)
SOCIAL PHOBIA (18%)
PANIC DISORDERS (12%)

6. Course
 Typically chronic, waxing and waning course.
 20 to 30 % of patients: significant improvement
 40 to 50 % : moderate improvement
 20 to 40 % : either remain ill or their symptoms
worsen.

7. Classification
 The classification of OCD is intriguing.
 OCD was a part of anxiety disorders not very long
ago.
 Now it gained an independent identity both in DSM
and ICD.
 In DSM 5th edition the major change for OCD is a
fact that it and related disorders have their own
chapters and no longer considered as anxiety
disorders. As the same ICD 11 also.

8. Obsessive-Compulsive and Related
Disorders in DSM 5 and ICD 11
DSM 5 ICD 11
1. OCD
2. BODY DYSMORPHIC
DISORDER
3. HOARDING DISORDER
4. TRICHOTILLOMANIA
5. EXCORIATION
6. BODY FOCUSED
REPETITIVE BEHAVIOUR
7. OBSESSIONAL JELOUSY
1. OCD
2. BODY DYSMORPHIC
DISORDER
3. HOARDING DISORDER
4. OLFACTORY REFERENCE
DISORDER
5. HYPOCHONDRIASIS
6. BODY FOCUSED
REPETITIVE BEHAVIOUR
1. TRICHOTILLOMANIA
2. EXCORIATION

9. DSM 5 CRITERIA

10. ICD 10 CRITERIA

11. Core features of obsessions
(ruuine)
 Intrusive quality
 Unacceptability
 Subjective resistance
 Uncontrollability
 Ego-dystonicity
 Neutralizing behaviors

12. Normal intrusions
 Less frequent
 Brief
 Less resistance
 Less unacceptable
 Considered irrelevant
 Less concern with
control
 Less emphasis on
neutralizing
 Less interference
Obsessions
 More frequent
 Time consuming
 Strong resistance
 More unacceptable
 Highly ego-dystonic
 Heightened concern
with thought control
 Strong focus on
neutralizing distress
 Significant interference

13. Core features of compulsions
 Repetitive, stereotypic, and intentional
 Subjective urge to perform
 Diminished sense of voluntary control
 Prevention or reduction of distress or a dreaded
consequence
 Considered exaggerated/excessive

14. M/C Obsessive-Compulsive Symptoms in
Adults
 OBSESSIONS
– Contamination
– Pathological doubt
– Somatic
– Need for symmetry
– Aggressive
– Sexual
– hoarding
 COMPULSIONS
– Checking
– Washing
– Counting
– Need to ask or confess
– Symmetry and precision
– Hoarding

15. Neurobiology of OCD
 BRAIN Abnormalities.
– Abnormalities in fronto striatal circuits (CSTC) and
fronto sub cortical circuits.
 BRAIN imaging studies
– Structural brain imaging
Decreased grey matter in
 Dorsomedial prefrontal cortex
 Anterior cingulate cortex
 Inferior frontal gyrus
 Anterior Insula
Absence of age related change in
 Putamen
 Insula
 OFC
– Functional brain-imaging studies-
– positron emission tomography (PET}-have shown
increased activity (e.g., metabolism and blood flow) in
the frontal lobes, the basal ganglia (especially the
caudate ), and the cingulum of patients with OCD.

16.  Magnetic resonance spectrosocpy
 Decreased NAA in ACC and caudate
 Decreased Glutamate
 Increased GLX
 NEUROIMMUNOLOGY
– Group A beta-hemolytic streptococcal infection can
cause rheumatic fever, and approximately 1 0 to 30
percent of the patients develop Sydenham's chorea and
show obsessive-compulsive symptoms.
 Neurotransmitters .
Role of neurotransmitters in OCD
– Serotonin:
– Evidence do not support a primary pathogenic role of serotonin
– Probably modulate networks or regions that are dysfunctional in OCD.
– Dopamine
• Dysregulated dopamine function
– Neuropeptides
• Elevation of stress mediating neuropeptides –
• AVP/CRH/OXYTOCIN
– Glutamate

17. Management of OCD
 Pharmacotherapy
 Psychotherapy
 Somatic therapies(brain stimulation strategies)
 Recent developments
– Pharmacological augumentation therapies
– Novel psychotherapies

18. Pharmacotherapy
 SSRI
 CLOMIPRAMINE
MEDICATION RECOMMENDED DOSE
FLUOXETINE 40-80 mg
SERTRALINE 100-200
FLUVOXAMINE 200-300
PAROXETINE 40-60
ESCITILOPRAM* 20-40
CLOMIPRAMINE 150-250

19. PSYCHOTHERAPY
 Cognitive - Behavioral therapy
– Exposure and response prevention (EX/RP)
– Desensitization,
– thought stopping,
– flooding,
– implosion therapy, and
– aversive conditioning

20. Recent developments
Pharmacological augmentation therapies
Anti psychotics:- Risperidone
aripiprazole
Glutamatergic agents:-Memantine
N –acetyl cysteine
Topiramate
Lamotrigine
Ketamine
Riluzole
Serotinergic agents:- Ondonsetron, granisetran
Novel psychotherapies:
Acceptance and commitment therapy
Mindfulness based cognitive therapy
Dialectical behavioural therapy
Meta cognitive therapy

21. Somatic therapies
(Brain stimulation strategies)
Electrical Stimulation of brain
Non invasive:
Trans cranial
Invasive:surgical
Intra cranial Preipheral
VNS
DEEPSUPERFICIAL
DBSCORTICAL
STIMULATION
DIRECT:
ELECTRICAL
INDIRECT:
MAGNATIC
CONVUL
SIVE
CONVUL
SIVE
NON- CO
NVULSIVE
NON-CO
NVULSIVE
ECT MST TMSCES
TES
TDCS

22. Neuromodulation therapies/ Brain stimulation
methods
 There is an increasing interest in the utilization of several
neuromodulation therapies (NTs) in the management of
psychiatric patients
 Psychopharmacological therapy exposes the entire body to a
potentially therapeutic substance in order to treat a relatively
small region of the brain
 NTs are designed to target specific brain circuits that are
important in the pathogenesis of psychiatric disorder
 NTs are not systemic and, therefore, the side-effect profile is
limited and different from medications, and there are
minimal, if any, drug interactions
 Data has been emerging continuously about FDA-approved
and yet-to-be-approved NTs in the psychiatric population
over the past decade

23. Neuromodulation therapies
 An electrically stimulated cell will primarily produce a
restricted range of responses inherent to its functionality
 Brain stimulation modulates the system’s endogenous
responsiveness and presumably, when delivered appropriately,
allows it to recruit adaptive strategies
 Long term potentiation (LTP) or long term depression (LTD)
can alter synaptic plasticity and learning

24. Therapeutic Neuromodulation: Treating
Psychiatric Disorders Through Brain
Stimulation
 Mechanism of Action
 Electrical Stimulation—Common Pathway
– The brain stimulation modalities just reviewed generate
either electrical or magnetic pulses.
– However, both of these share a common final pathway—
they affect the neurons electrically.
 That electrical effect may either be through the direct
application of electricity or through the indirect induction of
electricity via magnetic stimulation.
– The direct forms of electrical stimulation are exemplified in
either transcranial delivery, as with ECT, CES, and tDCS,
or intracerebral delivery, as in the case of DBS or direct
cortical stimulation (epidural or subdural).
– The indirect forms of electrical stimulation include TMS
and MST, which induce electrical fields in the brain
through the application of alternating magnetic fields.

25.  Of note, both the epidural and intracerebral modalities are more
focal than the transcranial application of electricity because
electrodes are placed directly in the neuronal tissue, bypassing
the impedance of the scalp and skull.
 The relatively more contemporary magnetic stimulation methods
(TMS and MST) also bypass the impedance of the scalp and skull
and are thus likewise more focal.
 Magnetic stimulation is working on principle of Faraday law and
maxwell equation.
 The magnetic modalities achieve their enhanced focality
noninvasively, in contrast to the intracerebral and epidural
methods, and are thus at the center of intensive research in that
they offer a promise of an unparalleled degree of spatial
specificity without the need for surgery.

26. Comparison of Brain Stimulation with
Psychopharmacology
Brain stimulation Psycopharmacolgy
Therapeutic agent Electrical (or
electromagnetic)
Neurochemical
Temporal characteristics Phasic Tonic
Delivery Automated or clinician
administered
Dependent on patient
compliance
Site of action Axonal depolarization Molecular target
Distribution Focally applied to the brain Systemic
Duration of availability Milliseconds to seconds Typical half-life of hours to
weeks
Dosing parameters Intensity, frequency,
intertrain interval, number
of pulses, site of stimulation
Milligrams, blood level
Metabolism None Hepatic
Clearance None Renal
Interactions with
metabolism of other
agents
None known Possible

27. Acute and Prolonged Mechanisms of Action
• Phasic activation of neural circuit.
• Observable motor responses (e.g., twitch)
• Temporary disruption (e.g., speech arrest) or
facilitation of ongoing processing (e.g.,
speeds reaction time
Acute
effects
• Neuroplasticity
• Change in synaptic efficacy, akin to long-
term potentiation or depression
• Alterations in neurotropic factors
• Modulation of cortical excitability
• Modulation of functional connectivity
Prolong
ed
effects

29. Role of Deep brain stimulation
and ablative neurosurgeries in
OCD

30. Need for alternate interventions in
OCD
• Response to standard treatments
• 40-60% of patients show inadequate response to SSRIs
• Around 50-60% of patients respond to CBT
• Around 30% of patients respond to antipsychotic
augmentation
Pallanti et al, 2002, Eddy et al, 2004, Dold, 2013
• 10-20% of patients are refractory to standard pharmacotherapy
and psychotherapy
Aouizerate et al., 2006; Denys et al, 2006
• Indication for invasive treatments – severe, chronic, disabling
and treatment refractory illness.

31. Surgery for psychiatric disorders
• Prefrontal lobotomy for psychiatric disorders
• Early to mid 20th century – marked personality changes*
• Fell into disrepute due to indiscriminate use and with
advent of other effective non-invasive treatments
vs
• Contemporary neurosurgical procedures -
• Advances in image guidance, & stereotactic procedures
• Gamma-knife surgery and Deep Brain Stimulation
• Advances in theoretical understanding
• Careful selection of patients

32. Rationale for surgery in OCD
• Earlier rationale – based on outdated theories
and serendipitous observations
• Techniques & targets improvised based on
experience – “learning curve”
• Effective targets lie on the CSTC circuits
• ACC, capsule, striatum and ventral striatum
• Similar to SSRIs & CBT, surgical techniques
decrease hyperactive fronto-striatal circuits
– Figee et al, 2013; Greenberg et al; 2010; Nakao et al, 2014

33. Selection criteria for surgery
1. Severe (YBOCS >25-30) and chronic unremitting OCD
2. Causing substantial distress and impairment in
functioning (GAF ≤50), a poor quality of life.
3. The following treatment options tried systematically
without appreciable effect on the symptoms
• 2 adequate SSRI trials for 3 months each
• Clomipramine trial for 3 months, unless poorly tolerated
• 2 augmentation trials, one of them being an atypical antipsychotic:
Risperidone/aripiprazole, clomipramine, memantine, ondansetron/granisetron
• 1 CBT trial (at least 20 ERP sessions) or demonstrated inability to tolerate the
anxiety due to therapy
• Previous treatment trials have not been abandoned prematurely due to solely
mild side effects
• Duration of the primary illness must exceed 1 year and typically exceeds 5
years.
4. Patient gives informed consent
5. Willing to participate in the pre-operative evaluation
and post-operative periodic follow-up
Reddy et al, Clinical practice guidelines for OCD, Indian J Psychiatry, 2017

34. Relative contraindications
1. Comorbid intellectual disability, psychosis,
bipolar disorder and severe personality disorders
2. Clinically significant and unstable neurologic
illnesses.

35.  Pre Surgery Work-Up
• Detailed clinical examination – to confirm diagnosis and
comorbidity
• Review of treatment history – establish refracoriness
• MRI brain, other routine pre-surgical investigations
• Neuropsychological testing
• Clearance from an independent committee – consisting of a
neurologist, neurosurgeon, and psychiatrist
• Final review by the head of the panel (independent
psychiatrist)

36. Informed consent
• Indication & rationale for surgery
• Possible benefits
• Latency of response
• Probability and extent of improvement
• Need to continue standard treatment techniques
• Adverse effects
• Alternatives
• Follow-up
• Post-surgery treatment options

37. Neurosurgical Approaches
Neurosurgical Approaches
Ablative Procedures Deep brain stimulation
Thermal coagulation Gamma-knife
radiosurgery
1. Capsulotomy
2. Anterior Cingulotomy
3. Subcaudate Tractotomy
4. Limbic Leucotomy
1. Ventral capsule/Ventral striatum
(VC/VS)
2. Nucleus Accumbens (NAcc)
3. Bed nucleus of stria terminalis
4. Sub-thalamic nucleus (STN)
5. Inferior thalamic peduncle (ITP)

38. Ablative surgery
Surgery Location
Anterior capsulotomy Anterior limb of internal capsule
Anterior cingulotomy Anterior cingulate cortex and
adjacent cingulum bundle
Subcaudate tractotomy Substantia innominata – inferior
to head of caudate nucleus
Limbic leukotomy Bilateral cingulotomy +
Subcaudate Tractotomy

39. Adverse effects
 Acute
 Chronic
Open surgeries headache, delirium, CNS infection,
hemorrhage, seizures
Gamma knife Radiation necrosis, brain edema
Personality changes – apathy, disinhibition, impulsivity,
aggression
Cognitive deficits – executive, visuospatial
Seizures
Urinary incontinence
Weight gain
Brain cyst – gamma knife surgery

43. Deep Brain stimulation

44. Deep Brain stimulation
 DBS has been use for treatment of movement
disorders.
 Recently there has been a surge of interest in
using this device for treatment of psychiatric
disorders, especially OCD.
 Although it is an invasive procedure , the risk of
operation is small, it is reversible in nature, and
the treatment can be optimized postoperatively.

45. Deep Brain stimulation, procedure
3 stages
1. Image guided insertion of electrodes (1mm)
inserted under LA
• Multiple contacts in to sub cortical nuclei(usually
4 per side)
• Intraoperative macrostimulation for monitoring
adverse effects
2. Subdermal implantation of neurostimulator
– Upper chest wall, connects it, via extension wires
tunneled under the skin, to the brain leads.
• Battery –replaceble vs rechargable
3. Programming -flexibility
• Polarity, amplitude, frequency and pulse duration

46. Mechanism
 Exact mechanism of action is not known
•DBS is thought to block neural activity within the
stimulated target area, producing similar to tissue
ablation.

47. Targets in OCD
• Ventral Anterior limb of the internal capsule
• Ventral capsule/ventral striatum (VC/VS)
• Nucleus Accumbens
• Bed nucleus of stria terminalis
• Subthalamic nucleus
• Inferior thalamic peduncle
In depression
Subgenual cingulate cortex

48. Adverse effects
• Complications of the surgical intervention
• Intracerebral hemorrhage - 0.2% to 5% -? higher in STN
• Postoperative infection
• Devise related
• Lead breakage
• Devise related discomfort
• Depletion of battery – increase in anxiety & depression
• Adverse effects of the stimulation itself
• Dyskinesia, dysarthria, eyelid apraxia, gait disturbances
• Depression/suicidal ideation
• transient hypomanic symptoms,fear,panic and occational forgetfulness,
• Word findng difficulties
• Persistent – increased libido, micturition problems, cognitive deficits

49. Outcome
 DBS can be considered an effective treatment
modality with few side effects.
 60% response in treatment resistant OCD
 FDA recently approved DBS for Rx resistant
OCD on Humanitarian Device Exemption
 DBS approved for MDD also

50. Pros & Cons of DBS
 Advantages
¨ Does not produce irreversible lesion
¨ Side effects may be reversible
¨ Stimulator is adjustable
¨ Sham stimulations possible
¨ Can change stimulation sites
 Disadvantages
¨ High cost
¨ May have to replace batteries periodically
¨ Highly skilled interdisciplinary team with intensive and
frequent monitoring
¨ Invasive

51. Summary
• Stereotactic ablation and Deep Brain Stimulation may be tried
in carefully selected patients with treatment refractory severe
OCD
• Ablative surgery – gamma ventral capsulotomy/anterior
cingulotomy
• DBS – ventral capsule/ventral striatum & subthalamic nucleus
• Around 40-60% of patients improve 6-12 months after procedure
• Extent of improvement – variable – mean 40-60%
• Not a standalone treatment - should be considered to be one of
the treatment modalities in a comprehensive package

52. Transcranial Direct Current
Stimulation

53. tDCS
 Transcranial direct current stimulation (tDCS) is a noninvasive
form of treatment that uses very weak (1 to 3 mA) direct electrical
current applied to the scalp.
 Because direct current polarizes rather than stimulates with
discrete pulses, its action does not appear directly to result in
action potential firing in cortical neurons.
 It is also this direct current (DC) form of electrical stimulation
that distinguishes it from devices that use alternating currents
(AC) as found in CES, ECT, VNS, and DBS, which produce
discrete pulse stimulation.
 In addition, because tDCS works via polarization and does not
affect action potential firing in cortical neurons, the term
“transcranial direct current polarization” is favored by some
modern investigators, and both terms appear interchangeably in
the literature today.
 The small device is very portable and usually operated by readily

54. History
 tDCS was initially investigated in the 1960s and
has experienced a recent resurgence of interest
because of its ease of application, small device
size, low cost, and relative lack of worrisome
risks and side effects as compared with
treatments like ECT and TMS

57. Mechanism of Action
 Direct current polarizes current, and tDCS is
believed to act via the alteration of neuronal
membrane polarization, but little is known about
the actual mechanism of action of tDCS.
 Polarization may affect the firing and conductance
of neurons by either lowering or raising the
threshold of activation.
 Because tDCS involves the application of low
currents to the scalp via cathodal and anodal
electrodes, depending on the direction of current
flow, polarization can either inhibit (cathodal) or
facilitate (anodal) function.

58. Transcranial direct current stimulation is a non-invasive
neuromodulatory technique that delivers low intensity, direct
current (1-2 mA) to cortical areas through application of
electrodes on the scalp facilitating or inhibiting spontaneous
neuronal activity

59. tDCS: Neurobiological Effects
•Firing rates recorded from neural populations in cats.
•Anodal stimulation results in positive shift of resting membrane
potential
•This can result in an elevated neuronal firing rate

60. tDCS: Neurobiological Effects
•Firing rates recorded from neural populations in cats.
•Cathodal stimulation - negative shift of resting membrane potential
•This can result in a decreased neuronal firing rate

61. tDCS: Neurobiological Effects
Anodal tDCS inhibits
GABAergic transmission
Cathodal tDCS inhibits
Glutamatergic transmission

62. Role of tDCS in OCD
 As OCD is related to hyper activity of cortico-striato-
thalamic-cortical circuits, tDCS could potentially
alleviate OC sypmtoms by modulating activity of
orbito-frontal cortex or dorsolateral prefrontal cortex.
 Till date, only a few case reports have been published
regarding the role of tDCS in OCD.
 In one case cathodal stimulation over DLPFC
produced no change in OC symptoms although
anxiety and depressive symptoms improved.
 In a recent report, cathodal stimulation over OFC
produced response in resistant OCD.
 Another series of two cases were reported from india
where anodal stimulation over supplementary motor
area(SMA) caused improvement in SSRI resistant
OCD.

63. Side Effects
 There are no known serious adverse effects of
tDCS.
 It is well tolerated,
 common side effects
 minimal tingling at the site of stimulation,
 skin irritation.

64. Current Status in Treatment
Algorithms
 tDCS is not approved by the FDA for psychiatric
treatments and is thus considered an
experimental research technology with much
work needed to demonstrate its efficacy.
 tDCS could represent an inexpensive and
relatively safe alternative form of treatment to
medications, prior to the more invasive
stimulation methods like ECT or VNS.

65. Future Directions
 Most of the current tDCS devices use large,
saline solution–soaked electrodes.
 Future device development will most likely
investigate electrode shape and contact material
to optimize the intended clinical effects and
further improve ease of use.
 However, basic questions of efficacy, indications,
and dose–response relationships, as well as
predictors of response, will need to be explored
first.

66. Transcranial Magnetic
Stimulation

67. rTMS
 Definition
 TMS is the application of a rapidly changing magnetic field
to the superficial layers of the cerebral cortex, which locally
induces small electric currents, also referred to as “eddy”
currents.
 This induction was originally discovered by Michael
Faraday through his experiments in 1831 and later
quantified in Maxwell's equations of electromagnetism.
 Thus, TMS may be referred to as electrical stimulation
without an electrode, in that it uses magnetic fields to
indirectly induce electrical pulses.

68.  TMS devices deliver strong magnetic pulses via a coil
that is held on the scalp.
 Because magnetic fields are unaffected by the
electrical impedance of the scalp and skull, this
method of stimulation enables the focal stimulation of
smaller areas of the brain than is possible with other
noninvasive devices that use either alternating (ECT,
CES) or direct (tDCS) electrical current for primary
stimulation.
 TMS is an example of noninvasive stimulation of focal
regions of the brain and, as such, can be used for
research or therapeutically without the need for
anesthesia.

69. History
 In 1985, Barker, Jalinus, and Freeston from the
University of Sheffield in the United Kingdom
reported the first use of TMS to stimulate the
human brain.
 In 1996, Alvaro Pascual-Leone and colleagues
reported that TMS might have prolonged
antidepressant properties after daily stimulation
for 5 days to the dorsolateral prefrontal cortex.
 1985 – Baker
1st Therapeutic reports of TMS in Mood Disorders

70. Mechanisms of Action
 Based on the principle Faraday's law
– the induced electromotive force in a closed
loop is directly proportional to the time
rate of change of magnetic flux through
the loop.
– As applied in TMS, a changing magnetic
field induces an electrical current in the
circuitry of the superficial cortex
underlying the TMS coil.
– This electrical current is commonly
referred to as “eddy current” for its
circulating motion in a plane
perpendicular to the plane of the magnetic
field, and is also known as Foucault
current
– At sufficient intensity, electrical currents
will stimulate neuronal depolarization,
which can result in an action potential

71.  For example, when the TMS coil is positioned
over the hand area of the cerebral cortex's motor
strip, the changing magnetic field generated by
the repetitive pulses induces local currents
immediately below the site of stimulation that
cause the neurons in area M1 to fire. In turn, this
action potential propagates through the
polysynaptic corticospinal tract and results in a
twitch in the contralateral hand muscle

72. Types of TMS
Single-pulse TMS Repetitive pulse TMS (rTMS)
Paired pulse TMS (ppTMS ) Repeated paired pulse TMS (rppTMS)
Theta Burst Stimulation (TBS)--------continuously (cTBS) and intermittent
(iTBS)

73. Dosing
Transcranial Magnetic Stimulation
Dosing Parameters
Scalp position, target localization method
Coil shape and orientation
Single pulse vs. repetitive vs. convulsive
Train: Frequency, duration, intensity, total
pulses
Intertrain interval
Number of trains/session
Number of sessions/day
Number of days/course
Taper/maintenance/reintroduction

74. r TMS Coils
 Circular Coil
Larger and deeper magnetic field
- when neuroanatomical targets are not precise
 Figure of 8 coil
stronger and more focused magnetic field
- Better spatial resolution of activation
- Penetration depth aprox 2 -3cms
 H Coil
Newer type
- Multiple coil windings
- Generate greater depth of penetration (dorsal ant
Cingulate, subgenual cingulate)

75. Role of rTMS in OCD
 After publicatin of the first positive results in
1997, several studies have investigated efficacy of
rTMS in OCD.
 The sites for cortical stimulation for
– DLPFC
– OFC
– SMA
 The results were mixed and some and some
benefit occurred on application of low frequency
rTMS over SMA and OFC though benefits seem
to disappear following discontinuation of rTMS.
 rTMS approved for MDD

76. Other Therapeutic use of r TMS
 Mood Disorders – Left DLPFC
 Movement Disorders – Motor Cortex
 Parkinson's – Motor cortex
 Tourette disease – Motor cortex
 Seizures – specific areas indicated by EEG
 Pain – motor cortex , OFC,
somatosensory cortex

77. Side Effects, Interactions with
Medications, and Other Risks
 Common side effects
– Transient headache
– Scalp discomfort
 Other side effects
– Dizziness
– Facial twitching
– Hypo manic switch
 Serious side effects
– Seizure (subject factors can be important, such as the
presence of a neurological disorder (epilepsy or a focal
brain lesion) or use of seizure-lowering medications.)

78. Current Status in Treatment Algorithms
 TMS is not currently approved by the FDA as a
clinical treatment modality, although an
application for an indication in the treatment of
depression is being considered by this agency.
 For that reason there is no specific treatment
algorithm for the use of TMS;
 however, if it is approved as an effective and safe
treatment, it would most likely be considered as
an alternative treatment modality to
medications, prior to more invasive methods like
ECT.

79. Future Directions
 TMS and other forms of magnetic stimulation
hold a tremendous promise in psychiatric
treatment due to their focality and
noninvasiveness.
 However, much research is needed to replicate
preliminary findings, improve optimal dosing,
establish the patient characteristics that predict
response, and examine the influence of
concomitant medications on TMS effect.

80. ECT
 It can be used only in cases of OCD
with comorbid severe mood
disorders.
 Ect has failed to find any place in the
current rx guidelines of OCD.

81. TAKE HOME MSG
 OCD is cronic debilitating psychiatric disorder.
 SSRI and CBT are the first line therapies.
 Brain stmulation methods and surgical methods
(Stereotactic ablation and Deep Brain Stimulation) may be
tried in carefully selected patients with
treatment refractory severe OCD.
 Only DBS is approved for OCD by FDA.
 ECT has limited use in OCD, Low efficacy and
more adverse effects
 TMS and other forms of magnetic stimulation
hold a tremendous promise in psychiatric
treatment due to their focality and
noninvasiveness

82. References
 Kaplan and sadock’s 9th edition of CTP
 Kaplan and sadock’s 10TH edtion of
synopsis of psychiatry.
 Indian consensus document on OCD
by IPS.
 Reddy et al, Clinical practice guidelines for
OCD, Indian J Psychiatry, 2017