BRAIN STIMULATION METHODS IN OCD
- 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
- 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
- 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
- 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.
- 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
Editor's Notes
- #6: The lifetime prevalence for major depressive disorder in persons with OCD is about 67 percent and for social phobia about 18 percent.
- #7: 20 to 30 % of patients have significant improvement in their symptoms, and 40 to 50 percent have moderate improvement. The remaining 20 to 40 percent of patients either remain ill or their symptoms worsen
- #10: ADDED SPECIFIERS AND DELETED CRITERIA B AS At some point during the course of the disorder, the person has recognized that the obsessions or compulsions are excessive or unreasonable
- #17: NAA N acetyl l aspartate GLX GLUTAMINE
- #19: Initial effects are generally seen after 4 to 6 weeks of treatment, although 8 to 1 6 weeks are usually needed to obtain maximal therapeutic benefit. GUIDELINES RECOMMEND CONTINUATION OF MEDICATION AT LEAST 1 -2 YEARS
- #20: The principal behavioral approaches in OCD are exposure and response prevention.
- #22: TDCS, transcranial direct current stimulation; TES, Transcranial electrical stimulation; TMS, transcranial magnetic stimulation; VNS, vagus nerve stimulation. CES : Cranial electrical stimulation
- #23: NEURO MODULATION IS THE PHYSIOLOCAL PROCESS BY WHICH A GIVEN NEURON USES ONE OR MORE CHEMIVALS TO REGULATE DIVERSE POPULATION OF NEURONS
- #28: A single electrical pulse delivered at sufficient intensity can induce depolarization, trigger an action potential, release neurotransmitters at the synapse, and result in transsynaptic propagation with subsequent activation of a functional circuit. For example, brain stimulation applied to the hand area of the primary motor cortex may activate the corticospinal tract and induce a muscle twitch in the contralateral hand --Persistent activation of a brain circuit can induce prolonged changes in the subsequent activities of that circuit. For example, repeated stimulation of the perforant pathway at high electrical frequency induces a lasting increase in the efficacy that circuit, whereas low frequencies depress it. These phenomena are termed long-term potentiation (LTP) and long-term depression (LTD), respectively
- #31: What is the
- #32: During mid 20 th century mc performed adverse effects included 6 percent mortality, seizures in 1 percent, and disinhibition syndromes in 1.5 percent
- #46: 1.The procedure involves placement of small-diameter brain “leads” (e.g., approximately 1.3 mm) with multiple electrode contacts into subcortical nuclei or specific white matter tracts. The surgeon drills burr holes in skull bone under local anesthesia and then places the leads, guided by multimodal imaging and precise stereotactic landmarking. Usually this is done bilaterally. The subject is typically sedated but awake during surgery. 2.Later, the “pacemaker” (also known as an implantable neurostimulator or pulse generator) is implanted subdermally (e.g., in the upper chest wall) and connects it, via extension wires tunneled under the skin, to the brain leads. 3.Since various combinations of electrodes can be activated, at adjustable polarity, intensity, and frequency, DBS permits more flexible modulation of brain function, referred to as neuromodulation. Thus, parameters can be optimized for individual patients. The process of optimizing parameters for individual patients, typically performed by a specially trained psychiatrist in the outpatient setting, can be quite time-consuming and requires attentive, long-term follow-up. 4. In cases where no beneficial settings can be identified despite extensive efforts, the electrodes can be inactivated, and devices may be removed. In that event, devices are usually only partly explanted, with the brain electrodes left in place given the small risk of hemorrhage upon removal
- #73: when given one pulse at a time without regular rhythm and at low rates of delivery, is referred to as single-pulse TMS When repeated at regular rhythmic intervals that usually range from 1 to 25 Hz, this stimulation method is described as repetitive TMS (rTMS), which can be further functionally divided into “low-frequency rTMS” when the stimulation frequency is 1 Hz or less and “high-frequency rTMS” when higher frequencies are used, usually 5 to 20 Hz. Theta burst stimulation (TBS) refers to high-frequency bursts (e.g., 3 pulses at 50 Hz) applied at a regular frequency (e.g., 5 bursts per second).
- #74: Each device's technical parameters, such as stimulation intensity, pulse frequency, and total number of pulses administered, are the most basic adjustable elements of TMS dosing