Dr.S.Santhosh Goud
Chairperson Dr.D.Ragadeepthi
 Brain stimulation therapies involve activating
or touching the brain directly with electricity,
magnets, or implants to treat neuro psychiatric
illness
 Other names- neuromodulation/non-
pharmacological somatic therapies
 16th century seizure induction in psychiatric
conditions
 1785 therapeutic use of seizure induction
inLondon Medical Journal
 Father of electrotherapy-G.B.C Duchenne
 ELECTRO CONVULSIVE THERAPY
 VAGUS NERVE STIMULATION
 TRANSCRANIAL MAGNETIC
STIMULATION
 DEEP BRAIN STIMULATION
 MISCELLANEOUS
S.no. Year Procedure Introduced by
1 1934 Chemical convulsive therapy Von Meduna
2 1938 Electro convulsive therapy Cerlette&Bini
3 1940 Curare modified therapy Bennet
4 1945 Oxygenation during ect Holovachka
5 1949 Unilateral non dominant ect Goldman
6 1952 Succinylcholine-modified ect Holmberg&Thesleff
7 1942 Ect in india Brig.E.A.Bennet
8 1979 FDA approval for Depression
 The aim of ECT -to induce generalised
cerebral seizure activity with an electrical dose
that is sufficiently above the seizure threshold
to maximize the clinical efficacy of treatment,
but not so high that it needlessly contributes to
the cognitive effects of treatment
 Electrical aspects
Parameter Brief Pulse wave Sine wave
Current
amplitude
0.8A 0.6A
Voltage 160V 120V
Frequency 100PPS 50Hz
Width 1msec
Duration 1sec 0.5sec
Impedence 200ohm 200ohm
Energy 12.8J 36J
charge 80mC 300mC
Electrode placement
 Unilateral vs Bilateral
 Bi temporal
 Bi frontal
 Unilateral(d’Elia RUL)
Frequency of treatment
 Thrice or twice a week
 Matelzky’s multiple monitored ECTs-2 or more
ECTs per treatment session, at a frequency of 2 or more
sessions per week
Regressive ECTs-repeated ECTs to produce vegetative state
Stimulus aspects
 Threshold stimulus-lowest stimulus at which
seizure is produced
 Effectiveness with supra threshold
stimulus(150%)
 Threshold is increased with number of ECT
sessions
 Determining the stimulus strength
 Based on age,sex,anesthetic dosage and
concomitant medication
 Trial method
 Fixed high charge for all patients
EEG changes-electro cerebral silence
Neurochemical changes-
 Upregulation of 5-HT receptors
 Decreased DA autoregulation
 Increased opiods in brain
 Increased GABA
 Increased CSF Acetylcholine
Action on second messangers
Neuro endocrine changes HPA axis
Blood Brain Barrier permeability
Increased expression of growth factors
 Informed consent
 Pre-ect investigations
 Pre anesthetic precautions
 NBM for 6 hours prior
 Void urine
 Not to apply hair oil,remove hair pins
 Remove jewellery,contact lens,hearing aids,
dentures
 Establish venous and airway access
Pre medication,anesthesia and muscle relaxant
 Atropine 0.3-0.6mg/i.m 30-45 mins before
 Methohexitol(0.75-
1.0mg/kg)/thiopentone(2.5mg/kg)Profopol(1.
5mg/kg)
 Scoline with in a minute of anesthetic
agent(0.5-1mg/kg)
 Oxygenation(100% 5L/min) through out the
procedure
Unmodified ECT
 With out prior muscle relaxant
 Common in India, Japan and Nigeria
 Union health ministry recommended to ban
direct ECT in mental health care bill 2013
 Benzodiazepine-modified ECT
 Duration of seizure
 Atleast 25 sec(15secs of motor seizures(30-60sec
optimal)
 Monitering
 Seizures(motor seizure duration 30% shorter
than EEG seizure)
 Ecg
 vitals
 Missed seizures-25-100% increase in dose with
proper oxygenation and a 20-40second
delay(max 4/session)
 Abortive seizures-restimulation after a 60-90
seconds delay
 Prolonged seizures-more than 120secs(>90secs
of motor seizures)
 Terminate by giving iv anesthetic/Benzo with
adequate ventilation
 ECT emergent delirium-give iv
benzo/haloperidol
 Prolonged confusion ->1 hour
 Reduce ect sessions/stop ECT/Switch to
unilateral ECT
 Headache-analgesics, bodyache-curare
 Prolonged apnoea –assisted respiration for 1
hour; Rarely fresh plasma transfusion
 The major risks of ECT are those of brief
general anesthesia.
 There are virtually no absolute health
contraindications precluding its use where
warranted (Potter & Rudorfer, 1993; Rudorfer
et al., 1997).
 The most common adverse effects are
confusion and memory loss for events
surrounding the period of ECT treatment.
 The confusion and disorientation seen upon
awakening after ECT typically clear within an
hour.
 Mortality 1 per 10,000
Contraindications
 Only relative contraindications
 Raised ICT
 Recent MI(<3 months) > 6 months not aCI
 Unstable vascular aneurysm
 Retinal detachment
 Pheochromocytoma
 Anesthetic risk
 Cardiac pacemaker is not a contraindication
 Thyroid dysfunction should be corrected
Indications
 Major depressive disorder with
Suicidal attempt
Severe suicidal plans
Severe illness refusing food/fluids
Stupor
Psychomotor retardation
psychosis
 ECT may be considered as a second- or third-
line treatment of a depressive illness that has
not adequately responded to antidepressant
drug treatment and where social recovery has
not been achieved (e.g. an inability to return to
work).
 70% efficacy in MDD
Mania
 The treatment of choice for mania is a mood-
stabilising drug plus antipsychotic drug.
 ECT may be considered for severe mania
associated with:
life-threatening physical exhaustion
treatment resistance (i.e. mania that has not
responded to the treatment of choice).
 A combination of ECT and a moderate dose of
a neuroleptic is extremely effective in rapidly
aborting an acute episode of mania
 ECT can be recommended for any manic
patient,irrespective of the severity or the
duration of the illness (Sikdar et al 1994)
Acute schizophrenia
 The treatment of choice for acute schizophrenia
is antipsychotic drug treatment. ECT may be
considered as a fourth-line option, that is, for
patients with schizophrenia for whom
clozapine has already proven ineffective or
intolerable
 Effective in 10% cases
Catatonia
 Catatonia is a syndrome that may complicate
several psychiatric and medical conditions. The
treatment of choice is a benzodiazepine
drug;most experience is with lorazepam.
 ECT may be indicated when treatment with
lorazepam has been ineffective.
 Delusional disorder
Other neuropsychiatric conditions
 PD and movement disorders
 Intractable seizures
 NMS
 Hypopituitarism
 Delirium
 There is no evidence to indicate what number
of sessions of ECT gains the best response.
Neither is there any evidence to support the
practice of giving two extra ECT sessions after
the patient is considered to be well enough to
discontinue ECT.
 Frequency 3 times weekly/Twice weekly
 Total 6-12 or more when needed
 No response with 6 sessions-stop ect
ECT in elderly patients with depression
 Electroconvulsive therapy is a highly effective
treatment for major depressive disorder in the
elderly, perhaps even more so than in younger
age groups (Benbow, 1987; Devenand &
Kruger, 1994).
 It is also effective and well tolerated in the old-
old(Tew et al, 1999).
 Older people tend to have higher seizure
thresholds
 Older patients may be more susceptible to
confusion after ECT
 Cognitive function should be assessed at least
24 hours following ECT
 If confusion proves to be a problem,
consideration should be given to switching
from bilateral to unilateral ECT
 There is no significant difference in the
cognitive outcome of elderly patients with
depression treated with ECT or tricyclic
antidepressant medication
 ECT can be given to patients with dementia
and depression without ill effect but they may
be at increased risk of post-ECT delirium
 ECT in pregnancy the recommended (Heath &
Yonkers, 2001):
 Obstetric consultation before referral for ECT
 Routine fetal heart monitoring before and after
each individual treatment when gestational age
is beyond the first trimester(obstetric
consultation may suggest earlier monitoring in
high-risk pregnancies)
 case-by-case consideration of intubation,
because of the risk of regurgitation, particularly
beyond the first trimester.
ECT in children and adolescents
 No studies only case reports
 Differ in opinions
 Safe in 15-17
 Case report in 8 year child with successful
resolution of depression
 Risk benefit ratio
 There is evidence that ECT can cause persistent
or permanent memory loss (Squire et al,
1981;Weiner et al, 1986; McElhiney et al, 1995;
Sobin et al, 1995), which is difficult to
distinguish from that caused by illness.
 Deficits are usually in recall of both
autobiographical memory and public
information(knowledge of events in the world)
ECT and Psychotropics
 No isssues with any anti depressant
 Antipsychotics except clozapine are safe
 Reduce anti epileptic dose if possible(only for
mania)
 Reduce benzodiazepine dose(or shift to non
benzo anxiolytic/for sleep add low dose CPZ)
 Lithium???
 Focal electrically adminstered seizure
therapy(FEAST)-Spellman,2009
 Uses direct current/monophasic pulses
 Different electrode configuration
 Unidirectional stimulation
 Focal seizures in prefrontal cortex with
secondary generalization
 Few side effects
 Primarily developed for seizure disorder(1997
FDA approval)
 In 2005 approved for MDD
 Response rate 30%
 Approved for chronic use only>2yrs
 Vagus nerve is a mixed nerve
 Afferents had connection with NTS and many
other vital centers
 Zabara(1992) discovered anti convulsant action
of VNS in experimental seizures(pentylene
tetrazole) in dogs
 His hypothesis VNS prevents or controls motor
and autonomic components of epilepsy
 Action on mid brain centers
 Regulation of NE and GABA
A device called a pulse generator, about the size
of a pocket watch, is surgically implanted in
the upper left side of the chest. (left had few
cardiac efferents so low risk of arrhythmias)
 Connected to the pulse generator is a lead wire,
which is guided under the skin up to the neck,
where it is attached to the left-sided vagus
nerve.
 VNS generator can be controlled by personal
computer or digital infra red wand
 Typically, electrical pulses that last about 30
seconds are sent about every five minutes from
the generator to the vagus nerve
 The vagus nerve, in turn, delivers those signals
to the brain.
 The pulse generator, which operates
continuously, is powered by a battery that lasts
around 10 years, after which it must be
replaced.
 The device also can be temporarily deactivated
by placing a magnet over the chest where the
pulse generator is implanted. A person may
want to deactivate it if side effects become
intolerable, or before engaging in strenuous
activity or exercise because it may interfere
with breathing. The device reactivates when
the magnet is removed.
 VNS is indicated for the adjunctive long-term
treatment of chronic (more than 2 years) or
recurrent depression for patients 18 years of
age or older who are experiencing a major
depressive episode and have not had an
adequate response to four or more adequate
antidepressant treatments
Side effects
 Infection
 Voice changes or hoarseness(SLN&RLN
stimulation)
 Cough or sore throat
 Neck pain
 Discomfort or tingling in the area where the
device is implanted
 Breathing problems, especially during exercise
 Difficulty swallowing, dyspepsia
Other uses
 Anxiety disorders
 Migraine
 Alzheimer's disease
 Fibromyalgia
 Tinnitus
 Obesity
 Lennox-gastaut syndrome
 Multiple sclerosis
Thompson 1910
Barker, 1984
Cadwell
DantecMagstim
Common rTMS machines
 Repetitive transcranial magnetic stimulation
(rTMS) uses a magnet instead of an electrical
current to activate the brain.
 Typical rTMS session lasts 30 to 60 minutes and
does not require anesthesia.
 An electromagnetic coil is held against the target
area of the brain that is thought to be involved in
deserved function. Then, short electromagnetic
pulses are administered through the coil.
 The magnetic pulse easily passes through the skull,
and causes small electrical currents that stimulate
nerve cells in the targeted brain region. And
because this type of pulse generally does not reach
further than two inches into the brain, scientists
can select which parts of the brain will be affected
and which will not be.
 Generally, the person will feel a slight knocking or
tapping on the head as the pulses are administered
1. Non invasive procedure
2. Fewer cognitive side effects
3. Patient can drive in and drive out
4. No risk of anesthesia
5. No stigma
6. Less risk for clinician
Low frequency rTMS
 < 1 Hz. frequency stimulation
 Low frequency stimulation for
long duration, induces long
lasting inhibition of neuronal
excitation called as Long term
depression (LTD)
 Reduces cerebral metabolism
 Reduction in cerebral blood flow
 Application on Lt. PFC causes
deterioration of mood
High Frequency rTMS
 > 1 Hz frequency stimulation
 High frequency stimulation for
short duration, induces long
lasting increase of neuronal
excitation called as Long term
Potentiation (LTP)
 Increases cerebral metabolism
 Increase in cerebral blood flow
 Application on Lt. PFC causes
elevation of mood
 Protocol A
 low frequency stimulation (1 Hz)
 Used for auditory hallucinations on left temporo
parietal region at 90% of MT
 Protocol B
 High frequency stimulation ( 2Hz)
 Used for anxiety disorders, somatisation disorder,
OCD, moderate depressive disorder on left prefrontal
region at 110% of MT
 Protocol C
 High frequency stimulation(3Hz)
 Used for severe depression on left prefrontal region at
110% of MT
 TMS diagnostic uses-to measure activity and
function of specific brain circuits in humans.
 measuring the connection between the
primary motor cortex and a muscle to evaluate
damage from stroke, multiple sclerosis,
amyotrophic lateral sclerosis, movement
disorders, motor neuron disease and injuries
and other disorders affecting the facial and
other cranial nerves and the spinal cord.
 The use of single-pulse TMS was approved by
the FDA for use in migraine
 For neuropathic pain, for which there is high-
frequency (HF) repetitive TMS (rTMS) appears
effective
 For loss of function caused by stroke LF-rTMS
of the corresponding brain region has probable
efficacy
 For treatment-resistant major depressive
disorder, HF-rTMS of the left dorsolateral
prefrontal cortex(DLPFC) appears effective and
low-frequency (LF) rTMS of the right DLPFC
has probable efficacy.
 For negative symptoms of schizophrenia, HF-
rTMS of the left DLPFC has probable efficacy
 Hoffman used daily LF-rTMS over temporal
lobes to treat hallucinations
Areas of research
 Rehabilitation of aphasia and motor disability
after stroke
 Anxiety disorders,obsessive-compulsive
disorder, schizophrenia,substance
abuse,addiction, and posttraumatic stress
disorder (PTSD)
 Amyotrophic lateral sclerosis, multiple
sclerosis,epilepsy,Alzheimer's disease,
Parkinson's disease, Tinnitus
Side effects
 The muscles of the scalp, jaw or face may contract
or tingle during the procedure.
 Mild headache or brief light headedness
 Possibility of seizure(1 in 1000 patients or 1 in
30,000 treatments)
 Transient induction of hypomania, transient
cognitive changes
 Transient hearing loss, transient impairment of
working memory,
 Induced currents in electrical circuits in implanted
devices
 Contraindications
Patients with any type of non-removable metal
in their heads (with the exception of braces or
dental fillings), or within twelve inches of the
coil should not receive rTMS
 Deep brain stimulation (DBS) was first
developed as a treatment for Parkinson's
disease to reduce tremor, stiffness, walking
problems and uncontrollable
movements(Limousin 1995)
 Internal globus pallidus & Sub thalamic
nucleus are the target areas
 In DBS, a pair of electrodes is implanted in the
brain and controlled by a generator that is
implanted in the chest. Stimulation is
continuous and its frequency and level is
customized to the individual.
 DBS has only recently been studied as a
treatment for depression or obsessive
compulsive disorder
 No FDA approval for depression
 DBS requires brain surgery. The head is shaved
and then attached with screws to a sturdy
frame that prevents the head from moving
during the surgery. Scans of the head and brain
using MRI are taken. The surgeon uses these
images as guides during the surgery. Patients
are awake during the procedure to provide the
surgeon with feedback, but they feel no pain
because the head is numbed with a local
anesthetic
 Once ready for surgery, two holes are drilled into the
head. From there, the surgeon threads a slender tube
down into the brain to place electrodes on each side of
a specific part of the brain.
 In the case of depression, the part of the brain targeted
is called Area 25(Rostral anterior cingulate). This area
has been found to be overactive in depression and
other mood disorders.
 Another approach bilateral high frequency stimulation
of nucleas accumbens
 In the case of OCD, the electrodes are placed at anterior
limb of internal capsule ,bilaterally (Greenberg)
 After the electrodes are implanted and the
patient provides feedback about the placement
of the electrodes, the patient is put under
general anesthesia.
 The electrodes are then attached to wires that
are run inside the body from the head down to
the chest, where a pair of battery-operated
generators are implanted.
 From here, electrical pulses are continuously
delivered over the wires to the electrodes in the
brain.
Epidural cortical stimulation
 Based on principle of cortical regulation of sub
cortical ,limbic regions
 Shown good results
Other indications of DBS
 Tourette’s disorder
 Substance use
 Obesity
 schizophrenia
Side effects
• Bleeding in the brain or stroke
• Infection
• Disorientation or confusion
• Unwanted mood changes
• Movement disorders
• Lightheadedness
• Trouble sleeping
 Magnetic seizure therapy (MST) borrows certain
aspects from both ECT and rTMS.
 Like rTMS, it uses a magnetic pulse instead of
electricity to stimulate a precise target in the brain.
However, unlike rTMS, MST aims to induce a
seizure like ECT. So the pulse is given at a higher
frequency than that used in rTMS(100Hz,2T)
 Therefore, like ECT, the patient must be
anesthetized and given a muscle relaxant to
prevent movement.
 The goal of MST is to retain the effectiveness of
ECT while reducing the cognitive side effects
usually associated with it.
 It is currently being investigated for the treatment
of treatment-resistant depression (TRD),
schizophrenia and obsessive-compulsive disorder
 Application of constant weak(<
1mA) for 20mins through scalp
electrodes
 Induces subthreshold changes in
membrane potential thus alters the
cortical excitability
 Most research for neuro
rehabilitation(post stroke aphasia
rehabilitation)
 Studies in pain and depression
 Burns over scalp is the only side
effect if current >2mA
THANK YOU FRIENDS

Brain stimulation therapies

  • 1.
  • 2.
     Brain stimulationtherapies involve activating or touching the brain directly with electricity, magnets, or implants to treat neuro psychiatric illness  Other names- neuromodulation/non- pharmacological somatic therapies  16th century seizure induction in psychiatric conditions  1785 therapeutic use of seizure induction inLondon Medical Journal  Father of electrotherapy-G.B.C Duchenne
  • 3.
     ELECTRO CONVULSIVETHERAPY  VAGUS NERVE STIMULATION  TRANSCRANIAL MAGNETIC STIMULATION  DEEP BRAIN STIMULATION  MISCELLANEOUS
  • 4.
    S.no. Year ProcedureIntroduced by 1 1934 Chemical convulsive therapy Von Meduna 2 1938 Electro convulsive therapy Cerlette&Bini 3 1940 Curare modified therapy Bennet 4 1945 Oxygenation during ect Holovachka 5 1949 Unilateral non dominant ect Goldman 6 1952 Succinylcholine-modified ect Holmberg&Thesleff 7 1942 Ect in india Brig.E.A.Bennet 8 1979 FDA approval for Depression
  • 5.
     The aimof ECT -to induce generalised cerebral seizure activity with an electrical dose that is sufficiently above the seizure threshold to maximize the clinical efficacy of treatment, but not so high that it needlessly contributes to the cognitive effects of treatment
  • 6.
     Electrical aspects ParameterBrief Pulse wave Sine wave Current amplitude 0.8A 0.6A Voltage 160V 120V Frequency 100PPS 50Hz Width 1msec Duration 1sec 0.5sec Impedence 200ohm 200ohm Energy 12.8J 36J charge 80mC 300mC
  • 7.
    Electrode placement  Unilateralvs Bilateral  Bi temporal  Bi frontal  Unilateral(d’Elia RUL) Frequency of treatment  Thrice or twice a week  Matelzky’s multiple monitored ECTs-2 or more ECTs per treatment session, at a frequency of 2 or more sessions per week Regressive ECTs-repeated ECTs to produce vegetative state
  • 8.
    Stimulus aspects  Thresholdstimulus-lowest stimulus at which seizure is produced  Effectiveness with supra threshold stimulus(150%)  Threshold is increased with number of ECT sessions
  • 9.
     Determining thestimulus strength  Based on age,sex,anesthetic dosage and concomitant medication  Trial method  Fixed high charge for all patients
  • 10.
    EEG changes-electro cerebralsilence Neurochemical changes-  Upregulation of 5-HT receptors  Decreased DA autoregulation  Increased opiods in brain  Increased GABA  Increased CSF Acetylcholine Action on second messangers Neuro endocrine changes HPA axis Blood Brain Barrier permeability Increased expression of growth factors
  • 11.
     Informed consent Pre-ect investigations  Pre anesthetic precautions  NBM for 6 hours prior  Void urine  Not to apply hair oil,remove hair pins  Remove jewellery,contact lens,hearing aids, dentures  Establish venous and airway access
  • 12.
    Pre medication,anesthesia andmuscle relaxant  Atropine 0.3-0.6mg/i.m 30-45 mins before  Methohexitol(0.75- 1.0mg/kg)/thiopentone(2.5mg/kg)Profopol(1. 5mg/kg)  Scoline with in a minute of anesthetic agent(0.5-1mg/kg)  Oxygenation(100% 5L/min) through out the procedure
  • 13.
    Unmodified ECT  Without prior muscle relaxant  Common in India, Japan and Nigeria  Union health ministry recommended to ban direct ECT in mental health care bill 2013  Benzodiazepine-modified ECT
  • 14.
     Duration ofseizure  Atleast 25 sec(15secs of motor seizures(30-60sec optimal)  Monitering  Seizures(motor seizure duration 30% shorter than EEG seizure)  Ecg  vitals
  • 15.
     Missed seizures-25-100%increase in dose with proper oxygenation and a 20-40second delay(max 4/session)  Abortive seizures-restimulation after a 60-90 seconds delay  Prolonged seizures-more than 120secs(>90secs of motor seizures)  Terminate by giving iv anesthetic/Benzo with adequate ventilation
  • 16.
     ECT emergentdelirium-give iv benzo/haloperidol  Prolonged confusion ->1 hour  Reduce ect sessions/stop ECT/Switch to unilateral ECT  Headache-analgesics, bodyache-curare  Prolonged apnoea –assisted respiration for 1 hour; Rarely fresh plasma transfusion
  • 17.
     The majorrisks of ECT are those of brief general anesthesia.  There are virtually no absolute health contraindications precluding its use where warranted (Potter & Rudorfer, 1993; Rudorfer et al., 1997).
  • 18.
     The mostcommon adverse effects are confusion and memory loss for events surrounding the period of ECT treatment.  The confusion and disorientation seen upon awakening after ECT typically clear within an hour.  Mortality 1 per 10,000
  • 19.
    Contraindications  Only relativecontraindications  Raised ICT  Recent MI(<3 months) > 6 months not aCI  Unstable vascular aneurysm  Retinal detachment  Pheochromocytoma  Anesthetic risk  Cardiac pacemaker is not a contraindication  Thyroid dysfunction should be corrected
  • 20.
    Indications  Major depressivedisorder with Suicidal attempt Severe suicidal plans Severe illness refusing food/fluids Stupor Psychomotor retardation psychosis
  • 21.
     ECT maybe considered as a second- or third- line treatment of a depressive illness that has not adequately responded to antidepressant drug treatment and where social recovery has not been achieved (e.g. an inability to return to work).  70% efficacy in MDD
  • 22.
    Mania  The treatmentof choice for mania is a mood- stabilising drug plus antipsychotic drug.  ECT may be considered for severe mania associated with: life-threatening physical exhaustion treatment resistance (i.e. mania that has not responded to the treatment of choice).
  • 23.
     A combinationof ECT and a moderate dose of a neuroleptic is extremely effective in rapidly aborting an acute episode of mania  ECT can be recommended for any manic patient,irrespective of the severity or the duration of the illness (Sikdar et al 1994)
  • 24.
    Acute schizophrenia  Thetreatment of choice for acute schizophrenia is antipsychotic drug treatment. ECT may be considered as a fourth-line option, that is, for patients with schizophrenia for whom clozapine has already proven ineffective or intolerable  Effective in 10% cases
  • 25.
    Catatonia  Catatonia isa syndrome that may complicate several psychiatric and medical conditions. The treatment of choice is a benzodiazepine drug;most experience is with lorazepam.  ECT may be indicated when treatment with lorazepam has been ineffective.
  • 26.
     Delusional disorder Otherneuropsychiatric conditions  PD and movement disorders  Intractable seizures  NMS  Hypopituitarism  Delirium
  • 27.
     There isno evidence to indicate what number of sessions of ECT gains the best response. Neither is there any evidence to support the practice of giving two extra ECT sessions after the patient is considered to be well enough to discontinue ECT.  Frequency 3 times weekly/Twice weekly  Total 6-12 or more when needed  No response with 6 sessions-stop ect
  • 28.
    ECT in elderlypatients with depression  Electroconvulsive therapy is a highly effective treatment for major depressive disorder in the elderly, perhaps even more so than in younger age groups (Benbow, 1987; Devenand & Kruger, 1994).  It is also effective and well tolerated in the old- old(Tew et al, 1999).
  • 29.
     Older peopletend to have higher seizure thresholds  Older patients may be more susceptible to confusion after ECT  Cognitive function should be assessed at least 24 hours following ECT  If confusion proves to be a problem, consideration should be given to switching from bilateral to unilateral ECT
  • 30.
     There isno significant difference in the cognitive outcome of elderly patients with depression treated with ECT or tricyclic antidepressant medication  ECT can be given to patients with dementia and depression without ill effect but they may be at increased risk of post-ECT delirium
  • 31.
     ECT inpregnancy the recommended (Heath & Yonkers, 2001):  Obstetric consultation before referral for ECT  Routine fetal heart monitoring before and after each individual treatment when gestational age is beyond the first trimester(obstetric consultation may suggest earlier monitoring in high-risk pregnancies)  case-by-case consideration of intubation, because of the risk of regurgitation, particularly beyond the first trimester.
  • 32.
    ECT in childrenand adolescents  No studies only case reports  Differ in opinions  Safe in 15-17  Case report in 8 year child with successful resolution of depression  Risk benefit ratio
  • 33.
     There isevidence that ECT can cause persistent or permanent memory loss (Squire et al, 1981;Weiner et al, 1986; McElhiney et al, 1995; Sobin et al, 1995), which is difficult to distinguish from that caused by illness.  Deficits are usually in recall of both autobiographical memory and public information(knowledge of events in the world)
  • 34.
    ECT and Psychotropics No isssues with any anti depressant  Antipsychotics except clozapine are safe  Reduce anti epileptic dose if possible(only for mania)  Reduce benzodiazepine dose(or shift to non benzo anxiolytic/for sleep add low dose CPZ)  Lithium???
  • 35.
     Focal electricallyadminstered seizure therapy(FEAST)-Spellman,2009  Uses direct current/monophasic pulses  Different electrode configuration  Unidirectional stimulation  Focal seizures in prefrontal cortex with secondary generalization  Few side effects
  • 37.
     Primarily developedfor seizure disorder(1997 FDA approval)  In 2005 approved for MDD  Response rate 30%  Approved for chronic use only>2yrs
  • 38.
     Vagus nerveis a mixed nerve  Afferents had connection with NTS and many other vital centers  Zabara(1992) discovered anti convulsant action of VNS in experimental seizures(pentylene tetrazole) in dogs  His hypothesis VNS prevents or controls motor and autonomic components of epilepsy  Action on mid brain centers  Regulation of NE and GABA
  • 39.
    A device calleda pulse generator, about the size of a pocket watch, is surgically implanted in the upper left side of the chest. (left had few cardiac efferents so low risk of arrhythmias)  Connected to the pulse generator is a lead wire, which is guided under the skin up to the neck, where it is attached to the left-sided vagus nerve.  VNS generator can be controlled by personal computer or digital infra red wand
  • 40.
     Typically, electricalpulses that last about 30 seconds are sent about every five minutes from the generator to the vagus nerve  The vagus nerve, in turn, delivers those signals to the brain.  The pulse generator, which operates continuously, is powered by a battery that lasts around 10 years, after which it must be replaced.
  • 41.
     The devicealso can be temporarily deactivated by placing a magnet over the chest where the pulse generator is implanted. A person may want to deactivate it if side effects become intolerable, or before engaging in strenuous activity or exercise because it may interfere with breathing. The device reactivates when the magnet is removed.
  • 42.
     VNS isindicated for the adjunctive long-term treatment of chronic (more than 2 years) or recurrent depression for patients 18 years of age or older who are experiencing a major depressive episode and have not had an adequate response to four or more adequate antidepressant treatments
  • 43.
    Side effects  Infection Voice changes or hoarseness(SLN&RLN stimulation)  Cough or sore throat  Neck pain  Discomfort or tingling in the area where the device is implanted  Breathing problems, especially during exercise  Difficulty swallowing, dyspepsia
  • 44.
    Other uses  Anxietydisorders  Migraine  Alzheimer's disease  Fibromyalgia  Tinnitus  Obesity  Lennox-gastaut syndrome  Multiple sclerosis
  • 45.
  • 46.
  • 47.
     Repetitive transcranialmagnetic stimulation (rTMS) uses a magnet instead of an electrical current to activate the brain.  Typical rTMS session lasts 30 to 60 minutes and does not require anesthesia.
  • 48.
     An electromagneticcoil is held against the target area of the brain that is thought to be involved in deserved function. Then, short electromagnetic pulses are administered through the coil.  The magnetic pulse easily passes through the skull, and causes small electrical currents that stimulate nerve cells in the targeted brain region. And because this type of pulse generally does not reach further than two inches into the brain, scientists can select which parts of the brain will be affected and which will not be.  Generally, the person will feel a slight knocking or tapping on the head as the pulses are administered
  • 49.
    1. Non invasiveprocedure 2. Fewer cognitive side effects 3. Patient can drive in and drive out 4. No risk of anesthesia 5. No stigma 6. Less risk for clinician
  • 50.
    Low frequency rTMS < 1 Hz. frequency stimulation  Low frequency stimulation for long duration, induces long lasting inhibition of neuronal excitation called as Long term depression (LTD)  Reduces cerebral metabolism  Reduction in cerebral blood flow  Application on Lt. PFC causes deterioration of mood High Frequency rTMS  > 1 Hz frequency stimulation  High frequency stimulation for short duration, induces long lasting increase of neuronal excitation called as Long term Potentiation (LTP)  Increases cerebral metabolism  Increase in cerebral blood flow  Application on Lt. PFC causes elevation of mood
  • 51.
     Protocol A low frequency stimulation (1 Hz)  Used for auditory hallucinations on left temporo parietal region at 90% of MT  Protocol B  High frequency stimulation ( 2Hz)  Used for anxiety disorders, somatisation disorder, OCD, moderate depressive disorder on left prefrontal region at 110% of MT  Protocol C  High frequency stimulation(3Hz)  Used for severe depression on left prefrontal region at 110% of MT
  • 52.
     TMS diagnosticuses-to measure activity and function of specific brain circuits in humans.  measuring the connection between the primary motor cortex and a muscle to evaluate damage from stroke, multiple sclerosis, amyotrophic lateral sclerosis, movement disorders, motor neuron disease and injuries and other disorders affecting the facial and other cranial nerves and the spinal cord.
  • 53.
     The useof single-pulse TMS was approved by the FDA for use in migraine  For neuropathic pain, for which there is high- frequency (HF) repetitive TMS (rTMS) appears effective  For loss of function caused by stroke LF-rTMS of the corresponding brain region has probable efficacy
  • 54.
     For treatment-resistantmajor depressive disorder, HF-rTMS of the left dorsolateral prefrontal cortex(DLPFC) appears effective and low-frequency (LF) rTMS of the right DLPFC has probable efficacy.  For negative symptoms of schizophrenia, HF- rTMS of the left DLPFC has probable efficacy  Hoffman used daily LF-rTMS over temporal lobes to treat hallucinations
  • 55.
    Areas of research Rehabilitation of aphasia and motor disability after stroke  Anxiety disorders,obsessive-compulsive disorder, schizophrenia,substance abuse,addiction, and posttraumatic stress disorder (PTSD)  Amyotrophic lateral sclerosis, multiple sclerosis,epilepsy,Alzheimer's disease, Parkinson's disease, Tinnitus
  • 56.
    Side effects  Themuscles of the scalp, jaw or face may contract or tingle during the procedure.  Mild headache or brief light headedness  Possibility of seizure(1 in 1000 patients or 1 in 30,000 treatments)  Transient induction of hypomania, transient cognitive changes  Transient hearing loss, transient impairment of working memory,  Induced currents in electrical circuits in implanted devices
  • 57.
     Contraindications Patients withany type of non-removable metal in their heads (with the exception of braces or dental fillings), or within twelve inches of the coil should not receive rTMS
  • 59.
     Deep brainstimulation (DBS) was first developed as a treatment for Parkinson's disease to reduce tremor, stiffness, walking problems and uncontrollable movements(Limousin 1995)  Internal globus pallidus & Sub thalamic nucleus are the target areas
  • 60.
     In DBS,a pair of electrodes is implanted in the brain and controlled by a generator that is implanted in the chest. Stimulation is continuous and its frequency and level is customized to the individual.  DBS has only recently been studied as a treatment for depression or obsessive compulsive disorder  No FDA approval for depression
  • 61.
     DBS requiresbrain surgery. The head is shaved and then attached with screws to a sturdy frame that prevents the head from moving during the surgery. Scans of the head and brain using MRI are taken. The surgeon uses these images as guides during the surgery. Patients are awake during the procedure to provide the surgeon with feedback, but they feel no pain because the head is numbed with a local anesthetic
  • 62.
     Once readyfor surgery, two holes are drilled into the head. From there, the surgeon threads a slender tube down into the brain to place electrodes on each side of a specific part of the brain.  In the case of depression, the part of the brain targeted is called Area 25(Rostral anterior cingulate). This area has been found to be overactive in depression and other mood disorders.  Another approach bilateral high frequency stimulation of nucleas accumbens  In the case of OCD, the electrodes are placed at anterior limb of internal capsule ,bilaterally (Greenberg)
  • 63.
     After theelectrodes are implanted and the patient provides feedback about the placement of the electrodes, the patient is put under general anesthesia.  The electrodes are then attached to wires that are run inside the body from the head down to the chest, where a pair of battery-operated generators are implanted.  From here, electrical pulses are continuously delivered over the wires to the electrodes in the brain.
  • 64.
    Epidural cortical stimulation Based on principle of cortical regulation of sub cortical ,limbic regions  Shown good results Other indications of DBS  Tourette’s disorder  Substance use  Obesity  schizophrenia
  • 65.
    Side effects • Bleedingin the brain or stroke • Infection • Disorientation or confusion • Unwanted mood changes • Movement disorders • Lightheadedness • Trouble sleeping
  • 67.
     Magnetic seizuretherapy (MST) borrows certain aspects from both ECT and rTMS.  Like rTMS, it uses a magnetic pulse instead of electricity to stimulate a precise target in the brain. However, unlike rTMS, MST aims to induce a seizure like ECT. So the pulse is given at a higher frequency than that used in rTMS(100Hz,2T)  Therefore, like ECT, the patient must be anesthetized and given a muscle relaxant to prevent movement.  The goal of MST is to retain the effectiveness of ECT while reducing the cognitive side effects usually associated with it.  It is currently being investigated for the treatment of treatment-resistant depression (TRD), schizophrenia and obsessive-compulsive disorder
  • 68.
     Application ofconstant weak(< 1mA) for 20mins through scalp electrodes  Induces subthreshold changes in membrane potential thus alters the cortical excitability  Most research for neuro rehabilitation(post stroke aphasia rehabilitation)  Studies in pain and depression  Burns over scalp is the only side effect if current >2mA
  • 69.