This document discusses various classes of drugs used to treat neuropathic pain, including anticonvulsants and antidepressants. It begins by defining nociceptive and neuropathic pain. It then discusses various antiepileptic drugs (AEDs) such as valproic acid, clonazepam, gabapentin, pregabalin, felbamate, topiramate, and phenytoin. It explains their mechanisms of action, which commonly involve enhancing GABA activity or blocking sodium channels. Dosing, metabolism, and side effects are provided for each drug. The document aims to outline treatment options for neuropathic pain conditions using AEDs.

1. ANTIDEPRESSENTAND
ANTICONVULANT AS
ANALGESICS
Ravi shankar sharma
Moderator- Dr. Ajit kuma r

2. A/T IASP:
• "Nociceptive pain" -- "Pain that arises from actual or threatened
damage to non-neural tissue and is due to the activation of
nociceptors."
• "Pain caused by a lesion or disease of the somatosensory nervous
system." -?"Neuropathic pain"

3. Nociceptive Vs Neuropathic pain
P•ln types Nocfceprive Nturop.athk
Dttnition Paincaustd by physlologlal
ictiv1tionof pain receptors
Pain cal.Mdby lesion or
dysfunctionof the
tosensory system,cspteially
the nociceptive pathway
MKhanlsm Natural physlologlcol ,
,.nsductlon Ectopic Impulse generation. amoog
others
Loalii
atlon Local+ referred piln C
onfined toI
nnervation territory of
the lesioned nervous structure
Quality of symptoms Orchna1y painful sensation N
tw str.ange sensations
(good v01bal descriptors) (poor ••
rb•I dewlpton)
Treatment Good response Poor•mocferate response
(conventional analgesics) (antldopress>nt1,anti•plleprics)

4. Antiepileptic drugs (AEDs)
• Used in the treatment of chronic pain syndromes for more than 50
years.
• Neuropathic syndromes have been treated with AEDs, including:
• Diabetic neuropathy
• Postherpetic neuralgia
• Glossopharyngeal neuralgia
• Postsympathectomy neuralgia
• Postthoracotomy pain syndrome

5. CLSSIFICATION:
F
irst-generation antiepilept ics
• Benzodiazepines
Carbamazepine
• Ethosuximlde
• Phenobarbital
• Phenytoin
• Primidone
• valproic acid
Second-generation antiepi leptics
• Fe
lbamate
• Gabapentin
• Lacosamide
• Lamotrig
i
ne
• Levetiracetam
• Oxcarbazepine
• Pregaballn
• Tiagabine
• Topiramate
• Vigabatrin
• Zonisamide

6. Peripheral nerve damage
• With intact connective tissue
sheath - axons grow in formally
innervated area
• With damage connective tissue
sheath - axon extensions grow in
any direction, become tangled to
form neuroma.
......._
......._
-

7. • Neuromas generate ectopic electrical impulses at the regenerating
tips.
• Causes disruption in the balance of the excitatory (e.g.,glutamate)
and inhibitory (e.g., y-aminobutyric acid [GABA]) neurotransmitters.
• eads to hyperexcitability of the neuronal membrane sodium
channels and voltage-dependent calcium channels, causing rapid
ectopic firing.

8. AEDs Mechanism of action
-".
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Clobwa It

9. VALPROIC ACID
Uses-
• broad-spectrum AED used to treat a number of epileptic syndromes
• preventive treatment of migraine, cluster & tension-type headaches.
• Mood stabilizer

10. Mchan1sm ot action
• Inhibit GABA aminotransferase and succinic semialdehyde dehydrogenase.
• Selectively enhancing postsynaptic GABA responses.
• Direct effects on neuronal membranes.

11. Valproate increases brain GABA levels
- w ..
..
.....
.....
suppress events in the cortex, perivascular
parasympathetics or trigeminal nucleus caudalis.
•
suppresses neurogenic inflammation and directly
attenuates nociceptive neurotransmission
•
Relief of headache
.....
_
...................
--

12. Dose-
• Available as 250-mg capsules and 250 mg/5 m
l syrup.
• starting dosage- is usually 250 mg/day.
• Titrated slowly upward to a maximum dosage of 1000 to 2000
mg/day, in divided doses.

13. Metabolism -
• Absorbed rapidly orally
• Peak concentrations in 1 to 4 hours.
• About 90% bound to plasma proteins.
• Hepatic metabolism
• 15-hour half-life.

14. S
/E-
• CNSdepression
• Hepatotoxicity
• Hematologic toxicity

15. CLONAZEPAM
Uses-
• Chronic malignant and nonmalignant pain syndromes:
• Headaches & Temporomandibular joint dysfunction
• Phantom limb pain & other neuropathic states
• Fibromyalgia

16. INTRACELLUtAR SIDE
Increases frequency of chloride channel opening

17. EnhancedGABA
Activity
MOA-
• Enhance GABAreceptor-mediated chloride channels opening.
• particularly effective when used in combination with other
neuropathlc analgesics

18. Dose-
• Available as 0.5-, 1-, and 2-mg tablets.
• Starting dose 0.5 mg at bedtime, with the dose being slowly increased to
0.5 to 1 mg three times per day.
• Antiepileptic dose - 20 mg/day have been used in epilepsy.
• Headache and pain 1 to 6 mg/day.

19. Metabolism -
• Rapid oral absorption.
• Peak concentrations in 1 to 4 hours.
• 85% bound to plasma proteins.
• Hepatic metabolism
• Half life of about 24 hours.

20. S
/E-
• Drowsiness
• Dizziness
• Fatigue
• Sedation
• Physical and psychological dependence
• Abrupt discontinuation is prohibited.

21. • Gabapentin
• Pregablin
A2o Ligands

22. • a2o-1,-7 VGCC subunit, (binding site of GPN 's)
• NMDAR activity increased by nerve injury
• a2o-1 + NMDARs -7 heteromeric complex in spinal cords
promotes surface trafficking and synaptic targeting of NMDARs
Gabapentin or an a2o-1 Cterminus-interfering peptide normalizes
NMDAR synaptic targeting
'1,-neuropathic pain by - forward trafficking of a2o-1-NMDAR complexes

23. a2l5-is an NMDAR-interacting protein that increases NMDAR synaptic delivery in
neuropathic pain
Normal
lf NMOAr.ceplOr
i .
....
W
o 2 1.NMOAreceptot

24. GABAPENTIN
Uses-
• Postherpetic neuralgia
• Diabetic neuropathy
• Refractory CRPS type 1
• M igraine headaches
• Other neuropathic states

25. Dose-
• Available as 100-, 300-, 400-, 600-, and 800-mg capsules and 250
mg/5 ml syrup.
• reported adequate pain relief dose- 900 to 2400 mg/day

26. Metabolism
• well absorbed orally
• argely unbound to plasma proteins.
• It is not metabolized and is renally excreted.
• Half-life of 5 to 9 hours.

27. S/E-
• Somnolence,
• Diarrhea
• mood swings
• Ataxia
• Fatigue
• Nausea
• Dizziness

28. PREGABALIN
• Fibromyalgia
• Diabetic neuropathy
• Spinal cord injury nerve pain
• PHN
• Other neuropathic States

29. MOA-
EA
f l..exdtatory a
add mnspon·
er

30. Dose-
• Available in 2S, SO, 7S, 100, SO, 200 & 300mg capsules & 20 mg/ml oral
solution.
• 7S to SOmg B.D, or SOto 100 mg TDS ( lS0-300 mg/day) in patients with C.Cr
of at least 60 m l/min.
• Start at 7S mg od/B.O., or SOmg TDS ( lSO mg/day).
• Increase up to 300 mg/day within 1 week based on efficacy and to lerability.

31. Fibromyalgta
Postherpetlc nouralgla
Palnlul diabetic nouropathy
•
central neuropathlc pain
r ,
- - - -
I
I 2 4 6 8 10 12 14 16 18 20
N"1T (95°k Cl) for at least 50% pain
I
ntensity redlJCllon

32. Metabolism-
• Eliminated by renal excretion as unchanged drug
• Half-life of 6.3 hours in subjects with normal renal function.

33. S/E-
• Angioedema Table 1: L
yrica's More Common Adverse Effect Profile Based on Trial Data '!'
Hypersensitivity
Peripheral edema
Dizziness
• Somnolence.
Prq•b•lln Adv•rse Effect "o{P'atJentsTakln1 Preaaballn
Dizziness Up to 30%
Somnolonca Uo to 23%
Ory Mouth Up to S%
PeripheralEdema Up to 1
6%
Ocular/Visual Field Changes Up to 13%
Accidenta lInjury Up to 11"

34. Gablin·
Comparative Pharmacokinetics
Pregaballn Gabapentln
FDA Appfovod
IMicol:ions
OPN,Fibromya9a, PHN
.
Pan ISoitutOI
PHH. Epilctpsy
M
...o
..c
.h
..a
.n
l
sm of
SMedtvely bind '°lho alpl'la2·
defl8 subun
l
l
ot Ca channel
Selectlvely bind to me a!pha2-delta
11t1bunit ot Ca channel
P
......na
l.inebl'(p
l
;aama concentrationI
s
dole lllO)
Non- ,
eat (.P&Mm.n
conCOMl'llbon l
ncreuet
disproportiontiioly 1
0dose)
Oral bloavallabllity >90% aldoses
."
."
,,,' ·2
-
AOOmg
60% 900mg
33% 3600mg
Dosing 810 TIO
1day (
effective s.t.1rung dose
or ay)
> 9days (btrate 1
0ettee1ive dos& of
1800mgld)

35. FELBAMA
TE
.. <'
.
.
.-
,
..
.
.
.
,.
_
.
,_
..
.
.
Uses-
• Trigeminal neuralgia - ........ J ....... 1-
llrCil"t
. ...cr
MOA-
• Inhibition of NMDA and AMPA
• Potentiating GABA receptor- mediated chloride channels
• Inhibiting spontaneous discharges from the voltage dependent sodium
channels.

36. Dose-
• Available as 400- and 600-mg tablets and 600 mg/5 ml suspension.

37. S
/E-
• plastic anemia
• Fulminant hepatic failure.
• Frequent monitoring with CBCs and LFT
s

38. TOPIRAMATE
Uses-
• Post-thoracotomy pain syndrome
• lntercostal neuralgia and other neuropathic pain states.
• Headaches,

39. ;...roplramate blocks voltage-depend ent sodium and calcium channels.
;...it also inhibits the excitatory gluta mate pathway while enhancing effect of GABA.

40. Dose-
• Available as 25-, 100
·
, and 200-mg tablets.
• Starting dosage -- 25 to 50 mg/day
• Dosage can be increased to 400 mg/day in two divided doses over 8
weeks.

41. S
/E-
• kidney stones because of the inhibition of carbonic anhydrase.

42. Sodium channels:
• .l -
-
- ]
- -
-
·-
•
l
• •
ANTIEPILEPTIC DRUGS
.,.
Phtnyloin. C1rb1n111A
'lllnr 1
1nd
'1
1fpro1lt' •« b) prolonitl nJt
lht ln11c1h1atlonor Na eh;annel1

43. Types of VGSC:
Essential
Sodium Peripheral Neurooal
°"'"""'
Nav1
.
7
S
- lallon
Nav1.8-negatfve
sensory neurons
Nav1S-poslttve
sensory neurons
Nav1
.
8-poolllvo
sensory neurons
Nav1
.
8-pooltlllo
.sonsory neurons
"""1
.
7
"""1
.
8
Nav1
.
7
- - - - - - - - - - - - - -
- - - - - - - - - - - - - -
- - - - - - - - - P
ain Moda
l
i1
y
- -
'
-
------- --
'
-
'
-
-
-
--
- - - - - - - - C
I
assicaI noc:lceptive pain pathways
Primary Location Acute (spinal)hea1 pain
-----------------'
-
-
-
-
-
Na11.1
- •l
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.
)
.......
.
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Y
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I
......
"'l'O<)'!n
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ro
'oc9"'9lioo Nonr<>ciCOplMI poln polhways
l)ofNI tO
O
C
.91"'9lon Nouropathlc moctiatlica lallodynia Nav'l 7
-------------------
Acute odd paSl
1
nnamma10<y hyponilgosla
Nav1.
8-nogative
sympattlefic neurons
SOOSC>rf
nourons
Navl
.
7 Nav1.
8-posi1M>
sensory
neurons
Sympnlhotloally maintained pnln Navl
.
7 Nav1
.
7 poolUYe

44. PHENYTOIN
Use -
• Diabetic neuropathy
• Trigeminal neuralgia
• Neuropathic cancer pain
• Postherpetic neuralgia
• Complex regional pain syndrome (CRPS) types 1 and 2
• Postsympathectomy neuralgia

45. MOA
• Prolongs inactivated state of VSSC
• Reduction of neuronal hyperexcitability
• Stabilizing the neural membrane.
h
PROLONGAT
I
ON OF
Na
·CHANNEL
INACTIVATION
Phenytoin

46. Dose -
• Phenytoin is supplied as 30- and 100-mg capsules.
• The recommended dosage is up-to 300 mg/day.
• An exact dosage needed to achieve adequate analgesia has not been
define

47. Metabolism-
• Absorption orally is slow and variable
• peak concentrations - 3 hours or as long as 12 hours.
• 90% bound to plasma proteins
• Metabolized primarily by the liver.
• Half-life of 20 to 60 hours at therapeutic concentrations.
• Narrow therapeutic window and its short- and long-term side effects
limit use.

48. Adverse effects of Phenytoin
·a
-A
-
t the-
rap
-
eu
-
tic levels
a Gum hypertrophy
a Hirsutism
a Hypersensitivity reactions
a Megaloblastic anaemia
a Osteomalacia
a foetal hydantoin syndrome(hypoplastic phalanges, cleft
palate, hare lip, microcephaly)
a At high plasma levels (dose related toxicity)
a (a) Cerebellar and vestibular manifestations:ataxia,
vertigo, diplopia, nystagmus.
CBCs, LFT
s, and serum drug levels need to be closely monitored

49. CARBAMAZEPINE
Uses
•Trigeminal neuralgia
• Best neuropathic analgesic for lancinating or electric-like pain.
• Other neuropathic pain syndromes such as
• GPN, DPN& pain syndromes A/W multiple sclerosis.
• M igraine headaches in pediatric populations

50. Open
Na+
Inactivated
Na+
Na+
A = activation gate
I = inactivation gate
Carbamazepine G) Lamotrigine
phenytoin Na+ valproate
binds to VSSNin their inactive conformation thus prevents repetitive and
sustained firing of an action potential

51. Dose
Available as 100-mg chewable tablets
100-, 200-, and 400-mg extended-release tablets
100 mg/5 m l suspension.
• Starting dosage between 100 and 300 mg/ day
• Dose can be slowly increased over several weeks as needed to a
maximum total dose of 1200 mg/day

52. Metabolism-
• Slow absorbed orally, Active metabolite - 10,1 1
-epoxycarbamazepine
• Peak concentrations - 4 to 8 hours but may be delayed 24 hours
• 75% bound to plasma proteins.
• Half-life is between 10 and 20 hours.
• Narrow therapeutic window.

53. S
/E-
• Agranulocytosis and aplastic anemia ( advised to report episodes of fever)
• Hypersensitivity reactions , Stevens-Johnson syndrome
• liver failure.
• hyponatremia
• A baseline CBCand LFT
s should be obtained
• Frequent monitoringthereafter, particularly in the first 6 months.

54. OXCARBAZEPINE
• Chemically similar to carbamazepine
• trigeminal neuralgia.

55. Oxcarbazepine versus carbamazepine
• OXC is similar lo CBZ in its anti-epileptic efficacy and
main mechanism of action.
• OXC is better tolerated and has fewer interacl ons with
other drugs becausei
t does not undergo metabolism to
epoxide.
• OXC does not I
nvolve hepatic CYP enzymes for i
ts
metabolism.
• OXC has al
oweri
ncidence of idiosyncratic reactions than
CBZ.
• Hyponatremla Is more common with OXC.

56. NUMBER NEEDED-TO-TREAT (NNT)
• T
o obtain a clinically meaningful response to treatment
• Lower NNT suggests better efficacy, higher doses associated with
lower NNT
s
Table lit
S e1n
;itk rcYlewso( nlk?pUepdc drug. (or paintcllc:(
Cond
i
tion RC(
('rCnct' Study Drug (No.'J'rials) NNT
Varlou<
.t neuropa1hlc [23) G1
.!Y.lpenlln (l•i) 4.3-6.4
condJUons Pr"S"b:alln (14) 3.8-il.8
·
rrigc1nln1tl ncur;ilgla [87) Carban1a1;cplnc(2) 1.4-2.8
P
osdw"
. f)>elicnt'
.Uralgi;i [s9r Prcg;obolln )300-600mg)(8) 3.9-5.31
[60) Gob:apcnlln (4) 4.. -7
.
71
Diabt.-c.k:neurop:ithy [5
9) Prcg;itx.Un.300-600
n1
g(17)
S-l l t
[60) G1
.hllpt
'1uln(a) 4.
7-281
Ccntr.alncUrQi)alhlc
pain
[5
9) Pr<s'l>llln,600mg(2) 35
-14

58. Antidepressa nts as Analgesics
TRICYCLIC ANTIDEPRESSANTS
• Amitriptyline
• Clomipramine
• Desipramine
• Dothiepin
• Doxepin
• lmipramine
• Nortriptyline

59. MOA of Antidepressants
.-.......
•
·
-
-
-
J!HT)
-
--
-

60. Site of action of Anti-depress ants in pain
- ,
- - t
---
TCA'S
SNRI
SSRI

61. Indications
• Post-herpetic Neuralgia
• Painful Diabetic Neuropathy
• Painful Mononeuropathy and Polyneuropathy
• Pain Associated with Spinal Cord Injury
• Fibromyalgia
• Osteoarthritis
• Low Back Pain
• Cancer-Related Neuropathic Pain
• HIV related Sensory Neuropathy

62. Analgesic effects of TCAs:
• Occur more rapidly (a week or less after initiating TCA therapy),
• At lower serum blood levels
• At lower doses than those used for antidepressive effects.
• Pain-relieving properties can be observed at much lower doses, even
1/ l Oth to 1/30th of their FDA-approved maximum.

63. Mode of Action of Tricyclic Antidepressa nts
EFFECTS MODE OFACTION
Serotonergic
Noradrenerg
l
c
Opioidergie
N Methyl·D·aspartatc
(NMDA) receptor
Adenosine receptor
Sodium channel
C.alc:lum channel
Other receptors
I
nterferes with serotonin reuptakeAlters serotoninbinding to
receptors I
nteractswith n2 adrenoreceptors
Modifies opioid receptor densit es
I
ncreases opioid levelsin some brain areas
Bindsto the NMOA receptor complex Alters NMDA binding character stics
Inhibits adenoslne uptake
Bloc.kssodium channels
l
ntteases det1
.s1t esof L type cale:lumchannels
Inhibits histam
i
n c, cholinergic, muscarinic,and nicotinic receptors

64. S/E-
• Sedation
• Constipation
• Dry mouth
• Sexual dysfunction
• Weight gain
• Arrhythmogeni c and may induce seizures in overdose
• Risk for major fetal malformation.

65. Con1mon side effects associated Vith
tricyclic antidepressants
I
Seda1lon Anti·
chollnitrglc
effects
Hypo•
tension
Cardiac
cffetts
Seizures Weig
gain
•••
•• •
•
Oeslpramlne 01•
• • •
• • •
Nonrlptyl no
• • • •
• • •
O
-
t1d11lm
:
..i:••11lfhl; _..._..m11Cltr11lr, ++-11tedtt•ltl
)'UlTf ""
n--(.
'...,....-
(
ak
-.-. ,,,.,..
ltaitlfff'w"'fwwtln.,. "11!1M.

66. Antidepressants Used for Neuropathic Pain
Anlldepressant Suggested Dose for Neuropathlc Pa n
Secondary-Amine TCAs
Deslpramlne
Nonriptyllne
1025 mg/day; tttrate up 10300 mg/day
10
·
150 mg/day
T
ertlary Amlne TCAs
Amllrfptyllne
lm
lpramlne
10-25 mg/day; utrateup to 150 mg/day
t0·150 mg/day
SNRls
Duloxet1ne
Venlafaxlne
60·120mg/day
lnlhally 37.5·75 mg/day; meandose
225 mg/day: max 375 mg/day
• .rx· "''" "''*"';S/'1
lRt ,,,.
,,,,,,.,,""
!
""
'"'""' ""l''"'k
"
"11
t1'1l
n111r: r<:A
tntyt/1t iilffll it / ttYMNI
• usr"' " '- '·UNif111/0t-dM/M 1/w-tottuldk-.1"Pft(eilllilNuL J:JdnJ.Glffbood -1
0
11.iat.CO.
T"""nHm Mirr-f'dn; 'IWT

67. SELECTIVESERO
TONIN REUPT
AKE INHIBITORS
• Citalopram
• Escitalopram
• Fluoxetine
• Fluvoxamine
• Paroxetine
• Sertraline

68. Uses-
• Shown little effect on most types of pain
• Painful Diabetic Neuropathy
• Fibromyalgia
• Chronic pelvic pain

69. Dose-
• Sertraline -started at 25 mg/day and increased by 25- to 50-mg increments.
• Citalopram - Initial dose of 20 mg once daily- 40 mg/day
-?Doses above 40 mg/day are not recommended (risk of QT prolongation).
• Escitalopram- twice as potent. ,,, started at 10 mg
• Trazodone's - 400 mg in divided doses

70. - Maximum daily dose
rluoxc:tlaie 8-0""
? l
1
U1
il.
"°""
20""
3 r.
.... . , _
•• Scra-
.tlil!c
..
r MO'tlll
C
'
'°""
JOOmi:
6 r1
"'uu
..m.iot

71. • Dry mouth
• Daytime sedation
• Insomnia
• GI upset (particularly with sertralir
• Const ipation
• Tremors
• Weight gain
• Sexual dysfunction (decreased libido, decreased arousal, anorgasmia)
• increased risk for major fetal malformation
S
/E-
Adverse Effects Of SSRis
_,. SINflilllllllwltt :
1
... --·
. .....,...._.,
.........._
...v........
; r . ...

72. Serotonin syndrome -
• SSRls with monoamine oxidase inhibitors (MAOls) -serotonin syndrome.
• Hyperserotonemia
• C/f: -agitation or altered mental status,diarrhea, hyperthermia, ataxia,
myoclonus, hyperreflexia, and autonomic instability.
• Rx.-supportive, but cyproheptadine may be used to block further
serotonin production.

73. SEROTONIN -NOREPINEPHRINE REUPTAKE
INHIBITORS
• Ouloxetine
• M ilnacipran
• Nefazodone
• Venlafaxine
D rugn.tme S-HT:NE uptake
lnh1
bltk>n . . .do
V,,,,bhxine
Dulc»cedne
Desvenbbxlne
AmitriptyltnO
Milnxlpran
10:1••
10:1"
10:1"
$;1. .
t:Jtt
• Duloxetine is the first antidepressant to have a specific pain indication

74. Uses-
• Painful Diabetic Neuropathy (Duloxetine)
• Fibromyalgia (Duloxetine)
• Degenerative arthritis

75. MOA-
• Inhibit reuptake of serotonin but also norepinephrine from the
synaptic cleft.
Dose-
• Duloxetine may be started at 20 or 30 mg and then increased to 60 mg
after 1 week.
SNR/s
Ouloxe1
1n
e
Ven
l
alaxlne
60·120mg/day
ln
l
lfally37
.
5·75 mg/day; mean dose
225 mg/day; max 375 mg/day
-...n •""· 1VRI· KNUt1t1#·'"1Wft1Hp riM r r .,tJ.h 1#/.1'1tt•r: l'CA
tnrtrlk "
•'"'"
I
Y
'
A
J
l
ll.

76. Adverse effects:
• similar to those of the SSRls.
• Nausea (particularly with duloxetine in the first week)
• hypertension (particularly with venlafaxine), and diaphoresis.
• Do not combine SNRlswith MAOls and use caution with tramadol, SSRls.

77. Systematic reviews of antidepressant drugs for neuropathic pain
Condition Ref. Study Drug (No.Trials) NNT
Various neuropathic [691 Amitri ptyline (lO) 2.5-4.2
conditions Desipramine (2) 1.
9-4.5
lmipramine (3) 1.7-3.2
Various neuropatllic [231 TCAs (23) 1.9-3.8
conditions SSR
!
s(4) 3.
9-27
SNR!s(7) 3.
4-14
Diabetic neuropathy (491 Duloxetine (3) 5-10

78. Pain Treatment Guidelines Regarding
Antidepressant Drugs
P'allllll WiC'tCtlt0fll¢
111
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81. Th.ankyou