1

BAB 1
PRELIMINARY

1. Background
Pain can be described as a sensory and emotional experience unpleasant
associated with tissue damage that has or could potentially occur, or explained on
the basis of such damage. This definition pengkorelasian avoid pain by a stimulus
(stimulus). This definition also emphasizes that pain is subjective and is a
sensation at once emotions.1,2,3
In pathological pain grouped on adaptive pain or acute pain or nociceptive
pain and maladaptive pain as chronic pain are also referred to as neuropathic pain
and psychological pain or idiopathic pain. Acute or nociceptive pain caused by
tissue damage, is one of the signals to accelerate the repair of damaged tissue.
Whereas neuropathic pain referred to as functional pain is an abnormal sensory
processing disorder, also known as an alarm system. Idiopathic pain which is not
associated with pathology both neuropathic and nociceptive and display
symptoms such somatoform disorders meet the psychological stress, depression,
anxiety, etc.1,2,3
Classification of chronic pain are classified in three categories: pain
caused by disease or damage to the network itself (pain nociceptive, such as
osteoarthritis), pain caused by disease or damage to the somatosensory system
(neuropathic pain), and a combination of pain nociceptive and neuropathic ( joint
pain).1,2,3
International Association for the Study of Pain (IASP) defines neuropathic
pain is pain resulting from disease or damage of the peripheral or central nervous
system, and come from dysfunction of nerve system. Initially, neuropathic pain is
used only to describe the pain associated with peripheral neuropathic and central
pain in lesions in the central nervous system that is associated with pain.
Neurogenic pain concerns all causes, both peripheral and central.1,2,3

Neuropathic pain is defined as pain due to nerve tissue lesions either

peripheral or central can be attributed to several causes such as amputation, toxic
(due to chemotherapy) metabolic (diabetic neuropathy) or infections such as
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shingles also in post-herpetic neuralgia and others. Neuropathic Pain can arise
spontaneously (without stimulus) as well as with the stimulus or a combination.1,2,3

BAB 2
LITERATURE

2.1 Definition
Pain post herpeticum (Post herpetic neuralgia = NPH / Post Herpetic
Neuralgia = PHN) is a persistent pain that comes after Shingles rash has healed
(usually within one month). This pain occurs along the nerve fibers that follow the
pattern of segmental rash of Herpes Zoster.3
Neuralgia is characterized as pain, burning, or pain disetetik cut that last
for months or even can be up to several years. Dworkin, 1994, defines neuralgia
post herpetika as neuropathic pain that persists after rash onset (or 3 months after
healing of herpes zoster). The most common definition used is the definition
 3

according to Dworkin. In accordance with the previous definition, the The

International Association for the Study of Pain (IASP) classifies neuralgia post
herpetika as chronic pain is pain that arises after the healing is over or pain that
lasts more than three months without malignitas.4
NPH is generally defined as pain that arises more than 3 months after the
onset (early symptoms) zoster eruption occurs. Pain is generally expressed as a
burning sensation (burning) or punctured-puncture (shooting) or pruritus (itching).
This pain is also associated with more severe symptoms more like disestesia,
paresthesias, hiperstesia, allodynia and hyperalgesia. In patients with NPH,
usually there is a change of sensory function in the affected area. In one study,
almost all patients have the eruption area which is very sensitive to pain, abnormal
sensation to light touch, pain or temperature on the affected skin area. Pain is
generally precipitated by movement (mechanical allodynia) or a change in
temperature (thermal allodynia). While the other study revealed that the degree of
sensory deficits associated with severe pain. In addition, patients with NPH are
more likely to experience sensory changes than patients with zoster neuralgia
cured without.5

2.2 Prevalensi
In the United States, the frequency of PHN which occurred one month
after onset was reported as much as 9 to 14.3%, and 3 months after the onset of as
much as 5%, while within 1 year, 3% will experience more severe pain.5
Incidence varies by age and immunological status, range from 0.4 to 1.6
cases per 1,000 population below normal at the age of 20 years, and 4.5 to 11
cases per 1,000 population of normal at the age of 80 years or lebih.7 A study in
Iceland showed that the risk variation PNH is associated with a particular age
group. Of the sample showed that no samples were aged under 50 years were
reported suffering severe pain, and patients older than 60 years reported
experiencing more severe pain: 6% 1 month after onset, and as much as 4% 3
months after onset.5
The second attack risk as high as the risk that occurred in the first attack.
The number of events several times higher than in adult patients with HIV
 4

infection or in patients with malignancy and 50 to 100 times higher in children

with leukemia compared with healthy people of the same age. The risk of post-
herpetic pain increased as age. The incidence of post-herpetic pain increased in
patients with Zoster Ophtalmic and possibly higher in women than in men.6

2.3 Etiology
Post herpetic neuralgia caused by herpes zoster virus infection. Varisella
zoster virus is one of the eight herpes viruses that infect humans. This virus
belongs to the family Herpesviridae. The structure consists of an icosahedral virus
nucleocapsid surrounded by a lipid sheath. Ditengahnya are double-stranded
DNA. Varisella zoster virus has a diameter of about 150-200 nm. The primary
infection is clinically known as Varicella (chicken pox), generally occurs in
children. Virus types that are pathogenic in humans is herpes virus 3 (HHV-3),
also called the varisella zoster virus (VZV) .7 This virus settles in a ganglion
posterior edge of the nervous system and cranial ganglion mainly cranial nerve V
(trigeminal) on gasseri ganglion and the ophthalmic branch vervus VII cranial
(facial) ganglion genikulatum.
2.4 Pathophysiology
Primary infection varisella zoster virus known as varicella or chicken pox.
First exposure usually occurs in childhood. This virus enters the body through the
respiratory system. In the nasopharynx, varisella zoster virus replicates and
spreads through the bloodstream, causing viremia with manifestations of skin
lesions scattered throughout the body. The incubation period of about 14-16 days
after the initial exposure. After primary infection passed, the virus lodged in the
dorsal root ganglia, live dormant for years.2,3,7
Pathogenesis of herpes zoster is caused by reactivation of the virus
varisella zoster who live dormant in the ganglion. Cellular immunity plays a role
in the prevention of recurrent clinical appearance of varicella zoster virus by an
unknown mechanism. The loss of cellular immunity against the virus by age or
status imunokompromis reactivation associated with clinical. When reactivation,
the virus runs along the axon to the skin. On the skin inflammation process and
has undergone partial denervation. In epidermal cells, the virus replicates causes
 5

swelling, vacuolization and lysis of cells that result from this process is formed
vesicles known as the 'Lipschutz inclusion body'.2,3,7

Picture 1 : Patologi Herpes Zoster7

Post herpetic neuralgia have different pathophysiology with acute herpes zoster
pain. NPH, a complication of herpes zoster, is a neuropathic pain syndrome
resulting from a combination of inflammation and damage caused by viruses in
primary afferent sensory nerve fibers. Following the resolution of primary
varicella infection, the virus stays dormant in sensory ganglia. The virus is
reactivated or reactivated, herpes zoster manifests as acute, and is associated with
damage to the ganglion, primary afferent nerves, and skin. Studies histopathology
showed fibrosis and loss of neurons (the ganglion dorsal), scarring, and loss of
axons and myelin (the peripheral nerves involved), atrophy (of the dorsal horn of
the spinal cord), and inflammation (around the spinal cord) with infiltration and
the accumulation of lymphocytes. In addition, there is a reduction in large-
diameter nerve inhibitor and a small increase in neuronal excitation, peripheral
nerves.8,9
The mechanism of post-herpetika neuralgia can be different for each
individual so that the manifestation of pain associated with neuralgia
 6

pascaherpetika also different. Replication of the virus in the dorsal root ganglion
causes an inflammatory response in the form of swelling, hemorrhage, necrosis
and cell death of neurons. The journey of this virus causes damage to the nerves.
Inflammation of the peripheral nerves can take several weeks to several months
and can cause demyelination, degeneration wallerian and process sclerosis.6,7
Then the virus will spread centrifugally along the nerves leading to the
skin, causing inflammation and damage to peripheral nerves. Sometimes the virus
spread centripetal direction of the spinal cord (the sensory and motor areas) as
well as the brain stem. This causes sensitization or deaferenisasi peripheral and
central neural elements.10

Picture 2 : Desensitasi dan Deaferenisasi

Peripheral nerve sensitization mainly occurs in nociceptors C nerve fibers

are smooth and not bermyelin. This sensitization causes sensory threshold to
temperature decreases, causing heat hyperalgesia, which is like a burning pain.
There was also an outbreak of nociceptors C ectopic damaged causing allodynia,
which is pain due to a stimulus which in normal circumstances do not cause pain.
In response to the disappearance of most of the C nerve fibers input for the
damage, formed shoots A nerve fibers that receive stimuli non-noksius
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mekanoseptor in the superficial layer of the dorsal horn of the spinal cord. This
causes the budding relationship between A nerve fibers that does not conduct
pain with nerve fibers C, so it does not cause pain stimuli (light touch) are
perceived as pain.10
In addition to the peripheral sensitization of central sensitization may also
occur that cause spontaneous pain or pain that is provoked, such as allodynia and
hyperalgesia. Central sensitization caused by ectopic activity of afferent nerve
fibers. The main excitatory neurotransmitter in the spinal cord is glutamate binds
to the receptor N-methyl-D-aspartate (NMDA). Glutamate is produced by primary
afferent nerve fibers in the dorsal horn. In the resting state of glutamate activates
receptors ionotropik -amino-3-hydroxy-5-methyl-4-isoksazol propionate
(AMPA) receptor Kainat, and receptors metabotropik glutamate (mGluRs),
whereas NMDA receptors are blocked by magnesium ions thus preventing the
entry of ions sodium and calcium that will occur when glutamate binds to the
NMDA receptor. Pascasinap repeated activation will cause the summation
potential and the synaptic membrane depolarization progressive. This causes the
NMDA receptor freed from a block of magnesium ions which in turn causes an
influx of cations into the cell and membrane depolarization increasingly
progresif.5,9 Neuralgia pascaherpetika can also occur due to the deaferenisasi,
namely the loss of afferent sensory nerve fibers both large and small diameter ,
Lesions of the peripheral or central nerve fibers can stimulate remodeling and cell
membrane hyperexcitability. Lesions that are still connected to the body cells will
form new shoots. New shoots have nothing reaches the target organ, while not
reaching the target organ will form neuroma, at neuroma will accumulate various
ion channels, especially channels, sodium ions, molecules transducer and
receptors of new, so it will eventually lead the occurrence of ectopic burst,
mekanosensitivitas abnormal sensitivity to temperature and chemicals. Ectopic
burst and sensitization of various receptors will cause spontaneous pain and pain
provoked. Spontaneous burst on central neurones that terdeaferenisasi will cause
constant pain in the area.3,4,8,10
 8

Picture 3 : Central sensitization mechanisms and Peripheral

At autopsy of patients who have had shingles and neuralgia post herpetika
found atrophy of the dorsal horn, whereas in patients with herpes zoster neuralgia
but did not experience post-herpetika not found atrophy of the dorsal horn.3,9

2.5 Clinical manifestations

Typical signs of herpes zoster in the prodromal phase is pain and
parasthesia in areas affected dermatome. Dworkin post herpetic neuralgia split
into three phases:1,9,11
1.
Acute phase: phase concomitant pain / accompanying skin lesions. It usually
lasts <4 weeks.
2.
F 2. Subacute Phase: Phase pain persists> 30 days after the onset of skin
lesions but <4 months.
3.
N Post herpetic neuralgia: where pain persists> 4 months after the onset of
skin lesions or lesions 3 months after healing of herpes zoster.
In general, people with herpes zoster visit to the doctor dermatologist
because of the presence of bubbles herpes. Complaints of patients accompanied
by a sense of fever, headache, nausea, weak body. 48-72 hours later, after the
prodromal symptoms arise erythematous maculopapular lesions unilateral
dermatomal skin and quickly transformed into vesicular lesions. Pain arising on
 9

an intensity that varies from mild to severe that only a light touch causes pain that
is so disturbing sufferers. After 3-5 days of early skin lesions, lesions usually will
begin to dry. The duration of the disease is usually 7-10 days, but usually for skin
lesions returned to normal may take up to weeks.1,8,11
This disease can be very annoying sufferers. Sensory disturbance caused
exacerbated by stimulation of the skin with the result hiperestesia, allodynia and
hyperalgesia. The pain experienced can disrupt the work of the patient, sleep even
mood so that pain can affect the quality of life of short-term and long-term
patients. Pain may be felt a few days or a few weeks before the onset of skin
eruption. The most commonly reported complaint is pain as burning, paresthesias
that may be accompanied by pain (disestesi), hiperestesia which is exaggerated
pain response to stimuli, or pain like exposed / electric shock. Pain itself be
provoked partly by stimulus light / normal (allodynia), flavor-gata unbearable
itching and pain that continues to grow in response to repeated stimuli.1,8,11
During the herpes incased bubbles become dry, the pain began to suffer
from severe pain that is felt on exposed skin areas. Severe pain that is neuralgik.
Where the pain is very hot and sharp, painful nature of this neuralgik neuralgik
resembles idiopathic pain, especially in the case of attacks that appear every attack
arrived - arrived and each attack consists of a group of attack - small and large
attacks. People sick with headaches behind or above the ear and unwell. But when
people come before the bubble - the bubble herpes arise, to predict that it will
appear herpes is difficult. The difference with idiopathic trigeminal neuralgia are
the symptoms of sensory deficits. And the paradoxical phenomenon that is the
hallmark of post herpatik neuralgia, namely anesthesia in place - the place where
the herpes but at the onset of an attack of neuralgia, precisely where the anesthetic
herpes -the former was perceived as the most painful. Neuralgia post herpatik
often occurs in the face and head. If there is in the forehead called neuralgia
postherpatikum oftalmikum and in the ear neuralgia postherpatikum otikum.1,8,11
Classical clinical manifestations that occur in the prodromal symptoms of
shingles are burning, itching with mild to moderate skin according to the affected
dermatome. Patient complaints usually accompanied by a sense of fever,
headache, nausea, weak body. 48-72 hours later, after the prodromal symptoms
 10

arise erythematous maculopapular lesions unilateral dermatomal skin and quickly

transformed into vesicular lesions. Pain arising on an intensity that varies from
mild to severe that only a light touch causes pain that is so disturbing sufferers.
After 3-5 days of early skin lesions, lesions usually will begin to dry. The duration
of the disease is usually 7-10 days, but usually for skin lesions returned to normal
may take up to several weeks. The intensity and duration of the eruption of the
skin due to herpes zoster infection can be reduced by administration of acyclovir
(5x800mg / day) or with famciclovir or valacyclovir. Clinical manifestations of
post herpetika neuralgia is a disease that can be very annoying sufferers. Sensory
disturbance caused exacerbated by stimulation of the skin with the result
hiperestesia, allodynia and hyperalgesia. The pain experienced can disrupt the
work of the patient, sleep even mood so that pain can affect the quality of life of
short-term and long-term patients. Pain may be felt a few days or a few weeks
before the onset of skin eruption. The most commonly reported complaint is pain
as burning, paresthesias that may be accompanied by pain (disestesi), hiperestesia
which is exaggerated pain response to stimuli, or pain like exposed / electric
shock. Pain itself be provoked partly by stimulus light / normal (allodynia),
flavor-gata unbearable itching and pain that continues to grow in response to
repeated stimuli.1,8,11

2.6 Diagnosis
2.6.1 Anamnesis
Painful vesicular eruption accordance with dermatom area is the typical
symptom of shingles. Along with the resolution of the skin eruption, pain arises
continues until 3 months or more, or what is known as post-herpetic pain. This
pain is often described as burning, stabbing tingling, itching or shock.7,12
2.6.2 Physical examination7,12
1. Headache, which arose as a response of viremia
2. The emergence of the flushing area after 2-3 days
3. Areas previously infected with herpes zoster may be a cutaneous scarring

4. Sensations may include hypersensitivity to touch and temperature, which

often misdiagnosis as myositis, pleuritik, as well as cardiac ischemia, as
well as itching and numbness that misdiagnosis as urticaria
 11

5. Appears blister containing pus, which will become crusts (2-3 weeks
later)
6. Crusts are healed and the disappearance of itching, but the pain appears
not lost and settled in accordance nerve distribution (3-4 weeks later).
7. Allodynia, which is caused by non-noxious stimuli, such as light touch
8. Changes in the function of anatomy, such as increased perspiration in the
area affected by this pain.
2.6.3 Supporting investigation
Pemeriksaan penunjang yang dapat dilakukan, yaitu: 7,12
1. Neurological examination of the trigeminal nerve and other
neurological examination.
2. Electromyography (EMG) to look at the electrical activity in nerve
3. Cerebrospinal fluid (CSF) abnormal dlm 61% of cases
4. Pleocytosis found in 46% of cases, an increase of 26% protein and
22% of cases of VZV DNA.
5. Pleocytosis found in 46% of cases, an increase of 26% protein and
22% of cases of VZV DNA.
6. Viral culture or immunofluorescence staining can be used to
differentiate herpes simplex with herpes zoster
7. Measuring antibodies to herpes zoster. 4-fold increase in the diagnosis
of herpes zoster subclinical support.

2.7 Management
In general the therapy we can do against cases of patients with post-
herpetika neuralgia is divided into two types, namely non-pharmacological
therapy and pharmacological therapy.1,13
a. Therapy farmakologis:1,13
1. Antivirus
The intensity and duration of cutaneous eruption and acute pain in herpes
zoster arising from viral replication can be reduced by administration of
acyclovir, Valacyclovir, famciclovir. Acyclovir is given with the
recommended dosage of 5 x 800 mg / day for 7-10 days given in the first 3
days since the side muncul.Efek lesions that can be found in the use of this
drug are nausea, vomiting, headache, diarrhea, dizziness, weakness,
anorexia, edema, and sore throat. Valaciclovir given the recommended
dosage of 1 mg / day orally for 7 days. The side effects can be found da;
 12

lam use of this drug are nausea, vomiting, headache, and abdominal pain.
Famciclovir given the recommended dosage of 500 mg / day for 7 days for
7 days. The side effects in the use opbat are nausea, vomiting, headache,
dizziness, pain.
2. Analgesik
Systemic therapy is generally symptomatic, given analgesics for pain. If
accompanied deberikan secondary infection antibiotics. Non-opioid
analgesics such as NSAIDs and paracetamol have peripheral and central
analgesic effect although little effectiveness against neuropathic pain.
While the use of opioid analgesics provide better effectiveness. Tramadol
has been shown to be effective in the treatment of neuropathic pain.
Working as a mu-opioid agonist that also inhibits reuptake of
norepinephrine and serotonin. In a study, if the tramadol dose titrated up to
a maximum of 400 mg / day in 4 divided doses. However, the effect on the
central nervous system can lead to the occurrence of amnesia in the
elderly. It should be noted that the administration of powerful opiates
better devoted to cases of severe or refractory pain due to the effects of
tolerance and takifilaksisnya. The dose used a maximum of 60 mg / day.
1.22. Oxycodone is based on research showing a better effect than placebo
in relieving pain, allodynia, sleep disorders, and disability.

3. Anti epilepsi
Mechanism of action of epilepsy drugs No 3, ie by 1) modulates the
voltage-gated sodium channels and calcium channels, 2) increasing the
inhibitory effects of GABA, and 3) hinder the glutaminergik that are
excitatory transmission. Gabapentin works on axon terminals by
modulating the influx of calcium in calcium channels, resulting in a
bottleneck. Because works centrally, gabapentin can cause fatigue,
confusion, and somnolence. The recommended dose of 1800-3600 mg / d.
Carbamazepine, lamotrigine work on axon terminals by blocking the
sodium channels, resulting in a bottleneck. Pregabalin work resembling
gabapentin. Faster onset of action. Just as gabapentin, pregabalin, but not a
 13

GABA agonist binds to a subunit of voltage-gated calcium channel, thus

reducing calcium influx and release of neurotransmitters (glutamate,
substance P and calcitonin gene-related peptide) in primary afferent nerve
terminals. It said the provision of pregabalin has good analgesic efficacy in
cases of post-herpetika neuralgia, neuropathic pain diabetikorum and
patients with CNS due to spinal cord injury. Found also the result of
improvements in sleep and anxiety.
4. Anti depressan
Tricyclic anti-depressants suggest an important role in the case of post-
herpetika neuralgia. These drugs have a mechanism to block the reuptake
(retrieval) of norepinephrine and serotonin. These drugs can reduce pain
through inhibition of spinal nerves involved in pain perception. In several
clinical trials of drugs tricyclic antidepressants amitriptyline, reported 47-
67% of patients experienced a reduction in pain of moderate to very good.
Amitriptyline lowered nerve reuptake of norepinephrine and serotonin
both. by administering a tricyclic antidepressant such as amiitriptyline
with dose, 25-150 mg / d orally. These drugs will be more effective when
combined with phenitiazine. TCA has been proven effective in the
treatment of neuropathic pain compared to SSRIs (selective serotonine
reuptake inhibitors) such as fluoxetine, paroxetine, sertraline, and
citalopram. The reason may be due to TCA inhibits both serotonin and
norepinephrine reuptake, whereas SSRIs only inhibit the reuptake of
serotonin. TCA side effects such as sedation, confusion, constipation, and
cardiovascular effects such as conduction block, tachycardia, and
ventricular arrhythmias. These drugs also can promote weight loss,
lowering the threshold of stimulation seizures, and orthostatic
hypotension. Anti-depressants are commonly used for cases of neuralgia
pot herpetika is amitriptyline, nortriptiline, imipramine, desipramine and
more.
5. Topical therapy
Local anesthetics modify axonal conduction by blocking voltage-gated
sodium channels. Inactivation cause obstacles to the spontaneous ectopic
 14

impulses. These drugs work better if the damage to neurons occurs only
partially, the functions of nociceptors remained, and the amount of excess
sodium channels. Another mechanism is to modify the activity of NMDA.
Topical Lidocaine is a drug that is often studied with good results in
treating neuropathic pain. A study showed a good effect with the use of lidocaine
patch 5% for the treatment of NPH. This drug is placed on the symptomatic area
for 12 hours and released to 12 hours later. These drugs can be used for many
years and used as an additional therapeutic option in elderly patients. The use of
topical creams such as capsaicin quite widely reported. Capsaicin cream to date is
the only FDA-approved drug for post-herpetika neuralgia. Capsaicin affects the
sensory neuron fibers C (C-fiber). It is known that these neurons release
neuropeptides such inflammatory pain substantia P is initiated. With high doses,
capsaicin mendesensitisasi these neurons. But unfortunately capsaicin has the
effect of a burning sensation that often can not be tolerated wearer (1/3 patients in
the clinical trial).

b. Therapy non farmakologis 1,13

1. Akupunktur
Acupuncture is widely used as a treatment for pain relief. There are several
studies on acupuncture therapy for post-herpetika neuralgia cases.
However, these studies are still using the number of cases is not too much
and the therapy is also combined with pharmacological therapy.
2. TENS (stimulasi saraf elektris transkutan)
The use of TENS has been reported to reduce pain by partial to complete
in some patients with post-herpetic neuralgia. But the use of TENS-was
recommended only as an adjuvant therapy / extra besides pharmacological
therapy.
3. Vaksin
The use of vaccines to prevent Postherpertika neuralgia in the elderly were
age 60 years and older with a dose of 1 ml administered sub-cutaneous
turned out to be effective. Of the 107 people who suffered from neuralgia
post herpetika then given the vaccine was found to reduce pain caused up
to 66.5%.
 15

2.8 Prevention
How to prevent pain Post herpeticum this is to prevent the Zoster virus
infection sendiri.7 Prevention pascaherpetika neuralgia can be operated with a
combination of antiviral agents and aggressive efforts reduce acute pain in
patients with herpes zoster. This combination is expected to reduce nerve damage
and acute pain. Antiviral therapy should be initiated immediately after diagnosis,
and better if it started on the first three or four days. Antiviral therapy is expected
to stop the replication of the virus, so it will be shorter disease duration, and
decrease the incidence of neuralgia pascaherpetika. Antivirals can be used are
acyclovir, valacyclovir, or famciclovir. Analgesic therapy will reduce the pain
which is a major risk factor neuralgia pascaherpetika.9,10
Has developed preventive shingles vaccine recommended by the Centers
for Disease Control and Prevention (CDC) for those aged 60 years or more. In
clinical studies involving thousands of elderly aged 60 years or older, the vaccine
reduced the risk of shingles by 51% and the risk pascaherpetika neuralgia by 67%.
The protective effects of the vaccine were reported up to 6 years or even
lebih.9,11 In addition, the United States Advisory Committee on Immunization
Practices (ACIP) has recommended the elderly diatasumur 60 years to get the
shingles vaccine as part of routine health care. Oka-strain live vaccine has recently
been approved by the Food and Drug Administration to prevent Varicella.6,14

2.9 Prognosis
Pain syndrome that occurs in PNH is likely to slow denagn resolution. In
patients with PNH, most respond well to analgesic drugs, such as tricyclic
antidepressants, but in the majority of cases, the pain felt worse and do not
respond to treatment.5
Generally the prognosis is good, which is dependent on the maintenance
action early on. in general, patients with neuralgia post herpetika response to
analgesics such as tricyclic antidepressants. If there is a patient with persistent
pain and a long time and no response to medication therapy is needed advanced
search to look for appropriate therapy.5
 16

The prognosis ad vitam said bonam for post herpetic neuralgia does not
cause death. The damage that occurs locally and just disrupt sensory function.
Prognosis functionam said bonam ad for real improvements obtained after
treatment, and the patient can move as good as usual.5
Prognosis ad sanactionam bonam because although the risk of recurrence
HZ may still occur as described in the literature, as long as the patient has a good
body resistance may arise small back.5

BAB 3
CONCLUSION

Post herpeticum pain is a condition of pain is felt in the body that ever had
herpes zoster infection. Herpes zoster is a reactivation of the virus itself Varicella
dwelling in nerve tissue. NPH can be classified as acute herpetic neuralgia (30
days after the rash on the skin), subacute herpetic neuralgia (30-120 days after the
rash on the skin) and NPH (pain that occurs at least 120 days after the rash on the
skin).
NPH is more common in the elderly and people with weak immune. When
on aging, especially at the age of 60 years and above, or in a state of
imunokmpromise the herpes virus will be reactivated.
NPH occurs because of injury neurons of the peripheral nervous system or
central well. This injury resulted in peripheral and central neurons discharge
spontaneously hold while also lowering the activation threshold to produce pain
that does not fit on a stimulus that does not cause pain.
Clinical manifestations are often encountered is the pain as burning,
paresthesias that may be accompanied by pain (disestesi), hiperestesia which is
exaggerated pain response to stimuli, or pain like exposed / electric shock. The
management of this disease can be done with pharmacological and non-
 17

pharmacological therapies. Investigation of this disease is not very meaningful,

enough with the history and physical examination, diagnosis of this disease is
already established. The prognosis is not bad, can generally be cured with regular
therapy.

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