Case Report

HERNIATED NUCLEUS PULPOSUS

By:
Wahyu Wijayanti
1608438194

Supervisor:

dr. Riki Sukiandra, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL SCHOOL RIAU UNIVERSITY
RSUD ARIFIN ACHMAD
PEKANBARU
2018

KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN

 FAKULTAS KEDOKTERAN UNIVERSITAS RIAU
SMF/ BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000
E-mail : saraffkur@gmail.com
PEKANBARU

I. Patient’s Identity

Name Mr. BS
Age 25 years old
Gender Male
Address Surian Kampung Padang street – Rokan Hulu
Religion Islam
Marital Status Married
Occupation Entrepreneur
Entry Hospital October, 12th 2018
Medical Record 9983XX

II. ANAMNESIS :
Auto anamnesis with patient (October, 12th 2018)

Chief Complain
Lower back pain radiating to both of the leg since 10 days before admitted to the
hospital.

Present illness history

10 days before admitted to the hospital patient complained of back pain
radiating to both of the legs until the patient was difficult to walk and felt numb.
Pain is sharp and felt like a burning pain, intermittent, triggered by static sitting
and standing position. The intensity of the pain increased when sneezing or
coughing and didn’t decreased with rest. The numbness from the upper leg to toes
and feels intermittent. No complaints on the bladder and bowel. Fever before the
complaint denied, weight loss quickly denied, prolonged cough denied, and taking
drugs denied.

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 Back pain was first felt 3 month ago after lifting a heavy weigh. Pain felt
intermittent. Pain triggered when changes in body position such as bending or
lifting a heavy object. The intensity of the pain decreased with rest. Pain didn’t
radiating to both of the legs. Numbness (-).

Past Illness History

 History of fall from stairs 1,5 years ago on sitting position.
 History of backbone surgery (-).
 History of loss weight (-), paroxysmal diaphoresis and blood cough (-).

Socioeconomic History
 The patient working as a construction laborers, and often does a heavy lifting of
object.
 History of smoking (+), comsumes alcohol (-)

The Family Disease History

 No family history with the same complains.
 History of Tuberculosis (TB) in family denied.
 A history of cancer or tumors (-).

ANAMNESIS RESUME
Mr. BS, 25 years old came to hospital with chief complain of lower back
pain radiating to both of the leg since 10 days ago until the patient difficult to
walk. The pain is intermittent, triggered by static sitting and standing position.
The intensity of the pain increased when sneezing or coughing and didn’t
decreased with rest. The numbness from the upper leg to toes and feels
intermittent. Back pain was first felt 3 month ago after lifting a heavy weigh. Pain
felt intermittent. Pain triggered when changes in body position such as bending or
lifting a heavy object. The intensity of the pain decreased with rest. Pain didn’t
radiating to both of the legs. Numbness (-), history of trauma 1.5 years ago.

III. Physical Examination (October, 12th 2018)

A. Generalized Condition
Blood Presure : Dextra :130/70 mmHg, sinistra : 130/70 mmHg

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Heart Rate : Dextra : 84 bpm, sinistra : 84 bpm, regullar
Respiratory rate : 22 x/I, type : abdominotorakal
Temperature : 36,7°C
Weight : 85 kg
Height : 170 cm
Body Mass Index (BMI) : 29,4 kg/m2 (Obesity grade I)
Numerical Rating Scale (NRS) : 6-7

B. Neurological status
1) Consciousness : Composmentis, GCS : E4V5M6
2) Noble Function : Normal, no interference with the function of
language, memory and orientation
3) Neck Rigidity : Negative
4) Cranial Nerves

1. N. I (Olfactorius )
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. N.II (Opticus)
Right Left Interpretation
Visual Acuity Normal Normal
Visual Fields Normal Normal Normal
Colour Recognition No test No Test

3. N.III (Oculomotorius)
Right Left Interpretation
-
Ptosis -
isokor
Pupil isokor
Round
Shape Round
Φ3mm Normal
Side Φ3mm
Pupillary reaction to light
+
direct +
+
Indirect +

4
4. N. IV (Trokhlearis)
Right Left Interpretation
Extraocular movement Normal Normal Normal

5. N. V (Trigeminus)
Right Left Interpretation
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal reflex + +

6. N. VI (Abduscens)
Right Left Interpretation
Extraocular Normal Normal
movement Strabismus (-) (-) Normal
Deviation (-) (-)

7. N. VII (Facialis)
Right Left Interpretation
Tic Motor (-) (-)
- Frowning Normal Normal
- Raised eye brow Normal Normal
- Close eyes Normal Normal
- Corners of the Normal Normal
Normal
mouth
- Nasolabial fold Normal Normal

Sense of Taste Normal Normal

8. N. VIII (Akustikus)
Right Left Interpretation
Hearing sense Normal Normal Normal

9. N. IX (Glossofaringeus)
Right Left Interpretation
Arcus farings Normal Normal
Flavour sense Normal Normal Normal
Gag Reflex Normal Normal

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 10.N. X (Vagus)
Right Left Interpretation
Arcus farings Normal Normal
Normal
Dysfonia - -

11.N. XI (Assesorius)
Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Normal Normal

12.N. XII (Hipoglossus)

Right Left Interpretation
Motoric Normal Normal
Trophy Eutrophy Eutrophy Normal
Tremor - -
Disartria - -

5) MOTORIC
Right Left Interpretation
Upper Extremity
Strength
Distal 5 5
Proximal 5 5
Normal
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Clonus (-) (-)
Lower Extremity
Strength
Distal 5 5 Normal, but
Proximal 5 5 Patient feels
Tone Normal Normal pain
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Clonus (-) (-)
Body
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-) Normal
Abdominal Reflex (-) (-)

6) SENSORY
Right Left Interpretation

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 Touch Normal Normal
Normal,
Pain Normal Normal
except the
Temperature No test No test
temperature
Proprioceptive
and vibration
 Position Normal Normal
test was
 Two point Normal Normal
difficult to
discrimination
assess
 Stereognosis Normal Normal
 Graphestesia Normal Normal
 Vibration No test No test

7) REFLEX

Right Left Interpretation

Physiologic
Biseps + +
Physiologic reflex (+)
Triseps + +
Patella + +
Achilles + +

Patologic
(-) (-)
Babinski
(-) (-)
Chaddock Pathological Reflex
(-) (-)
Hoffman Tromer (-)
(-) (-)
Openheim
(-) (-)
Schaefer

8) COORDINATION

Right Left Interpretation

Point to point movement (+) (+)
Walk heel to toe No test No test
Normal
Gait Normal Normal
Tandem No test No test
Romberg No test No test

9) AUTONOM
Urinate : Normal
Defecate : Normal
10) OTHERS EXAMINATION

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 a. Laseque : Limited mobility due to pain/ Limited mobility due to pain
b. Kernig : Limited mobility due to pain/ Limited mobility due to pain
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test :+
f. Naffziger :+
g. CVA : -/-

11). EXAMINATION RESUME (October, 12th 2018)

Generalized Condition
Blood Presure : 130/70 mmHg
Heart Rate : 84 bpm regullar

Respiratory rate : 22 x/minute, abdominothoracal

Temperature : 36,8°C
Weight : 85 kg
Height : 170 cm

Body Mass Index (BMI) : 29,4 (Obesity Grade I)

Numerical Rating Scale (NRS) : 6-7
Noble Function : Normal
Meningeal Sign : (-)
Cranial Nerve : Normal

Motoric : Normal
Sensory : Normal
Coordination : Normal
Otonom : Normal
Reflex
Physiologic : Normal
Patologic : (-)
Others Examination
a. Laseque : +/+
b. Kernig : +/+
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test :+
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 f. Naffziger : +

C. WORKING DIAGNOSE
CLINICAL DIAGNOSE : Lumbal Radiculophaty
TOPICAL DIAGNOSE : Ischiadica Nervus Radix
ETIOLOGICAL DIAGNOSE : Suspect Herniated Nukleus Pulposus regio
Lumbal
DIFFERENTIAL DIAGNOSE : Radiks Trauma

D. SUGGESTION EXAMINATION
 Blood routine
 Blood chemistry
 Lumbal Magnetic Resonance Imaging (MRI)

E. MANAGEMENT
1) Bed rest
2) Pharmacology
 Meloxicam 2 x 7,5 mg
 Omeprazole 1 x 40 mg
 Mecobalamin 3 x 500 mg
 Eperisone HCL 3 x 50 mg
3) Physiotheraphy

FINAL DIAGNOSE : Ischialgia bilateral et causa suspect HNP

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 DISCUSSION

1. Pain
1.1 Definition
The International Association for Study of Pain (IASP) defines pain as “an
unpleasant sensory and emotional experience” associated with actual or potential
tissue damage or described in terms of such damage. Pain classified as acute or
chronic. Acute pain is frequently associated with anxiety and hyperactivity of the
sympathetic nervous system (eg, tachycardia, increased respiratory rate and BP,
diaphoresis, dilated pupils). Chronic pain does not involve sympathetic
hyperactivity but may be associated with vegetative signs (eg, fatigue, loss of
libido, loss of appetite) and depressed mood. People vary considerably in their
tolerance for pain.

1.2 Mechanism of pain

There are four processes that occur on a trip that pain transduction,
transmission, modulation and perception.
1. Transduction, is an evolutionary process pain stimuli into an electrical activity
that will be accepted in nerve endings. This excitatory stimulation can be either
physical, chemical, or heat. And can occur throughout the pain pathways.
2. Transmission, is the process of distributing the electrical impulses generated by
transduction process along the lines of pain, where molecules in the synaptic
cleft transmit information from one neuron to the next neuron
3. Modulation, is the process of modification to stimuli. These modifications can
occur at all points of since the first transmission to the cerebral cortex. These
modifications may include augmentation (increase) or inhibitory (inhibitory).
4. Perception, is the process the last time it had reached the cortex stimulation so
as to achieve the level of consciousness, it is then translated and followed up in
the form of a response to the pain

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 Figure 1. Mechanism of pain

1.3 Classification and Pathofisiology

a) Acute pain , which usually occurs in response to tissue injury, results from
activation of peripheral pain receptors and their specific A delta and C
sensory nerve fibers (nociceptors).
b) Chronic pain related to ongoing tissue injury is presumably caused by
persistent activation of these fibers. However, the severity of tissue injury
does not always predict the severity of chronic or acute pain. Chronic pain
may also result from ongoing damage to or dysfunction of the peripheral or
central nervous system.
c) Nociceptive pain may be somatic or visceral. Somatic pain receptors are
located in skin, subcutaneous tissues, fascia, other connective tissues,
periosteum, endosteum, and joint capsules. Stimulation of these receptors
usually produces sharp or dull localized pain, but burning is not uncommon
if the skin or subcutaneous tissues are involved. Visceral pain receptors are
located in most viscera and the surrounding connective tissue. Visceral pain
due to obstruction of a hollow organ is poorly localized, deep, and cramping
and may be referred to remote cutaneous sites. Visceral pain due to injury of
organ capsules or other deep connective tissues may be more localized and
sharp. Nociceptive pain is generally because it prevents further injury and/or
promotes healing.
d) Inflammatory pain is maladaptive, pathologic with no protective function,
and results from tissue damage (eg, trauma, surgery, OA, and rheumatoid
arthritis). Damaged tissue inflammation and causing the function of various

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 components of nociceptive changed. Inflamed tissue secrete a variety of
inflammatory mediators, such as bradykinin, leukotrienes, prostaglandins,
purine and cytokines that can activate or sensitize nociceptors directly or
indirectly.
e) Neuropathic pain results from direct injury or dysfunction of the nervous
system, eg, postherpetic neuralgia, diabetic neuropathy, complex regional
pain syndrome, trauma, compression and poisoning toxins.
f) Functional pain is associated with abnormal neural processing in the
absence of neurologic deficit or peripheral abnormalities, eg, fibromyalgia
and irritable bowel syndrome. Characteristic of simple pain is the presence
of a positive correlation between the strength and perception of pain stimuli,
such as the stronger stimuli, the more severe the pain experienced. Of note,
there is usually an overlap between the different pain states (Table 1).

Table 1. Types of Pain and Their Characteristics

Nociceptive Pain
Transient pain in response to noxious stimulus
Arises from a stimulus outside of the nervous system
Pain proportionate to the stimulation of nociceptors
Serves as a protective function
Inflammatory Pain
Initiated by tissue damage and/or inflammation
Arises from a stimulus that is outside of the nervous system
Spontaneous pain and hypersensitivity to noxious stimulus
Disproportionate to the stimulation of nociceptors
Serves no protective function
Neuropathic Pain
Initiated or caused by a primary lesion or dysfunction in the nervous system
No nociceptive stimulation
Disproportionate to the stimulation of receptors
Other evidence of nerve damage (eg, postherpetic neuralgia)

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Functional Pain
Hypersensitivity to pain resulting from abnormal central processing of normal
input
No nociceptive stimulation or nervous system lesion
Data from Woolf CJ. Ann Intern Med. 2004;140:441-451.
Although inflammatory, neuropathic, and functional pain syndromes have
different causes, they have some common characteristics through similar pain
pathophysiology Tissue injury results in the release of a variety of
neurotransmitters from damaged and inflammatory cells, including macrophages,
mast cells, and lymphocytes. The punitive substances that are released from the
pain response are also referred to as a "sensitizing soup" and act to further
sensitize the nerve endings leading to peripheral sensitization. This inflammatory
response results in a reduced threshold of the pain receptors, ie, nociceptors; an
increase in response magnitude to further stimuli; an increase in spontaneous pain;
and an increase in the area from which stimuli can evoke action potentials. This
phenomenon is referred to as peripheral sensitization.
Peripheral sensitization increases the transmission of pain stimuli to the
dorsal horn of the spinal cord, which can amplify pain response. In addition, there
is modification of the neurons in the dorsal horn, which include changes in
transmission, receptors, and structural reorganization -- a phenomenon known as
central sensitization. Overall, peripheral and central sensitizations represent the
plasticity of the nervous system, wherein the nerves change their function and
structure to new functions in response to changing inputs, such as pain. This leads
to spontaneous pain without any noxious stimuli and expansion of pain beyond
the original site of tissue damage as well as exaggerated and/or prolonged
response to a noxious stimulus or evoked pain from stimuli that are usually not
painful (eg, light touch) (Table 2).

Table 2. Sensation of pain

Paresthesias Spontaneous sensations that are not unpleasant

Dysesthesias Spontaneous and unpleasant pain sensations
Hyperalgesia Stimulus-evoked heightened response to painful stimulus

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Allodynia Ongoing stimulus-evoked painful response to nonpainful stimulus
Data from Woolf CJ. Ann Intern Med. 2004;140:441-451.

1.4 Classification of Scale Pain

Pain is a very subjective matter which is influenced by psychological,
cultural and other things, so measuring the intensity of pain is a relatively difficult
problem. There are several methods commonly used to measure the intensity of
pain, among others:
a. Visual Analog Scale (VAS)
The scale is a straight line that extends 10 cm (or 100 mm), with verbal
depiction on each end. The score is divided into four categories:
• 0 = No Pain
• 1-3 = mild pain
• 4-6 = moderate pain
• 7-10 = severe pain

Figure 2. Visual Analog Scale (VAS)

b. Numerical Rating Scale (NRS)

This method uses numbers to describe the range of pain intensity.
Generally the patient will describe the intensity of the pain felt from the numbers
0-10 where starting from the number "0" is no pain and "10" is a great pain.

Figure 3. Numerical Rating Scale (NRS)

c. Verbal Rating Scale (VRS)
Patients were asked how the nature of the pain she felt. Score consists of
four points, namely:

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 • 0 = No pain or feeling unwell when asked
• 1 = mild pain were reported to the patient when asked
• 2 = moderate pain reported patient when asked
• 3 = pain associated with voice response, hands or arms, face
whimpering or crying
For patients with cognitive impairment, verbal pain scale is difficult to use.
d. Faces Pain Rating Scale
Widely used in pediatric patients with verbal difficulties or limitations.
Explained to the patients regarding appropriate changes to mimic facial pain and
select appropriate patients the pain she felt.

Figure 4. Faces Pain Rating Scale

1.5 Therapy
The pathophysiologic approach to pain classification has diagnostic and
therapeutic implications. Nociceptive and inflammatory pain syndromes are
generally responsive to analgesics, such as acetaminophen, nonsteroidal anti-
inflammatory drugs (NSAIDs, both nonselective [NS]-NSAIDs and
cyclooxygenase [COX]-2 selective inhibitors), and opioids; however, neuropathic
and functional pain syndromes often require the use of adjuvant analgesics, such
as anticonvulsants (eg, gabapentin and pregabalin) and antidepressants (eg,
tricyclic antidepressants [TCAs] and serotonin-norepinephrine reuptake
inhibitors). Because there is usually an overlap between pain states, optimal
therapy may require combining different drug therapies (Table 3).

Table 3. Mechanism of Action of Analgesics

Drugs Mechanism of Action

Acetaminophen Exact mechanism of action unknown. Proposed
mechanisms include a donor of a moiety of an

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 endogenous cannabinomimetic and activation of the
cannabinoid CB1 receptors in the central nervous system
Nonselective Inhibition of prostaglandin synthesis through inhibition of
nonsteroidal anti- COX-1 and COX-2 isoenzymes
inflammatory drugs
Cyclooxygenase Inhibition of prostaglandin synthesis through selective
(COX)-2 selective inhibition of COX-2 isoenzyme spares COX-1 isoenzyme
drugs
Tramadol Opioid receptor agonist and serotonin-norepinephrine
reuptake inhibitors
Opioids Opioid receptor agonists
Tricyclic Exact mechanism of action unknown. Proposed
antidepressants mechanisms include norepinephrine and serotonin
reuptake inhibition, H1 receptors, NMDA receptors, and
peripheral sodium channels
Serotonin- Norepinephrine and serotonin reuptake inhibition
norepinephrine
reuptake inhibitors
Local anesthetics Sodium channel blockade
Gabapentinoids Modulation of the alpha-2/delta-1 subunit of the voltage-
(gabapentin and dependent calcium channels in the dorsal horn of the
pregabalin) spinal cord
Capsaicin Irritation of peripheral nerve endings resulting in
peripheral nerve desensitization

2. Ischialgia or sciatica
2.1 Definition
Ischalgia or sciatica is a common type of pain affecting the sciatic nerve,
which extends from the lower back all the way through the back of the thigh and
down through the leg. Depending on where the sciatic nerve is affected, the pain
may also extend to the foot or toes. Usually only one side of the lower body is
affected.

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2.2 Ethiology
Ischialgia most commonly occurs when a herniated disk or a bone spur on
the spine compresses part of the nerve causing inflammation, pain and numbness
in the affected leg.
•Irritation of the roots of the lower lumbar and lumbosacral spine
•Lumbar spinal stenosis (narrowing of the spinal canal)
•Degenerative disc disease (breakdown of discs, which act as cushions between
the vertebrae)
•Spondylolisthesis (a condition in which one vertebra slips forward over another
one)
•Piriformis Syndrome.
 More rarely, the nerve can be compressed by a tumor or damaged by a disease
such as diabetes.

2.3 Risk factor

Risk factors for ischialgia include:
 Age. Age-related changes in the spine, such as herniated disks and bone spurs,
are the most common causes of sciatica.
 Obesity. By increasing the stress on your spine, excess body weight can
contribute to the spinal changes that trigger sciatica.
 Occupation. A job that requires you to twist your back, carry heavy loads or
drive a motor vehicle for long periods might play a role in sciatica, but there's
no conclusive evidence of this link.
 Prolonged sitting. People who sit for prolonged periods or have a sedentary
lifestyle are more likely to develop sciatica than active people are.
 Diabetes affects the way your body uses blood sugar, increases your risk of
nerve damage.

2.4 Symptom
 Pain - vary widely from a mild ache to a sharp, burning sensation or
excruciating discomfort. Sometimes it may feel like a jolt or electric shock. It

17
 may be worse when you cough or sneeze, and prolonged sitting can aggravate
symptoms.
 Tingling, weakness and numbness
 Difficulty moving the leg or foot

2.5 Diagnosis
 The most applied diagnostic test is the straight leg raise to produce , which is
considered positive if pain in the distribution of the sciatic nerve is reproduced
with between 30 and 70 degrees passive flexion of the straight leg. While this
test is positive in about 90% of people with sciatica, approximately 75% of
people with a positive test do not have sciatica.
 Imaging tests such as CT or MRI can help with the diagnosis of lumbar disc
herniation.

2.6 Treatments and drugs

 Medications: Anti-inflammatory, Muscle relaxants.
 Steroid injections: Corticosteroids help reduce pain by suppressing
inflammation around the irritated nerve.
 Surgery
 Physical therapy:
- Posture correction - Pay special attention to your core muscles — the muscles
in your abdomen and lower back that are essential for proper posture and
alignment.
- Back support
- Good body mechanics
- Exercise is usually better for relieving sciatic pain than bed rest. Patients may
rest for a day or two after their sciatic pain flares up, but after that time period,
inactivity will usually make the pain worse.
- Active exercise is important for the health of the spinal discs. Movement helps
exchange nutrients and fluids within the discs to keep them healthy and prevent
pressure on the sciatic nerve.
- Incorporate strengthening, stretching and aerobic activities -they are central
components of almost any sciatica treatment plan.
- Stretching is usually recommended to alleviate sciatic pain (Piriformis and
hamstrings)

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- Strengthen the spinal column and the supporting muscles, ligaments and
tendons,the abdominal muscles, gluteus and hip muscles. (McKenzie exercises
and Dynamic Lumbar Stabilization)
- Ultrasound– decrease healing time and relieve stiff and inflexible muscles by
improving the circulation and gently heating the muscles.
- Massage –deep and firm massage will not only help soothe those cramped
muscles but can actually make the nerves and ligaments both relax.
- Transcutaneous Electrical Nerve Stimulation – In some cases using a very
small and controlled amount of electricity can decrease the intensity and
number of muscle spasms and can help release pain blocking endorphins, much
like aerobics.

3. Herniated Nucleus Pulposus (HNP)

3.1 Definition
Herniated nucleus pulposus (HNP) is a disease in which bearings are
between vertebrae commonly called the nucleus pulposus is compressed at the
posterior or lateral, the compression causes the nucleus pulposus rupture resulting
protrusion through the annulus fibrosus into the spinal canal and lead to irritation
and suppression of nerve root irritation in the area of pain that menjalar.1 Here is a
painful nature of the HNP is:
1. Under an intermittent back pain (in a few weeks to several years). Pain spreads
in accordance with the distribution of the sciatic nerve.
2. Nature of the typical pain of lying to a sitting position, pain from the buttocks
and continue to spread to the back and then to the lower limbs.
3. Pain intensified as the originator of such movements of the waist when
coughing or straining, standing or sitting for long periods of time and reduced
pain with a rest.
4. Patients often complain of tingling (parostesia) or numbness even decreased
muscle strength in accordance with the distribution of innervation involved.
5. Pain increases when the area L5-S1 (the line between the two iliac crest) is
pressed

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 Figure 5 . Herniation of the nucleus pulposus

The spinal cord is part of the central nervous system which is entirely
located within the vertebral canal and surrounded by cerebrospinal fluid. In
humans there are 31 pairs of spinal nerves which each pair of these nerves going
into certain parts of the body segments. Here is the distribution segment of the
spinal cord:2
 8 pairs of cervical nerves (C1-C8)
 12 pairs of nerves thoracic (T1-T12)
 5 pairs of lumbar nerve (L1-L5)
 5 pairs of sacral nerves (S1-S5)
 1 pair of coccygeal nerve

Figure 6. The division of the spinal cord 2

The spinal cord ends at the conical medularis high as L1 or L2. Below this
level, there is a lumbar sac (teca) who just lack the nerve root filament called
cauda equina (horsetail). 3
The spinal cord consists of gray matter (grisea) and white matter (alba).
White matter containing the ascending and descending tracts, whereas gray matter

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contains various types of neurons; especially the anterior horn contains motor
neurons, particularly lateral cornua contain autonomous and dorsal horn neurons
containing mainly somatosensory neurons. Ascending tract is a tract in the body
that carry information to the brain such as excitatory touch, temperature, pain and
movement position and tract descenden are tracts that carry information from the
brain to the limbs and control functions of the body).2

Figure 7: Conus medularis and cauda equina 3

3.2 Etiology and Predisposition

Herniation of the discs intervertrebalis form protrusions of the annulus

fibrosus. Under normal circumstances the annulus fibrosus protect from the
location of the nucleus contained therein. In the event of herniation in the nucleus,
there is compression of the nerve pathways adjacent to the site of disc herniation
causing irritation, causing pain that can be called sciatica, if more severe to the
neuron system may occur to dysfunction .4
The HNP risk factor consists of changed and can not be changed the risk
factors, there are:
 Risk factors that can not be changed:
1. Age: increasingly higher risk age
2. Gender: male more than female
3. History of back injury or trauma
 Risk factors that can be changed:
1. Employment and activities: prolonged sitting, lifting or pulling heavy
items, often bending or twisting motion at the back, strenuous exercise,
exposure to constant vibration such as drivers.

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 2. Sports irregular, started training after a long practice, strenuous exercise in
the long term.
3. Smoking. Nicotine and other toxins can interfere with the ability of the
disc to absorb the necessary nutrients from the blood.
4. Excessive weight, especially extra weight in the abdominal area can cause
a strain on the lower back.

Figure 8. Figure the process of herniation

3.3 Pathophysiology
Factors that contributed to the HNP:
1. The reduced blood flow to discus.
2. Heavy load.
3. Narrows of the posterior longitudinal ligament.
If the increased load on the disc, the annulus fibrosus not hold the nucleus
pulposus (gel) will come out, there will be pain because the gel which is in the
root canal of the vertebral pressing. Buildings containing sensitive pain receptors
nociception (pain) provided stimulation by various local stimulus (mechanical,
thermal, chemical). This stimulus will be responded by spending a variety of
inflammatory mediators that will cause the perception of pain. Pain is the
protection mechanism aimed at preventing the movement so that the healing
process is possible. One form of protection is muscle spasm, which in turn can
lead to ischemia. Pain that arises can be a painful inflammation of the tissues with
the involvement of a variety of inflammatory mediators; or neuropathic pain is
caused by a primary lesion of the nervous system.
Neuropathic nerve fiber irritation can lead to two possibilities. First, the
emphasis only occurs in the nerve-rich membranes covering the nociceptors of
nervi nevorum by painful inflammation. Pain is felt along the nerve fibers and
nerve fibers grow by stretching for example because of the movement. The second
possibility, the emphasis on the nerve fibers. In this condition there is a change
biomolecular where the accumulation of Na ion channels and other ion. This

22
buildup causes mechanical stimuli heat very sensitive to mechanical and thermal
stimuli.4,5
Degrees of HNP :
1.Disc degeneration: a change in the composition of the annulus pulposus, so
that if there is a load nucleus pulposus stand to one side of the annulus fibrosus
is still intact, and no herniation.
2.Prolapse or bulging disc or disc protrution: going protrusion nucleus
pulposus and annulus fibrosus, the annulus fibrosus and posterior longitudinal
ligament is intact, already herniation and began suppression padaradix or spinal
cord
3.Extrusion disc: the annulus fibrosus rupture, so the gel of the nucleus
pulposus out from the intervertebral discs, but still intact posterior longitudinal
ligament.
4.Sequesteration disc: there has been a rupture of posterior longitudinal
ligament, so that the nucleus pulposus gel out through the gap heading into the
spinal canal ligaments.

Figure 9. Stage of disc herniation

Classification of Lower Back Pain (LBP)

The classification system that is simple and practical to the LBP can be
divided into three categories; LBP Non-Specific, LBP for Neurological Disorders
(canal stenosis and radiculopathy) and low back pain caused by a serious spinal
disease (red flags). The first priority in doing triage diagnosis during digging
anamnesis of patients is to identify the condition of the red flags and the
possibility of potential yellow flags.

LBP Non Specific6
- Age: 20-55 years
- The general state of the patient well.

23
 - Pain in the thigh area, buttocks and lumbosacral.
- Mechanical pain.

LBP for Neurological Disorders (canal stenosis and radiculopathy)6
- The existence of radicular pain / iscialgia.
- Pain spread to below the knee, not only on the back of the thigh.
- History pain / tingling old.
- Signs of positive LASEQUE.
- History of micturition disorders / defecation / sexual function.
- The existence of a back saddle anesthesia / hypesthesia.
- The weakness of the limbs and other styles disorders.

LBP caused by a serious spinal disease (red flags)6
Serious spinal pathological disorders include malignancies vertebrae,
spinal inflammation and cauda equina syndrome. Red flags are signs and
symptoms that may indicate the possibility of a serious spinal pathological
condition. Here is the criteria for red flags:6

Abnormality Red Flags

Cancer or infection  Age> 50 or <20 years

 History of cancer
 Weight loss for no apparent reason
 immunosuppressant therapy
 UTI, IV drug abuse, fever, chills
 Back pain does not better with rest
Vertebral Fractures  History of significant trauma
 Long-term use of steroids
 Age> 70 years
Cauda equina syndrome or  Acute urinary retention or overflow incontinence
severe neurologic deficits  Alvi incontinence or anal sphincter atony
 Saddle anesthesia
 Progressive paraparesis or paraplegia
Table 4. Red Flag on lower back pain

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 Yellow flags are factors that increase the risk for development of chronic
pain conditions and long-term disability. Factors related to work, psychosocial
stress, depressive mood, to influence the severity of pain and functional, episodes
of low back pain before, and hopes pasien.7
Clinical symptoms of lower back pain can be seen in the following table:

Table 5. Overview Pain in Various Diseases.

3.4 Diagnosis
a. Anamnesis
In anamesis obtained discogenic pain will increase when sitting, bending,
coughing, sneezing or activities that can increase intradiscal pressure. Then
watch out when to start of presentation, how to start the onset of complaints,
pain location, nature of pain, quality of pain, whether the pain suffered by
starting physical activity, factors that aggravate or extenuate, there is a history
of previous trauma and whether there are family people with the same disease.
It should also prompted complaints that lead to nerve lesions as their radicular
pain, history of micturition disorders, weak limbs and their saddle anestesi.8

25
b. Physical examination
1. Standing:
a. Notice how the person is standing and attitude of the establishment.
b. Note the rear of the body: is there any deformity, Gibus, scoliosis,
lumbar lordosis (normal, flat, or hiperlordosis), the pelvis is tilted
left and right pelvic bones are not the same height, muscle atrophy.
c. The degree of movement (range of motion) and muscle spasm.
d. Denervation hypersensitivity (piloerection to cold).
e. Palpation for trigger zone, myofascial nodes, pain in the sacroiliac
joints, and others.
f. Notice how the patient walk / gait.
2. Seat Position:
a. Notice how people sit and attitude of his seat.
b. Pay attention to her backside.
3. Lie down Position:
a. Notice how people lie.
b. Measuring the length of the lower extremities.
c. Examination of the abdomen, rectal, or urogenital.
4. Neurologic examination:
a. Sensory testing
b. Motor examination: look for if there is a weakness, muscle atrophy
or fasciculations
c. Tendon examination
d. Frequently examination:
1. Test to stretch the nerves ischiadicus (laseque test)
2. Test to raise the pressure of intrathecal (Nafzigger test,
Valsalva test)
3. Patrick and Contra Patrick test
4. Distraction Test and compression test8

26
 Figure 10. Patrick and Laseque Test
c. Supporting Examination

Elekrofisiologic Inspection
- Elecromyography (EMG): Needle EMG and H-reflex recommended when
the alleged root dysfunction of more than 3-4 weeks. When the diagnosis of
radiculopathy is definitely in the clinical examination, electrophysiological
examination is not dianjurkan.8
- Somatosensory Evoked Potential (SSEP). Useful for canal stenosis and
myelopathy spinal.8

Radiological examination
- Plain: Not recommended for routine evaluation of NPB. Recommended to
waive their bone disorders and patients at high risk of fracture vertebral
compression such as a history of trauma, osteoporosis and use steroid.6,8
- Myelography, Mielo-CT, CT scan, MRI: Indicated to find the causes of
pain include tumors, HNP, adhesions. MRI is superior to CT Scan. In
patients with persistent low back pain with complaints and symptoms of
radiculopathy or spinal stenosis, MRI or CT examination Spinal only
recommended in patients who are candidates for action operasi.6,8
- MRI can depict soft tissue and is helpful in the diagnosis of cauda equina
syndrome. MRI with gadolinium contrast at the lumbosacral region is a
diagnostic examination of the option to look for abnormalities pathology in
conus medullaris and cauda equina.9

Laboratorium Examination8

27
 - Erythrocyte sedimentation rate, complete peripheral blood, C-reactive
protein (CRP), rheumatoid factor, alkaline phosphatase / acid, calcium
(above indication)
- Urinalysis, useful for non-specific diseases such as infections, hematuria.
- Examination of cerebrospinal fluid (above indication)
d. Gold standard Examination
For the best examination is to use Magnetic Resonance Imaging (MRI)
because with these checks can diagnose the occurrence of spinal compression.

3.5 Management
a. Pharmacology
NSAIDs may help reduce the pain experienced by the patient. NSAIDs
can be selected is dependent on the dose to be used and the price will be given. If
the pain is excruciating, analgesics can be given steroids to reduce pain quickly.
Examples of non-steroidal anti-inflammatory drugs that can be given is:
1. Calecoxib
2. Ibuprofen
3. Naproxen
4. Ketoprofen
In addition to drug therapy can also be performed surgical therapy.
Surgical therapy that can be done in case of disc herniation intravertebralis is
microdiscectomy and laminotomy.
Chronic low back pain: Anti anticonvulsants (Pregabalin, gabapentin,
carbamazepine, okskarbasepin, phenytoin), antidepressants (amitriptyline,
duloxetin, venlafaxin), alpha blockers (clonidine, prazosin), opioids (if so
required). The combination of pregabalin and celecoxib is more effective at
lowering pain scores compared with monterapi NPB pregabalin or celecoxib.6,8

b. Non- Pharmacology
Medical rehabilitation in patients HNP:
1. Physical therapy: diathermy, electrotherapy, lumbar traction, exercise
2. Occupational therapy: teach proper body mechanic
3. Orthotic prosthetic: the provision of a lumbar corset, walker

28
4. Education dan advice
Providing rehabilitation program for 3 different times, namely:
1. The acute phase can be done to conservative therapy for the provision of initial
treatment such as providing analgesic, anti-inflammatory, and physical therapy.
2. The recovery phase is the focus of therapy in this phase is a function of
biochemical and connective tissue deficit. Can also begin light physical exercises
to strengthen the muscles.
3. Maintenance phase is the focus of therapy in phase is to prevent back pain not
to recurrence.

c. Surgical therapy
Surgical therapy requires a strict indication for preventing the occurrence
of failed back syndrome (failure and recurrence after surgery). Surgical treatment
should be considered in the following circumstances: 6
 No progress after one month of being treated conservatively
 Ischialgia severe that the patient is able to withstand the pain
 Ischialgia settle or increase.
 Disturbance of micturition / defecation and sexual
 There is clinical evidence of root dysfunction
 There is a lower limb muscle weakness

3.6 Prognosis
1. The majority of patients will recover improve within 6 weeks with conservative
therapy.
2. A small percentage can develop into chronic despite being treated.
3. In the operated patient: 90% recover improved notably of leg pain, the
possibility of recurrence is 5%.

29
 THE BASIC OF DIAGNOSE

1. Basic Diagnose
1.1 Clinical diagnose : Radiculopathy Lumbal
According to anamnesis and physical examination we have found the patient
complained felt lower back pain radiating to both of the leg (ischialgia). Pain is
sharp and felt like a burning pain, intermittent, triggered by static sitting and
standing position. The intensity of the pain increased when sneezing or coughing
and didn’t decreased with rest. And patient also felt numbness. The numbness
from the upper leg to toes and feels intermittent.

1.2 Topical diagnose : Radix nervus ischiadica

It is based on the anamnesis and physical examination we found on the
patient complaining about felt lower back pain radiating to the both of the leg
from upper leg to toes (N. ischiadica).

1.3 Etiological diagnose : Susp. Herniated Nucleus Pulposus (HNP)

Etiological diagnose on this patient is leads to HNP, obtained by
anamnesis that the patient has ischialgia, Pain is sharp and felt like a burning pain,
intermittent, triggered by static sitting and standing position. The intensity of the
pain increased when sneezing or coughing and didn’t decreased with rest, and of
the physical examination found the Laseque (+), Kernig (+), Valsava test (+),
Naffziger (+).

1.4 Differential diagnose : radix trauma

The gold standard for diagnose the Herniated Nucleus Pulposus (HNP) is
with MRI. Considered the radix trauma because it almost have the same
manifestation and on this patient has history of fall from stairs 1,5 years ago on
sitting position.

1.5 Basic treatment

30
1. Bed rest to reduce the compression of nerve root

2. Farmacology

 Meloxicam 2 x 7,5 mg is a anti-inflamatory.

 Omeprazole 1 x 40 mg to prevent increase gastric acid .
 Mecobalamin 3 x 500 mg is a neurotropic.
 Eperisone HCL 3 x 50 mg is a muscle relaxan.

3. Physiotheraphy

31
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1. Benjamin C. 2011.Herniated Disk.University of

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http://www.umm.edu/imagepages/9700.html
2. Kahle W. Spinal cord and spinal nerves in Color
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3. Baehr M, Fotscher M. Diagnosis topic neurologi

Duus: anatomi, tanda, gejala. Jakarta: Penerbit Buku Kedokteran EGC;
2010.h.60-80.

4. Sahrakar, Kamran. 2011. Lumbar Disc Disease.

Medscape Reference. Available at
http://emedicine.medscape.com/article/249113-overview#a0112

5. Foster Mark. 2012. Herniated Nucleus Pulposus.

Medscape Reference. Available at
http://emedicine.medscape.com/article/1263961-overview#aw2aab6b3

6. Suryamiharja A [et al]. Nyeri neuropatik di daerah

punggung bawah (Low back pain) dalam Konsensus nasional 1: Diagnostik
dan penatalaksanaan nyeri neuropatik. Jakarta: Perhimpunan Dokter
Spesialis Saraf Indonesia (PERDOSSI); 2011.h.29-33

7. Ropper H.A, Brown R H. Adam’s and Victor

Principles of Neurology. USA ; McGrawHill : 2005.

8. Mumenthaler M, Mattle H. Neurology 4th edition.

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10. Dewanto G, dkk. Panduan Praktis Diagnosis &
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