Case Report

HERNIA NUCLEOUS PULPOSUS

Presented by:

Annisa Tiara Putri

2208438031

Supervisor :
Dr.dr. Riki Sukiandra, Sp.S (K)

CLINICAL CLERKSHIP
NEUROLOGY DEPARTEMENT
MEDICAL FACULTY UNIVERSITY OF RIAU
ARIFIN ACHMAD GENERAL HOSPITAL
PEKANBARU
2023
 KEMENTERIAN RISET, TEKNOLOGI, DAN PENDIDIKAN TINGGI
UNIVERSITAS RIAU
FAKULTAS KEDOKTERAN
BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000, Email :[email protected]

PATIENT STATUS

Co-ass’ Name Annisa Tiara Putri

NIM 2208438031

Supervisor dr. Riki Sukiandra, Sp.S

I. PATIENT’S IDENTITY

Name Mrs. R
Age 53 years old
Gander Famale
Address Lintas Bagan Siapi-api labuhan tangga kecil, Rokan Hilir
Religion Islam
Marital’s status Married
Occupation Housewife
Day of admission February 14th 2023
Medical record 0111xxx

II. ANAMNESIS (Autoanamnesis)

Autoanamnesis with patient and alloanamnesis with patient’s child
(February 14th,2023 on 12:00 p.m in poli room, Arifin Achmad Hospital)

Chief Complain
Low Back pain that radiates to the left leg which has been getting worse since 3
months before come to the hospital.

2
Present Ilness History
3 months before come to the hospital, the patient complained of lower
back pain that was getting worse. The pain feels like being stabbed, radiates to the
left leg and lasts continuously. The pain will increase if the patient stands for a
long time, is active, bends (bowing during worship), or rests and will decrease
when the patient is massaged by the waist. Patients also complain of difficulty
walking and numbness, feeling heavy when walking and pain in the neck and
head. Complaints do not get worse at night. There are no complaints of defecation
and urination. Patients denied fever and weight loss.
3 months before come to the hospital the patient also complained of low
back pain that radiated to the left leg, the patient then went to Dr. RM. Pratomo
Rokan Hilir, and the patient was diagnosed with a pinched nerve. The patient
received analgesic medication and vitamins but because the complaint did not
improve and the patient was referred to Arifin Achmad Hospital for further
examination.

Treatment history
- Go to dr. RM. Pratomo Rokan Hilir hospital 3 months before come to the
hospital, given analgesic medication and vitamins but complaints did not
decrease.

Past Ilness History

- There is a history of kidney stones since 2 years ago
- History is no history Diabetes Melitus
- History is no history of trauma
- History is no history of pulmonary TB
- History is no history of malignancy
- History is no history of spinal surgery

The Family Disease History

- The are not family with same complained
- History is no history diabetes melitus

3
 - History is no history of pulmonary TB
- History is no history of malignancy
- History is no history of stroke
Social Economic History
- The patient is a housewife
- Has a history of often lifting heavy weights at a young age and working in
non-ergonomic positions
- There is no history of alcohol consumption and drug abuse

SUMAMARY
Mrs. R 53 years came to the neurology polyclinic with the main complaint
of low back pain radiating to the left leg continuously which has been aggravating
since 3 months efore come to the hospital. The pain is exacerbated by prolonged
standing, activities, bending (bowing during worship), as well as rest and will
decrease when the patient is massaged by the waist. Complaints are accompanied
by difficulty walking, numbness, and feeling heavy when walking and arising
pain in the neck radiating to the head. The patient first complained of low back
pain radiating to the left leg since 3 months before come to the hospital. The
patient has a history of often lifting heavy weights at a young age and working in
non-ergonomic positions. The patient seeks treatment at Dr. RM. Pratomo Rokan
Hilir since 3 months before come to the hospital, was given anti-pain medication
and vitamins but the complaints did not decrease, then the patient was referred to
the neurologist polyclinic at Arifin Achmad Hospital for further examination.

4
III. PHYSICAL EXAMINATION
A. General state
General State : Moderate illness
Consciousness : Composmentis
Blood Pressure : 139/88 mmHg
Heart Rate : 78 bpm
Respiratory Rate : 20 tpm
Temperature : 36,8oC
Numeric Rating Scale: 5/10
Eye : anemic conjunctiva (-/-), icteric sclera (-), direct light
reflex (+/+), indirect light reflex (+/+)
Cardiovascular : HR : 78 bpm, regular, murmur (-), gallop (-)
Lungs : Respiratory : Vesikuler (+) ronchi (-) wheezing (-)
Nutritional status : Height : 154 cm
Weight : 57 kg
BMI : 24,7 kg/m2 (Normal)

B. Neurological Status
1) Consciousness : Composmentis, GCS 15 E4M5V6
2) Cognitive Function : Normal
3) Meningeal Sign : Not found
4) Cranial Nerves

1st Cranial Nerve (Olfactory)

Right Left Interpretation
Sense of smell Normal Normal Normal
2nd Cranial Nerve (Optic)
Right Left Interpretation
Visual Acuity Normal Normal
Visual Fields Normal Normal Normal

5
Colour Recognition Normal Normal
3rd Cranial Nerve (Oculomotor)
Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Bulat Bulat
Size 3 mm 3 mm
Normal
Move the eyeballs Normal Normal
Pupillary reactions to light
Direct
(+) (+)
Indirect
(+) (+)
4th Cranial Nerve (Trochlear)
Right Left Interpretation
Extraocular Normal Normal Normal
Movements
5th Cranial Nerve (Trigeminal)
Right Left Interpretation
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal Reflex (+) (+)
6th Cranial Nerve (Abducens)
Right Left Interpretation
Eye Movement Normal Normal
Strabismus (-) (-) Normal
Deviation (-) (-)

6
7th Cranial Nerve (Facial)
Right Left Interpretation
Tic (-) (-)
Motoric :
- Frowing Normal Normal
- Raised eyebrow Normal Normal
- Closed eyes Normal Normal
Normal
- Corners of the Normal Normal
mouth Normal Normal
- Nasolabial fold Normal Normal
Sense of taste Normal Normal
Chvostek sign (-) (-)
8th Cranial Nerve (Acoustic)
Right Left Interpretation
Hearing sense Normal Normal Normal
9th Cranial Nerve (Glossopharyngeal)
Right Left Interpretation
Pharyngeal Arch Normal Normal
Sense of taste Normal Normal Normal
Gag Reflex (+) (+)
10th Cranial Nerve (Vagus)
Right Left Interpretation
Pharyngeal Arch Normal Normal
Normal
Dysphonia (-) (-)
11th Cranial Nerve (Accessory)
Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Eutrophy Eutrophy
12th Cranial Nerve (Hypoglossal)
Kanan Left Interpretation

7
Motoric Normal Normal
Trophy Eutrophy Eutrophy
Normal
Tremor (-) (-)
Disartria (-) (-)

IV. MOTORIC SYSTEM

Right Left Interpretation
Upper Extremity
Strength
Distal 5 5
proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary Movements (-) (-)
Clonus
Lower extremities Normal

Strength
Distal 5 5
proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary Movement (-) (-)
Clonus (-) (-)
Body
Trophy Eutrophy Eutrophy
Normal
Involuntary Movement (-) (-)
Abdominal reflex (+) (+)

8
V. SENSORIC SYSTEM
Right Left Interpretation
Touch Normal Normal
Pain Normal Normal Normal
Temperature Normal Normal
Proprioceptive Normal Normal
VI. REFLEX
Right Left Interpretation
Physiological
Biceps + +
Physiological reflex (+)
Triceps + +
patella + +
Achilles + +

Pathological (-) (-)

Babinski (-) (-)
Chaddock (-) (-) Pathological reflex (-)
Hoffman Tromer (-) (-)
Openheim (-) (-)
Schaefer

VII. COORDINATION
Right Left Interpretation
Point to point movement (+) (+)
Walk heel to toe Normal Normal
Gait Normal Normal Normal
Tandem Normal Normal
Romberg Normal Normal
VIII. AUTONOM
Miction : Normal
defecation : Normal
IX. SPECIAL EXAMINATION
Spine examination :
1. Inspection : Symmetrical(-), redness (-), tumor (-), deformity (-)
2. Palpation : Swelling (-), tanderness(+) at vertebrae lumbal 5
and vertebre sacral 1, crepitation (-)
9
 3. Examination to assess function
a. Range of motion (ROM)
- Flex : limited
- Extention : limited
- Internal rotation : limited
- External rotation : limited
b. Straight leg raising (SLR) / Laseque : -/+ limited and painful <70°
c. Bragard test : -/+
d. Kernig : -/-
e. Patrick : -/+
f. Contrapatrick : -/+
g. Valsava test : -/+
h. Naffziger test : -/-
Urologic status examination :
a. Area flank
• Trauma sign : -/-
• Inflammation sign : -/-
• Mass Sign : -/-
• Ballotement : -/-
• CVA :
Tenderness : -/-
Knock Pain : -/-
b. Suprapubis
• Trauma sign :-
• Inflammation sign :-
• Mass Sign :-

X. EXAMINATION RESUME
Consciousness : Composmentis, GCS 15 E4M5V6
Numeric Rating Scale : 5/10
Blood Pressure : 139/88 mmHg

10
 Heart Rate : 78 bpm
Respiratory Rate : 20 tpm
IMT : 24,7 kg/m2
sublime function : -
Meningeal sign : -
Cranial nerves : Normal
Motoric : Normal
Sensory : Normal
Coordination : Normal
Autonom : Normal
Reflex
Physiological : Normal
Pathological : (-/-)
Spine check :
Palpation : Tanderness (+)at the level of the L5-S1 vertebre
Range of movement : Limited
Straight leg raising (SLR) / Laseque : +/+, limited and painful <70°
Bragard test : -/+
Kernig : -/-
Patrick : -/+
Kontrapatrick : -/+
Valsava test : -/+
Naffziger test : -/+
Urologic status examination :
Flank Area : -/-
Suprapubic : -/-

XI. WORKING DIAGNOSED :

Clinical Diagnosed : Lumbosacral radiculopathy
Topical Diagnosed : Radiks nervus ischiadika
Etiologic Diagnosed : Suspect. Hernia nukleus pulposus
Differential Diagnosed: Spondilosis

11
XII. SUGESSTED EXAMINATION
- Routine blood (hemoglobin, hematocrit, leukocytes, platelets)
- Rontgen X-ray lumbosacral AP/lateral
- MRI lumbosacral

XIII. RESULTS OF SUPPORTING EXAMINATION

1. AP/lateral lumbosacral vertebral X-ray

Interpretation :
 Appears Paralumbal muscle spasm
 Spondylosis is seen in the thoracolumbar vertebrae
 There is narrowing of the neural foramen of the 5th lumbar
vertebra and 1st sacral vertebra
 The intervertebral spaces are narrowed
Impression :
• Degenerative lumbar spine
• susp. Lumbosacral HNP

12
XIV. FINAL DIAGNOSE
Ischialgia sinistra Susp. Hernia nucleus pulposus lumbar region 5 and
sacral 1

XV. SUGESSTED MANAGEMENT

1. Non-pharmacological :
• Explain to the patient and family about the illness
• Bed rest
• Don't lift heavy weights and don't stand for too long
• Medical rehabilitation specialist consultant
• Follow the physiotherapy exercise program regularly
2. Pharmacology
• Anti Convulsant : Gabapentin 100 mg 2 x 1
• Muscle relaxant : Eperisone HCL 2 x 1 mg
• Anti-inflammatory : Meloxicam 15 mg 1x 1 mg

13
 LITERATURE REVIEW
1. Pain
1.1 Definition
According to the International Association for the Study of Pain (IASP),
pain is an unpleasant sensory and emotional experience resulting from tissue
damage or that tends to damage tissue, or as is meant by the word tissue damage.
Pain consists of two main components, namely sensory (physical) and emotional
(psychological). The sensory component is a neurophysiological mechanism that
translates nociceptor signals into information about pain (duration, intensity,
location, and quality of stimuli). While the emotional component is the
component that determines the severity of the individual's discomfort, can initiate
emotional disorders such as anxiety and depression if they become chronic pain,
and is played by nociceptive stimulation through limbic system activation and
environmental conditions (origin of disease, unclear treatment results, and
social/family support).1

1.2 Pain Mechanism

The mechanism of pain onset is based on multiple processes, namely
nociception, peripheral sensitization, phenotypic changes, central sensitization,
ectopic excitability, structural reorganization, and decreased inhibition. Between
the tissue injury stimulus and the subjective experience of pain there are four
separate processes, viz:2,15
1. Transduction is a process by which afferent nerve endings translate a stimulus
(eg a needle prick) into nociceptive impulses. Three types of nerve fibers are
involved in this process, namely A-beta, A-delta, and C fibers. Those that
respond maximally to non-noxious stimulation are combined as pain-
conducting fibers, or nociceptors. These fibers are the A-delta and C. This
excitatory stimulation can be physical, chemical, or thermal. Tissue damage
due to trauma either traumatic damage or other trauma causes the synthesis of
prostaglandins, where these prostaglandins will cause sensitization of
nociceptive receptors and release pain mediators such as histamine, serotonin
which will cause the sensation of pain. This condition is known as peripheral
sensitization.
14
2. Transmission, is the process of transmitting impulses through sensory nerves
as a continuation of the transduction process through A-delta fibers and C
fibers from the periphery to the spinal cord, where these impulses undergo
modulation before being forwarded to the thalamus by the spinothalamic tract
and partly to the spinoreticular tract. The spinoreticular tract carries mainly
stimulation from the deeper and visceral organs and is associated with pain that
is more diffuse and emotionally involved. In addition, the nerve fibers here
have interneuron synapses with large diameter and myelinated nerves.
Furthermore, the impulses are channeled to the thalamus and somatosensory in
the cerebral cortex and are felt as pain perception.
3. Modulation is the process of amplifying pain-related neural signals. This
process occurs primarily in the dorsal horn of the spinal cord, and may also
occur at other levels. A series of opioid receptors such as mu, kappa, and delta
can be found in the dorsal horn. The nociceptive system also has a descending
pathway from the frontal cortex, hypothalamus, and other brain areas to the
midbrain and medulla oblongata, then to the spinal cord. The result of this
descending inhibitory process is amplification, or even inhibition (blocking) of
nociceptive signals in the dorsal horn.
4. Perception, is the end result of a complex interaction process of transduction,
transmission and modulation processes which will eventually produce a
subjective process known as the perception of pain, which is thought to occur
in the thalamus with the cortex as discrimination from sensory.

15
 Pigure 1. Mechanism of pain 15

1.3 Pain Pathways in the Central Nervous System15

1.3.1 Ascendent Path
C and A fine delta nerve fibers, which carry sharp acute pain and chronic
slow pain, respectively, synapse in the substantia gelatinosa of the dorsal horn,
cross the spinal cord and ascend to the brain in the neospinothalamic or
paleospinothalamic branches of the anterolateral spinothalamic tract. The
neospinothalamic tract, activated primarily by peripheral A delta afferents,
synapses in the ventroposterolateral nucleus (VPN) of the thalamus and continues
directly to the somatosensory cortex of the postcentral gyrus, where pain is
perceived as a sharp, well-defined sensation. The paleospinothalamic branch,
which is primarily activated by peripheral afferents of C-nerve fibers, is a diffuse
pathway that sends collaterals to the brainstem reticular formation and other
structures. These fibers affect the hypothalamus and limbic system as well as the
cerebral cortex.
1.3.2 Descending Path
One of the descending paths that has been identified includes 3
components namely:

16
 a. The first is the periaquaductal gray matter (PAG) and the periventricular
gray matter of the mesencephalon and upper pons which surround the
aqueduct of Sylvius.
b. Neurons in area one send impulses to the ravemacnus nucleus (NRM)
located in the lower pons and upper medulla oblongata and to the
paragigantocellular reticular nucleus (PGL) in the lateral medulla.
c. Impulses are transmitted downward through the dorsal column of the
spinal cord to a pain inhibitory complex located in the dorsal horn of the
spinal cord..

1.4 Pain Classification

Based on time, pain is divided into:
a) Acute pain is defined as a complex unpleasant experience related to
sensory, cognitive and emotional related to tissue trauma, disease process,
or abnormal function of muscles or viscera. Acute pain acts as a protective
alarm against tissue injury. Protective reflexes (reflexes away from the
source of stimuli, muscle spasms, and autonomic responses) often
accompany acute pain. The underlying pathophysiology can be
nociceptive pain or neuropathic pain
b) Chronic pain, defined as pain that lasts until it exceeds the course of an
acute illness, runs continuously until it exceeds the time needed to heal a
trauma, and occurs repeatedly at intervals of several months or several
years. Many clinicians limit the duration of pain to 3 or 6 months. The
severity of tissue injury does not always predict the severity of chronic or
acute pain. Chronic pain can also result from ongoing damage or
dysfunction of the peripheral or central nervous system.

Based on the type, pain is divided into:16

a. Nociceptive pain may be somatic or visceral. Somatic pain receptors are
located in the skin, subcutaneous tissue, fascia, other connective tissues,
periosteum, endosteum, and joint capsule. Stimulation of these receptors
usually produces a local sharp or dull pain, but burning is not uncommon
when the skin or subcutaneous tissue is involved. Visceral pain receptors
17
 are located in most internal organs and surrounding connective tissue.
Visceral pain due to obstruction of the hollow organs is poorly localized,
deep, and cramping and may be referred to distant skin sites. Visceral pain
from injury to organ capsules or other deep connective tissue may be more
localized and sharp. Nociceptive pain is generally due to preventing
further injury and/or speeding healing.
b. Pain is inflammatory, pain is maladaptive, pathological without a
protective function, and results from tissue damage (eg, trauma,
rehabilitation, OA, and rheumatoid arthritis). Inflammation of the
damaged tissue and causes the function of various nociceptive components
to change. Inflamed tissues secrete various inflammatory mediators, such
as bradykinins, leukotrienes, prostaglandins, purines, and cytokines that
can activate or sensitize nociceptors directly or indirectly.
c. Neuropathic pain due to direct injury or dysfunction of the nervous
system, eg postherpetic neuralgia, diabetic neuropathy, complex regional
pain syndrome, trauma, compression and poison toxins.
d. Functional pain related to abnormal nerve processes in the absence of
neurologic deficits or peripheral abnormalities, eg fibromyalgia and
irritable bowel syndrome. The hallmark of simple pain is a positive
correlation between the strength and perception of painful stimuli, such as
the stronger the stimulus, the more severe the pain is experienced.

Table 1. Types and characteristics of pain 16

Nociceptive Pain
• Transient pain in response to noxious stimulus
• Arising from stimuli outside the nervous system
• Pain proportional to nociceptor stimulation
• Serves as a protective function
Inflammatory Pain
• Based on tissue damage or inflammation
• Arising from a stimulus that is outside the nervous system
• Pain and spontaneous hyperactivity to noxious stimuli

18
 • Does not function as a protector
Neuropathic Pain
• Initiated or caused by a primary lesion or dysfunction in the nervous system
• No nociceptive stimulation
• Disproportionate to receptor stimulation
• Other evidence of nerve damage (eg, postherpetic neuralgia)
Functional Pain
• Hypersensitivity to pain due to abnormal central processing of normal input.
• No nociceptive stimulation or nervous system lesions

Although inflammatory, neuropathic, and functional pain have

different causes, these syndromes share several common characteristics
through a similar pathophysiology of pain. Tissue injury results in the
release of various neurotransmitters from damaged and inflammatory cells,
including macrophages, mast cells, and lymphocytes. Substances released
from the pain response are also referred to as the "sensitizing soup" and act
to further sensitize the nerve endings causing peripheral sensitization. This
inflammatory response results in a decrease in the threshold for pain
receptors, namely nociceptors; an increase in the magnitude of the response
to further stimulation; spontaneous increase in pain; and an increase in the
area in which a stimulus can generate an action potential. This phenomenon
is referred to as peripheral sensitization.

19
 Figure 2. Types of pain 16

Peripheral sensitization enhances the transmission of pain stimuli to

the dorsal horn of the spinal cord, which can amplify the pain response. In
addition, there are modifications of the neurons in the dorsal horn, which
include changes in transmission, receptors, and structural reorganization – a
phenomenon known as central sensitization. Taken together, peripheral and
central sensitization represents the plasticity of the nervous system, in which
nerves change function and structure to new functions in response to
changing inputs, such as pain. This causes spontaneous pain without

20
 noxious stimuli and extension of pain beyond the original site of tissue
damage as well as exaggerated and/or prolonged responses to noxious
stimuli or pain elicited from normally painless stimuli (eg, light touch).

Table 2. Pain Sensation 16

Paresthesias Unpleasant spontaneous sensations

Dysesthesias Unpleasant spontaneous sensation of pain

Hyperalgesia Responses that arise to painful stimuli

Allodynia A response that is persistently arousing a stimulus to a non-painful

stimulus

1.4 Pain Scale Classification 11

Pain is a very subjective problem that is influenced by psychological,
cultural and other factors, so measuring pain intensity is a relatively difficult
problem. There are several methods commonly used to measure pain intensity,
including:
a. Visual Analog Scale (VAS)
The scale is a straight line that extends 10 cm (or 100 mm), with a verbal
description at 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 3. Visual Analog Scale (VAS)

21
b. Numerical Rating Scale (NRS)
This method uses numbers to describe the range of pain intensity.
Generally, sufferers will describe the intensity of pain that is felt from the number
0-10 where starting from the number "0" there is no pain and "10" is severe pain.

Figure 4. Numerical Rating Scale (NRS)

c. Verbal Rating Scale (VRS)

The patient is asked how the nature of the pain he feels. The score consists
of four points, namely:
 0 = No pain or unwell when asked
 1 = Mild pain on asking
 2 = Moderate pain when asked
 3 = Pain associated with voice, hands and face response
moaning or crying.
For patients with cognitive impairment, verbal pain scales are difficult to use.
d. Faces Pain Rating Scale
Widely used in pediatric patients with verbal difficulties or limitations.
Explained to the patient about the appropriate changes to mimic facial pain and
choose a patient according to the pain he feels.

Figure 5. Faces Pain Rating Scale

22
1.5 Governance
The pathophysiological approach to pain classification has
diagnostic and therapeutic classifications. Inflammatory and nociceptive
pain syndromes are generally responsive to analgesics, such as
acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs, both
nonselective [NS]-NSAIDs and cyclooxygenase [COX]-2-locking
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 overlap between pain states, optimal
therapy may require a combination of different drug therapies.3

2. Hernia Nukleus Pulposus (HNP)

2.1 Definition
Hernia nucleus pulposus (HNP) is a disease in which the pads that
are between the vertebrae, commonly called the nucleus pulposus, are
compressed in the posterior or lateral parts, this compression causes rupture
of the nucleus pulposus which results in protrusion through the annulus
fibrosus into the spinal canal and results in irritation and pressure. on the
nerve roots so that in the area of irritation there is pain that radiates. The
following is the nature of pain in HNP:4
1. Intermittent low back pain (within weeks to years). Pain spreads according
to the distribution of nerves.
2. The nature of the pain is typical lying down in a sitting position, pain from
the buttocks and continues to radiate to the back and then to the lower legs.
3. The pain gets worse when it is triggered by movements of the waist such as
when coughing or straining, standing or sitting for a long time and the pain
decreases with rest.
4. Patients often complain of tingling (paresthesia) or numbness and even
decreased muscle strength according to the distribution of nerves involved.
5. Pain increases when the area L5-S1 (the line between the two iliac crests) is
pressed.
23
 Figure 6. Hernia nukleus pulposus
The spinal cord is the part of the central nervous system that lies
entirely within the vertebral canal and is surrounded by cerebrospinal fluid.
In humans, there are 31 pairs of spinal nerves, each of which enters a certain
part of the body. Following are the distribution segments of the spinal cord:5
 8 pairs of cervical nerves (C1-C8)
 12 pairs of thoracic nerves (T1-T12)
 5 pairs of lumbar nerves (L1-L5)
 5 pairs of sacral nerves (S1-S5)
 1 pair of coccygeal nerves

Figure 7. Spinal division 5

24
 The spinal cord terminates at the medullary cone at the level of L1 or
L2. Below this level, there is a lumbar sac (teca) lacking only nerve root
filaments called the cauda equina (horse tail).6 The spinal cord is composed of
gray matter (grisea) and white matter (alba). White matter contains ascending
and descending channels, while gray matter contains different types of
neurons; Mainly the anterior horn contains motor neurons, mainly the lateral
horn contains autonomic neurons and the dorsal horn contains mainly
somatosensory neurons. Ascending tracts are tracts in the body that carry
information to the brain such as touch stimuli, temperature, pain and
movement positions and descending tracts are tracts that carry information
from the brain to the limbs and body control functions.5

Figure 8 Conus medularis dan cauda equina6

2.2 Etiology and Risk Factors

Herniation of the intervertrebal disc forms the bulge of the annulus
fibrosus. Under normal circumstances, the annulus fibrosus protects from the
location of the nucleus it contains. When a herniation occurs in the nucleus,
there is compression of the nerve pathway adjacent to the location of the disc
herniation, causing irritation to occur, causing pain which can be called
sciatica, if it is more severe, dysfunction can occur in the neuronal system.

25
HNP risk factors consist of modifiable and non-modifiable risk factors,
namely non-modifiable risk factors:7
1. Age. The increasing age will occur degenerative changes that result in less
flexibility and thin nucleus pulposus. Annulus fibrosus changes because it
is used continuously. As a result, the annulus fibrosus usually in the
lumbar region can pop or rupture.
2. Gender. Men are more often affected by HNP than women (2:1), this is
related to the work and activities carried out in men tend to be physical
activities that involve the vertebral column.

3. Traumatic process. The onset of disc degeneration affects intervertebral

joint mechanics, which can lead to further degeneration. In addition to
degeneration, repetitive movements, such as flexion, extension, lateral
flexion, rotation, and lifting weights can place abnormal pressure on the
nucleus. If this pressure is great enough to injure the annulus, the nucleus
pulposus leads to herniation. Acute trauma can also cause herniation, such
as lifting things the wrong way and falling.

Modifiable risk factors include::

1. Occupation and activity: prolonged sitting, lifting or pulling heavy objects,

frequent bending or twisting of the back, strenuous exercise, exposure to
constant vibrations such as driving.
2. Irregular exercise, exercise begins after a long exercise, strenuous exercise
in the long term.
3. Smoking. Nicotine and other toxins can interfere with the ability of the
discs to absorb necessary nutrients from the blood.
4. Excessive weight, especially excess weight in the abdominal area can
cause tension in the lower back

Figure. Herniation process 4

26
2.3 Pathophysiology
Factors that contribute to HNP:
1. Blood flow to the disc is reduced.
2. Heavy load
3. Narrowing of the posterior longitudinal ligament.
If there is an increase in the load on the disc, the annulus fibrosus which
does not hold the nucleus pulposus (gel) will come out, pain will occur because
the gel inside the root canal presses on the vertebrae. spaces containing
nociception-sensitive pain receptors (pain) are stimulated by various local
stimuli (mechanical, thermal, chemical). This stimulus will be responded to by
releasing various inflammatory mediators which will cause the perception of
pain. Pain is a protective mechanism aimed at preventing movement so as to
allow the healing process to occur. One form of protection is muscle spasm,
which in turn can lead to ischemia. The resulting pain may be painful tissue
inflammation with involvement of various inflammatory mediators; or
neuropathic pain caused by a primary lesion of the nervous system. 4,5
The irritation of neuropathic nerve fibers can result in two possibilities.
First, pressure is placed only on the nerve-rich membrane covering the
nociceptors of the nervi nevorum by painful inflammation. Pain is felt along
the nerve fibers and the nerve fibers grow with stretching, for example due to
movement. The second possibility, emphasis on nerve fibers. In this condition
biomolecular changes occur where there is an accumulation of Na ion channels
and other ions. This buildup causes mechanical stimulation heat is very
sensitive to mechanical and thermal stimulation. 7,8
HNP degrees:
1. Disc degeneration: there is a change in the composition of the annulus
pulposus, so that when there is a load the nucleus pulposus stands on one
side of the annulus fibrosus it is still intact, and herniation does not occur.
2. Prolapse or bulging disc or disc protrusion: there is a protrusion of the
nucleus pulposus and annulus fibrosus, the annulus fibrosus and the
posterior longitudinal ligament are still intact, have herniated and are
starting to put pressure on the radix or spinal cord.

27
3. Disc extrusion: the annulus fibrosus is ruptured, so that the nucleus
pulposus protrudes from the intervertebral disc, but the posterior
longitudinal ligament is intact.
4. Disc sequestration: there has been a rupture of the posterior longitudinal
ligament, so that the nucleus pulposus gel exits through the ligament gap
of the spinal canal towards the vertebral canal.

Figure 10. HNP degrees

2.3 Clinical Manifestations

The main clinical manifestation that appears is pain in the lower back
accompanied by the muscles around the lesion and tenderness. HNP is divided
into central and lateral HNP. Central HNP will cause flaccid paraparesis,
paresthesia and urinary retention. Whereas lateral HNP manifests in pain and
tenderness which is located in the lower back, in the middle of the buttocks and
calves area, behind the heels and soles of the feet.
The clinical symptoms that appear in HNP are very dependent on the
affected nerve roots. Pain or more commonly pain along the course of the
sciatic nerve (ischialgia). This pain is sharp like a burning feeling, symptoms of
tingling can also appear and decreased tendon reflexes, especially the achilles
reflex if the S1 root is affected. This pain will increase when the sufferer
strains, coughs and sneezes. Motor disturbances or muscle weakness are rare,
these symptoms appear when there is already root damage, the HNP has been
chronic and the pain has not reappeared. Likewise, vegetative disorders such as
BAK and BB disorders are also rare.17

28
2.4 Diagnosis

Nerve
Discus Radicular pain Sensory disturbances
Radix
L3 L2-3 Butt  hind thigh  Knee
front knee
L4 L3-4 Butt  hind thigh  Medial part of the lower
medial part of the lower leg
leg
L5 L4-5 Butt  dorsum pedis  Dorsum pedis and big toe
big toe
S1 L5-S1 Butt  soles and heels Heel the lateral part of
the foot
a. Anamnesis
Anamesis found that the pain will increase when sitting, bending, coughing,
sneezing or activities that can increase intradiscal pressure. Then pay attention to
when starting the presentation, how to start the complaint, the location of the pain,
the nature of the pain, the quality of the pain, whether the pain is experienced
when starting physical activity, aggravating or aggravating factors, there is a
history of previous trauma and whether there are relatives of people with the same
disease. It should also trigger complaints suggestive of a nerve lesion such as
radicular pain, history of urinary disturbances, and weakness in the limbs. 9

b. Physical examination
1. Stand up:
a. Notice how the person is standing and stance.
b. Pay attention to the back of the body: is there any deformity, scoliosis,
lumbar lordosis (normal, flat, or hyperlordosis), left and right tilted
pelvis hip bones are not the same height, muscle atrophy.
c. Degree of movement (range of motion) and muscle spasms.
d. Denervation hypersensitivity (piloerection to cold).
e. Palpate for trigger zones, myofascial nodes, pain in the sacroiliac
joints, etc.

29
 f. Watch how the patient walks.
2. Sitting Position :
a. Pay attention to how you sit
b. Watch the back.
3. Lying position :
a. Watch how people lie down
b. Measure the length of the lower extremities.
c. Abdominal, rectal and urogenital examination.
4. Neurological Examination:
a. Sensory Examination
b. Motor Examination: look for weakness, muscle atrophy or
fasciculation
c. Tendon Examination.
d. Another check:
1. Test to stretch the sciatic nerve (laseque test)
2. Tests to increase intrathecal pressure (Nafzigger test, Valsalva test)
3. Patrick's Test and Patrick's Cons.
4. Distraction test and compression test 9

Figure 11. Patrick and Laserque's examination

c. Supporting investigation
 Electrophysiological Examination
 Electromyography (EMG) and Nerve Conduction Studies (NCS):
recommended if root dysfunction is suspected for more than 3-4 weeks. In
HNP patients with neurological signs and symptoms, EMG and NCS can
help to reveal the presence of lumbosacral radiculopathy, pepipheral

30
 polyneuripathy, myopathy or peripheral nerve entrapment. If the diagnosis
of radiculopathy is certain on clinical examination, electrophysiological
examination is not recommended.9
 Somatosensory Evoked Potential (SSEP). Useful for canal stenosis and
spinal myelopathy.9
 Radiological Examination
 Plain photo of the spine. In old (chronic) HNP, this plain photo usually
helps establish the diagnosis.
 Caudography, myelography and CT-myelo: This examination provides
significant accuracy to help establish the diagnosis of HNP. Besides that,
this examination can also determine the location of the HNP, making it
easier for surgeons when surgical treatment is necessary. However, this
examination is invasive and only owned by type B and A health care
centers/hospitals.11
 Laboratory examination 9
 Erythrocyte sedimentation rate, complete peripheral blood, C-reactive
protein (CRP), rheumatoid factor, alkaline phosphatase / acid, calcium
(indication above), Urinalysis, useful for non-specific diseases such as
infection, hematuria. Cerebrospinal fluid examination.

 Urinalysis, useful for non-specific diseases such as infection or hematuria

d. Gold Standard Examination

The best examination is to use Magnetic Resonance Imaging (MRI)
because this examination can diagnose spinal compression.9 This examination
can also detect soft tissues such as muscles, ligaments, tendons and discs that
are less obvious on caudigraphy and CT-myelo examination..17
2.5 Governance
a. Conservative Therapy 12,13,14
The goals of conservative therapy are to reduce nerve irritation, improve
the patient's physical condition and protect and improve overall spinal function.
The main treatment for a herniated disc is to begin with rest with pain and anti-
inflammatory medications, followed by physical therapy. In this way, more

31
than 95% of sufferers will recover and return to their normal activities. A few
percent of sufferers need to continue to receive further treatment which
includes steroid injections or surgery.
Conservative therapy includes:
1. Bed rest
The purpose of bed rest is to reduce mechanical pain and intradiscal
pressure, the recommended duration is 2-4 days. Bed rest for too long will
cause the muscles to weaken. The patient is gradually trained to return to
normal activities. The recommended bed rest position is to lean your back,
knees and lower back in a slightly flexed position. Slight flexion of the
lumbosacral vertebrae separates the joint surfaces and separates the
approximations of inflamed tissue.
2. Medikamentosa
- Analgesics and NSAIDs
- Muscle relaxants: used to treat muscle spasms
- Opioids: not proven to be more effective than regular analgesics. Long
term use can cause dependence
- Oral corticosteroids: use is still controversial but may be considered in
cases of severe HNP to reduce inflammation.
- Adjuvant analgesics: used in chronic HNP
3. Terapi fisik
 Pelvic traction
According to a panel of studies in America and England pelvic
traction has not proved beneficial. Studies comparing bed rest, corset and
traction to bed rest and corset alone have shown no difference in healing
rates.
 Diathermy/hot/cold compress
The goal is to treat pain by overcoming inflammation and muscle
spasms. In acute conditions, cold compresses can usually be used,
including if there is edema. For chronic pain, hot or cold compresses can
be used.
 Lumbar corset

32
 Lumbar corset is not useful in acute HNP but can be used to
prevent exacerbations of acute or chronic HNP pain. As a support for the
corset, it can reduce the burden on the disc and can reduce spasms.
 Physical training
Doing exercises with minimal back stress such as walking, riding a
bicycle or swimming is recommended. Other exercises include flexibility
and strengthening. Exercise aims to maintain physiological flexibility,
muscle strength, joint and soft tissue mobility. With exercise, the
elongation of muscles, ligaments and tendons can occur so that blood flow
increases.
 Proper body mechanics
Patients need to get knowledge about good posture to prevent
injury and pain. Some principles in maintaining the position of the back
are as follows:
1. In a sitting and standing position, the abdominal muscles are tense, the
back is straight and straight. This will keep the spine straight.
2. When going to get out of bed position your back closer to the edge of the
bed. Use your hands and arms to lift your pelvis and return to a sitting
position. When standing, place your hands on your thighs to help you
stand up.
3. Sleeping position use hands to help lift and shift the position of the pelvis.
4. When sitting, the arms help support the body. When standing up, the body
is lifted with the help of the hands as a support.
5. When lifting something from the floor, bend your knees as if you are
going to squat, keep your back straight by tightening your abdominal
muscles. With a straight back, the weight is lifted by straightening the
legs. The weight lifted by hand is placed as close to the chest as possible.
6. If you want to change position, do not turn around. The head, back and
legs must change position simultaneously.
7. Avoid movements that twist the vertebrae. If necessary, replace the squat
toilet with the sitting toilet so that it makes movement easier and doesn't
burden your back when you get up.

33
b. Operative Therapy 12,14
Surgical therapy is useful for removing pressure and nerve
irritation so that pain and impaired function will disappear. HNP
operations must be based on good reasons, namely worsening neurologic
deficits, autonomic disturbances (micturition, defecation, sexual) and
lower limb muscle paresis.
1. Laminectomy
Laminectomy, which is an operative procedure to remove the
vertebral lamina, can be performed as a decompression of the spinal roots
which are compressed or pinched by the protrusion of the nucleus
pulposus.

Figure 12. Laminectomy

2. Discectomy
In a discectomy, part of the intervertebral disc is removed to relieve
pressure on the nerves. Discectomy is performed to remove the protruding
part under general anesthesia. Only about 2-3 days stay in the hospital.
You will be advised to walk on the first day after surgery to reduce the risk
of blood pooling. Full recovery may take several weeks. If more than one
disc to be treated if there is a problem other than disc herniation. More
extensive surgery may be required and it may take longer to heal.12,14

3. Microdiscectomy
Other surgical options include microdiscectomy, a procedure to
remove fragments of nucleated disks through very small incisions using a
34
 ray-ray and chemonucleosis. Chemonucleosis involves injecting an
enzyme (called chymopapain) into the herniated disc to dissolve the
protruding gelatinous substance. This procedure is an alternative to
discectomy in certain cases.

Figure 13. Microdiskectomy

2.6 Prognosis 14.16

1. Most patients will improve within 6 weeks with conservative therapy.
2. A small proportion develop into chronic despite being treated.
3. Patients who were operated on: 90% improved, especially leg pain, the
possibility of recurrence is 5%.

35
 THE BASIC OF DIAGNOSIS

1.1 Clinical diagnosis: Lumbosacral radiculopathy

Based on the history of a 53 year old woman complaining of pain in the
lower back that radiates to the left leg, where the pain feels like stabbing, radiates
to the left leg and lasts continuously. Complaints increase if the patient stands for
a long time, is active, bends (bowing during worship), or rests and decreases when
the patient is massaged by the waist. The existence of pain in the lower back can
be caused by two mechanisms, namely the mechanism of compression and the
mechanism of the inflammatory reaction. The existence of this mechanism causes
the pain felt by the patient to spread to the knee, lower leg and around the thumb
which is felt continuously, the presence of this pain is a manifestation of
radiculopathy, which appears as pain that radiates according to the dermatome. In
addition, the patient also complained of numbness that was felt from the knee,
lower leg to the left big toe and felt intermittent. On physical examination during
the examination of the laseque test, patrick test, contra patrick test, bagard test,
and valsalva test, it was found that there was significant pain/+. Normally in HNP,
positive results are found in these examinations, in the form of finding pain in the
lower back that radiates to the left leg (ischialgia).
1.2 Topic Diagnosis: Radiks nervus ischiadica
This is based on the anamnesis found in the patient. The patient
complained of lower back pain that radiated to the left leg, accompanied by
impaired sensibility in the form of a feeling of numbness from the knee, lower leg,
to both feet, especially the thumb (N. ischiadica) and the physical examination
found a laseque test (+), patrick test (+), contra patrick test (+), bagard test (+),
and valsalva test (+).

1.3 Basic Etiological Diagnose: Suspek. Herniated Nucleus Pulposus (HNP)

The etiological diagnosis in this patient leads to herniated nucleus
pulposus (HNP) due to the patient's age of 53 years and from the patient's history
of ischialgia, stabbing pain, the pain gets worse if the patient stands for a long
time, is active, bends (bowing during worship), or rests. and will decrease when
the patient is massaged by his waist. Physical examination in significant patients
36
found pain with some manuver as laseque, etc. The based of support examination
X-ray lumbosacral investigation which found bulging that appeared paralumbar
muscle spasm, spondylosis in the thoracolumbar vertebrae, narrowing of the
neural foramen in the 5th lumbar vertebrae and 1st sacral vertebrae, and a
narrowing of the intervertebral space which may also become cause of pain in the
patient’s legs and direct to HNP. On physical examination found a lasereque test
(+) <70°, a patrick test (+), contra patrick test (+), bagard test (+) and valsalva test
(+) the results were positive because there was pain in the waist area to the
patient's left leg as sign there are nerve compression cause HNP at lumbosacral
vertebra segment.

1.4 Diagnosis banding: Spondilosis

The gold standard for diagnosing HNP is an MRI examination. Differential
diagnosis with spondylosis because this disease is mostly found in older people
who at a young age often lift heavy loads and whose clinical manifestations are
similar to HNP, these two diseases can only be distinguished by investigations. In
HNP using Magnetic Resonance Imaging (MRI) you will see compression of the
vertebrae, while for spondylosis a plain lumbosacral photo examination with
anteroposterior, lateral and oblique directions shows spondylosis (osteophytes),
spondylolisthesis, while central canal stenosis can be determined by the MRI
method where it will be found symptomatic or asymptomatic stenosis of the
segment.

1.5 Treatment
1. Bed rest to reduce nerve compression
2. Don't lift heavy weights and don't stand for too long
3. Physiotherapy
4. Pharmacology
1. Anti inflammatory
Meloxicam 15 mg 1 x 1 mg. Meloxicam is a nonsteroidal anti-inflammatory
drug (NSAID), used as an anti-inflammatory to reduce pain felt by patients.
2. Muscle relaxant
37
 Eperisone HCL 2 x 1 mg, Eperisone is a muscle relaxant used to treat
muscle spasms.
3. Analgesic
Pregabalin 2 x 75 mg. Gabapentin is an anticonvulsant drug used as a
muscle relaxant and antispasmodic drug. It has potential as an
anticonvulsant drug and as an adjunct to more potent anticonvulsants. These
drugs are useful in controlling nerve pain. Can describe the indications,
mechanism of action, dosage, significant side effects, contraindications,
monitoring, and gabapentin toxicity.

38
 REFERENCE

1. Giger & Davidhizar. 2013. Transcultural Nursing Assessment and

Intervention. Missouri : Mosby Year Book.
2. Tansumri, Anas. 2007. Konsep dan Penatalaksanaan Nyeri. Jakarta: EGc
3. Bonica, J.J., Loeser, J.D., 2001. History of Pain Concepts and Therapies,
In: Loeser J.D., et al (eds)
4. Benjamin C. 2011.Herniated Disk.University of Maryland Medical Center.
Available at http://www.umm.edu/imagepages/9700.html
5. Kahle W. Spinal cord and spinal nerves in Color atlas of human anatomy.
Vol 3. New York: Thieme; 2003. p.48-69
6. Baehr M, Fotscher M. Diagnosis topic neurologi Duus: anatomi, tanda,
gejala. Jakarta: Penerbit Buku Kedokteran EGC; 2010.h.60-80.
7. Sahrakar, Kamran. 2011. Lumbar Disc Disease. Medscape Reference.
Available at http://emedicine.medscape.com/article/249113-
overview#a0112
8. Foster Mark. 2012. Herniated Nucleus Pulposus. Medscape Reference.
Available at http://emedicine.medscape.com/article/1263961-
overview#aw2aab6b3
9. Jacob A, Weinshenker B. An Approach to the Diagnosis of Acute
Transverse Myelitis. Semin Neurol 2008;28:105-120.
10. 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
11. Mumenthaler M, Mattle H. Neurology 4th edition. Germany : Thieme
Flexibook ; 2004.
12. Sidharta, Priguna. Sakit Neuromuskuloskeletal Dalam Praktek Umum.
Jakarta : PT Dian Rakyat. 2005: 182-212.
13. Nuarta, Bagus. Ilmu Penyakit Saraf. In: Kapita Selekta Kedokteran, edisi
III, jilid kedua, cetakan keenam. Jakarta : Media Aesculapius. 54-59. 2004
14. Mardjono Mahar dan Sidharta Priguna. 2004. neurologi Klinis Dasar. Dian
Rakyat:Jakarta.
15. Bahrudin M. Patofisiologi Nyeri (Pain). Fakultas kedokteran Universitas
Muhammadiyah Malang. 2017;13(1): 7-13.
16. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-
Specifific Pharmacologic Management Ann Intern Med. 2004;140:441-
451.
17. 2nd Bali Neurology Uodate (BANU). Update in Neuropathic Pain and
Headache. Bagian SMF Neurologi FK Unud, RSUP Sanglah Denpasar.
Denpasar: Udayana University Press. 2014:6-11.

39