Grand case report

SPONDYLITIS TB

By:
Liskhairia Abidin
1808436170

Supervisor:
dr. Riki Sukiandra, Sp.S

CLINICAL CLERKSHIP DEPARTMENT OF NEUROLOGY

RSUD ARIFIN ACHMAD
FACULTY OF MEDICINE UNIVERSITY OF RIAU
PEKANBARU
2020

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 KEMENTRIAN 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 Mrs. A
Age 45 years old
Gender Female
Address Pekanbaru
Religion Moeslim
Marital’s Status Married
Occupation enterpreneur
Day of admission January, 11th 2020
Medical Record 01031214

II.ANAMNESIS :
Autoanamnesis (January, 13th 2020 on 10.00 AM)
Chief complain
Weakness in both limbs since 2 month before admitted to hospital.
Present illness history
2 months before admitted to hospital patient feels weakness in both legs
but can still be moved and can still walk with the help of a cane. Weakness in
both legs has not been accompanied by numbness. There was not history of
trauma. 2 days before admitted to hospital patient felt both legs getting
weaker so that it was difficult to move and could only be shifted and unable
to walk, both legs felt weak from the waist down and felt heavy and numb.
There was history of long cough.

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 Weekness in both limb preceded patients feel low back pain continuously
7 months before admittted to hospital. Low back pain is felt especially when
walking and getting out of bed. But patients are still able to carry out their
daily activities and there are no other complaints. During that time the patient
had never received any treatment. The patient had history of low grade fever ,
malaise and weight loss of ± 20 kg for 7 months.

Past illness history

Diagnosed with tuberculosis since 1,5 months ago and the patient has
initiated antitubercular treatment.
Diagnosed with unstable angina pectoris

The family disease history

 Her sister also diagnosed with tuberculosis and had passed away

Socioeconomic history
 The patient is currently a laundry worker, she always work long standing.

SUMMARY
Mrs. A, 45 years old admitted to the hospital on Oct, 11th 2020. The patient
has complained weakness gradually on both legs 2 months before admission. She
Patient complained unable to work 2 days before admission. The patient had
history of low grade fever , malaise and weight loss of ± 20 kg for 7 months.

III. Physical examination

Blood Pressure : 130/90 mmHg
Heart Rate : 96 tpm
Respiratory rate : 24 tpm
Temperature : 37,0°C
Weight : 30 kg
Height : 155 cm
Body Mass Index (BMI) : 12,5 kg/m2 (underweight)

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VAS : 5-6
Eyes : Pale conjunctiva (-/-), isocoria 2mm/2mm,
direct light reflex (+/+), indirect light reflex
(+/+)
Cardiovascular : HR : 96 bpm, regular, murmur (-), gallop (-)
Respiratory : Vesicular (+/+), Rhonchi (+/+), Wheezing (-/-),
symmetrical lung expansion
Abdomen : Normal skin turgor, murphy sign (+), bowel
sounds : 8x/minutes.
Lymph nodes : Swollen lymph nodes (-)

A. NEUROLOGICAL STATUS (January, 13th2019 on 10.00 am)

1) Consciousness : Composmentis Cooperative
GCS : E(4)V(5)M(6)
2) Cognitive Function : Normal
3) Nuchal rigidity : Negative
4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. Cranial nerve II (Optic)

Right Left Interpretation
Visual Acity >3/60 >3/60
Visual Fields
Normal Normal Normal
Colour Recognition
+ +

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3. Cranial nerve III (Oculomotor)
Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Round Round
Size Φ2mm Φ2mm
Normal
Pupillary reactions to light
Direct (+) (+)
Indirect (+) (+)

4. Cranial nerve IV (Trochlear)

Right Left Interpretation
Extraocular
(+) (+) Normal
Movements

5. Cranial nerve V (Trigeminal)

Right Left Interpretation
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal reflex (+) (+)

6. Cranial nerve VI (Abducens)

Right Left Interpretation
Eyes movement Normal Normal
Strabismus (-) (-) Normal
Deviation (-) (-)

7. Cranial nerve VII (Facial)

Right Left Interpretation
Tic (-) (-) Normal
Motoric:
- Frowning Normal Normal
- Raised eye brow Normal Normal
- Closed eyes Normal Normal
- Corners of the
mouth Normal Normal

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 - Nasolabial fold Normal Normal
Sense of Taste Normal Normal
Chvostek Sign (-) (-)

8. Cranial nerve VIII (Acoustic)

Right Left Interpretation
Hearing sense Normal Normal Normal

9. Cranial nerve IX (Glossopharyngeal)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Sense of Taste Normal Normal Normal
Gag Reflex + +

10.Cranial nerve X (Vagus)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Normal
Dysphonia - -

11.Cranial nerve XI (Accessory)

Right Left Interpretation
Motoric Normal Normal
Normal
Trophy Eutrophy Eutrophy

12.Cranial nerve XII (Hypoglossal)

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

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IV. MOTORIC SYSTEM
Right Left Interpretation
Upper Extremity
Strength
Distal 5 5
Medial 5 5
Proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements - -
Clonus - -
Lower Extremity Paraparesis UMN
Strength
Distal 3 3
Medial 3 3
Proximal 3 3
Tone Hipertonus Hipertonus
Trophy Eutrophy Eutrophy
Involuntary movements - -
Clonus - -
Body
Trophy Eutrophy Eutrophy
Involuntary movements - - Normal

V. SENSORY SYSTEM
Right Left Interpretation
Touch
Normal Normal
Pain
Hipoestesia Hipoestesia
Hipoestesia 12- Th
Normal Normal
Temperature
Normal Normal
Propioseptive

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VI. REFLEX
Right Left Interpretation

Physiologic
(+)
Biceps (+)
(+)
Triceps (+) Physiologic reflex (+)
(+)
Knee (+)
(+)
Ankle (+)
(+)

Pathologic
Babinsky (-) (-)
Chaddock (-) (-) Pathological reflex(-)
HoffmanTromer (-) (-)
Openheim (-) (-)
Schaefer (-) (-)

VII. COORDINATION
Right Left Interpretation
Point to point movement
Walk heel to toe Difficult to Difficult to
Gait asses asses Not testable
Tandem
Romberg

VIII. AUTONOM

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 Urination : Catheterized
Defecation : Normal
IX. OTHERS EXAMINATION
a. Laseque : limited (<70)
b. Kernig : limited (<130)
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test : -
f. Brudzinski : -

X. EXAMINATION RESUME
Generalized condition
Blood Pressure : 130/90 mmHg
Heart Rate : 96 tpm
Respiratory rate : 24 tpm
Temperature : 37,0°C
Weight : 30 kg
Height : 155 cm
Body Mass Index(BMI) : 12,5 kg/m2 (underweight)
Cognitive Function : Normal
Meningeal sign : (-)
Cranial Nerves : Normal
Motoric : Normal
Sensory : Normal
Coordination : Difficult to asses
Autonomy : Normal
Reflex : Physiologic (+) normal , Pathologic (-)

XI. WORKING DIAGNOSIS :

CLINICAL DIAGNOSIS : Myelopati thoracic

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TOPICAL DIAGNOSIS : Medulla spinalis segmen thorakal
ETIOLOGIC DIAGNOSIS : Susp. Spondylitis TB
DIFFERENTIAL DIAGNOSIS : Spinal cord tumor .
SECONDARY DIAGNOSIS : TB on anti tubercular drug

SUGESSTION EXAMINATION :
o Blood routine test
o Blood chemistry test
o Electrolyte
o Thoracic X-Ray
o Spine CT Scan
o MRI
MANAGEMENT :
1) O2 3 lpm
2) IVFD RL + drip tramadol 1 ampul/24 hours
3) Ketorolac 3x30 mg IV
4) Ranitidine 2x50 mg IV
5) Pregabalin 1 x 75 mg
6) Tizanidine 2x 2 mg

LABORATORIUM FINDING :
1. Blood Routine (january, 11th 2020)
Hemoglobin :13,3 gr/dl
Hematocrit : 40,9%
Leucocytes : 9,740 /mm3
Platelets : 436.000/mm3
2. Blood Chemistry (January,11th 2020)

Creatinin : 0,80 mg/dl

Ureum : 34,0 mg/dl

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 Albumin : 3,3 g/dl
AST : 37 u/l
ALT : 29 u/l
3. Elektrolyte
Na+ : 136 mmol/L
K+ : 3,5 mmol/L

4. X-ray

Interpretation :
- X-Ray Thorax
Cor : CTR >50%
Pulmo : bronchovascular pattern is normal, infiltrate (-), honey comb
appearance in lung
Conclusion : Cor : cardiomegaly
Lung : bronkiectasis
- X-Ray Lumbosacral AP/Lateral
Bone structure normal
Alignment lordotic

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 Weight bearing line in promontorium anterior
Normal corpus and discus
There is not fracture
There is not listhesis
Osteofit (-)
Conclusion : there is not abnormality in lumbosakral
5 5
3 3
FINAL DIAGNOSIS
Myelopati ec Susp. Spondylitis TB dd spinal cord tumor + TB on Antitubercular
drug.

FOLLOW UP
1. Jan, 14th 2020
S : Weakness on extremities (+), numbness (+), back pain (+), fever (-), c
O : GCS E(4)V(5)M(6)
Composmentis
BP : 113/81mmHg
HR : 109 bpm
RR : 22 tpm
T : 36.7°C
Cognitive Function : Normal

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 Neck Stiffness : Negative
Cranial Nerves : Normal
Cranial Nerves : Within normal limits
Motoric : Paraparese inferior
Sensory : Hypoesthesia on Th-12 dermatome to lower
Coordination : NT
Autonomy : Micturition (+) with cateter, defecation (-)
Reflex : physiologic(+), Pathologic reflexes (-)
A : Thoracic myelopathy ec susp. Spondilitis TB + TB on antitubercular
treatment
P :
 IVFD RL + tramadol 1  Ketorolac 3x30 mg IV
amp  Ranitidin 2x50 mg IV
 Pregabalin 2x 75 mg  Plan: MRI Thoracal
 Tizanidin 2x2 mg

2. Jan, 15th 2020

S : Weakness on extremities (+), numbness (+), back pain (+), fever (-)
O : GCS E(4)V(5)M(6)
Composmentis
BP : 116/84 mmHg
HR : 100 bpm
RR : 22 tpm
T : 36.7°C
Cognitive Function : Normal
5 5
Neck Stiffness : Negative
3 3
Cranial Nerves : Normal
Motoric : Paraparese inferior
Sensory : Hypoesthesia on Th-12 dermatome to lower
Coordination : NT
Autonomy : Micturition (+) with cateter, defecation (+)

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 Laseque : limited <70
A : Thoracic myelopathy ec susp. Spondilitis TB+ TB on antitubercular
treatment
P :
 IVFD RL + tramadol 1  Ketorolac 3x30 mg IV
amp  Ranitidin 2x50 mg IV
 Pregabalin 2x 75 mg  Consul to Med Rehab
 Tizanidin 2x2 mg

3. Jan, 16th 2020

S : Weakness on extremities (+), numbness (+), back pain (+),fever (-)
O : GCS E(4)V(5)M(6)
Composmentis
BP : 131/91 mmHg 5 5
HR : 114 bpm 4 5
RR : 20 tpm
T : 36.6°C
Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Normal
Motoric : monoparese inferior
Sensory : Hypoesthesia on Th-12 dermatome to lower
Coordination : NT
Autonomy : Micturition (+) with cateter, defecation (+)
Reflex : physiologic reflex(+), pathologic reflexes (-)

A : Thoracic myelopathy ec susp. Spondilitis TB

P :
 IVFD RL + tramadol 1 amp
 Pregabalin 2x 75 mg

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 Tizanidin 2x2 mg
 Ketorolac 3x30 mg IV
 Ranitidin 2x50 mg IV

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 LITERATURE REVIEW

1. Myelopathy
1.1 Definition
The term myelopathy describes pathologic conditions that cause spinal
cord, meningeal or perimeningeal space damage or dysfunction. Traumatic
injuries, vascular diseases, infections and inflammatory or autoimmune processes
may affect the spinal cord due to its confinement in a very small space. Spinal
cord injuries usually have devastating consequences such as quadriplegia,
paraplegia and severe sensory deficits.1

1. 2 Etiology
There are cases where the etiology is never identified, and they are
classified as idiopathic myelopathy. In 2001, De Seze et al. found that 43% of
acute myelopathies were secondary to multiple sclerosis; 16.5% were due to a
systemic disease; 14% to a spinal cord infarct; 6% to an infectious disease; 4%
were secondary to radiation; and 16.5% were idiopathic. Moore et al. found that
in cases of non-traumatic injury, 23.6% were due to cervical spondylolysis; 17.8%
to multiple sclerosis; 16.4% to a neoplastic lesion; 4.1% to motor neuron disease;
and 18.6% were idiopathic or of unknown etiology.1

1.3 Classification
Based on the Sicard and Forstier classification that divides the disease into
compressive and non-compressive.
1.3.1 Compressive myelopathies
Compressive diseases of the spinal cord are divided into acute and chronic,
including degenerative changes, trauma, tumor infiltration, vascular
malformations, infections with abscess formation, and syringomyelia.
Compressive disease is the main cause of myelopathy in older patients. It has a
chronic course and usually does not recur. Kelley et al. found that none of the
patients with compressive myelopathy improved with intravenous corticosteroids,
while patients with inflammatory myelopathies did improve, invalidating the
hypothesis of traumatic inflammatory demyelination.2

1.3.2 Non-compressive myelopathies

Once compression is ruled out as the etiology of myelopathy, the clinical
history is analyzed in depth and a careful clinical examination is performed in
order to look for an inflammatory cause. The diagnosis of an inflammatory
myelopathy requires evidence of spinal cord inflammation. At the present time,
MRI and cerebrospinal fluid (CSF) analysis are the only tools available for
determining the presence of inflammation. There needs to be gadolinium
enhancement of the spinal cord, pleocytosis in the CSF or a high immunoglobulin
G index in the CSF, with a time course ranging between four hours and four
weeks. If none of these findings are present at the time of onset of symptoms,
MRI and lumbar taps must be repeated two to seven days later.2
1.4 Clinical Feature of Myelopathy
Pain is the most prominent complaint elicited from patients with spinal
cord disease. Local pain over the site of the spinal cord lesion usually arises from
involvement of the bone and ligaments surrounding the spinal cord. Pain may
extend into the paravertebral areas and into the shoulders or hips when there is
cervical or lumbar vertebral involvement. Acute pain is seen in fracture, spinal
hemorrhage, infarction, and herniation, whereas subacute pain is seen with
epidural abscess, tumor, and transverse myelitis (days to weeks). Spondylosis,
syringo- myelia, glioma, and intradural extramedullary tumor are causes of
chronic pain (weeks to years).
Local pain can be difficult to distinguish from radicular pain that only
rarely extends into the terminal distribution of the nerve root. Paresthesias in the
distal nerve territory have greater diagnostic value for radiculopathy. Central pain
is most frequently seen in patients with spinal cord injury and occurs long after
the onset of symptoms. It is usually felt in the buttocks, feet, and legs and is
characterized by poorly localized, diffuse, aching, or burning pain. Lhermitte's
sign, another type of central pain caused by irritation of the dorsal column, is an

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electric shock sensation descending down the spine from the neck and, at times
into the extremities, lasting only a few seconds.
Sensory complaints include paresthesias that may be experienced as
tingling, buzzing, or pins and needles usually caused by partial injury of the dorsal
roots or dorsal columns. Numbness or deadness, indicating a lack of sensation in a
part of the body, and dysesthesias, the experience of nonnoxious stimuli as
unpleasant, usually indicate dorsal column pathology. Sensations of warmth,
coldness, and itching tend to be caused by injury to the spinothalamic tracts.
Motor abnormalities include sudden weakness and, in its most extreme
form, paralysis, usually caused by spinal cord trauma, infarcion, and hemorrhage.
If the symptoms evolve slowly, the complaint may be clumsiness or fatigability.
The AIS further classifies injuries as a complete or incomplete spinal cord
injury. A complete spinal cord injury is defined as the absence of all motor and
sensory functions, including sacral roots, distal to the site of injury. These injuries
are designated as being Grade A on the AIS. Incomplete injuries are defined as
those with some degree of retained motor or sensory function below the site of
injury. These are graded B through E on the AIS. Patients with AIS Grade B
injuries have some sensory function but no motor function. AIS Grade C injuries
have a motor grade less than 3 below the neurologic level of injury while AIS
Grade D injuries have a motor grade of at least 3 below the neurologic level of
injury. Patients with Grade E injuries have normal motor and sensory
examinations, but still may have abnormal reflexes or other neurologic
phenomena.
2. Spondylitis TB

2.1 Definition

Tuberculosis spondylitis is a chronic infection in the form of

granulomatosis infection caused by a specific namely mycobacterium tuberculosa
which affects the vertebrae.1
2.2 Classification

To overcome the limitations described, Oguz et al. developed a new

classification system in which spinal TB is classified in to three main types, with

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type I lesions being subdivided in to two subtypes. In this classification system,

lesions are classified as follows: 1) Type I, one-level disc involvement and soft

tissue infiltration without abscess, collapse and neurologic deficit. 2) Type I-A,

lesions only limited to vertebra and therefore, manageable with fine needle biopsy

and medical therapy. 3) Type I-B, abscess formation exceeds the vertebra and the

treatment is debridement using an anterior, posterior or endoscopic approach. 4)

Type II, one- or two-level disc degeneration, abscess formation and mild kyphosis

correctable with anterior surgery. Although instability is not seen in this type,

neurological deficit may be present. The treatment includes debridement with an

anterior approach and fusion with strut tri-cortical graft. 5) Type III, one- or two-

level disc degeneration, abscess formation, instability and deformity that cannot

be corrected without instrumentation. Decompression and stabilization of the

deformity via an anterolateral, posterior, or combined approach is necessary.

Although this classification system provides a practical classification, it has no

special focus on posterior lesions and therefore, this can be considered as the main

limitation of this classification system.2

2.3 Pathogenesis

Spinal involvement is usually a result of hematogenous spread of M.

tuberculosis into the dense vasculature of cancellous bone of the vertebral bodies.

The primary infection site is either a pulmonary lesion or an infection of the

genitourinary system. Spread occurs either via the arterial or the venous route. An

arterial arcade, in the subchondral region of each vertebra, is derived from anterior

and posterior spinal arteries; this arcade form a rich vascular plexus.

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 This vascular plexus facilitates hematogenous spread of the infection in the

paradiskal regions. Batson's paravertebral venous plexus in the vertebra is a valve-

less system that allows free flow of blood in both directions depending upon the

pressure generated by the intra-abdominal and intrathoracic cavities following

strenuous activities like coughing. Spread of the infection via the intraosseous

venous system may be responsible for central vertebral body lesions. In patients

with noncontiguous vertebral tuberculosis, again it is the vertebral venous system

that spreads the infection to multiple vertebrae.

Spinal tuberculosis is initially apparent in the anterior inferior portion of the

vertebral body. Later on it spreads into the central part of the body or disk.

Paradiskal, anterior, and central lesions are the common types of vertebral

involvement. In the central lesion, the disk is not involved, and collapse of the

vertebral body produces vertebra plana. Vertebra plana indicates complete

compression of the vertebral body. In younger patients, the disk is primarily

involved because it is more vascularized. In old age, the disk is not primarily

involved because of its age-related avascularity.

In spinal tuberculosis, there is involvement of more than one vertebra

because its segmental arteries bifurcate to supply two adjacent vertebrae. Spread

of the disease beneath the anterior or posterior longitudinal ligaments involves

multiple contiguous vertebrae. A lack of proteolytic enzymes in mycobacterial

infections (in comparison with pyogenic infections) has been suggested as the

cause of the of the subligamentous spread of infection. In spinal tuberculosis,

characteristically, there is destruction of the intervertebral disk space and the

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adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging

leading to the characteristic angulation and gibbus (palpable deformity because of

involvement of multiple vertebrae) formation.

The upper lumbar and lower thoracic spine are most frequently involved

sites. More than one vertebra is typically affected, and the vertebral body is more

frequently affected than the posterior arch. Distortion of spinal column leads to

spinal deformities.3

2.4 Clinical feature

The characteristic clinical features of spinal tuberculosis include local pain,

local tenderness, stiffness and spasm of the muscles, a cold abscess, gibbus, and a

prominent spinal deformity. The cold abscess slowly develops when tuberculous

infection extends to adjacent ligaments and soft tissues. Cold abscess is

characterized by lack of pain and other signs of inflammation.3

2.5 Suggestive examinations to diagnose spondylitis TB

MRI is the neuroimaging of choice for spinal tuberculosis. MRI is more

sensitive than x-ray and more specific than CT in the diagnosis of spinal

tuberculosis. MRI allows for the rapid determination of the mechanism for

neurologic involvement. MRI readily demonstrates involvement of the vertebral

bodies, disk destruction, cold abscess, vertebral collapse, and spinal deformities.

In the early stages, however, only disk degeneration with alteration of bone

marrow signal intensity of vertebra is seen, which may not be sufficiently

diagnostic of spinal tuberculosis.

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 Abscess formation and collection and expansion of granulation tissue

adjacent to the vertebral body is highly suggestive of spinal tuberculosis. MRI is

also useful in detecting intramedullary or extramedullary tuberculoma, spinal cord

cavitation, spinal cord edema, and possibly unsuspected noncontiguous lesions of

the spine. The subligamentous spread of a paraspinal mass and the involvement of

multiple contiguous bones and intramedullary spinal changes can be very well

demonstrated by MRI.4

2.6 Treatment

World Health Organization (WHO) recommends a category-based treatment

for tuberculosis. Spinal tuberculosis falls under category-1 of the WHO treatment

category. The category-1 antituberculosis treatment regimen is divided into two

phases: an intensive (initial) phase and a continuation phase. In the 2-month

intensive phase, antituberculous therapy includes a combination of four first-line

drugs: isoniazid, rifampicin, streptomycin, and pyrazinamide. In the continuation

phase, two drugs (isoniazid and rifampicin) are given for 4 months. Because of

the serious risk of disability and mortality and because of difficulties of assessing

treatment response, WHO recommends 9 months of treatment for tuberculosis of

bones or joints.

The American Thoracic Society recommends 6 months of chemotherapy for

spinal tuberculosis in adults and 12 months in children. The British Thoracic

Society recommends 6 months of daily treatment with rifampicin and isoniazid,

supplemented in the initial 2 months with pyrazinamide and either ethambutol or

streptomycin (the 6-month four-drug regimen), irrespective of age. Although 6

months of treatment is considered sufficient, many experts still prefer a durations

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of 12–24 months or until radiological or pathological evidence of regression of

disease occurs.5,6

THE BASIC OF DIAGNOSIS

1. Basic clinical diagnosis
According to anamnesis and physical examination, we have found this
patient has paraparesis inferior (UMN Type), hypoesthesia from Th-12
dermatome to the lower. The several important things above mean that there is
damaging on complete spinal cord because of the involvement not of all the tracts7

2. Basic topic diagnosis

Based on anamnesis there are weakness on both legs and numbness in
patient’s lower extremities but from the examination of sensory system, we found
hypoesthesia from Th-12 dermatome to the lower. Based on the dermatomes, we
found that the level of disorder is 12nd thoracal spinal cord segments.
3. Basic etiological diagnosis
Basic etiological diagnose of this patient lead to spondylitis TB because
based on anamnesis and physical examination, we have found symptoms like
localized back pain, numbness on lower extremities, weakness on lower
extremities. On this patient, she also had history of low grade fever , malaise and
weight loss of ± 20 kg for 7 months.
4. Basic differential diagnosis
Spinal cord tumor is chosen as the differential diagnose because it almost
have the same manifestation, such as motor disturbance and numbness. To
establish the diagnosis, some adjunct examination are needed.

Basic workup
 Blood routine test (to find any change that show infection)
 Blood chemistry test and electrolyte (to find whether there is any
extraspinal process involved)
 Thoracic X-Ray (to find any other possible etiology)

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  Vertebra X-Ray (osteoporosis, osteolytics, vertebral corpus destruction,
narrowing of the intervertebral discs, and possibly a mass of paravertebral
abscesses).
 MRI evaluates intervertebral discs and spinal osteomyelitis infections and
shows nerve pressure
5. Basic treatment
 Ketorolac is an non steroidal anti inflamatory drug (NSAID) as an
analgetik for low back pain.
 Pregabalin is an antagonist of voltage gated Ca2+ channels and
specifically binds to alpha-2-delta subunit to produce antiepileptic and
analgesic actions. It successfully alleviates the symptoms of various types
of neuropathic pain and presents itself as a first line therapeutic agent with
remarkable safety and efficacy.
 Ranitidin is a competitive, reversible inhibitor of the action of histamine at
the histamine H2 receptors found in gastric parietal cells. This results in
decreased gastric acid secretion and gastric volume, and reduced hydrogen
ion concentration.
 Tizanidine use for the management of increased muscle tone associated
with spasticity.
 Tramadol is an opioid pain medication moderate to severe pain.

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Ortopedi. Ed.II. Makassar: Bintang Lamumpatue. p. 144-149.
4. Oguz E, Sehirlioglu A, Altinmakas M, et al. A new classification and
guide for surgical treatment of spinal tuberculosis. Int Orthop.
2008;32:127–133.
5. Kumar, Ravindra. 1996. Diagnose SOL. Lucknow: Department of
Neurology King George Medical College.
6. Hsu LC, Cheng CL, Leong JC. Pott's paraplegia of late onset: the cause of
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Br 1988;70(4):534–8
7. World Health Organization. Treatment of tuberculosis: guidelines. 4th ed.
(WHO/HTM/TB/2009.420) World Health Organization; 2010.
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Treatment of tuberculosis and tuberculosis infection in adults and children.
American Thoracic Society and the Centers for Disease Control and
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