Case Report Mielopati

Case Report
MYELOPATHY
By:
Earfistk Tim Vio Lovya
1508434470
Supervisor:
dr. Riki Sukiandra, Sp.S
DEPARTMENT OF NEUROLOGY
MEDICAL SCHOOL RIAU UNIVERSITY
RSUD ARIFIN ACHMAD
PEKANBARU
2017
1
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 : [email protected]
PEKANBARU
I. Patients Identity
Name Mrs. P
Age 58 years
Gender Female
Address Limbungan, Pekanbaru
Religion Moslem
Maritals Status Married
Occupation Housewife
Entry Hospital August,9th 2017
Medical Record 9587xx
II. ANAMNESIS :
Auto & Alloanamnesis (August,9th 2017)
A. Chief Complaint
The weakness on both legs since 1 months before admitted to the hospital
B. Present illness history

About 3 months before admitted to the hospital, previously patients
complained pain in the low back intermittently. It radiated to the abdomen and
was feeling like bounded by something. Patient felt so better when she used the
corset and there was a bottle of warm water in there. Pain felt when woke up in
the morning. Because her complaint didnt get any better, the patient went to
hospital. Pain didnt disappear after get some rest and drugs.
1 month before admitted to the hospital, the patient has complained
weakness on both legs, the weakness appears simultaneously on the right and left
legs but there wasnt numbness. Patient still could walk but wasnt good as usual.
2
Patient also complained breathlessness and left chest pain. Patient still could
control urination and defecation.
She was disclaims the history fever and spinal injury. There was history of
weight loss within 3 months (50kg 39kg) and also history of chronic cought
but not bloody cought.
C. Past Illness history

Hypertension (-), Diabetes mellitus (-)
A history of Cancer (-)
D. Family Illness History

A history of Cancer (-)
RESUME ANAMNESIS
Mrs. P, 58 years old admitted to the hospital on August, 9th 2017. The
patient has complained weakness on both legs suddenly since 1 month before
admission. She complained pain in the back when activity and it radiated to the
abdomen and was feeling like bounded by something since 3 months ago. Pain
didnt disappear after get some rest and drugs and felt when woke up in the
morning. Patient complained about breathlessness and left chest pain. Patient
still could control urination and defecation. There were history of weight loss
within 3 months and history of chronic cought but not bloody cought.
III. PHYSICAL EXAMINATION
A. Generalized Condition
Blood Presure : Right: 120/70 mmHg Left: 120/70 mmHg
Heart Rate : 82 bpm
Respiratory : Respiratory rate : 25 x/mnt Type : Abdominotorakal
Temperature : 36,5C
Weight : 39 kg Height : 143 cm
IMT : 19,07 kg/m2 (normal)
3
B. Neurological status
1) Consciousness : Composmentis GCS : 15 (E4V5 M6)
2) Cognitive Function : Normal
3) Neck Rigidity : Negative
C. Cranial Nerves
1. N. I (Olfactorius )
Right Left Interpretation
Sense of Smell Normal Normal Normal
2. N.II (Opticus)
Visual Acuity Normal Normal
Normal
Visual Fields Normal Normal
Colour Recognition Normal Normal
3. N.III (Oculomotorius)
Ptosis (-) (-)
Pupil
Shape Round Round
Side 3mm 3mm Normal
Extraocular movement Normal Normal
Pupillary reaction to light
Direct (+) (+)
Indirect (+) (+)
4. N. IV (Trokhlearis)
Extraocular movement Normal Normal Normal
4
5. N. V (Trigeminus)
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal reflex (+) (+)
6. N. VI (Abduscens)
Extraocular movement Normal Normal
Strabismus (-) (-) Normal
Deviation (-) (-)
7. N. VII (Facialis)
Tic (-) (-)
Normal
Sense of Taste Normal Normal
Chvostek Sign (-) (-)
8. N. VIII (Acusticus)
Sense of Hearing Normal Normal Normal
9. N. IX (Glossopharyngeus)
Pharyngeal Arch Normal Normal
Sense of Taste Normal Normal Normal
Gag Reflex (+) (+)
5
10. N. X (Vagus)
Pharyngeal Arch Normal Normal
Normal
Dysphonia (-) (-)
11. N. XI (Accesorius)
Normal
Trophy Eutrophy Eutrophy
12. N. XII (Hypoglossus)

Trophy Eutrophy Eutrophy Normal
Tremor (-) (-)
Disartria (-) (-)
D. Motoric
Upper Extremity
Strength
Distal 5 5
Proximal 5 5 Normal
Tone Normal Normal
Involuntary movements (-) (-)
Clonus (-) (-)
Lower Extremity
Strength
Distal 4 4
Proximal 4 4 Paraparase
Tone Spastic Spastic (UMN Type)
Involuntary movements (-) (-)
Clonus (-) (-)
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Body
Involuntary movements (-) (-) Normal
Abdominal Reflex (-) (-)
E. Sensory
Light Touch
Pain
Temperature
Hypesthesia
Proprioceptive
from T11
Position
dermatome to
Two point discrimination
the lower.
Stereognosis
Graphestesia
Vibration Not tested Not tested
F. Reflex
Physiologic
Biceps (+) (+)
Physiologic reflex
Triceps (+) (+)
()
Knee (+++) (+++)
Ankle (+) (+)
Pathologic
(-) (-)
Babinsky
(-) (-)
Chaddock
(-) (-)
Hoffman Tromer
(-) (-)
Openheim Pathologic reflex (-)
(-) (-)
Schaefer
(-) (-)
Gordon
Primitive Reflex
(-) (-)
Palmomental No Primitive Reflex
(-) (-)
Snout
G. Coordination
Point to point movements Normal Normal
Walk heel to toe Not Tested Not Tested
Difficult to assessed
Gait Not Tested Not Tested
Tandem Not Tested Not Tested
Romberg Not Tested Not Tested
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H. Autonom system
Urination : Normal
Defecation : Normal
I. Others Examination
a. Laseque : >700
b. Kernig : >1300
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test : -
f. Brudzinski : -
EXAMINATION RESUME
General Status :
Blood Pressure 120/70 mmHg
Heart Rate 82 bpm
Respiratory Rate 25 times per minute
Temperature 36,5C
Noble Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Normal
Motoric : Paraparese (UMN Type)
Sensory : Hypesthesia on T11 dermatome to the lower
Coordination : Difficult to assessed
Autonomy : Normal
Reflex : Physiologic reflex ()
IV. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS : Thoracic Myelopathy
Paraparese (UMN Type)
Hypesthesia on T11 dermatome to the lower
TOPICAL DIAGNOSIS : 11th thoracal spinal cord segments
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ETIOLOGICAL DIAGNOSIS:
Extradural Spinal Tumor ec. Suspect Vertebral Metastase
DIFFERENTIAL DIAGNOSIS :
Tuberculous Spondylitis
V. SUGGESTION EXAMINATION :
Blood routine
Blood chemistry
Thoracic spine X-ray
MRI thoracic spine with contrast and no contrast
VI. MANAGEMENT
Maintanance : IVFD NaCl 20 dpm
Anti inflamation : Methylprednisolone 3 x 125 mg per IV
Gastric Protector : Ranitidine 2 x 50 mg per IV
Neurotropic : Mecobalamin 3 x 500 mg
Consoul to Pulmonologist
VIII. LABORATORY AND RADIOLOGY FINDINGS

1. Blood Routine (August, 9th 2017)
- Hemoglobin : 14,78 g/dL
- Hematocrit : 32,3 %
- Leukocyte : 14.780/uL
- Thrombocyte : 493.000/uL
Interpretation: Leukocytosis
2. Blood Chemistry (August, 9th 2017)

- Glucose : 133 mg/dL
- Ureum : 36 mg/dL
- Creatinin : 0,74 mg/dL
Interpretation: In normal limit
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3. Thoracic X-ray (August, 10th 2017)
Interpretation:
- Pleura effusion sinistra.
- The absence of mass still couldnt be removed.
- Inhomogeneous opacity at superior sinistra lobes.
4. MRI thoracic spine with contrast and no contrast at Awal Bross

Hospital (August, 10th 2017)
Interpretation:
- The change of signal intensity looks at corpus vertebra Th 9,
Th12, L5, S1, S2 Suggestive of metastase.
- Bikonkaf fracture at corpus vertebra Th 12.
- Protuced disc intervetebral L4-5
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- Multiple disc bulging intervetrebrae L1-2, L2-3 and L3 3-4
- Spondylosis of vertebra lumbalis
- The change of signal hyperintensity at end plate corpus vertebra
L1, L, L4 and S1 Degenerative process.
IX. FINAL DIAGNOSIS

1. Myelopathy T11 ec Suspect Vertebral Metastase
2. Suspect Lung Cancer
X. MANAGEMENT
Maintanance : IVFD NaCl 20 dpm
Anti inflamation : Methylprednisolone 3 x 125 mg per IV
Gastric Protector : Ranitidine 2 x 50 mg per IV
Neurotropic : Mecobalamin 3 x 500 mg
XI. FOLLOW UP
August, 10th 2017
Subjective :
The patient has complained the weakness on both legs, pain in the low back (+),
breathlessness (+).
Objective :
GCS 15
Heart Rate 86 bpm
Respiratory Rate 25 tpm
Temperature 36.5C
Motoric : Paraparase (UMN Type)
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Autonomy : Normal
Assessment :
- Myelopathy T11 ec Suspect Vertebral Metastase
- Suspect Lung Cancer
Plan :
IVFD NaCl 20 dpm
Methylprednisolone 3 x 125 mg per IV
Ranitidine 2 x 50 mg per IV
Mecobalamin 3 x 500 mg
August, 11th 2017

Subjective :
breathlessness ( ).
Objective :
GCS 15
Heart Rate 87 bpm
Temperature 36.5C
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Autonomy : Normal
Assessment :
Plan :
IVFD NaCl 20 dpm
August, 12th 2017

Subjective :
breathlessness (-).
Objective :
GCS 15
Heart Rate 85 bpm
Temperature 36.5C
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Autonomy : Normal
Assessment :
Plan :
IVFD NaCl 20 dpm
August, 14th 2017

Subjective :
breathlessness (-).
Objective :
GCS 15
Heart Rate 87 bpm
Temperature 36.5C
14
Autonomy : Normal
Assessment :
Plan :
IVFD NaCl 20 dpm
15
DISCUSSION
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
It is important not to mistake myelopathy for myelitis. Although both terms
refer to spinal cord compromise due to a pathological event, myelopathy has
multiple etiologies, while myelitis is used to refer to inflammatory or infectious
processes.1,2 Acute transverse myelopathy (includes non-inflammatory etiologies)
and transverse myelitis have been used as synonyms in the published literature.2,3
Findings of spinal tract injuries, a certain degree of sensory dysfunction, or
urinary retention, point to a spinal cord injury. There are certain conditions that
may mimic myelopathy, such as myopathy or disorders of the neuromuscular
junction, but the absence of a sensory deficit rules them out. On the other hand,
bilateral frontal mesial lesions may mimic myelopathy but they are associated
with abulia or other signs of frontal dysfunction.4
Myelopathies may have a variable course and may manifest as a single
event or as a multi-phasic or recurrent disease. The latter is rare and is usually
secondary to demyelinating diseases, vascular malformations of the spinal cord, or
systemic diseases.2,3 The central nervous system (CNS) damage may be
monofocal as in transverse myelitis and optic neuritis, or multifocal as in acute
disseminated encephalomyelitis (ADEM) (brain and spinal cord), neuromyelitis
optica (optic nerve and spinal cord) and multiple sclerosis (MS) (any area of the
neural axis).2
Spinal cord pathologies may be classified as acute, subacute/intermittent
or chronic, depending on the time course, the extent of the involvement, the
clinical picture or syndrome, or the etiology. Patients with myelopathies but no
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evident lesions, or who present with multiple lesions of chronic appearance on
magnetic resonance imaging, must be questioned about prior subtle symptoms.4
Acute onset that worsens within hours or days points to a spinal cord
infarct or hemorrhage. When symptoms are recent, it is of paramount importance
to rule out a surgical emergency. This requires immediate imaging work-up,
ideally total spine magnetic resonance (MRI). If there is evidence of spinal cord
compression due to an acute lesion (epidural metastasis or abscess), definitive
management is required in order to avoid damage or to adequately manage all
other potential diagnoses. If the symptoms progress for more than three weeks,
transverse myelitis is improbable, and other conditions must be considered, such
as a spinal tumor, chronic compressive disease, dural arterio-venous fistula,
metabolic disorder, sarcoidosis, or a degenerative process.4
Spinal cord syndromes present with typical signs and symptoms caused by
a lesion of a specific tract in a specific location that may lead to the etiological
diagnosis. They are classified as follows:4-6
1. Complete spinal cord: involvement of all the tracts (trauma, compression or
acute transverse myelitis).
2. Brown Squard or hemi-spinal cord syndrome: ipsilateral cortico-spinal tract,
posterior columns and contralateral spinothalamic tract (multiple sclerosis and
compression).
3. Anterior spinal cord syndrome: anterior horns, corticospinal, spinothalamic
and autonomic tracts (anterior spinal artery infarct and multiple sclerosis).
4. Posterior spinal cord syndrome: posterior columns (vitamin B12 or copper
deficiency).
5. Central syndrome: spino-thalamic crossing, cortico-spinal and autonomic
tracts (syringomyelia, neuromyelitis optica).
6. Medullary cone: sacral emerging fibres (post-viral myelitis).
7. Cauda equina: cauda equina nerves (acute cytomegalovirus infection,
polyradiculitis and compression).
8. Tractopathies: selective disorders (vitamin B12 deficiency, paraneoplastic
myelopathy and multiple sclerosis).
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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. Chronic myelopathies
include, among others, spondylotic myelopathy, vascular malformations,
retrovirus-associated myelopathy (human immunodeficiency virus),
syringomyelia, chronic myelopathy due to multiple sclerosis, combined subacute
degeneration (vitamin B12 deficiency), tabes dorsalis, and familial spastic
paraplegia. Based on the Sicard and Forstier classification that divides the disease
into compressive and non-compressive, in relation to subarachnoid space
obstruction, Table 1 shows a list of the different etiologies.
Table 1. Etiologies5,7,8
Compressive Non-compressive
Degenerative Infectious transverse myelitis (viral,

bacterial, spirochetes, fungi)
Acute disseminated encephalitis

(demyelinating diseases, multiple
sclerosis, neuromyelitis optica, Eales
disease)
Vascular (spinal arterial thrombosis,

central nervous system vasculitis)
Traumatic (bone lesion, disc herniation, Toxic substances and physical agents
epidural hemorrhage) (lathyrism, arsenic, tri-ortho-cresyl
phosphate, nitric oxide, intrathecal
methotrexate, radiation, electric injury)
Infectious (abscess) Degenerative (primary lateral sclerosis,

familial spastic paraparesis,
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spinocerebellar ataxia, Friedriechs
ataxia)
Tumors (extradural, intradural) Metabolic (vitamin B12 deficiency,

vitamin E deficiency,chronic hepatic,
renal disease, hexosamidase deficiency)
Vascular (arterio-venous malformation) Paraneoplastic
Syringomyelia
1.2.1 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 (Table 1).
Patients with clinical findings of compressive myelopathy that show extensive
(more than three vertebral segments) fusiform spinal cord hyperintensity in T2
weighted sequences, are often mistakenly thought to have optic neuritis, or
classified as idiopathic. This delays surgical treatment when other causes such as
stenosis of the spinal canal are not taken into consideration.9
Compressive disease is the main cause of myelopathy in older patients. It
has a chronic course and usually does not recur.10 High intensity signals in T2
images is explained by myelomalacia, gliosis, tethering damage, vascular or
inflammatory edema, demyelination and vacuolar changes. Gadolinium
enhancement is limited to the region of maximum compression.11 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.
Surgery improved or stabilized all patients with compressive disease,
consistent with the hypothesis of spinal cord edema or reversible ischemia in
compression. These findings support the argument that the clinical and imaging
findings may differentiate those patients who will benefit from surgical
decompression.11 In 2007, Yukawa et al. found that the signal intensity in the pre-
operative T2 image correlates with patient age, chronicity of the disease, and post-
operative recovery. Patients with greater signal intensity in T2 weighted images
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recover poorly. Consequently, this parameter may be used as a predictor of
surgical prognosis.12 Matsumoto et al. found no relationship between hyperintense
signals and prognosis.13
1.2.2 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.14
2. Spinal Tumor
2.1 Definition
Spinal tumors are neoplasm located in the spinal cord. Tumors of the
spinal cord is divided as primary tumors and secondary tumors. The primary
tumor is a tumor originating from the spinal cord, while secondary tumors are the
mestastase of tumors in other body parts. Spinal cord tumors are generally benign
(onset is usually gradual) and two-thirds of patients operated on between 1-2 years
after the onset of symptoms. The first symptoms of spinocerebellar cord tumor is
important to know because the surgery as early as possible to prevent disability.6,7
2.2 Classification
Based on the origin and nature of the cells, the tumor in the spinal cord
tumors can be divided into primary and secondary tumors. Primary tumors can be
benign or malignant, while secondary tumors are always malignant because it is
the metastasis of malignant process in other places such as lung cancer, breast,
prostate, kidney, thyroid or lymphoma. Primary tumors are malignant
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astrocytomas example, neuroblastoma, and kordoma, while benign example
neurinoma, glioma, and ependimoma.8,9
Based on its location, a tumor of the spinal cord can be divided into two
groups, there are tumor intradural and extradural. Intradural tumor in which it is
itself subdivided into intramedular and extramedullary tumors. Various kinds of
spinal cord tumors is based on location can be seen in Table 2 .8
Image 1 (A) Intradural-intramedular Tumor, (B) Intradural-ekstramedular

tumor and (C) Ekstradural tumor.
Tabel 2. Spinal Tumor Classified by the Histologic Representation8
Intradural Intradural
Ekstra dural
ekstramedular intramedular
Chondroblastoma Ependymoma, type Astrocytoma
Chondroma myxopapillary Ependymoma
Hemangyoma Epydermoid Ganglioglyoma
Lymphoma Lypoma Hemangyoblastoma
Meningyoma Meningyoma Hemangioma
Neuroblastoma Neurofibroma Lyphoma
Neurofybroma Paraganglyoma Medulloblastoma
Osteoblastoma Schwanoma Neuroblastoma
Osteochondroma Neurofybroma
Osteosarcoma Oligodendroglioma
Sarcoma Teratoma
Vertebral hemangyoma
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2.3 Etiology
Causes of primary spinal cord tumors until now has not known for certain.
Some possible causes and are still in the research stage is a virus, a genetic
disorder, and chemicals that are carcinogenic. As for the secondary tumor
(metastasis) is caused by cancer cells that spread from other parts of the body via
the bloodstream which then penetrate the vascular wall, attached to the normal
spinal cord tissue and form a new tumor tissue in the area.9
2.4 Clinical Manifestation7-9

According to Cassirer, spinal cord tumor disease course is divided into
three :
1. The discovery of unilateral radicular syndrome in the long term
2. Brown Sequard Syndrome
3. The total compression of the spinal cord or bilateral paralysis
The first complaint of spinal cord tumors may be radicular pain, pain
vertebrae, or pain funikuler. Statistically the radicular pain is the first indication of
space occupying lesions in the spinal canal and called pseudo phase pre neuralgia.
Reported 68% of cases of spinal tumor properties radicular pain, another report
mentions 60% in the form of radicular pain, 24% and 16% funikuler pain pain is
not jelas3. Suspected radicular pain due to spinal cord tumor when:
1. Radicular pain is severe and prolonged, with pyramidal tract symptoms
2. Location radicular pain beyond the area of predilection HNP such as C5-7,
L3-4, L5 and S1.
Tumors of the spinal cord that often cause radicular pain are located at
intradural-extramedullary, was intramedular tumors rarely cause radicular pain. At
extradural tumor properties radikulernya usually severe pain and about some
radiks.
Tumors intrameduler and intradural-ekstrameduler can also be preceded
by symptoms of ICT such as hydrocephalus, headache, nausea and vomiting,
papilledema, visual disturbances, and impaired gait. Tumors neurinoma and
Ependymomas secrete large amounts of protein into the liquor, which can impede
the flow of liquor in spinal subarachnoid compartment, and this incident put
forward as a hypothesis to explain the incidence of hydrocephalus as clinical
22
symptoms of intraspinal neoplasms primer.5 General symptoms due compression,
among others:
1. Pain
Compression of a tumor may stimulate neural pathways-pathways found
in the spinal cord and cause pain that seemed to come from various parts of the
body (diffuse pain). This pain is usually sedentary, sometimes gain weight and
feels like a burn.
2. Sensory changes
Most patients with spinal cord tumors experience a loss of sensation.
Usually numbness and loss of skin sensitivity to temperature.
3. Problem Motor
Initial symptoms may include muscle weakness, spasticity, and the
inability to hold urine or defecate. If untreated can worsen symptoms including
muscle atrophy and paralysis. In fact, in some people can develop into ataxia.
Parts of the body that cause the symptoms vary depending on the location
of tumors along the spinal cord. In general, the symptoms appear on the body
level with the location of the tumor or below the location of the tumor. For
example, the tumor in the spinal cord (the segment thorakal) can cause chest pain
that spreads to the front (girdleshape pattern) and increased pain when coughing,
sneezing, or bending. Tumors that grow on cervical segment can cause pain that
can be felt up to the arm, while tumors that grow in the lumbosacral segment can
trigger back pain or pain in legs.
2.5 Diagnosis7-9
In addition to history and physical examination, diagnosis of tumors of the
spinal cord can be enforced with the help of investigations like the one below.
1. Laboratory
Spinal fluid (CSF) may show increased protein and xantokhrom, and
sometimes found the cell malignancies. In taking and obtain spinal fluid of
patients with spinal cord tumors should be careful because the blocks can be
partially transformed into a complete block of spinal fluid and cause complete
paralysis.
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2. Plain Photo vertebrae
Plain entire spine 67-85% abnormal. Discovered the possibility of erosion
of the pedicle (defects resembling "owl eyes" on the lumbosacral spine AP) or
dilation, pathological compression fractures, vertebral body scalloping, sclerosis,
changes in osteoblastic (perhaps terajdi myeloma, prostate Ca, Hodgkin, and
usually Ca breast).
3. CT-scan
CT scans can provide information on the location of the tumor, even
sometimes provide information on the type of tumor. This examination can also
help doctors detect the presence of edema, hemorrhage and other related
circumstances. CT scans can also help doctors evaluate the therapeutic results and
see the progression of tumors.
4. MRI
This examination can distinguish between healthy tissue and tissue
abnormalities accurately. MRI can also show images of tumor that is located near
the bone is more obvious than the CT-scan.
2.6 Management
Management for the most part either intramedular and extramedullary
tumors is by surgery. The aim is to remove the tumor completely with the rescue
of neurological function optimally. Most intradural-extramedullary tumors can be
resected completely with a neurological disorder that minimal or no postoperative.
Tumors that have a pattern of rapid growth and aggressive histologically and not
totally eliminated through surgery can be treated with radiation therapy post
operation.12
Therapies for the spinal cord tumors are13,14,15:
1. Deksamethason: 100 mg (reducing pain in 85% of cases, it may also result in
improved neurological).
2. Management based on evaluation of radiographic :
If there is no epidural mass: ambulatory primary tumor (eg with systemic
chemotherapy); local radiation therapy at the bony lesions; analgesics for
pain.
24
If there is an epidural lesions, perform surgery or radiation (typically
3000-4000 cGy at 10x care with the introduction of two levels above and
below the lesion); Radiation is usually as effective as laminectomy with
fewer complications.
3. Emergency Management (surgery / radiation) is based on the degree of the
block and the speed of deterioration :
If >80% complete block or worsening rapidly: the management as soon as
possible (when taking care of the radiation, deksamethason continue the
next day with 24 mg IV every 6 hours for 2 days, then lowered (tappering)
for radiation, for 2 weeks).
If <80% block: routine maintenance (for radiation, continue
deksamethason 4 mg for 6 hours, lowered (tappering) during treatment as
tolerated).
4. Radiation
Radiation therapy is recommended for intramedular tumor that can not be
removed completely.
5. Surgery
Tumors are usually removed with little surrounding tissue with myelotomy
techniques. Ultrasonic aspiration, laser, and microscopes used in surgery of the
spinal cord tumor.
Surgical indications12:
1. Tumor and tissue cannot be diagnosed (consider biopsy if the lesion can be
reached). Note: lesion such as epidural abscesses can occur in patients with a
history of tumors and can be misinterpreted as metastases.
2. The spinal cord is not stable (unstable spinal).
3. Failure radiation (radiation experiments usually for 48 hours, unless there are
significant or rapid deterioration); usually occurs with radioresistant tumors
such as renal cell carcinoma or melanoma.
4. Recurrence after the maximum radiation.
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2.7 Prognosis
Tumors with the aggressive histopathologic and clinical manifestation
have a poor prognosis to therapy. Radical surgery may be done in these cases.
Total resection of tumor can cure or at least the patient can be controlled for a
long time. Neurologic function after surgery is very dependent on the patient's
preoperative status. The prognosis gets worse with increasing age (> 60 years).13
3. Tuberculous Spondylitis
3.1 Definition
Tuberculous spondylitis or spinal tuberculosis are also known as name

Pott's disease of the spine or vertebral tuberculous osteomyelitisis a disease that is
prevalent throughout the world. Accounted for lessover 3 million deaths occur
annually due to this disease.16
This disease was first described by Percival Pott in1779 found an
association between lower locomotor weaknessthe curvature of the spine, but it is
not associated withtuberculosis bacillus until the discovery of the bacillus by
Koch in 1882,so the etiology of the incident became clear.16
In the past, tuberculosis spondylitis is a term that used for diseases of
childhood, which are mainly aged 3-5 year. Today, with the improvement of
health services, the incidence of age This experience changes that adult age
groups become more frequent affected than children.3 Conservative therapy given
to patients with spinal tuberculosis actually give good results, but in the case -
specific case the necessary operative measures and rehabilitation measures should
be carried out well before or after the patient underwent operative action.
3.2 Pathophysiology
Pott disease is usually secondary to an extraspinal source of infection. Pott

disease manifests as a combination of osteomyelitis and arthritis that usually
involves more than 1 vertebra. The anterior aspect of the vertebral body adjacent
to the subchondral plate is usually affected. Tuberculosis may spread from that
area to adjacent intervertebral disks. In adults, disk disease is secondary to the
26
spread of infection from the vertebral body. In children, the disk, because it is
vascularized, can be the primary site.16
Progressive bone destruction leads to vertebral collapse and kyphosis. The
spinal canal can be narrowed by abscesses, granulation tissue, or direct dural
invasion, leading to spinal cord compression and neurologic deficits.16
The kyphotic deformity is caused by collapse in the anterior spine. Lesions
in the thoracic spine are more likely to lead to kyphosis than those in the lumbar
spine. A cold abscess can occur if the infection extends to adjacent ligaments and
soft tissues. Abscesses in the lumbar region may descend down the sheath of the
psoas to the femoral trigone region and eventually erode into the skin.16
3.3 Diagnosis16
1. History of the disease and the clinical manifestation:
a. Onset of the disease usually several months - in the form of general
weakness, appetite decreased eating, weight loss, night sweats, body
temperature increased slightly in the afternoon and evening.
b. Pain in the back of the early symptoms and is often found.
c. Gibus.
d. Cold abscess.
e. Neurologic abnormalities occurred in 50% of cases and include spinal
compression cord disorders such as motor, sensory and autonomic
according to severity destruction spine, kyphosis and abscess formation.
f. Tuberculosis cervical vertebrae are rare but have more conditions serious
because of the severe neurological complications. This condition is
particularly followed with pain and stiffness. Patients with lower cervical
spine disease found with dysphagia or stridor. Symptoms also include
torticollis, hoarse and neurological deficits.
2. Investigations
a. Tuberculin skin test: positive

b. Erythrocyte sedimentation rate: increased
c. Microbiology (of bone tissue or abscess): acid-fast bacilli (+)
d. X-ray:
27
Destruction of the anterior portion of the vertebral body
An increase in anterior wedging
Collapse of the vertebral body
e. CT-Scan:
Describe in more detail with bone lytic lesions irregular, collapse disk and
bone damage
Low contrast resolution of soft tissue better describe, particularly the
paraspinal region
Detect lesions early and effective way to describe the shape and
calcification of soft tissue abscess
f. MRI
Standards for evaluating infection and most effective disk space in shows
the extent of disease in soft tissue and spread tuberculosis debris under the
anterior and posterior longitudinal ligament
The most effective way to demonstrate the neural compression
4. Lung Cancer
4.1 Definition
Lung cancer is a malignant tumour that grows in an uncontrolled way in
one or both of the lungs. Cancer that starts in the lungs is known as primary lung
cancer. It can spread to other parts of the body such as the lymph nodes, brain,
adrenal glands, liver and bones. Sometimes a cancer starts in another part of the
body and spreads to the lungs. This is known as secondary or metastatic cancer in
the lung.17
4.2 Risk Factors17

While the causes of lung cancer are not fully understood, a number of risk
factors are associated with developing the disease. These include:
1. Tobacco smoking : Smoking causes almost 9 out of 10 lung cancers.
Compared with nonsmokers, smokers are 25 times more likely to develop
28
lung cancer.4 In Australia, about 84% of lung cancer cases in males, and
74% in females, are estimated to be a result of tobacco smoking.5 The risk
of developing lung cancer is strongly linked to the age a person starts
smoking, how long they smoke and the number of cigarettes they smoke.
2. Second-hand smoking: Breathing in other peoples tobacco smoke (passive
or second-hand smoke) can cause lung cancer. People who have never
smoked but who have been frequently exposed to second-hand smoke are
2030% more likely to develop lung cancer than nonsmokers who have not
been exposed. People who have never smoked and have not been around
second-hand smoke have about a 0.5% risk of developing lung cancer.
3. Exposure to asbestos: People who are exposed to asbestos have a greater
risk of developing cancer, particularly pleural mesothelioma. Although the
use of asbestos in building materials has been banned nationally since 2003,
it may still be in some older buildings. People who have been exposed to
asbestos and are, or have been, a smoker are at even greater risk. It can take
many years after being exposed to asbestos for mesothelioma to develop.
This is called the latency period or latent interval, and it is usually between
20 and 60 years.
4. Exposure to other elements: Contact with the processing of steel, nickel,
chrome and coal gas may be a risk factor. Exposure to radiation and other
air pollution, such as diesel particulate matter, also increases the risk of
lung cancer.
5. Family history: Having a family member diagnosed with lung cancer
increases the risk.
6. Personal history: The risk of developing lung cancer is increased if you
have been previously diagnosed with another lung disease such as lung
fibrosis, chronic bronchitis, emphysema or pulmonary tuberculosis.
7. Older age: Lung cancer is most commonly diagnosed in people aged 60
years and older, though it can occur in younger people.
29
4.3 Classification17
There are several types of primary lung cancer, which are classified
according to the type of cells affected, and a number of less common subtypes.
Cancers are named for the way the cells appear when viewed under a microscope.
1. Non-small cell lung cancer (NSCLC)
Makes up over 80% of lung cancers. NSCLC may be classified as:
Adenocarcinoma (begins in mucus-producing cells and is more often
found in the outer part of the lungs).
Squamous cell carcinoma (most commonly develops in the larger airways)
Large cell undifferentiated carcinoma (the cancer cells are not clearly
squamous or adenocarcinoma).
2. Cancer Council Small cell lung cancer (SCLC)
Makes up about 1520% of lung cancers. SCLC tends to start in the
middle of the lungs, and usually spreads more quickly than NSCLC.
3. Other tumours starting in the space between the lungs (mediastinum) or
chest wall. Thymus gland tumours, germ cell tumours, tumours of nerve
tissue and lymph gland tumours (lymphoma) can arise in the mediastinum.
These are not strictly lung cancer. Primary tumours of bone, cartilage or
muscle can also arise in the chest wall but these are rare.
4. Mesothelioma: A type of cancer that affects the covering of the lung (the
pleura). It is different to lung cancer. There are two main types of
mesothelioma: pleural and peritoneal. In most cases, exposure to asbestos
is the only known cause of pleural mesothelioma.
4.4 Staging
Working out how far the cancer has spread is called staging, and it helps
your health care team recommend the best treatment for you. Both NSCLC and
SCLC are staged in similar ways. The most common staging system for lung
cancer is the TNM system. TNM stands for tumour-nodes-metastasis. Each letter
is assigned a number (and sometimes a or b) to show how advanced the cancer is.
This information may be combined to give the lung cancer an overall stage of I,
II, III or IV.17
30
Tabel 3. American Joint Committee on Cancer (AJCC) TNM System for Defining
Lung Cancer18
Tabel 4. AJCC Stage Grouping of Lung Cancer18
31
4.5 Diagnosis17
The main symptoms of lung cancer are a new cough or change in an
ongoing cough, breathlessness, chest pain, repeated bouts of pneumonia or
bronchitis coughing or spitting up blood. A person may have also experienced
symptoms such as fatigue, weight loss, hoarse voice, wheezing, difficulty
swallowing, and abdominal or joint pain.
Lung cancer symptoms can be vague and the disease is often discovered
when it is advanced (has spread to other parts of the body). Having any one of
these symptoms does not necessarily mean that you have cancer. Some of these
symptoms may be caused by other conditions or from the side effects of smoking.
However, if you have symptoms, see your doctor without delay.
Sometimes, there are no symptoms and the cancer is found during routine
tests (often an x-ray or CT scan) for other conditions. If so, the cancer is more
likely to be in an early stage of development (confined to the lungs).
1. Chest x-ray
A chest x-ray is painless and can show tumours 1 cm wide or larger. Small
tumours may not show up on an x-ray or may be hidden by other organs within
the chest cavity.
2. CT scan
It can detect smaller tumours than those found by chest x-rays, and provides
detailed information about the tumour, the lymph nodes in the chest and other
organs.
3. Lung function test (spirometry)
This test checks how well the lungs are working. It measures how much air
the lungs can hold and how quickly the lungs can be filled with air and then
emptied. You will be asked to take a full breath in and blow out into a machine
called a spirometer.
4. Sputum cytology
A sputum cytology test examines a sample of mucus (sputum) from your
lungs to see abnormal cells.. Sputum is different to saliva as it contains cells that
line the respiratory passages.
32
5. Biopsy
If a tumour is suspected after an x-ray or CT scan, a sample of tissue will be
taken to confirm whether you have lung cancer. The sample can be collected in
different ways such as bronchoscopy, mediatinoscopy, endobronchial ultrasound
or thoracoscopy
4.6 Treatment17
Treatment for lung cancer will depend on the type of lung cancer you have,
the stage of the cancer, your breathing capacity and your general health. NSCLC
and SCLC are treated in different ways.
1. Non-small cell lung cancer (NSCLC)
a. Early stage : Usually treated with surgery, including removal of nearby
lymph nodes. If surgery is not an option, radiotherapy is offered.
Sometimes, chemotherapy may be given after surgery or with radiotherapy
b. Locally advanced : Stage III cancer can be treated with surgery and
chemotherapy or with radiotherapy and chemotherapy. Treatment will
depend on the number and location of lymph nodes with cancer.
c. Advanced : Palliative chemotherapy and/or palliative radiotherapy may be
offered depending on symptoms. New targeted therapy drugs may also be
an option.
2. Small cell lung cancer (SCLC)
a. Stages IIII Chemotherapy and radiotherapy are the main treatments.
Surgery is not used.
b. Stage IV Palliative chemotherapy is the main treatment. Palliative
radiotherapy may also be given to the brain, spine, bone or other parts of
the body where the cancer has spread.
4.7 Prognosis
Prognosis means the expected outcome of a disease. You may wish to
discuss your prognosis and treatment options with your doctor, but it is not
possible for any doctor to predict the exact course of the disease. Instead, your
doctor can give you an idea about the general prognosis for people with the same
33
type and stage of cancer. As in most types of cancer, the results of lung cancer
treatment tend to be better when the cancer is found and treated early.17
5. The Basic of Diagnosis

5.1 Clinical Diagnosis : Thoracic myelopathy
According to anamnesis and physical examination, we have found:
1. Paraplegia (UMN Type)
2. Hypesthesia on T11 dermatome to the lower
The several important things above mean that there is damaging on
incomplete spinal cord because of the involvement not of all the tracts.
5.2 Topical Diagnosis : 11th thoracal spinal cord segments

Although based on anamnesis there isnt numbness in patients body but
from the examination of sensory system, we found hypesthesia on T11 dermatome
to the lower. Based on the dermatomes, we found that the level of disorder is 11th
thoracal spinal cord segments.
5.3 Basic Etiological Diagnosis

Basic etiological diagnosis of this patient is leads to extradural tumor,
because on this patient there are pain of the low back, it radiated to the abdomen
and like bounded by something. Then continued by weakness both of legs. Its
mean that something compression form the outter of medulla spinalis. The
metastase tumor is the most causing the medulla spinal tumor. And from
radiology findings (MRI), we found the change of signal intensity looks at corpus
vertebra suggestive of metastase. So we considered to vertebral metastase.
Based on anamnesis, this patient complained about breathlessness, chest
pain, history of chronic cought and weight loss until 11 kg within 3 months. That
are the manifestation clinic of malignancy. From thoracic x-ray also found
something at pulmo that suspected as mass although to ensure it, can do the CT
Scan Thoracic.
34
5.4 Basic differential diagnose
The gold standard for diagnose the spinal tumor is MRI. The tuberculous
spondylitis cause compression to the medulla spinalis by the abscess producing.
Considered the tuberculous spondylitis because it injury is in extradural too, so it
almost have the same manifestation that starting from the pain of low back then
weakness and numbness. But one the manifestation of infection is fever and this
patient didnt fever.
5.5 Basic supporting examination
a. Laboratory : to knowing risk factors factor for the tumors, infection and
the general condition of the patient.
b. Thoracal X-ray : to find the metastatic sign for the tumors
c. Thoracal MRI : to find the etiologic for this case at area of medulla
spinalis or vertebrae.
5.6 Basic treatment

a. IVFD (30cc/kgbb/day) NaCl 20 gtt/i to maintance the euvolemic
condition.
b. Methylprednisolone 2 x 125 mg per IV as to provides relief for inflamed
areas of the body.
c. Ranitidine 2 x 50 mg per IV as preventing side effects from use of
methylprednisolone in the stomach in the form of peptic ulcer
d. Mecobalamine 3 x 500 mg tab as neurotropic.
35
REFERENCE
1. Myelopathy. Diseases Database Ver 1.8. Medical lists and links [internet].
2006. http://www.diseasesdatabase.com
2. Scotti G, Gerevini S. Diagnosis and differential diagnosis of acute transverse
myelopathy. The role of neuroradiological investigations and review of the
literature. Neurol Sci. 2001;22Suppl 2:S69-73.
3. Kaplin AI, Krishnan C, Deshpande DM, et al. Diagnosis and management of
acute myelopathies. Neurologist. 2005;11:2-18.
4. Schmalstieg WF, Weinshenker BG. Approach to acute or subacute
myelopathy. Neurology. 2010;75:(18 Suppl 1):S2-8.
5. Hauser SL. Diseases of the spinal cord. In: Harrisons principles of internal
medicine. 16th ed. New York: McGraw-Hill; 2005. p. 2438-47.
6. Jacob A, Weinshenker BG. An approach to the diagnosis of acute transverse
myelitis. Semin Neurol. 2008;28:105-20.
7. Garca DR. Mielopatas. Manual de Prcticas Mdicas-Hospital Hermanos
Ameijeiras [internet]. 2008.
http://www.sld.cu/galerias/pdf/sitios/neurologia/pa_mielopatias.pdf.
8. Moore AP, Blumhardt LD. A prospective survey of the causes of non-
traumatic spastic paraparesis and tetraparesis in 585 patients. Spinal Cord.
1997;35:361-7.
9. De Seze J, Stojkovic T, Breteau G, et al. Acute myelopathies: Clinical,
laboratory and outcome profiles in 79 cases. Brain. 2001;124:1509-21.
10. Ghezzi A Baldini SM, Zaffaroni M. Differential diagnosis of acute
myelopathies. Neurol Sci. 2001;22(Suppl 2):S60-4.
11. Kelley BJ, Erickson BJ, Weinshenker BG. Compressive myelopathy
mimicking transverse myelitis. Neurologist. 2010;16:120-2.
12. Yukawa Y, Kato F, Yoshihara H, et al. MR T2 image classification in
cervical compression myelopathy: predictor of surgical outcomes. Spine.
2007;32:1675-8.
13. Matsumoto M, Toyama Y, Ishikawa M, et al. Increased signal intensity of the
spinal cord on magnetic resonance images in cervical compressive
36
myelopathy. Does it predict the outcome of conservative treatment? Spine.
2000;25:677-82.
14. Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria
and nosology of acute transverse myelitis. Neurology. 2002;59:499-505.
15. National Institutes of Health. Transverse Myelitis. Department of Health and
Human Services 2012;12: 1-14.
16. Hidalgo JA. Pott Disease (Tuberculous Spondylitis).
http://www.eMedicine.com
17. Cancer Counsil Australia. Understanding Lung Cancer.2016.
18. American Joint Committee on Cancer (AJCC). (2002). AJCC staging manual
(6th ed.). New York: Springer-Verlag.
37

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Case Report

B. Present illness history

C. Past Illness history

D. Family Illness History

III. PHYSICAL EXAMINATION

Sense of Hearing Normal Normal Normal

12. N. XII (Hypoglossus)

IV. WORKING DIAGNOSIS

VIII. LABORATORY AND RADIOLOGY FINDINGS

2. Blood Chemistry (August, 9th 2017)

4. MRI thoracic spine with contrast and no contrast at Awal Bross

IX. FINAL DIAGNOSIS

August, 11th 2017

August, 12th 2017

August, 14th 2017

Degenerative Infectious transverse myelitis (viral,

Acute disseminated encephalitis

Vascular (spinal arterial thrombosis,

Infectious (abscess) Degenerative (primary lateral sclerosis,

Tumors (extradural, intradural) Metabolic (vitamin B12 deficiency,

Vascular (arterio-venous malformation) Paraneoplastic

1.2.1 Compressive myelopathies

1.2.2 Non-compressive myelopathies

Image 1 (A) Intradural-intramedular Tumor, (B) Intradural-ekstramedular

Tabel 2. Spinal Tumor Classified by the Histologic Representation8

2.4 Clinical Manifestation7-9

Tuberculous spondylitis or spinal tuberculosis are also known as name

Pott disease is usually secondary to an extraspinal source of infection. Pott

a. Tuberculin skin test: positive

4.2 Risk Factors17

Tabel 4. AJCC Stage Grouping of Lung Cancer18

5. The Basic of Diagnosis

5.2 Topical Diagnosis : 11th thoracal spinal cord segments

5.3 Basic Etiological Diagnosis

5.5 Basic supporting examination

5.6 Basic treatment

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