MYELOPATHY

 Case Report

I. PATIENT’S IDENTITY

Name	Mr. AH
Age	56 years
Gender	Male

II. ANAMNESIS

Autoanamnesis (November, 26^th 2015)

Chief Complaint

The weakness on both legs

Present Illness History

§  1 month before admitted, the patient has complained the weakness on both legs. At first, the patient has complained the pain like bounded of waist. The pain didn’t disappear after get some rest and drugs bought from the stall. The pain has worsened day by day.

§  Furthermore, The numbness and then weakened gradually from the upper legs to both toes. The complaint has worsened since a week before admission, The patient can’t move both legs at all now and also feel the numbness on several parts of his body, from the chest to both legs. The patient can’t control his urination and defecation.

§  The patient disclaims the history of weight lifting (last weight : 40kg), spinal injury and fever. There was no chronic cought and feses bleeding history.

Past Illness History

§  Hypertension (-)

§  Diabetes mellitus (-)

Family Illness History

§  Cancer (-)

Socioeconomic History

§  Smoker since 25 years ago

THE SUMMARY OF ANAMNESIS

Mr. AH, 56 years old admitted to the hospital on November, 24^th 2015. The patient has complained the weakness on both legs gradually since 1 month before admission and worsened since a week before admission. He complained the pain like bounded from waist and also feel the numbness from the chest to both legs and can’t control his urination and defecation. There were no history of weight lifting, spinal injury , fever ,chronic cought and feses bleeding. There were no history of hypertension and diabetes mellitus.

III. PHYSICAL EXAMINATION

A.    General status

Blood Pressure   : 120/80 mmHg

Heart Rate          : 80 bpm

Respiratory Rate            : 20 times per minute

Temperature       : 36.8°C

B.     Neurological status

Consciousness               :  Alertness                     GCS   :   15      

Noble Function             :  Normal

Neck Stiffness               :  Negative

Cranial Nerves            : Normal

Motoric                       : Paraplegia (UMN Type)

Sensory                       : Hypesthesia on T5  dermatome to the lower

Coordination               : Can’t be assessed

Autonomy                   : Abnormal urination and defecation

Reflex                         : Pathologic ® Babinsky (+)

XI. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS : Thoracic Myelopathy

                                          §  Paraplegia (UMN Type)

                                          §  Hypesthesia on T5 dermatome to the lower

                                          §  Abnormal urination and defecation

TOPICAL DIAGNOSIS                      : T5 cord segment

ETIOLOGICAL DIAGNOSIS            : Extradural Spinal Tumor(vertebral metastase)

DIFFERENTIAL DIAGNOSIS           : Tuberculous Spondylitis 

XII. SUGGESTION EXAMINATION

§  Blood routine

§  Blood chemistry

§  MRI thoracic spine with contrast

XIII. MANAGEMENT

§  IVFD RL 20 dpm

§  Methylprednisolone 3 x 125 mg per IV

§  Ranitidine 2 x 50 mg per IV

§  Vitamine B complex 2 x 1 tab

XIV. LABORATORY AND RADIOLOGY FINDINGS

1.      Blood Routine (November, 24^th 2015)

-          Hemoglobin                : 5,9 g/dL

-          Hematocrit                  : 17,0 %

-          Leukocyte                   : 8.800/mm³

-          Thrombocyte               : 163.000/mm³

Interpretation: Anemia

2.      Blood Chemistry (November, 24^th 2015)

-          Glucose                             : 62 mg/dL

-          Ureum                        : 58 mg/dL

-          Creatinin                    : 0,86 mg/dL

-          AST                            : 25 U/L

-          ALT                           : 19 U/L

-          LDL- chol                  : 111 mg/dL

-          Cholesterol                 : 176 mg/dL

-          Bilirubin direct           : 0,07 mg/dL

MRI thoracic spine with contrast

 -          Medulla Spinalis Metastase of Thoraco 3-4-5

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.²

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.^2,3 Acute transverse myelopathy (includes non-inflammatory etiologies) and transverse myelitis have been used as synonyms in the published literature.^3,4

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.⁵

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.^3,4 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).³

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 evident lesions, or who present with multiple lesions of chronic appearance on magnetic resonance imaging, must be questioned about prior subtle symptoms.⁵

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 (MR). 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.⁵

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:^5-7

1.      Complete spinal cord: involvement of all the tracts (trauma, compression or acute transverse myelitis).

2.      Brown Séquard 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).

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.^6,8,9

Compressive	Non-compressive
Degenerative	Infectious transverse myelitis (viral, bacterial, spirochetes, fungi)
	Acute disseminated encephalitis (demyelinating diseases, multiple sclerosis, neuromyelitis optica, Eale’s disease)
	Vascular (spinal arterial thrombosis, central nervous system vasculitis)
Traumatic (bone lesion, disc herniation, epidural hemorrhage)	Toxic substances and physical agents (lathyrism, arsenic, tri-ortho-cresyl phosphate, nitric oxide, intrathecal methotrexate, radiation, electric injury)
Infectious (abscess)	Degenerative (primary lateral sclerosis, familial spastic paraparesis, spinocerebellar ataxia, Friedriech’s ataxia)
Tumors (extradural, intradural)	Metabolic (vitamin B12 deficiency, vitamin E deficiency,chronic hepatic, renal disease, hexosamidase deficiency)
Vascular (arterio-venous malformation)	Paraneoplastic
Syringomyelia

Table 1. Etiologies

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.¹⁰

Compressive disease is the main cause of myelopathy in older patients. It has a chronic course and usually does not recur.¹¹ 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.¹² 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.¹² 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 recover poorly. Consequently, this parameter may be used as a predictor of surgical prognosis.¹³ Matsumoto et al. found no relationship between hyperintense signals and prognosis.¹⁴

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.¹⁵

2. Spinal Tumor

2.1.      Definition

Spinal tumors are neoplasms 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.^7,8

1.    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 astrocytomas example, neuroblastoma, and kordoma, while benign example neurinoma, glioma, and ependimoma.^9,10

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 .⁹

Image 2.1 (A) Intradural-intramedular Tumor, (B) Intradural-ekstramedular tumor and (C) Ekstradural tumor.

Tabel 2. Spinal Tumor Classified by the Histologic Representation⁹

Ekstra dural	Intradural ekstramedular	Intradural intramedular
Chondroblastoma Chondroma Hemangyoma Lymphoma Meningyoma Neuroblastoma Neurofybroma Osteoblastoma Osteochondroma Osteosarcoma Sarcoma Vertebral hemangyoma	Ependymoma, type myxopapillary Epydermoid Lypoma Meningyoma Neurofibroma Paraganglyoma Schwanoma	Astrocytoma Ependymoma Ganglioglyoma Hemangyoblastoma Hemangioma Lyphoma Medulloblastoma Neuroblastoma Neurofybroma Oligodendroglioma Teratoma

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.¹⁰

2.4   Clinical Manifestation^8-10

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-ekstra¬meduler 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 gej¬ala of intraspinal neoplasms primer.5 General symptoms due compression, among others:

• 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.

• sensory changes

Most patients with spinal cord tumors experience a loss of sensation. Usually numbness and loss of skin sensitivity to temperature.

• 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       Diagnosis^8-10

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.

a. 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.

b. 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).

c. 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.

d. 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.¹³

Therapies for the spinal cord tumors are^13,14,15:

a. Deksamethason: 100 mg (reducing pain in 85% of cases, it may also result in improved neurological).

b. 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.

• 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.

c. 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.

d. Radiation

Radiation therapy is recommended for intramedular tumor that can not be removed completely.

e. 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 indications¹³:

·         Tumor and tissue can not 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.

·         The spinal cord is not stable (unstable spinal).

·         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.

·         Recurrence after the maximum radiation.

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).¹⁴

2.        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        Patophysiology

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 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:

v  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.

v  Pain in the back of the early symptoms and is often found.

v  Gibus.

v  Cold abscess.

v  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.

v  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:

·        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

3.    The Basic of Diagnosis

4.1 Clinical diagnosis : Thoracic myelopathy

According to anamnesis and physical examination, we have found:

§  Paraplegia (UMN Type)

§  Hypesthesia on T5 dermatome to the lower

§  Abnormal urination and defecation

            The several important things above mean that there is damaging on complete spinal cord because of the involvement of all the tracts. It usually happens on compression.

4.2 Topical Diagnosis : T5 cord segment

It is based on the examination of sensory system, we found hypesthesia on T5 dermatome to the lower. And for the radiology findings, we found that the metastase of spinal tumor sign on T3-4-5 spine effects the spinal cord on that level.

4.3 Basic etiological diagnose

Basic etiological diagnose of this patient is leads to extra dural tumor, because on this patient there are pain of the waist like bounded at first time. Then continued by numbess and weakness both of legs. Its mean that something compression form the outter of medulla spinalis. The metastase tumor is the most causing the medulla spinalistumor. So we considered to vertebral metastase, but from the supporting examination there are no found the primary tumors.

4.4 Basic differential diagnose

            The gold standard for diagnose the spinal tumor is with MRI. Considered the tuberculous spondylitis because it almost have the same manifestation, like pain from the waist, the numbess and weakness both of legs. The tuberculous spondylitis cause compression to the medulla spinalis by the abscess producing.

4.5  Basic supporting examination

a.       Laboratory :to find the risk factor for the tumors (tumor marker) and general condition of patient.

b.      Chest X ray :to find the metastatic sign for the tumors

c.       Vertebrae MRI : to find the tumor location and the area of medulla spinalis or vertebrae.

4.6  Basic treatment

a.       IVFD (30cc/kgbb/day)à RL 20 gtt/i  to maintance the euvolemik condition..

b.      Folat Acid 1x 300mg as the neurosupportif.

c.       Vitamin B complex 2 x 250 mg as the neurotropic.

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11.  Ghezzi A Baldini SM, Zaffaroni M. Differential diagnosis of acute myelopathies. Neurol Sci. 2001;22(Suppl 2):S60-4.

12.  Kelley BJ, Erickson BJ, Weinshenker BG. Compressive myelopathy mimicking transverse myelitis. Neurologist. 2010;16:120-2.

13.  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.

14.  Matsumoto M, Toyama Y, Ishikawa M, et al. Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopathy. Does it predict the outcome of conservative treatment? Spine. 2000;25:677-82.

15.  Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology. 2002;59:499-505.

16.  Hidalgo JA. Pott Disease (Tuberculous Spondylitis). http://www.eMedicine.com