Case Report Myelopathy - Noreba.docx

Case Report

MYELOPATHY

By:

Noreba 1508438072

Supervisor: dr. Enny Lestari, Sp.S

DEPARTMENT OF NEUROLOGY MEDICAL SCHOOL RIAU UNIVERSITY RSUD ARIFIN ACHMAD PEKANBARU 2017

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. PATIENT’S IDENTITY Name

Mrs. Y

Age

35 years

Gender

Female

Address

Rumbai, pekanbaru

Religion

Moslem

Marital Status

Married

Occupation

Housewife

Date of Admission

May 25nd 2017

Medical Record

75-90-XX

II. ANAMNESIS Autoanamnesis and alloanamnesis (May, 26th 2017)

Chief Complaint The paralyzed on both legs

Present Illness History 

Since 1 months before admission, the patient has complained the paralyzed on both of legs. The patient can’t elevate both of legs now and the pasien also complained the numbness on several parts of her body, from lower umbilical trought to the legs. The patient can’t control his urination and defecation.



Since 3 months before admission, the patient has complained the weakness on both of legs. Then went to hospital ibn sina.,Patient was pregnant so can’t get rontgen. Patient complained wound in the hump. Pain (-). Patient

1

also complained pain on his backbone, that wasn’t relieved by resting and medicine 

The patient was disclaims the history of weight loss, fever and spinal injury.

Past Illness History 

3 years ago, the patient had the history of breast cancer grade IV. The patient already get a chemotherapy in 6 Cycles, and then patient suggest to Mastectomy but

patient reject so patient not control again to

Oncologist.

Family Illness History 

Cancer (-)

Socioeconomic History 

The history of smoking (-)



The patient is a Housewife

THE SUMMARY OF ANAMNESIS Mrs. Y, 35 years old admitted to the hospital on May, 25th 2017. The patient has complained the paralyzed on both of legs since 1 months before admission.The patient can’t elevate both of legs now and she also complained the numbness on several parts of her body from hip to toe, from lower umbilical trought to the legs. The patient can’t control his urination and defecation. Since 3 months ago, she has complained the weakness on both of legs. There were history of breast cancer.

III. PHYSICAL EXAMINATION A. General status Blood Pressure : Right Heart Rate

: 120/80 mmHg

left

: 120/80 mmHg

: 86 bpm

2

TB

: 155 cm

BB

: 50 kg IMT : 22.2 ( normowight)

Thorax

:

Pulmo

: normal

Cor

: normal

Respiratory Rate: 20 times per minute, Temperature

: 37°C

B. Neurological status 1) Consciousness

: Alertness

2) Noble Function

: Normal

3) Neck Stiffness

: Negative

GCS : 15

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 Acuity Normal Normal Visual Fields Normal Normal Normal Colour Recognition Normal Normal 3. Cranial nerve III (Oculomotor) Right Ptosis (-) Pupil Shape Round Size Φ3 mm Extraocular movements Normal Pupillary reactions to light Direct (+) Indirect (+)

Left (-)

Interpretation

Round Φ3 mm Normal

Normal

(+) (+)

4. Cranial nerve IV (Trochlear) Right Left Interpretation Extraocular movements Normal Normal Normal 5. Cranial nerve V (Trigeminal) Right Left Interpretation Motor Normal Normal Normal

3

Sensory Normal Normal Corneal reflex (+) (+) 6. Cranial nerve VI (Abducens) Right Left Interpretation Extraocular movements Normal Normal Strabismus (-) (-) Normal Deviation (-) (-) 7. Cranial nerve VII (Facial) Right Left Tic (-) (-) Motor Normal Normal Sense of Taste Normal Normal Chvostek Sign (-) (-)

Interpretation Normal

8. Cranial nerve VIII (Acoustic) Right Left Interpretation Sense of Hearing 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 Motor Normal Normal Normal Trophy Eutrophy Eutrophy 12. Cranial nerve XII (Hypoglossal) Right Left Interpretation Motor Normal Normal Trophy Eutrophy Eutrophy Normal Tremor (-) (-) Dysarthria (-) (-)

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IV. MOTOR SYSTEM Upper Extremity Strength Distal Proximal Tone Trophy Involuntary movements Clonus Lower Extremity Strength Distal Proximal Tone Trophy Involuntary movements Clonus Body Trophy Involuntary movements Abdominal Reflex

Right

Left

5 5 Normal Eutrophy (-) (-)

5 5 Normal Eutrophy (-) (-)

0 0 hypotonus Atrophy (-) (-)

0 0 hypotonus Athrophy (-) (-)

Eutrophy (-) (-)

Eutrophy (-) (-)

Interpretation

Normal

Paraplegia (LMN Type)

Normal

V. SENSORY SYSTEM Right Light Touch Pain Temperature Proprioceptive  Position  Two point discrimination  Stereognosis  Graphestesia  Vibration

Left

Interpretation

Hypesthesia on T12 spinal cord segment

Not Tested

Not Tested

VI. REFLEX Right

Left

Physiologic Biceps Triceps Knee Ankle

(+) (+) (+) (-)

(+) (+) (+) (-)

Pathologic Babinsky Chaddock

(-) (-)

(-) (-)

Interpretation

Physiologic reflex (↓)

Pathologic reflex (-) 5

Hoffman Tromer Openheim Schaefer Primitive Reflex Palmomental Snout

(-) (-) (-)

(-) (-) (-)

(-) (-)

(-) (-)

No Primitive Reflex

VII. COORDINATION Point to point movements Walk heel to toe Gait Tandem Romberg

Right Normal Not Tested Not Tested Not Tested Not Tested

Left Normal Not Tested Not Tested Not Tested Not Tested

Interpretation Can’t be assessed

VIII. AUTONOMY SYSTEM Urination

: Incontinence

Defecation

: Incontinence

IX. Others Examination a. Laseque

: Unlimited

b. Kernig

: Unlimited

c. Patrick

: -/-

d. Kontrapatrick

: -/-

e. Valsava test

: -

f. Brudzinski

: -

X. THE SUMMARY OF EXAMINATION General Status

:

Blood Pressure 120/80 mmHg Heart Rate 86 bpm Respiratory Rate 20 times per minute Temperature 37°C Noble Function

: Normal

Neck Stiffness

: Negative

Cranial Nerves

: Normal

Motoric

: Paraplegia (LMN Type) 6

Sensory

: Hypesthesia on T12 cord segment

Coordination

: Normal

Autonomy

: Abnormal urination and defecation

Reflex

: Fisiologis ↓

XI. WORKING DIAGNOSIS CLINICAL DIAGNOSIS : Thoracic Myelopathy 

Paraplegia (LMN Type)



Hypesthesia on T12 spinal cord segment



Abnormal urination and defecation

TOPICAL DIAGNOSIS : Spinal cord segment T12-L1 ETIOLOGICAL DIAGNOSIS: Suspect spinal tumor (metastase) DIFFERENTIAL DIAGNOSIS : Spinal tumor (primary tumor) SECONDARY DIAGNOSE : -

Breast cancer

-

Decubitus

XII. SUGGESTION EXAMINATION 

Blood routine



Blood chemistry



Thoracic spine X-ray



MRI thoracic spine with contrast

XIII. MANAGEMENT 

IVFD RL 16 dpm



Methylprednisolone 3 x 125 mg per IV



Ranitidine 2 x 50 mg IV

XIV. LABORATORY AND RADIOLOGY FINDINGS 1. Blood Routine (May, 25th 2017) -

Hemoglobin

: 11.1 g/dL

7

-

Hematocrit

: 34 %

-

Leukocyte

: 6.600/mm3

-

Thrombocyte : 247.000/mm3

Interpretation: Normal

2. Blood Chemistry: Electrolyte -

Na+

: 138.0 mmol/L (135 - 145)

-

K+

: 3.7 mmol/L (3,5 - 4,5)

-

Cl

: 105.2 mmol/L (97 - 107)

Interpretation: Normal 3. Vertebra Thoraco lumbal X-ray (January,25th 2017)

Result : Proses metastasess in Th.12 Suggested MRI

4. Thorac X-ray

8

Interpretation: Cor : normal Pulmo : Multiple nodul in pulmo bilateral suspect metastase

5. FINAL DIAGNOSIS Myelophaty T12 ec Suspect Spinal tumor (metstase) + Breast Cancer +Decubitus

Follow up May, 26th 2017 S

: The patient can’t move both legs

O : GCS 15 (E4M6V5) Blood Pressure :120/70 mmHg Heart Rate: 86 bpm Respiratory Rate : 20 x/i Temperature 36,7 °C Noble Function : Normal Neck Stiffness : Negative Cranial nerves : Normal Motoric

: Paraplagi (LMN Type)

Sensory : Hypesthesia on T12 dermatome to the lower Coordination: can’t be assessed Autonomy: Abnormal urination and defecation Reflex Pathologic (-) Physiology : (+)

9

A

: Myelopathy T12 ec suspect spinal tumor (metastase) + Breast Cancer +

Decubitus

P

: 

IVFD RL 16 dpm



Methylprednisolone 3 x 125 mg per IV



Ranitidine 2 x 50 mg IV



Debridement

Follow up May, 27th 2017 S

: The patient can’t move both legs

O : GCS 15 (E4M6V5) Blood Pressure :110/70 mmHg Heart Rate: 76 bpm Respiratory Rate : 22x/i Temperature 36,5 °C Noble Function : Normal Neck Stiffness : Negative Cranial nerves : Normal Motoric

: Paraplagi (LMN Type)

Sensory : Hypesthesia on T12 dermatome to the lower Coordination: can’t be assessed Autonomy: Abnormal urination and defecation Reflex Pathologic (-) Physiology : (+)↓

10

A

: :Myelopathy T12 ec suspect spinal tumor (metastase) + Breast Cancer +

Decubitus

P

: 

IVFD RL 16 dpm



Methylprednisolone 3 x 125 mg per IV



Ranitidine 2 x 50 mg IV



Debridement

Follow up May, 29th 2017 S

: The patient can’t move both legs

O : GCS 15 (E4M6V5) Blood Pressure :120/80 mmHg Heart Rate: 84 bpm Respiratory Rate : 22 x/i Temperature 36 °C Noble Function : Normal Neck Stiffness : Negative Cranial nerves : Normal Motoric

: Paraplagi (LMN Type)

Sensory : Hypesthesia on T12 dermatome to the lower Coordination: can’t be assessed Autonomy: Abnormal urination and defecation Reflex Pathologic (-) Physiology : (+)↓

11

A

: Myelopathy T12 ec suspect spinal tumor (metastase) + Breast Cancer +

Decubitus

P

: 

IVFD RL 16 dpm



Methylprednisolone 3 x 125 mg per IV



Ranitidine 2 x 50 mg IV



Debridement

Follow up May, 30th 2017 S

: The patient can’t move both legs

O : GCS 15 (E4M6V5) Blood Pressure :110/70 mmHg Heart Rate: 72 bpm Respiratory Rate : 21 x/i Temperature 36,3C Noble Function : Normal Neck Stiffness : Negative Cranial nerves : Normal Motoric

: Paraplagi (LMN Type)

Sensory : Hypesthesia on T12 dermatome to the lower Coordination: can’t be assessed Autonomy: Abnormal urination and defecation Reflex Pathologic (-) Physiology : (+) ↓

12

A

: Myelopathy T12 ec suspect spinal tumor (metastase) + Breast Cancer +

Decubitus

P

: 

IVFD RL 16 dpm



Methylprednisolone 3 x 125 mg per IV



Ranitidine 2 x 50 mg IV



Debridement Planing MRI

Follow up June, 2nd 2017 S

: The patient can’t move both legs

O : GCS 15 (E4M6V5) Blood Pressure :110/70 mmHg Heart Rate: 78 bpm Respiratory Rate : 22 x/i Temperature 36C Noble Function : Normal Neck Stiffness : Negative Cranial nerves : Normal Motoric

: Paraplagi (LMN Type)

Sensory : Hypesthesia on T12 dermatome to the lower Coordination: can’t be assessed Autonomy: Abnormal urination and defecation Reflex Pathologic (-)

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Physiology : (+)↓

I nterpretation : Extensive process metastases on the spine in level Thoracal, Lumbal, sacrum and os iliaca dextra Severe stenosis canal in level Th.11 and moderate in level Th.12, L1, L2

A

: :Myelopathy T12 ec

spinal tumor (metastase) + Breast Cancer +

Decubitus P

: IVFD RL 16 dpm Methylprednisolone 3 x 125 mg per IV Ranitidine 2 x 50 mg IV Debridement

14

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

15

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.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 (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.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 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).

16

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.5,7,8 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

17

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.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

18

findings may differentiate those patients who will benefit from surgical decompression.11 In 2007, Yukawa et al. found that the signal intensity in the preoperative T2 image correlates with patient age, chronicity of the disease, and postoperative recovery. Patients with greater signal intensity in T2 weighted images 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 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.6,7

2.2.

Classification

19

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.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 2.1 (A) Intradural-intramedular Tumor, (B) Intraduralekstramedular tumor and (C) Ekstradural tumor. Tabel 2. Spinal Tumor Classified by the Histologic Representation8 Ekstra dural

Intradural ekstramedular

Chondroblastoma

Ependymoma, type

Chondroma Hemangyoma Lymphoma

myxopapillary Epydermoid Lypoma

Intradural intramedular Astrocytoma Ependymoma Ganglioglyoma Hemangyoblastoma

Meningyoma

20

Meningyoma

Neurofibroma

Hemangioma

Neuroblastoma

Paraganglyoma

Lyphoma

Neurofybroma

Schwanoma

Medulloblastoma

Osteoblastoma

Neuroblastoma

Osteochondroma

Neurofybroma

Osteosarcoma

Oligodendroglioma

Sarcoma

Teratoma

Vertebral hemangyoma

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 Clinical Manifestation7-9

2.4

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

21

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

22

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. 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

23

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 are12-14: 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

24

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: 

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.



2.7

Recurrence after the maximum radiation.

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. The Basic of Diagnosis 3.1 Clinical diagnosis : Thoracic Lumbal myelopathy According to anamnesis and physical examination, we have found: 

Paraplegia (LMN Type)



Hypesthesia on T12 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.

3.2 Topical Diagnosis : Spinal cord segment T12-L1

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It is based on anamnesis that numbness on several parts of his body from the waist to both legs and the examination of sensory system, we found hypesthesia on T12 dermatome to the lower.

3.3 Basic etiological diagnose Basic etiological diagnose of this patient is leads to suspect spinal tumor. Based on anamnesis and physical examination, we have found chronic symptoms like paraplegia lower extremity (LMN type), dissociated sensory loss, and abnormal urination and defecation. Its mean that something compression of medulla spinalis. The metastase tumor is the most causing the medulla spinalis tumor. According to anamnesis, we found that the patient has history of Breast Cancer. And for the examination, we found that the level of disorder is on T12 cord segment.

3.4 Basic differential diagnose Considered the spinal tumor ( primary tumor) because it almost have the same manifestation, like weakness on both legs, pain like bounded from waist and also feel the numbness from the waist to both legs, can’t control his urination and defecation.

3.5 Basic supporting examination a. Laboratory : to knowing risk factors whether infection exists, and knowing the general condition of the patient b.

Chest and vertebra thoraco lumbal X-ray :to find the metastatic sign for the tumors.

3.6 Basic treatment a. IVFD (30cc/kgbb/day) RL 20 gtt/i

to maintaince the euvolemic

condition. b. Methylprednisolone 3 x 125 mg per IV as to provides relief for inflamed areas of the body.

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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.

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: Harrison´s 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. García DR. Mielopatías. Manual de Prácticas Médicas-Hospital Hermanos Ameijeiras [internet]. 2008. http://www.sld.cu/galerias/pdf. 8. Moore AP, Blumhardt LD. A prospective survey of the causes of nontraumatic 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.

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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 myelopathy. Does it predict the outcome of conservative treatment? Spine. 2000;25:677-82.

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