Case Report Myelopathy.docx

Grand Case Report MYELOPATHY

Presented by: Wella Fadillah NIM : 1608438233

Supervisor : dr. Riki Sukiandra, Sp.S

CLINICAL CLERKSHIP NEUROLOGY DEPARTEMENT FACULTY OF MEDICINE RIAU UNIVERSITYOF RIAU ARIFIN ACHMAD GENERAL HOSPITAL PEKANBARU 2018

0

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. L

Age

38 years old

Gender

Female

Address

Tembilahan

Religion

Moslem

Marital’s Status

Married

Occupation

Housewife

Hospital Admission

Nov, 07th 2018

Medical Record

997010

II.

ANAMNESIS : Auto with the patient’s and Alloanamnesis with patient’s husband (Nov,

14th2018 on 11.00 AM) Chief complain Weakness on both lower extremities since 5 month before admitted to the hospital Present illness history 

Since 5 month before admitted to the hospital,

patient complained

weakness on both lower extremities. Patient has difficulty to lift both lower extremities and can’t stand by her own. Patient complained about numbness in her both lower extremities. She still could not her lower

1

extremities. Patient also can’t control her needs for urinating and defecating. weight loss until 20 kg. 

Since 1 year before, Patient had intermittent lower back pain which radiated to both lower limbs. The pain feels sharp, worsen by activity and relieved with analgesic drug. Patient also complained about numbness in her both lower extremities which gradually worsen. Sometimes, patient got fever, night sweat denied, getting better with medication.



Patient doesn’t have neck pain and weakness on her upper extremities. Prolong cough, trauma, lumps in her breasts or other organs, leucorrhea are denied. Past illness history



History of malignancy (-)



History of stroke (-)



History of using long term medication (such as TB drugs) (-)



Hypertension (-)



Diabetes mellitus (-) The family disease history



History of malignancy(-)



History of TB(-) Socioeconomic history

History of smoking (-) Dietary habit is regular Occupation Housewife

2

SUMMARY Mrs. L, 38 years old, admitted to the hospital on Nov 7 th 2018, with weakness on lower extremites since 5 months ago. She also has involuntary urinating and defecating, lose her weight up to 20 kg. 1 year before, she got radiating pain from her back to her lower extremities accompanied with numbness. She also had intermittent fever.

III.

Physical examination

A.

Generalized state (Nov, 14th2018 on 11.00 AM)) Blood Pressure : 120/80 mmHg Heart Rate

: 80 times/min

Respiratory rate : 16 times/min Temperature

: 36,8°C

Weight : 40 kg Height : 160 cmBMI : 15,62 kg/mm2( Under weight ) B.

NEUROLOGICAL STATUS

1)

Consciousness

: Composmentis-cooperative

2)

GCS

: E(4)V(5)M(6)

3)

Cognitive Function: Normal

4)

Meningeal Sign

5)

Cranial Nerves

: Negative

1. Cranial nerve I (Olfactory) Senseof Smell

Right +

Left +

Interpretation Normal

Right Normal

Left Normal

Interpretation

Normal

Normal

Normal

+

+

2. Cranial nerve II (Optic) Visual Acuity Visual Fields Colour Recognition

3

3. Cranial nerve III (Oculomotor) Right (-)

Left (-)

Isochoric

Isochoric

Φ3mm

Φ3mm

Direct

(+)

(+)

Indirect

(+)

(+)

Normal

Normal

Ptosis

Interpretation

Pupil Shape Size Pupillary reactions to light

Extraocular movement

Normal

4. Cranial nerve IV (Trochlear) Extraocular movements

Right

Left

Interpretation

Normal

Normal

Normal

5. Cranial nerve V (Trigeminal) Right Normal

Left Normal

Interpretation

Motoric Sensory

(+)

(+)

Normal

Corneal reflex

(+)

(+)

6. Cranial nerve VI (Abducens) Right Normal

Left Normal

Interpretation

Strabismus

(-)

(-)

Normal

Deviation

(-)

(-)

Eyes movement

7. Cranial nerve VII (Facial) Right

Left

Interpretation

4

Tic

(-)

(-)

Motor: -

Frowning

Normal

Normal

-

Raised eye

Normal

Normal

brow -

Closed eyes

Normal

Normal

-

Corners of

Normal

Normal

Normal

Normal

Sense of Taste

Normal

Normal

Chvostek Sign

-

-

Normal

the mouth -

Nasolabial fold

8. Cranial nerve VIII (Acoustic) Hearing sense

Right Normal

Left Normal

Interpretation Normal

9. Cranial nerve IX (Glossopharyngeal) Right Normal

Left Normal

Interpretation

Pharyngeal Arch Sense of Taste

Normal

Normal

Normal

+

+

Gag Reflex 10.Cranial nerve X (Vagus) Pharyngeal Arch

Right Normal

Left Normal

-

-

Dysphonia

Interpretation Normal

11.Cranial nerve XI (Accessory) Motoric

Right Normal

Left Normal

Trophy

Eutrophy

Eutrophy

Interpretation Normal

12.Cranial nerve XII (Hypoglossal) Right

Left

Interpretation

5

IV.

Motoric

Normal

Normal

Trophy

Eutrophy

Eutrophy

Tremor

-

-

Disartria

-

-

Normal

MOTORIC SYSTEM Right

Left

Distal

5

5

Medial

5

5

Proximal

5

5

Normal

Normal

Eutrophy

Eutrophy

-

-

-

-

Interpretation

Upper Extremity Strength

Tone Trophy Involuntary movements Clonus Lower Extremity

Paraparesis inferior

Strength Distal

4

4

Medial

4

4

Proximal

4

4

Tone

Atoni

Atoni

Trophy

Atrofi

Atrofi

-

-

-

-

Eutrophy

Eutrophy

Involuntary movements

-

-

Abdominal Reflex

+

+

Involuntary movements Clonus Body Trophy

V.

Normal

SENSORY SYSTEM Touch Pain

Right ↓onL2

Left ↓onL2

Interpretation Hypoesthesia

↓on

↓on

on L2 – S5

6

VI.

Temperature

Not identified

Not identified

Propioseptive

Negative

Negative

dermatome

REFLEX Right

Left

Interpretation

Biceps

+

+

Physiologic

Triceps

+

+

inferior

Knee

-

-

(-)

Ankle

-

-

Babinsky

(-)

(-)

Chaddock

(-)

(-)

HoffmanTromer

(-)

(-)

Oppenheim

(-)

(-)

Schaefer

(-)

(-)

Physiologic reflex

extremities

Pathologic

VII.

Pathological reflex(-)

COORDINATION Point to point movement

Right Normal

Left Normal

Difficult to

Difficult to

asses

asses

Walk heel to toe Gait Tandem

Interpretation

Difficult to Interpretate

Romberg VIII. AUTONOM

IX.

Urination

: Incontinence

Defecation

: Incontinence

OTHERS EXAMINATION a. Laseque

: Unlimited (>70)

b. Kernig

: Unlimited (>135)

c. Patrick

: -/-

d. Kontrapatrick : -/-

7

X.

e. Valsava test

:+

f. Brudzinski

:-

g. Naff ziger

:+

EXAMINATION RESUME Generalized condition Consciousness

: CM (GCS:E(4)V(5)M(6))

Blood Pressure

: 120/80 mmHg

Heart Rate

: 80 times/min

Respiratory Rate

: 19 times/min

Temperature

: 36,8°C

Cognitive Function

: Normal

Meningeal sign

: Negative

Cranial Nerves

: Normal

Motoric

: Paraparese inferior

Sensory

: Hypoesthesia on L2 – S5 dermatome

Coordination

: Difficult to interpretate

Autonomy

: Abnormal urination and defecation

Reflex

: Physiologic reflex inferior extremities (-) Pathologic reflex (-)

Others examination XI.

: Valsava test (+), Naff ziger (+)

WORKING DIAGNOSIS : CLINICAL DIAGNOSIS : -

Ischialgia bilateral

-

Paraparese inferior with LMN type

-

Hypoesthesia from L2 – S5 dermatome

-

Autonomic dysfunction TOPICAL DIAGNOSIS

: L2 spinal cord segments

ETIOLOGIC DIAGNOSIS

: Lumbal myelopathy caused suspect Spinal cord tumor

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DIFFERENTIAL DIAGNOSIS XII.

: Suspect Spondilitis Tuberculosis

ADJUNCT EXAMINATION : o Blood routine o Blood chemistry o Electrolytes o Chest X-ray o Thoracal spine X-ray o MRIthoracal spine o Lumbar puncture

MANAGEMENT : 

IVFD NaCl 0.9 (30cc/kgBW/day)  20 dpm



Corticosteroid

: Metilprednisolon 3x125 mg IV



Analgetic

: Ketorolac 3x30 mg IV , Tramadol 1x50 mg IV



Neuroprotector

: Mecobalamin 3x500 mg IV



Gastric protector : Ranitidin 2 x50 mg IV

LABORATORIUM FINDING : 1. Blood Routine (Nov, 07rd 2018) Haemoglobin

: 11,5 gr/dl

Haematocrit

: 36,2%

Leucocytes

: 9.420 /mm3

Platelet

:444.000 /uL

2. Blood Chemistry (Nov, 07rd 2018) Glucose

: 93 mg/dl (<200 mg/dl)

Ureum

: 32 mg/dl (15 – 41)

Creatinin

: 0,62 mg/dl ( 0,55 – 1,30)

3. MRI(N0v, 12th 2018)

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Interpretation :There is mass in the spinal canal as high as VTh 12 - L2 caused spinal suspect schwanoma FINAL DIAGNOSE Lumbal myelopathy caused Spinal cord tumor FOLLOW UP 1.

Nov, 15th2018 S : Weakness on extremities (+),back pain (+), fever (-) O : GCS E(4)V(5) M(6)

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Blood Pressure Heart Rate

:140/90 mmHg : 90 times/min, reguler

Respiratory Rate

: 20 times/min

Temperature

: 37,2°C

Cognitive Function

: Normal

Neck Stiffness Cranial Nerves Motoric

: Not found : Within normal limits : Paraparese inferior with LMN type

Sensory

5 5 4 4 : Hypoesthesia on L2 – S5 dermatome

Coordination

: Not testable

Autonom

: Micturition (+) with cateter, Defecation(+)

Reflex

: Physiologic reflex inferior extremities (-) Pathologic reflex (-)

A

: Lumbal myelopathy caused Spinal cord tumor

P

:

11

2.



IVFD NaCl 20 dpm



Metilprednisolon 3x125 mg IV



Mecobalamin 3x500 mg IV



Ketorolac 2x30 mg IV



Ranitidin 3x50 mg IV



Gabapentin 1x100 mg



Consul to neuro surgeon surgery plan: laminectomy Nov, 16th 2018

S : Weakness on extremities (+),back pain (+),fever (-) O : GCS E(4)V(5)M(6) Blood Pressure

:140/80 mmHg

Heart Rate

:82 times/min, reguler

Respiratory Rate

: 20 times/min

Temperature

: 37,4°C

Cognitive Function :Normal Neck Stiffness

: Not found

Cranial Nerves

: Within normal limits

Motoric

:Paraparese inferior with LMN type

Sensory

5 5 4 4 : Hypoesthesia on L2 – S5 dermatome

Coordination

: NT

Autonom

: Micturition (+) with cateter, Defecation (+)

Reflex

: Physiologic reflex inferior extremities (-) Pathologic reflex (-)

A

: Lumbal myelopathy caused Spinal cord tumor

P

:

12



IVFD NaCl 20 dpm



Metilprednisolon 3x125 mg IV



Mecobalamin 3x500 mg IV



Ketorolac 2x30 mg IV



Ranitidin 3x50 mg IV



Gabapentin 1x100 mg

Transfer in neuro surgeon divide 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 hasmultiple etiologies, while myelitis is used to refer to inflammatoryor infectious processes.1,2Acute 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, suchas myopathy or disorders of the neuromuscular junction, butthe absence of a sensory deficit rules them out. On the otherhand, bilateral frontal mesial lesions may mimic myelopathybut they are associated with abulia or other signs of frontaldysfunction.4 Myelopathies may have a variable course and may manifestas a single event or as a multi-phasic or recurrent disease. Thelatter 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

12

monofocalas in transverse myelitis and optic neuritis, or multifocalas 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 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 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).

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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 etal. 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, retrovirusassociated 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

(demyelinating

diseases,

encephalitis multiple

sclerosis, neuromyelitis optica, Eale’s

14

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

spinocerebellar

ataxia,

paraparesis, 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

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.

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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 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 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 16

(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 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 Ekstra dural

Intradural

Chondroblastoma

ekstramedular Ependymoma,

Chondroma

myxopapillary

Intradural intramedular type Astrocytoma Ependymoma

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Hemangyoma

Epydermoid

Ganglioglyoma

Lymphoma

Lypoma

Hemangyoblastoma

Meningyoma

Meningyoma

Hemangioma

Neuroblastoma

Neurofibroma

Lyphoma

Neurofybroma

Paraganglyoma

Medulloblastoma

Osteoblastoma

Schwanoma

Neuroblastoma

Osteochondroma

Neurofybroma

Osteosarcoma

Oligodendroglioma

Sarcoma

Teratoma

Vertebralhemangyoma 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 Manifestation6-9 a. Extradural Tumors Most of the tumors are metastatic, which cause compression of the spinal

cord and are located in the thoracic segments. Radicular pain can be an initial symptom in 30% patients but then after a few days, weeks or months followed by symptoms of myelopathy. Pain is usually more than one root, which initially disappears with rest, but the longer it will become more persistent, so it can be the main symptom eventough there are symptoms associated with the primary tumor. Pain in the metastatic tumor can occur spontaneously and often increases with mild percussion of the vertebrae, such pain is better known as vertebral pain. Metastatics tumor extradural malignancy has the following characteristics:

18

a) Most spinal tumors (>80%) are malignant metastases mainly from the lungs, breast, kidney, prostate, colon, thyroid, melanoma, lymphoma or sarcoma. b) The first involved is the vertebral body. Predilection for the location of metastatic lung, breast and colon tumors is the thoracic region, whereas prostate, testicular and ovarian tumors usually go to the lumbosacral region. c) Symptoms of spinal cord compression mostly occur at the thoracic level, because of the small diameter of the canal (approximately only 1 cm) d) Symptoms due to spinal metastases begin with local pain that is sharp and sometimes radiates (radicular) and is more intense at emphasis or palpation. b. Intradural-Extramedular Tumor This tumor is grow in the root and causes progressive chronic radicular pain. It is ± 70% of intradural tumors, and the most common type is neurinoma in men and meningioma in women. a) Neurinoma (Schwannoma) Has the following characteristics: 

Derived from the dorsal root



It occurs ± 30% of extramedullar tumors



2/3 cases have a major complaint of radicular pain, usually on one side and felt within a few months to years, while advanced symptoms are pyramidal tract sign



39% of the location is in the thoracic segments.

b) Meningioma Meningioma has the following characteristics: 

± 80% are located in the thoracic region and ±60% in the middleaged woman



Slow growth

19



In 25% of cases there is radicular pain, but more often with symptoms of the pyramidal tract below the lesion, and the nature of radicular pain is usually bilateral with a shorter duration of symptoms.

c. Intradural-Intramedular Tumor a) Ependymomas are associated with the following: 

Mean age at presentation of 43 years



Slight female predominance



Pain localized to the spine (65%)



Pain worse at night or upon awakening



Dysesthetic pain (burning pain)



Long history of symptoms



Myxopapillary variant (mean age of presentation of 21 years old, slight male predominance)

b) Astrocytomas are associated with the following: 

Equal male and female prevalence



Pain localized to spine



Pain worse at night or upon awakening



Paresthesias (abnormal sensation)

c) Hemangioblastomas are associated with the following: 

Onset of symptoms by the fourth decade of life, 80% symptomatic by age 40 years



Familial disorder (ie, von Hippel-Lindau syndrome) present in a third of patients



Decreased posterior column sensation



Back pain localized over lesion.10

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

20

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

Diagnosis7,8,9 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. 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,

21

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 4,13,: 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.



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

22

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.

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THE BASIC OF DIAGNOSIS 1.

Basic clinical diagnose According to anamnesis and physical examination, we have found this

patient has paraparesis inferior (LMN Type), hypoesthesia from L2 dermatome to the lower and autonomic dysfunction (abnormal urination and defecation). The several important things above mean that there is damaging on complete spinal cord because of the involvement not of all the tracts. 2.

Basic topic diagnose Based on anamnesis there are weakness on both lower extremities and

numbness in patient’s lower extremities but from the examination of sensory system, we found hypoesthesia from L-2 dermatome to the lower. Based on the dermatomes, we found that the level of disorder is 2th lumbal spinal cord segments. 3.

Basic etiological diagnose Basic etiological diagnose of this patient lead to spinal cord tumor because

based on anamnesis and physical examination, we have found symptoms like localized back pain, numbness on lower extremities, weakness on lower extremities, autonomic dysfunction (abnormal urination and defecation), and weight loss. These symptoms were gradually occur. This classic features suitable to spinal cord tumor which is a chronic progressive disease. 4.

Basic differential diagnosis Spondilitis TB is chosen as the differential diagnose because it almost

have the same manifestation, such as motor disturbance and numbness.On this patient, she also had history of fever. To establish the diagnosis, some adjunct examination are needed. 5.

Basic Workup

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-

Laboratory : to know the risk factors whether the infection exis and knowing the general condition of the patient for therapeutic purpose.

-

Chest X-ray : to find the etiologic for this case whether the infection exist.

-

Thoracal spine X-ray : to find the abnormality at thoracal vertebrae.

-

Thoracal MRI : to find the etiologic for this case at apinal cord area or vertebrae.

-

Lumbar puncture : to find the etiologic for this case whether the infection exist.

6.

Basic final diagnose The final diagnose of this patient is spinal cord tumor. This diagnose is

considered by history taking, general and neurological examination and adjunct examination. From history taking, we have found symptoms like localized back pain, numbness on lower extremities, weakness on lower extremities, autonomic dysfuction (abnormal urination and defecation). From physical examination there was paraparesis inferior with LMN type, hypoesthesia on L2 – S5 dermatome. From adjunct examination we found from MRI’s result there is the mass in the spinal canal as high as VTh 12 - L2 caused suspect schwanoma 7.

Basic treatment a. The aim of IVFD Ringer Lactate 20 dpm is to maintain the euvolemic condition b. The aim of Metilprednisolon 3x125 mg per IV to provide relief for inflamed areas of the body. c. The aim of Mecobalamin3 x 500 mg as a neurotropic d. The aim of Ketorolac 2x30 mg, Tramadol 1x50 mg IV as an analgetic e. The aim of Ranitidine 50 mg/12 hours per IV to preventing side effects from the use of methylprednisolone in the stomach in the form of peptic ulcer.

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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. Raj VS and Lofton LT. Invited review: rehabilitation and treatment of spinal cord tumors. The Journal of Spinal Cord Medicine. 2013; 36(1):1-8. 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/sitios/neurologia/pa_mielopatias.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. 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.

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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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