Contents

IDENTITY............................................................................................................................................2
PHYSICAL EXAMINATION (December 1th 2014)..............................................................................6
General Status....................................................................................................................................6
Antropometry Status..........................................................................................................................8
Head to Toe Examination...................................................................................................................9
Neurological Examination...............................................................................................................10
Meningeal Sign............................................................................................................................10
Motoric Examination...................................................................................................................10
Autonom Examination.................................................................................................................11
Laboratory Investigation..............................................................................................................11
FOLLOW UP..................................................................................................................................13
LITERATURE REVIEW.....................................................................................................................18
DEFINITION..................................................................................................................................19
EPIDEMIOLOGY...........................................................................................................................19
PATOFISIOLOGY...........................................................................................................................20
CLINICAL MANIFESTATIONS....................................................................................................21
DIAGNOSIS....................................................................................................................................22
TREATMENT.................................................................................................................................23
PREVENTION................................................................................................................................24
PROGNOSIS...................................................................................................................................26
REFERENCES....................................................................................................................................27

IDENTITY
Patient
Name
: FM
Birth Date
:November 1 th 2004
Age
: 11 years old
Gender
: Male
Address
: street Panca Warga 2 No 005/2, East Jakarta
Nationality : Indonesia
Religion
: Islam
Date of admission: December 04th 2014.
Date of examination: December 04th 2014- Januari 22th 2014

Father

Mother

Name

Mr. I

Mrs. E

Age

43 years old

40 years old

Job

Guruh gramedia

Housewife

Nationality

Javanese

Javanese

Religion

Islam

Islam

Education

Senior High School

Senior High School

Earning/month

Approximately Rp3.000.000,-

Address

street Panca Warga 2 No 005/2, East Jakarta

ANAMNESIS
The anamnesis was taken on December 04th 2014, by alloanamnesis (from patients mother).

Chief complain : Massive headache eight days before admission to the hospital.
Additional complains : Fever, Urinating and right leg starting to lose sensation, shacking
and numb, abdominal pain.

History Of Present Ilness

A 11 years old came to Raden Said Sukanto Police Center Hospital with his mother
patients complained of dizziness was heavy on his head back, the patient feels better when
2

lying down and when walking or sitting head feels heavier, and feels better when both eyes
closed. Since 8 days before msuk hospital patients also experience fever, fever up and down
and increased late in the afternoon and midnight, when the house temperature is not
measured. Already given paracetamol fever just down momentarily but increased to 6 days
before admission. Patients treated in hospital depok expectations. During the treatment the
patient felt no improvement. 4 days before admission the patient urinate more than 10x
colored clear day. 3 days before admission paien complained find it difficult to urinate. 12
hours before admission the patient complained of right leg can not be moved, trembling and
tingling. Patients present with a referral from hospital depok expectations.
History Of Past Illness
Pharyngitis/Tonsilitis

Bronchitis

Pneumonia

Morbilli

Pertussis

Varicella

Diphteria

Malaria

Polio

Enteritis

Bacillary Dysentry

Amoeba Dysentry

Diarrhea

Thypoid

Worms

Surgery

Brain Concussion

Fracture

Drug Reaction

Birth History
Mothers Pregnancy History
The mother routinely checked her pregnancy to the midwife and Rs. Ibu dan anak. She
denied any problem noted during her pregnancy. She took vitamins routinely given.
Childs Birth History
Labor

: RS. Ibu dan anak

Birth attendants

: midwife

Mode of delivery

: sc

Gestation

: 40 weeks

Infant state

: healthy

Birth weight

: 3100 grams

Body length

: 50 cm

According to the mother, the baby started to cry and the baby's skin is red, no
congenital defects were reported
Development History
First dentition: 6 months
Psychomotor development

Head Up

: 1 month old

Smile

: 1 month old

Laughing

: 1- 2 month old

Slant

: 2,5 month old

Speech Initation

: 5 month old

Prone Position

Food Self

Sitting

Crawling

: 8 month old

Standing

: *not able to until present time*

Walking

: *not able to until present time*

: 5 month old
: 5 6 month old
: 6 month old

 Mental Status:Normal
Conclusion: Growth and development status is still in the normal limits and was
appropriate according to the patients age
History of Eating

Breast Milk : Exclusively 6 month..

Formula milk : Bebelac since 1 month ago

Baby biscuits : Biscuits regal

Fruit and vegetables : Banana, Papaya

Solid foods and side dishes : White ricee, Carrots, Potatoes

Immunization History
Immunization

Frequency

Time

BCG

1 time

1 month old

Hepatitis B

3 times

0, 1, 6 months old

DPT

3 times

2, 4, 6 months old

Polio

4 times

Morbilli

0, 2, 4, 6 months old
-

Family History

Patients both parents were married when they were 21 years old and 19 years old,
and this is their first marriage.

There are not any significant illnesses or chronic illnesses in the family declared.

History of her brothers

No
1.

Childbirth
Spontan pervaginam,

Age

Boy

Age Died

Sumption Died

6 years old

gestation aterm
Spontan pervaginam,

2.

Gender

Girl

4 years old

gestation aterm

Spontan pervaginam,

3.

gestation aterm

Girl

10 month

The patient is the third child of three brothers.

Born died : ( - )
Child dies : ( - )
Miscarriage : ( - )

History of Disease in Other Family Members / Around the House

There is no one living around their home known for having the same condition as the patient.

Sosial and Economic History

The patient lived at the house with size 10 m x 8 m together with father and mother.
There are 1 door at the front side, 1 toilet near the kitchen and 3 rooms, in which 1
room is the bedroom of three of them and 1 room is for guest. There are 4 windows

inside the house. The windows are ocassionaly opened during the day.
Hygiene:
o The patient changes his clothes everyday with clean clothes.
o Bed sheets changed every two weeks.

PHYSICAL EXAMINATION (December 1th 2014)

General Status
-

General condition
Awareness
Pulse
Breathing rate
Temperature

: mild ill
: Compos Mentis
: 105 x/min, regular, full, strong.
: 26x/min
: 38,7oC (per axilla)

Antropometry Status
- Weight
- Height

: 9 kilogram
: 69 cm

Nutritional Status based NCHS (National Center for Health Statistics) year 2000:
WFA (Weight for Age): 9/8,9 x 100 % = 101 % ( good nutrition)
HFA (Height for Age): 69/71 x 100 % = 97 % (good nutrition)
WFH (Weight for Height): 9/8 x 100 % = 112 % (normal)
Conclusion: The patient has good nutritional status.
6

Head to Toe Examination

Head
Normocephaly, hair (black, normal distributon, not easily removed ) sign of trauma (-),
large fontanelle closed.
Eyes
Icteric sclera -/-, pale conjunctiva -/-, hyperaemia conjunctiva -/- , lacrimation -/-,
sunken eyes -/-, pupils 3mm/3mm isokor, Direct and indirect light response ++/++
Ears
Normal shape, no wound, no bleeding ,secretion or serumen
Nose
Normal shape, midline septum, secretion +/+
Mouth

Lips: dry
Teeth: no caries
Mucous: moist
Tongue: Not dirty
Tonsils: T1/T1, No hyperemia
Pharynx: No hyperemia

Neck
Lymph node enlargement (-), scrofuloderma (-)
Thorax
:
7

i.
ii.
iii.
iv.
1.
2.

i.

Inspection
: symmetric when breathing , no retraction, ictus cordis is not visible
Palpation
: mass (-), tactile fremitus +/+
Percussion
: sonor on both lungs
Auscultation :
Cor
: regular S1-S2, murmur (-), gallop (-)
Pulmo : vesicular +/+, Wheezing -/- , Rhonchy -/Abdomen
:
Inspection
: Convex, epigastric retraction (-), there is no a widening of the veins, no
spider nevi.

ii. Palpation

: supple, liver and spleen not palpable, fluid wave (-), abdominal mass

(-)

iii. Percussion
iv. Auscultation
Vertebra

: The entire field of tympanic abdomen, shifting dullness (-)

: normal bowel sound, bruit (-)
: There does not appear scoliosis, kyphosis, and lordosis, do not look

any mass along the line of the vertebral

Ekstremities : warm, capillary refill time < 2 second, edema(-)
Skin
: Good turgor.

Neurological Examination
Meningeal Sign

Motoric Examination
Power
Hand
Feet
Tonus
Hand
Feet
Trophy
Hand
Feet
Physiologic Reflex
Upper extrimities
Biceps
Triceps

5 5 5 5/ 5 5 5 5
5 5 5 5/ 5 5 5 5
Normotonus / Normotonus
Normotonus / Normotonus
Normotrophy / Normotrophy
Normotrophy / Normotrophy
+/+
+/+
8

Lower extrimities
Patella
Achilles

+/+
+/+

Pathologic Reflex
Upper extrimities
Hoffman
Trommer

-/+
-/+

Lower extrimities
Babinsky
Chaddock
Oppenheim
Gordon
Schaeffer

-/+
-/+
-/+
-/+
-/+

Clonus
Patella
Achilles

-/+
-/+

Autonom Examination
Defecation
Urination
Sweating

Normal ( 1 times daily, normal consistency )

Normal ( 4-5 times daily )
Normal

Laboratory Investigation
Hematology December 1th 2014

Thorax Photo (December 3th 2014)

Right hilar rough
Infiltrate (+) at suprahilar dextra and sinistra.
Cor, Sinus, Diaphragma is on a normal state.
Bone and Tissue are on normal limits.
Conclusion: Susp. TB.
DD/ Bronchopneumonia
WORKING DIAGNOSIS
Myelitis Transversa
DD/ - Guillain barre
- Chikungunya

MANAGEMENT

IVFD KAEN 3B, micro drip, 14 dpm 1000cc / 24 Hours.

Inj. Cefotaxime 2x500 mg IV
Paracetamol syrup 3x1 cth
Ambroxol syrup 3x1 cth

PROGNOSIS

10

Quo ad vitam
: dubia ad bonam
Quo ad functionam : dubia ad bonam
Quo ad sanactionam : dubia ad bonam

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LITERATURE REVIEW
DEFINITION
Transverse myelitis (MT) is an acute inflammatory process affecting a focal area of the spinal
cord with the clinical characteristics of the development of acute or subacute of signs and
symptoms of neurological dysfunction in motor nerves, sensory and autonomic nerves and
tracts in the medulla spinalis2. Disturbances in the spinal cord is usually involve
spinothalamic tract, pyramidal tract, posterior columns, and funikulus anterior3.
In 1948, a neurological dr.Suchett-Kaye of England, acute transverse myelitis terminology
introduced in its report on a case of transverse myelitis complications after pneumonia.
Transverse describe the clinical presence of a band-like horizontal area of altered sensation in
the neck area or piston. Since then, the syndrome of progressive paralysis due to
inflammation in the spinal cord known as transverse myelitis. Inflammation means that there
is activation of the immune system that existed at the lesion area and potentially cause
kerusakan2.

ETIOLOGY
Etiology MT is a combination of several factors. However, in some cases, the
clinical syndrome is the result of damage MT nerve tissue caused by an
infectious agent or by the immune system, or both. In some other cases, MT
caused by direct microbial infection in the CNS. MT 30-60% of patients reported
suffering from an infection in 3-8 weeks earlier and serological evidence of acute
infection by rubella, measles, infectious mononucleosis, influenza, enteroviruses,
mycoplasma or hepatitis A, B, and C. The other pathogen that herpesviruses
(CMV, VZV, HSV1, HSV2, HHV6, EBV), HTLV-1, HIV-1 that directly infects the
spinal cord and cause clinical symptoms MT. Borrelia burgdorferi (Lyme
neuroborreliosis) and Treponema pallidum (syphilis) were also associated with
direct CNS infection and MT1.
MT has been associated with systemic autoimmune diseases such as LES. Some
patients reported having focal spinal vasculitis associated with symptoms that
aktif1 LES.

PATHOPHYSIOLOGY
Acute transverse myelitis post-vaccination
15

Evaluation of spinal cord autopsy showed severe axonal loss with mild
demyelination and infiltration of mononuclear cells, especially T lymphocytes in
the nerve roots and spinal ganglion. In the spinal cord there is infiltration of
lymphocytes in the perivascular and parenchymal in gray matter, especially in
the anterior horns. Some studies conclude vaccination can induce autoimmune
process that develops into MT5.

MTA parainfectious
As many as 30-60% of cases of idiopathic transverse myelitis, there is the
presence of respiratory complaints, gastrointestinal, or systemic disease earlier.
The word "parainfectious" has been used for neurological injury caused by direct
microbial infection and injury caused by infection, direct microbial infection with
immune-mediated damage, or infection are asymptomatic and followed by a
systemic response that induces neuronal damage. Some of the herpes virus has
been associated with myelitis, and may be the cause of the infection directly to
nerve cells in the spinal cord. Other agents, such as Listeria monocytogenes
brought into the axon to the nerve in the spinal cord. By using some ways, an
agent can achieve access to rich location of the immune system, avoiding the
immune system that are on other organs. Such a mechanism may explain the
inflammation is limited to a focus area in the spinal cord that can be seen in
patients with MT5.

molecular mimicry
Molecular mimicry as a mechanism to explain the nervous system inflammatory
nice sting implemented in cases of GBS. Campilobakter jejuni infection proven to
be an important cause that precedes the occurrence of GBS. Human neural
tissue contains several subtypes of ganglioside moieties such as GM1, GM2, and
GQ1b in the cell wall. Typical components of human ganglioside, sialic acid, also
found on the surface antigens of C. jejuni lipopolysaccharide in the outer sheath.
Ganglioside antibodies which react with C. jejuni was found in the serum of
patients with GBS, and has been demonstrated to bind to peripheral nerves,
complement binding, and damaging nerve transmission. Molecular mimicry in

16

the MTA can also occur due to the formation of autoantibodies in response to
infection that occurs before.
Microbial superantigen-mediated inflammation
Another relationship between a history of previous infection with the MTA that
the fulminant activation of lymphocytes by microbial superantigens. Microbial
superantigens a peptide that has a unique capacity to stimulate the immune
system, and contribute to autoimmune disease that varies. Superantigen that
has been studied is Staphylococcal enterotoxin A to I, toxin-1 toxic shock
syndrome, and exotoxin piogen streptococci. Superantigens activate T
lymphocytes with a unique pathway compared with conventional antigens.
Moreover, unlike conventional antigens, superantigens can activate T
lymphocytes in the absence of co-stimulant molecules. With the existence of this
ssperbedaan, superantigens can activate between 2-20% of circulating
lymphocytes compared with conventional antigens. Moreover, superantigens
often cause expansion followed by deletion of T lymphocyte clones which causes
the formation of "holes" on T lymphocytes for a while after aktivasi5.
Stimulation of a large number of lymphocytes may trigger autoimmune disease
by activating autoreactive T cell clones. In humans, many reports expansion Vb
selected group of patients with autoimmune disease, which indicates previous
exposure to superantigens. Autoreactive T cells activated by superantigens
entering and being retained in the network of networks with repeated exposure
to the autoantigen. In the central nervous system, which is isolated from
Staphylococcal superantigen-induced paralysis in mice experiments. In humans,
patients with acute disseminated ensefalomyelitis and necrotizing myelopathy
piogen streptococci were found to have superantigen-induced T cell activation
against myelin5 basic protein.

Humoral abnormalities
One of the above process can lead to abnormalities in the function of the
humoral system, with reduced ability to distinguish between "self" and "noncell". The formation of abnormal antibodies can activate other components of the
immune system or attract additional cellular elements to the spinal cord.

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Circulating antibodies may form immune complexes and deposited in an area in

the medulla spinalis5.

CLINICAL MANIFESTATION
Transverse myelitis may arise stand alone or together with other diseases. Acute
transverse myelitis said when signs and symptoms develop within hours to a few
days, while the sub-acute clinical symptoms develops over 1-2 weeks. Transverse
myelitis symptoms evolve rapidly from a few hours to several weeks.
Approximately 45% of patients experience worsening maximally within 24 jam2.
Diagnostic in this patient is clinically characterized by the development of signs
and symptoms of neurological dysfunction in motor nerves, sensory and
autonomic nerves and tracts in the spinal cord either acute or subacute.
Inflammation in the spinal cord pathways break-this pathway and lead to the
presence of the common symptoms of myelitis transversalis2.
Weakness is described as a rapidly progressive paraparesis lasting, starting from
the feet and in addition can also be followed involvement hand. The weakness
may be the first recorded with signs of pyramidal tract involvement picture that
progresses slowly in the second week after the OS sakit2.
The involvement of the sensory level can be found in nearly all cases. Pain can
arise on the back, extremities or abdomen. Paresthesia is the most common
early signs of transverse myelitis in adults and not in children. Reduced
sensation below the level of spinal cord involvement in the majority of patients,
as well as pain and temperature.
Autonomic symptoms varies consists of an increase in urinary urgency, urinary
incontinence and Alvi (difficulty or unable to urinate), incomplete emptying of the
stomach or constipation. Also often found as a result of the involvement of
sensory and autonomic nervous system of sexual dysfunction. More than 80% of
patients received clinical signs at the most severe level within 10 days after
onset of symptoms, although the deterioration of neurological function varied
and lasting progressive, usually takes place in the 4-21 day 2.

DIAGNOSIS
The diagnostic criteria for acute transverse myelitis Idiopathic can be seen in
Table 2.1. Diagnosis MTA must meet all the inclusion criteria and none of the
exclusion criteria are met. Diagnosis MTA associated with other diseases must
18

meet all the inclusion criteria and patients also had clinical manifestations of the
disease are included in the criteria ekslusi6.
Table 2.1. Diagnostic Criteria transverse myelitis
inclusion criteria
1) Development of sensory, or autonomic dysfunction motors attributable to the
spinal cord
2) Bilateral signs or symptoms (Although not necessarily symmetric)
3) Clearly-defined sensory level
4) Exclusion of extra-axial compressive etiology by neuroimaging (MRI or
myelography; CT of the spine is not adequate)
5) Inflammation within the spinal cord demonstrated by CSF pleocytosis or
elevated IgG index or gadolinium enhancement. If none of the inflammatory
criteria is met at symptom onset, repeat MRI and LP evaluation between 2 and 7
days after symptom onset meets criteria
6) Progression to nadir between 4 h and 21 days after the onset of symptoms (if
patient awakens with symptoms, symptoms must Become more pronounced
from the point of awakening)
exclusion criteria
1) History of previous radiation to the spine within the past 10 years
2) Clear arterial distribution clinical deficit consistent with thrombosis of the
anterior spinal artery
3) Abnormal flow voids on the surface of the spinal cord consistent with AVM
4) serological or clinical evidence of connective tissue disease (sarcoidosis,
Behcet's disease, Sjogren's syndrome, SLE, mixed connective tissue disorder,
etc.) a
5) CNS manifestations of syphilis, Lyme disease, HIV, HTLV-1, mycoplasma, other
viral infection (eg HSV-1, HSV-2, VZV, EBV, CMV, HHV-6, enteroviruses) a
(a) Brain MRI abnormalities suggestive of MSA
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(b) History of clinically apparent optic neuritisa

AVM, arteriovenous malformation; CMV, cytomegalovirus; CNS, central nervous
system; CSF, cerebrospinal fluid; CT, computed tomography; EBV, Epstein Barr
virus; HHV, human herpesvirus; HSV, herpes simplex virus; HTLV, human T cell
leukemia virus; LP, lumbar puncture; MRI, magnetic resonance imaging; MS,
multiple sclerosis; SLE, systemic lupus erythematosus. ADO not exclude diseaseassociated acute transverse myelitis.
(Quoted from: Transverse myelitis Consortium Working Group. Proposed
diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002;
59: 499-5

TREATMENT

No consensus guidelines

Mainstays include:

corticosteroids: no randomized trials

plasmapheresis: moderate to severe cases, or those who do not

respond to steroids after 3-5 days

Pulse dose IV cyclophosphamide

CSF filtration therapy: spinal fluid is filtered for inflammatory factors

(not available in US)

For severe, refractory cases: 2 year course of azothioprine, methotrexate,

mycophenolate, or oral cyclophosphamide

PREVENTION
immunotherapies initials
The goal of therapy during the acute phase of myelitis is to inhibit progression and initiating
resolution inflamed spinal lesions that can accelerate clinical improvement. Corticosteroids
are the first-line therapy. Approximately 50-70% of patients experienced a partial or complete
repair. High-dose intravenous regimen (1000 mg methylprednisolone every day, usually for
3-5 days) given to the patient. Oral regimen can be used in cases of mild episodes myelitis
20

patients who do not require hospitalization. Undesirable effects on corticosteroid therapy are
gastrointestinal symptoms, insomnia, headache, anxiety, hypertension, manic, hyperglycemia,
and impaired elektrolit4.
With plasma exchange therapy beneficial in patients who do not respond to corticosteroids.
Hypotension,

electrolyte

disturbances,

coagulopathy,

thrombocytopenia,

thrombosis

associated with catheter placement, and infection as a complication of action ini4.

Plasmapharesis useful in patients who still have residual sensorimotor function when the first
attack, but the patients who lost sensorimotor function improved only when treated with
cyclophosphamide and plasmapharesis. In patients with demyelination, or long-acting
immunomodulatory therapy showed a reduction in the risk of attack imunosupressan
berulang4.
Respiration and Oropharyngeal Support
Transverse myelitis can cause respiratory failure if the upper cervical spinal cord and brain
stem has been involved. Therefore, regular examination of the respiratory function and
oropharynx are needed during the course of the disease. Dyspnea, use respiratory muscles, or
a weak cough require further examination of lung function and capacity of forced respiration.
Intubation with mechanical ventilation is required.
abnormalities Tonus
Severe myelitis cause hypotonia in the acute phase (spinal shock), but it is usually followed
by increased resistance to movement (spasticity tone), together with involuntary muscle
spasms (spasticity wicked). Spasticity is an adaptive response, but if excessive, painful or
intrusive, requiring treatment with physiotherapy or drugs. The study controlled trials
examining that baclofen, Tizanidine, and benzodiazepines as a therapy for patients with
spasticity due to brain disorders and spinalis4 cord.
painful
Pain is a frequent manifestation appeared during and after the attack myelitis and can be
caused by direct injury to the nerves (neuropathic pain), orthopedic factor (pain due to a
change in position or bursitis), spasticity, or a combination of these factors. Neuropathic pain
responds well to anticonvulsant agents, drugs anti-depressants (tricyclic antidepressants and
selective reuptake inhibitors of serotonin and norepinephrine), NSAIDS, and narkotik4.
malaise
21

Limited movement, medications, pain, and other factors contribute to excessive malaise after
myelitis attacks. Data from randomized controlled trials demonstrated the efficacy of
amantadine for the treatment of malaise due to multiple sclerosis, and in one study of
modafinil may be the treatment of choice. Stimulants such as methylphenidate
Dextroamphetamine or been used for the treatment of severe and refractory malaise occurring
after the episode myelitis, but the benefits of these agents for the treatment of patients with
myelitis has not been studied in randomized, controlled trials4.
Bowel dysfunction and Genitourinary
Catheter is usually required during the acute phase of transverse myelitis due to urinary
retention. After the acute phase, detrusor hyperreflexia usually appear with the characteristics
of frequent urination frequency, incontinence, and perception of bladder spasm. These
symptoms are usually reduced by administration of anticholinergics (oxybutinin and
tolterodine). Ultrasound to check the remaining volume of urine after micturition useful to
rule out urinary retention, but studies may be needed to assess urodinamis urinary
dysfunction. Drugs that inhibit 1-adrenergic receptors may help urinary sphincter relaxation
and discharge of urine in patients with sphincter hyperactivity, but some patients require
intermittent catheterization to empty the bladder kemih4.
In acute and chronic phases of transverse myelitis, bowel dysfunction characterized by
constipation and impaction risk, difficulty emptying the bowel, and in some cases of
incontinence are usually caused by interference programming to reduce constipation and
bowel control defekasi4 time.
Sexual dysfunction is a frequent consequence of transverse myelitis. Manifestations are
reduced genital sensation, pain, and reduced ability to orgasm, or anorgasmia4.
consulting psychiatrist
Mood and anxiety disorders often become long-term complications in patients with
transverse myelitis and can affect other symptoms, such as pain and sexual dysfunction.
Pharmacotherapy is often prescribed, as monotherapy or combined with consultation with
psikolog4.
PROGNOSIS
Recovery must begin within six months, and most patients showed recovery of function
neurologinya in 8 weeks. Recovery may occur rapidly during 3-6 weeks after onset and may
22

continue even can take place at a slower pace until 2 years. In these patients treatment
progress seen in 2 weeks terapi2.

REFERENCES
1. Kerr, D, 2001. Current Therapy in Neurologic Disease: Transverse myelitis. 6th ed.
[Accessed 20 November 2011]
2. Tapiheru LA, Sinurat PPO, Rintawan K. 2007. Case report: transverse myelitis. Magazine
Medical Nusantara 2007; 40; E235 [Accessed 20 November 2011]
3. Al Deeb SM, Yaqub BA, Bruyn GW, Biary NM. 1997. Acute transverse myelitis: A
Localized Form of Postinfectious encephalomyelitis. Brain 1997; 120; 1115-1122 [Accessed
20 November 2011]
4. Frohman EM, DM Wingerchuk. 2010. Transverse myelitis. The New England Journal of
Medicine 2010; 363: 564-72. [Accessed 20 November 2011]
5. Kerr DA, Ayetey H. 2002. Immunopathogenesis of acute transverse myelitis. Current
Opinion in Neurology 2002, 15: 339 347 [Accessed 20 November 2011]
6. Transverse myelitis Consortium Working Group. 2002. Proposed Diagnostic Criteria and
Nosology of Acute Transverse myelitis. Neurology 2002; 59; 499-505. [Accessed 20
November 2011]
7. Jacob A, Weinshenker BG. 2008. An Approach to the Diagnosis of Acute Transverse
myelitis. Semin Liver Dis 2008; 1; 105-120. [Accessed 20 November 2011]
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