ContentsIDENTITY2PHYSICAL EXAMINATION (December 1th 2014)6General Status6Antropometry Status8Head to Toe Examination9Neurological Examination10Meningeal Sign10Motoric Examination10Autonom Examination11Laboratory Investigation11FOLLOW UP13LITERATURE REVIEW18DEFINITION19EPIDEMIOLOGY19PATOFISIOLOGY20CLINICAL MANIFESTATIONS21DIAGNOSIS22TREATMENT23PREVENTION24PROGNOSIS26REFERENCES27

IDENTITY

Patient Name : FMBirth Date:November 1 th 2004 Age: 11 years oldGender: MaleAddress: street Panca Warga 2 No 005/2, East JakartaNationality: IndonesiaReligion: Islam Date of admission: December 04th 2014.Date of examination: December 04th 2014- Januari 22th 2014

FatherMother

NameMr. IMrs. E

Age43 years old40 years old

JobGuruh gramediaHousewife

NationalityJavaneseJavanese

ReligionIslamIslam

EducationSenior High SchoolSenior High School

Earning/monthApproximately Rp3.000.000,--

Addressstreet Panca Warga 2 No 005/2, East Jakarta

ANAMNESISThe 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 IlnessA 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 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 IllnessPharyngitis/Tonsilitis-

Bronchitis-

Pneumonia-

Morbilli-

Pertussis-

Varicella-

Diphteria-

Malaria-

Polio-

Enteritis-

Bacillary Dysentry-

Amoeba Dysentry-

Diarrhea-

Thypoid-

Worms-

Surgery-

Brain Concussion-

Fracture-

Drug Reaction-

Birth HistoryMothers Pregnancy HistoryThe 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: 5 month old Food Self: 5 6 month old Sitting: 6 month old Crawling: 8 month old Standing: *not able to until present time* Walking: *not able to until present time*

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, PotatoesImmunization HistoryImmunizationFrequencyTime

BCG1 time1 month old

Hepatitis B3 times0, 1, 6 months old

DPT3 times2, 4, 6 months old

Polio4 times0, 2, 4, 6 months old

Morbilli--

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 brothersNoChildbirthGenderAgeAge DiedSumption Died

1.Spontan pervaginam, gestation atermBoy

6 years old--

2.Spontan pervaginam, gestation atermGirl

4 years old--

3.Spontan pervaginam, gestation atermGirl10 month--

The patient is the third child of three brothers. Born died : ( - ) Child dies : ( - ) Miscarriage : ( - )

History of Disease in Other Family Members / Around the HouseThere 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: The patient changes his clothes everyday with clean clothes. Bed sheets changed every two weeks.PHYSICAL EXAMINATION (December 1th 2014)General Status General condition: mild ill Awareness: Compos Mentis Pulse: 105 x/min, regular, full, strong. Breathing rate: 26x/min Temperature: 38,7oC (per axilla)Antropometry Status Weight: 9 kilogram Height: 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.

Head to Toe Examination

HeadNormocephaly, hair (black, normal distributon, not easily removed ) sign of trauma (-), large fontanelle closed. EyesIcteric sclera -/-, pale conjunctiva -/-, hyperaemia conjunctiva -/- , lacrimation -/-, sunken eyes -/-, pupils 3mm/3mm isokor, Direct and indirect light response ++/++ EarsNormal shape, no wound, no bleeding ,secretion or serumen NoseNormal shape, midline septum, secretion +/+ Mouth Lips: dry Teeth: no caries Mucous: moist Tongue: Not dirty Tonsils: T1/T1, No hyperemia Pharynx: No hyperemia NeckLymph node enlargement (-), scrofuloderma (-) Thorax:i. Inspection: symmetric when breathing , no retraction, ictus cordis is not visibleii. Palpation: mass (-), tactile fremitus +/+iii. Percussion: sonor on both lungsiv. Auscultation:1. Cor: regular S1-S2, murmur (-), gallop (-)2. Pulmo: vesicular +/+, Wheezing -/- , Rhonchy -/- Abdomen:i. 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: The entire field of tympanic abdomen, shifting dullness (-)iv. Auscultation: normal bowel sound, bruit (-) Vertebra: 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 ExaminationMeningeal Sign

Motoric ExaminationPower Hand Feet5 5 5 5/ 5 5 5 55 5 5 5/ 5 5 5 5

Tonus Hand FeetNormotonus / NormotonusNormotonus / Normotonus

Trophy Hand FeetNormotrophy / NormotrophyNormotrophy / Normotrophy

Physiologic Reflex Upper extrimities Biceps Triceps

Lower extrimities Patella Achilles

+ / ++ / +

+ / ++ / +

Pathologic Reflex Upper extrimities Hoffman Trommer

Lower extrimities Babinsky Chaddock Oppenheim Gordon Schaeffer

- / +- / +

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

Clonus Patella Achilles- / +- / +

Autonom Examination Defecation Urination SweatingNormal ( 1 times daily, normal consistency )Normal ( 4-5 times daily )Normal

Laboratory InvestigationHematology December 1th 2014

Thorax Photo (December 3th 2014)Right hilar roughInfiltrate (+) 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 DIAGNOSISMyelitis TransversaDD/ - 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 Quo ad vitam: dubia ad bonam Quo ad functionam: dubia ad bonam Quo ad sanactionam: dubia ad bonam

LITERATURE REVIEWDEFINITIONTransverse 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.ETIOLOGYEtiology 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.PATHOPHYSIOLOGYAcute transverse myelitis post-vaccinationEvaluation 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 parainfectiousAs 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 mimicryMolecular 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 the MTA can also occur due to the formation of autoantibodies in response to infection that occurs before.Microbial superantigen-mediated inflammationAnother 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 abnormalitiesOne of the above process can lead to abnormalities in the function of the humoral system, with reduced ability to distinguish between "self" and "non-cell". The formation of abnormal antibodies can activate other components of the immune system or attract additional cellular elements to the spinal cord. Circulating antibodies may form immune complexes and deposited in an area in the medulla spinalis5.CLINICAL MANIFESTATIONTransverse 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.DIAGNOSISThe 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 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 myelitisinclusion criteria1) Development of sensory, or autonomic dysfunction motors attributable to the spinal cord2) Bilateral signs or symptoms (Although not necessarily symmetric)3) Clearly-defined sensory level4) 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 criteria6) 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 criteria1) History of previous radiation to the spine within the past 10 years2) Clear arterial distribution clinical deficit consistent with thrombosis of the anterior spinal artery3) Abnormal flow voids on the surface of the spinal cord consistent with AVM4) serological or clinical evidence of connective tissue disease (sarcoidosis, Behcet's disease, Sjogren's syndrome, SLE, mixed connective tissue disorder, etc.) a5) 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(b) History of clinically apparent optic neuritisaAVM, 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 disease-associated acute transverse myelitis.(Quoted from: Transverse myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002; 59: 499-5TREATMENT 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

PREVENTIONimmunotherapies initialsThe 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 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 SupportTransverse 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 TonusSevere 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.

painfulPain 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.

malaiseLimited 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 GenitourinaryCatheter 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 psychiatristMood 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.

PROGNOSISRecovery 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 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]Google Translate for Business:Translator ToolkitWebsite TranslatorGlobal Market Finder

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