This document discusses infections of the central nervous system, including meningitis and encephalitis. It provides details on:
1. The types and causes of meningitis such as bacterial, viral, fungal and tuberculosis meningitis.
2. The pathology, signs and symptoms, diagnostic criteria and treatment for different types of meningitis.
3. Risk factors, routes of transmission, pathology and clinical presentation of tuberculosis meningitis.
4. Differential diagnoses and complications for tuberculosis meningitis.
This document discusses infections of the central nervous system, including meningitis and encephalitis. It provides details on:
1. The types and causes of meningitis such as bacterial, viral, fungal and tuberculosis meningitis.
2. The pathology, signs and symptoms, diagnostic criteria and treatment for different types of meningitis.
3. Risk factors, routes of transmission, pathology and clinical presentation of tuberculosis meningitis.
4. Differential diagnoses and complications for tuberculosis meningitis.
This document discusses infections of the central nervous system, including meningitis and encephalitis. It provides details on:
1. The types and causes of meningitis such as bacterial, viral, fungal and tuberculosis meningitis.
2. The pathology, signs and symptoms, diagnostic criteria and treatment for different types of meningitis.
3. Risk factors, routes of transmission, pathology and clinical presentation of tuberculosis meningitis.
4. Differential diagnoses and complications for tuberculosis meningitis.
Departement of Neurology Medical Faculty of University of Sumatera Utara CNS INFECTION MENINGITIS - Inflamation of the meningeal covering of Brain and spinal cord. - LEPTOMENINGITIS (arachnoid + pia) PACHYMENINGITIS (duramater) - TYPE OF MENINGITIS : Bacterial, TB, Viral, fungal. ENCEPHALITIS VIRAL MYELITIS ABSCESS CEREBRI CEREBRAL MALARIA NCC ANATOMI MENINGS Acute Pyogenic Meningitis = Bacterial meningitis Is an inflamatory response to bacterial infections involving the pia and arachnoid membrane covering the brain and spinal cord. Many org. can produce pyogenic meningitis It can be categorised into: a. Spontaneous community acquired meningitis b. Post traumatic meningitis following neurosur- gery or fx of the skull. c. Device associated meningitis particularly in assoc. With CSF Shunts and drain. The causative org. of meningitis can be predicted based on the patients age, exposure to an epidemic, vacc. Against common agents (eg. H. Influenza, Streptococcus pneumonie, N. meningitidis) and Immune state.
Pathology is characterized by inflammation of the meninges and cortical blood vessels. Etiology of Bacterial meningitis Age Microorg. - Neonate ( 0-2 bln) Streptococ group B, E coli, list. Stap. Aureus, Enterobacter, Pseudomonas, Haemofilus - Child S. pneumonie, N. meningitidis, H. influenzae. - Youth ( 6-20 th ) N. meningitidis, S. pneumonie,H. infl. - Adult ( > 20 thn) S. pneu, N. meningi, Streptococ,Staph.
Clinical Picture The conditions occurs equally in both sexes Children aged 6 month to 1 year are at the greatest risk and children under 15 years of age comprise 75% of all cases. Patients aged 60 and older may be atypical. Symptoms and signs I. early infection: fever, headache, malaise,vomite II. Higher ICP: vomite, headache, seizure, alteration of consciousness, papiledema III. Meningeal irritation: nuchal rigidity, Kernig and Brudzinski + IV. CSF:neutrophilic pleocytosis, low glucose level, elevated protein concentration CSF Findings CSF Parameter Bacterial meningitis WBC Count > 2000/ ul, >60% PMN Glucose < 40 mg/ dl Protein > 200 mg/ dl Gram stain + 80% Culture + > 90%
Diagnostic Prosedure Lumbal Puncture Blood should be drawn for blood culture before administration of antibiotic. Bacterial antigen Chest, skull mastoid and paranasal sinus x rays MRI or CT Neuroimaging shoul be performed before LP in the following settings:60 yo or older, Depressed LOC, Focal neurologic signs, papilledema, Patients is immunocompromised. Treatment 1.Antibiotic therapy should be administrated. A minimum of 2 weeks of therapy is recommended. Age Antibiotic 0 4 mgg Cefotaxim + Ampi 4-12 mgg Gen III. Cephalos+ Ampi 3 bln- 18 thn Gen III. Ceph + Ampi atau Ampi + chloramph. 18 thn 50 thn Gen III. Ceph + Ampi 50 thn Gen III. Ceph + ampi.
2. When possible etiologies for meningitis include H. Influenza or S Pneumoniae in child, or S Pneumoniae in adults, give dexamethasone 0,15 mg/kg (IV) every 6 hours for 2-4 days in child and 10 mg IV every 6 hours for 4 days in adults.
Complication Bacterial meningitis Cerebral abscess Empyema subdural Convulsie Shock septic Cerebral edema Infarck serebral Herniation Sequele bacterial meningitis Mental retardation Hydrocephalus Convulsie, psikose Parese, deafness, blind. Tuberculous meningitis The first clinical description of tuberculous meningitis in the late 18th Century is credited to the Scottish physiologist Sir Robert Whytt , even before Robert Koch isolated mycobacterium tuberculosis in 1882. Almost 40 years later, Rich and McCordock demonstrate the presence of minute caseous tubercles known as Rich-foci within the brain or meninges, which formed the basis for understanding the pathogenesis of CNS tuberculosis.
Tuberculosis of the central nervous system (CNS) is the most serious complication of tuberculosis, especially in children.
TB hematogenous spread infection to the brain parenchyma or meninges. TB meningitis (TBM) Definition: TBM is an infection of the meninges caused by the acid-fast bacillus Mycobacterium tuberculosis. In the west country,the first make not much difference again, but lately incident mount drastically in all the world. TBM happened at all of age. Before important HIV factor in prevalens is age + 1,7 milyar people ( 1/3 worldwide people) Mycobacterium tuberculosa infected. Reported CDC 2002 was 5,36 cases per 100.000 people, but worldwide the infection rate is much higher. TB in Indonesian occupy 3 rd rank from 22 high burden countries. Indonesia 22 High Burden Countries 1. India 2. China 3. Indonesia 4. Bangladesh 5. Nigeria 6. Pakistan 7. South Africa 8. Philippines 9. Russia 10. Ethiopia 11. Kenya 12. DR Congo 13. Viet Nam 14. UR Tanzania 15. Brazil 16. Thailand 17. Zimbabwe 18. Cambodia 19. Myanmar 20. Uganda 21. Afghanistan 22. Mozambique Indonesia 10% Bangladesh 4% China 15% India 30% Other 28% Philippines 3% Pakistan 4% Nigeria 3% South Africa 2% Russia 1% 3% of All Deaths in Developed Countries Are Due to Tuberculosis HIV/AIDS = human immunodeficiency virus/acquired immunodeficiency syndrome. Other 27% Cancer 12% Stroke 10% Injury 9% Respiratory tract infection 7% HIV/AIDS 5% Chronic obstructive pulmonary disease 5% Perinatal causes Diarrheal disease Tuberculosis 3% 3% 4% 2% Malaria Coronary heart disease 13% Adapted with permission from MacKay J, Mensah GA. The Atlas of Heart Disease and Stroke. Available at: http://www.who.int/cardiovascular_diseases/en/cvd_atlas_16_death_from_stroke.pdf Accessed February 27, 2006. Etiologi Mycobacterium tuberculosis gol ordo Actinomycetales, famili Mycobacteriaceae, genus Mycobacterium Sifat : aerob, spora (-), motil (-), berkembang biak lambat Mati dgn pemanasan & sinar UV Bakteri batang tahan asam dgn pewarnaan ZiehlNeelsen /Auramin leading to nickname red snapper.
Size :0,3-,0,6 to 1-4 um Shape: Rods, straight or slightly curved, occurring singly or in occasional threads Temperature: 33-39 o C pH 6,6-6,8 PATHOLOGY
Aerosol transmission of Tuberculosis Tuberculosis is spread by droplet nuclei which are expelled when a person with infectious TB coughs, sneezes, speaks, or sings Pathology TBM is always secondary to TB elsewhere in the body. The primary focus of infection is usually in the lungs but may be in the lymph glands, bones, nasal sinuses, GIT, or any organ in the body. The bacilli usually enter the body by inhalation. Transmission through the skin or by ingestion are rare cause of infection. The organisms undergo multiflication and hematogenous dissemination and it is during this stage that the meninges are most likely to become involved. Cell mediated immunity with migration of macrophages at the site of infection leads to the development of tubercles. When the immune response fails, the subarachnoid space is infected by rupture of meningel tubercles followed by release of bacilli and the development of meningitis. The presence of bacilli in the subarachnoid space is followed by an intense granulomatous inflamation of the leptomeninges and subjacent cortex.
A thick, heavy fibrous and necrotic exudate is produced, which tends to collect at the base of the brain.
The arteries at the base of the brain are involved, and there is inflamation of the adventitia and media, with narrowing and thrombosis of the lumen. CN II and III, occasionally CN VII, VIII, are subject to compression by the heavy exudate. Clinical features TBM The disease occurs in all ages, but the incidence is higher in infants, young children, and the aged. It is more common amomg the undernourished and in those areas of the world characterized by poor hygiene and overcrowding. History of contact with an infected individual or a history previous active tuberculosis in 30 to 50 percent of patients.
Clinical staging of patients with TBM (terminus/ advance) The course of the illness depends: - on the extend of meningeal involvement, - the immune response of the host, - the virulence of the organism, - and the stage at which treatment is administered. Kategori diagnosis Ogawa Definite - bila kultur positi - otopsi positip, atau keduanya Probable - likuor pleiositosis (>5/mm 3 ), kultur bak- teri dan jamur negatip + salah satu: 1. test tuberkulin positip 2. TB diluar SSP atau TB aktip sebelumnya 3. glukosa likuor < 40 mg/dl 4. protein likuor > 60 mg/dl Complication Arteritis thrombosis of a major artery cerebral infarction. Hydrocephalus Seizures Focal motor deficits and impaired cognitive Hypopituitarism in childhood. Differential DX Viral encephalitis Partially treated pyogenic meningitis Fungal infection Other inflammatory disorders The presence of active TB elsewhere, and the results of CSF examination are usually sufficient to establish the dx. Diagnostic Prosedures 1. Lumbal Puncture CSF Parameter TB meningitis WBC Count < 500/ ul, MN Gluco moderate or marked decrease Protein marke increse Gram stain + +.- CSF lactic acid > 35 mg/dl.
2. Laju endap Darah 3. Radiologic 3a. Chest x ray: detect pulmonary involvement 3b. CT scan8 enhancement of the basal cistern. 3b. MRI are more sensitive than CT sans in detecting basal meningitis infarction owing to arteritis hydrocephalus and parenchymal tuberculomas often in combination in AIDS patient. 4. Arteriografi Images of CT Scans file 1: Contrast- enhanced computed tomography (CT) scan in a patient with tuberculous meningitis demonstrating marked enhancement in the basal cistern and meninges, with dilatation of the ventricles. file 2: Petechial hemorrhages in the subcortical white matter of the brain as a result of tuberculous meningitis associated vasculitis. file 3: Extensive infarcts of the right basal ganglia and internal capsule after the appearance of vasculitis in the thalamoperforating arteries in a child treated for tuberculous meningitis. Treatment 1. Combination of antituberculous drug Therapy WHO GILROY ATS - Initial INH+R+PZA+E INH+R+PZA INH+R+PZA atau S atau R+ PZA+S -2MO - 2 MO - 2 MO - Continued INH+R INH+R INH+R -7 MO - 9 MO - 9 MO Pyridoxine 50 mg/ hr 2. Spinal arachnoiditis and arteritis may show improvement when terated with corticosteroid. 3. Seizure anticonvulsant 4. ventriculoperitoneal shunt. Prognosis Mortality 10 & 20% The prognosis is poor in infants, the elderly, when treatment is delayed, and in patients with poor nutrition or debilation from HIV infection or other chronic disease. The outcome is clearly associated with the stage of the disease at dx and the introduction of early treatment. Those who are conscious and without neurological deficits have a good prognosis; those in coma at the beginning of treatment have 20% mortality and only 20 oercent make complete recovery. Viral meningitis Viral meningitis shares clinical features with bacterial meningitis, but patients appear less ill and the disease follows a more benign course. Headache, often meningismus and photophobia, is often the presenting symptoms. The most pathogens include herpes simplex-1 (HSV1), mumps, enterovirus, herpes zoster, adenoviruses and Epstein barr virus. Dx procedure Viral meningitis Lumbal Puncture Cells Glucose Protein Smear CSF lactic < 500 Normal Mild incr No org < 35 mg/dl MN /mm3 PCR MRI predominant temporal lobe and insular changes in HSE-1 and basal ganglia lesion in japanese encephalitis. Treatment Aciclovir 10 mg/ kg iv every 8 hours for 10- 14 days. FUNGAL MENINGITIS ETIOLOGY Fungi invade of CNS producing meningitis in a small fraction of patients with systemic fungal infection (mycoses)
The most pathogens are Cryptococcus neoformans, Coccidiodes immitis, Candida albicans, Aspergillus, H. Capsulatum, Blastomyces, and Mucor
Mucormycosis and aspergillosis usually spreads to the CNS from infected sinuses and generally cause local inflamation and necrosis rather than a diffuse meningitis Fungi can cause infection in patients with: 1. Cancer 2. Receiving corticosteroids 3. Other immunosuppressive drugs (Diabetes, malignancy, immunosuppressive th., or AIDS) 4. IV drug abuse.
Route of entry A. Haematogenous: from the heart, lung, GIT and skin B. Direct: from the orbit and paranasal sinuses. Clinical Picture Symptoms progress over days, sometimes weeks, with headache, nausea, vomiting and mild encephalopathy. Neurologic examination: 1. meningeal irritation (+) 5, Visual loss 2. papilledema 6. Confusional state 3. Cranial nerve palsies 7. Focal paralysis 4. Ptosis Investigations Lab investigations: 1. Blood culture 2. Serum glucose 3.Arterial blood gases 4. Electrolyte 5. Liver function test 6. Urinalysis CSF Examinations: Imaging Invest.. CSF Exam: - Pressure: Increased - Appearance: varies with organism - White Blood cells: 50 10.000 (mixed or lymphocytic). - Glucose :Normal - Protein: increased - Cryptoccal antigen is more sensitive - Fungal culture of CSF(+)
Invest. Chest X-ray : Hilar lymphadenopathy, cavitation, effusion. CT or MRI: mass lesion (Cryptococcus) Treatment Amphotericin B - Protocol, starting with 1 mg/ day - doubling the dose daily until reaching 16 mg per day, than increasing at increments of 10 mg until reaching full therapeutic dose of 0,5 to 1,5 mg/ kg per day IV. Myelitis Inflamation of the spinal cord I. Transverse Myelitis, II. Disseminata, III. Difussa Transverse myelitis (MYELOPATHY) is a syndrome characterized by acute spinal cord dysfunction both halves the cord in transverse section. Myelitis transversalis inflamasi akut atau sub akut mengenai suatu area fokal di medula spinalis karakteristik klinis disfungsi neurologis pada saraf motorik, sensorik dan otonom dan traktus saraf di medula spinalis
MYELITIS Gray matter Poliomyelitis. White matter . Leukomyelitis. The whole crossectional areTranversemyelitis. Lesions are multiple and wide spreadOver a long vertical extent.. DiffuseOr Disseminated. Combined meninges and spinal cordMeningomyelitis. Combined meninges and root--- meningpradiculitis. Inflammatory disease limited to the spinal dura. Pachymeningitis. Infected material collects in the epidural or subdural space Epidural spinal Or subdural spinal abcess or Granulomatous. CLASSIFICATION OF INFLAMMATORY DISEASE OF THE SPINAL CORD SEE TRANSPARANTS ACUTE TRANSVERSE MYELITIS IS USUALLY BILATERAL AND TENDS TO CAUSE MORE SEVERE WEAKNESS THAN THE TYPICAL ATTACKS OF PARTIAL MYELITIS. The condition may be peri infectious or postinfectious process and has been associated with many viral infection, including poliovirus, echovirus and coxsackieviruses.
Etiologie Transverse myelitis 1. Congenital vascular malformation 2. Infectious viral infection 3. Autoimune- peri or post infection or vaccinial myelitis. 4. Multiple sclerosis 5. Neoplastic 6. Toxic- secondary to heroin injection 7. Vascular 8. Degenerative- irradiation 9. Idiopathic. PATOLOGI JHTMC (John Hopkins Transverse Myelitis Center) kondisi inflamasi yang berhubungan dengan mekanisme immune-mediated
Pasien myelitis transversalis perubahan inflamasi pada medula spinalisnya
Abnormalitas patologi ( bervariasi ) infiltrasi lokal oleh limfosit dan monosit dalam segmen medula spinalis dan daerah perivaskuler adanya aktifitas yang bervariasi dari mikroglia dan astroglia
Besar dan luasnya gambaran inflamasi faktor etiologi dan profile perubahan myelopati : Myelitis post infeksius perubahan white matter, demielinasi, gangguan aksonal myelitis transversalis gambaran yang melibatkan keduanya secara bersamaan baik white maupun grey matter
Viral causes of acute myelitis Herpesvirus: HSV2, Varicella Zoster, HSV1, Epstein barr, Cytomegalo, human herpes6. Enterovirus: Poliovirus, Enterovirus 70, Echovirus, Coxsackievirus. Arbovirus: west nile virus Other: Mumps, HIV, Dengue. Affinities virus in myelitis Enterovirus anterior horn or nuclei of the brain stem Herpes zoster dorsal root ganglion Clinical manifestation Acute paraplegic or Quadriplegic. Urinary retention. Sensory disturbances Diagnostic prosedure CSF examination: - mild to moderate lymphocytic pleocytosis (10-1000 cell/mm3), elevated protein (100-500 mg/dl), and normal or mildly depressed glucose level. PCR- virus spesific PCR and antibody titer should be performed. MRI-T2 weighted shows increased signal intensity involving gray matter and surronding white matter. DIAGNOSIS BANDING :
Treatment Viral myelitis Antiviral treatment: Glucocorticoid Spasticity: baclofen (lioresal) 10 mg q6h, benzodiazepin and tizanidine. BRAIN ABSCESS Definition Brain abscess is a focal intracerebral infection that begin as a localized area of cerebritis and develops into a collection of pus surrounded by a weil-vascularized capsule. Abscess of the brain has been known for over 200 years, and surgical treatment started with MacEwen in 1893 [published: pyogenic infective disease of the Brain]. Parenchymal brain infection can arise from hematogenous delivery of infected material, which often results in multiple abscess. Especially at risk are patients with congenital heart disease or valve infection. Pathogenesis: abscess begin with local cerebritis, causing necrosis and surronding edema. Epidemiology: 0,3 1,3 per 100.000 / tahun Male to female ratio of 2:1 to 3:1 Common etiologic factors Common etiologic factors Distingushing characteristics Middle ear,paranasal sinus, or mastoid infection Ear inf: temporal lobe abscess, sinus inf: frontal lobe abscess, mastoid inf: cerebellar abscess Metastatic embolic from lung, pulmonary abscess, bronchietasis, or chronic empyema Multiple abscess Head trauma or Neurosurg. Gunshot wounds are the most common head trauma assc. With abscess Endocarditis Drug abuser Rare cause: dental procedures, Metastatic emboli from abdominal inf. Or PID, osteomyelitis of skull - Common etiologic factors Microorgnism involved Aerobes Anaerob Middle ear,paranasal sinus, or mastoid infection Streptococci, Streptococci Staph aureus Bacteriodes Metastatic embolic from lung, pulmonary abscess, bronchietasis, or chronic empyema Staph aureus, Klebsiela Streptococci, S.Pneumoniae Fusobacteria Head trauma or Neurosurg. Staph aureus, streptococci Pseudomonas Endocarditis Staph aureus - Rare cause: dental procedures, Metastatic emboli from abdominal inf. Or PID, osteomyelitis of skull - RISK FACTORS AND PATHOGENESIS CEREBRAL ABSCESS Directly from the paranasal sinuses, mastoid, middle ear or via hematogenous spread e.g. colonic diverticulae, pulmonary infection, periodontal infection, bacterial endocarditis, except rabies (infiltration along peripheral nerve), Naegleria and herpes via the olfactory bulbs Bacterial caused by aerobic and anaerobic gram negative/positive The source of inoculation of CNS remain unknown in up to one-third Head trauma : CSF leak, reoperation, delay in care or basilar skull fracture Implantation of a foreign body : shunt, high-grade glioma, irradiation Immunocompromised : transplant, cancer, chemotherapy, retroviral infection Neuropatologi (4 stages) 1. Early cerebritis ( days 1-3) infection of the brain with surronding white matter edema. 2. Late cerebritis ( days 4-9) The core of the cerebritis becomes necrotic and enlarges and capsular fibroblasts begin to form. 3. Early capsule formation ( days10-13) The capsule is well developed, with proliferation of fibroblasts, a surronding astrocytic proliferation, and edema 4. Late capsule formation (days 14 or more). A mature, thick capsule surronds the central cavity containing debris and PMN cells. There is usually marked cerebral edema in the surronding brain tissue in the presence of a mature abscess. Gejala dan tanda klinis: Sakit kepala (70-90%) Muntah (25-50%) Kejang(30-50%) Gejala pusing, vertigo, ataksia ( pd abses cerebelli) Ggn bicara (19,6%), hemianopsia (31%), unilateral midriasis (20,5%) Gejala fokal (61%) pd penderita abses supratentorial. Pemeriksaan utk Diagnosa: Glasgow coma scale : utk kesadaran penderita Rontgen foto kepala, sinus, mastoid, thoraks. EEG CT Scan/ MRI Cerebritis results in a non homogeneous mass with irregular margins and diffuse enhancement Angiografi : utk menentulan lokasi abses (24%). Lab: jlh leukosit 10.000-20.000/ cm3 (60-70%) LED meningkat 45 mm/jam (75-90%). Head Ct San A. Multiple brain abscesses associated with bacterial endocarditis (Staphylococcus aureus) in a 55-year-old man. The large abscess in the left hemisphere shows a characteristic ring enhancement. B. Contrastenhanced CT scan 4 months after institution of antibiotic treatment. The abscesses have resolved. A B TEMPORAL LOBE ABSCESS CT scan showing ring enhancement in temporal sinistra (hyperdense capsule differentiated from central low density (pus) and marked surronding edema) Komplikasi Abses Otak Robeknya kapsul abses kedalam ventrikel atau keruangan subarakhnoid. Penyumbatan cairan serebrospinal hidrosefalus Edema otak Herniasi tentorial oleh massa abses otak. 72 Pengobatan abses otak Konservatif: - Pemberian AB yg tepat : 6-8 mgg mengecilkan abses. - Prinsip pemberian AB: bakterisid thdp organisme hasil kultur, dapat melewati BBB. - Pemberian kortikosteroid: dewasa : loading dose 10-12 mg secara IV maintenance dose 4 mg secara IV setiap 6 jam anak : loading dose 10-12 mg/kg diberikan satu kali IV maintenance dose 1-1,5 mg/kg/hari IV - Pemberian antikonvulsan Operatif: Aspirasi dan eksisi. konsul Bedah Saraf , jika terapi konservatif gagal. SURGICAL MANAGEMENT CEREBRAL ABSCESS Stereotactic aspiration Advantages : Avoidance of general anesthesia Access to multiple lesions without an increase in surgical complexity Ability to decompress lesions in eloquent areas such as the thalamus and basal ganglia Simple cystic structure ; size <1.5 cm ; deep gray matter ; no air/fluid level ; no fistula Complication : intracerebral hematoma 0.4% to 1.6% Mortality less than 0.2% ; morbidity 1-4%
Open craniotomy with or without excision of the capsule Posterior fossa masses indicate for open craniectomy ; encapsulated ; silent cortex or white matter Multiloculated abscesses, which are difficult to fully decompress stereotactically, should open ; size >2.5 cm ; air/fluid level in abscess ; fistula Mortality 1% to 11% ; morbidity 4% to 30%
The goal treatment in brain abscesses :
Reduce mass effect Decrease intracranial pressure Prevent herniation or intraventricular rupture and ventriculitis Identify the causative microorganism Establish antibiotic sensitivities Antibiotic treatment for brain abscess Rational Administration :Timing of initial therapy, Choice of agents, Penetration of various agents into the brain, Duration of therapy
Ear, mastoid, sinus Streptococcal species, Ps anaerobes, Enterobaceteriacea Metronidazole 7.5 mg IV every 6 h + Cefepime 2 gr IV every 6 h or meropenem 2gr IV every 8 h Lung S. pneumoniae Same as above AB treatment Teeth, mouth Anaerobic streptococci, Eikenella, Prevotella, Actinomyces Metro 7,5 mg/kg IV every 12 h + PNC G 4million units IV every 4 h or ceftizoxime 3 gr IV every 6 h Post operative infection, furuncles or decubiti Staphiloc Cefepime 2 gr IV every 8 h, or Nafcillin or oxacillin 2 g IV every 4 h NEUROLOGICAL SEQUELAE Most likely due to : Delayed diagnosis Poor initial neurological conditions Larger size Common neurological sequelae are cognitive defisits, hemiparesis, and seizures Infants and children have a worse outcome than adults ,IQ lower than 80, 70% children had difficulties with school performance, 38% had severe hemiparesis Adult : 87% were able to continue their normal work and none had severe hemiparesis
Seizure disorders 3 to 4 years after treatment (15% to 92%) Children are more likely than adults Most common lesion at frontal and temporal lobes ; occipital lobe are unusual ; cerebellar do not predispose to seizures Anticonvulsant for at least 6 months Rates of recurrence 10% to 50% PROGNOSIS Cerebral Abscess Mortality > 60% if sign of brain herniation are present Mortality rate <29% among alert patients 90% among comatose patients Mortality rate 12.5% in posttrauma without signs of herniation Mortality rate 4.3% since CT became a routine diagnotic test Sex and ethnic origin is no evidence for mortality High mortality rate in : Patients related to immaturity Virulence of the gram-negative organisms Coexistent systemic disease Defenition Viral encephalitis Is an acute febrile illness with evidence of damage to the parenchymal tissue of the CNS, producing alteration of consciousness, focal neurological signs and seizures. Etiology:viral infection of the nervous system, Herpes simpleks Eastern equine Venezuela St Louis Japanese B Russian tick-borne Rabies
Etiology viral encephalitis Viral is the most common cause The commonest is HSV type I in adults and type 2 in neonates. It may occur sporadically or in epidemics 50-70% mortality if untreated So establishment of on early specific diagnosis and early initiation of antiviral chemotherapy is of great importance 2/3 of cases involve patients over 40 yo. Patogenesis. Bila virus patogen masuk kedalam tubuh pada SSP dapat terjadi: Radang akut Radang kronis Neoplasma Virus hidup dalam keadaan laten Cara penyebaran ke SSP: Cara penyebaran Contoh virus Hematogen herpes simplex sitomegalovirus Epstein-Barr Coxsackie HIV Morbilli Echovirus khoriomeningitis limfositik paravirus Neurogen Herpes simpleks B-virus Varisela-Zoster Rabies Gambaran klinik: Tanda dan gejala bervariasi tergantung virus penyebab. Umumnya: demam akut disertai tanda rang- sang meningeal, sakit kepala, mual, fotofobi, muntah, ggn kesadaran, defisit neurologik fokal dan kejang2. Mortalitas bervariasi dari tinggi (eastern equine encephalitis) sampai rendah (Vene- zuelan equine encephalitis). Gejala sisa termasuk kejang2 Komplikasi : - perubahan kepribadian - ggn ekstrapiramidal - demensia - ggn motorik - sensorik Kriteria diagnosis ensefalitis viral 1. Bentuk asimptomatik analisis LP 2. Bentuk abortif : Nyeri kepala, demam yg tdk tinggi, kaku kuduk. ISPA/ Infeksi GIT 3. Bentuk fulminan: Berlangsung bbrp jam sampai dengan beberapa hari yg berakhir dengan kematian. 4. Bentuk khas ensefalitis: NK, demam, keasadaran menurun, kejang fokal atau umum, hemiparesis, ggn koordinasi, disorientasi, ggn bicara, ggn mental Prosedur diagnostik. LP : CSF jernih, tekanan normal atau meningkat, Pleositosis limfositik < 1000/ul, glukosa dan klorida nornal, protein normal atau sedikit meninggi ( 80-200 mg/dl MRI atau CT scan SOL (?) EEG Liquor virus DNA dg polymerase chain reaction (prosedur cepat, sensitif, akurat) Virus kadang2 dikultur dari liquor,feces,urine nasofaring atau darah. Titer antibodi thd virus tertentu. Pengobatan. Tidak bisa diidentifikasi dianggap sebagai ensefalitis herpes simpleks dan terapi dgn. Acyclovir atau ganciclovir Jalan nafas diawasi Keseimbangan cairan dan elektrolit dijaga Atasi kejang Atasi peninggian ICP Spektrum NeuroAIDS Primary complication (non- opportunistic disease) HIV-Dementia HIV-Sensory neuropathy Secondary complication (opportunistic disease) Cerebral Toxoplasmosis TB Meningitis / tuberculoma Cryptococcal meningitis Other opportunistic diseases.... Komplikasi neurologi HIV Brain Predominantly nonfocal AIDS dementia complex Acute HIV-related encephalitis Cytomegalovirus encephalitis Varicella-zoster virus encephalitis Herpes simplex virus encephalitis Metabolic encephalopathies Predominantly focal Cerebral toxoplasmosis Primary CNS lymphoma Progressive multifocal leukoencephalopathy Cryptococcoma Brain abcess / tuberculoma Neurosyphilis (meningovascular) Vascular disorders Spinal cord Vacuolar myelopathy Herpes simplex or zoster myelitis Meninges Aseptic meningitis (HIV) Cryptococcal meningitis Tuberculous meningitis Syphilitic meningitis Metastatic lymphomatous meningitis Peripheral nerve and root and root infectious herpes zoster cytomegalovirus lumbar polyradiculopathy Virus or immune-related acute and chronic inflammatory HIV poly- neuritis mononeuritis multiplex sensorimotor demyelinating polyneuropathy distal painful sensory polyneuritis Muscle polymyositis and other myopathies Perjalanan penyakit infeksi HIV Infeksi virus (2-3 minggu) sindroma retro- viral akut (2-3 minggu) gejala menghilang + serokonversi infeksi kronis HIV asimpto matik (rata2 8 thn) infeksi HIV / AIDS simptomatik (rata2 1,3 thn) kematian. Window period masa dimana pemeriksa- an test serologis utk antibodi HIV masih negatif, tapi virus sdh ada dlm darah (sudah mampu menularkan kpd orang lain) HIV dementia (AIDS Dementia Complex) This progressive dementia occurs in AIDS, owing to a direct primary HIV infection of neurons or an indirect neurotoxicity induced by presence of the virus in the brain Pathology: the virus may be transported into the brain by infected peripheral monocytes (Trojan horse theory).
Manifestasi klinis demensia HIV:
Cognititive disorders Gangguan kognitif, kesulitan konsentrasi, forgetfullness, cognitive slowing. Kadang2 agitasi, mania. Pd std awal sulit membedakan dgn keluhan psikiatri. Motor abnormalities: ataksia, hiperreflels. Babinski refleks srg muncul. Pada std lanjut : paraparese dgn inkontinansia urin et alvii Behavioural dysfunction : Apathy, altered personality, disorientasi. Std akhir Mutism CEREBRAL TOXOPLASMOSIS Reactivation of latent infection Toxo seroprevalence 12-46% (SA) IgG indicates past infection (FN <3-6%)
CD4 > 200 virtually excludes Toxo Over 80% have CD4 < 100
Typically multiple ring enhancing lesions on CT/MRI 27-43% have single lesions Up to 10% may have diffuse encephalitis without any visible focal lesions
The course of HIV/AIDS Notes: Normal MRI CT Scan Atrofi Meningeal enhancement hidrosefalus SOL Evaluasi LCS Shunt (kalau perlu) Positif Negatif Terapi sesuai etiologi Observasi Lesi massa(-) Lesi massa (+) Skema 2 Keluhan intrakranial Skema-1. Algoritme Penatalaksanaan Keluhan Intraserebral bagi Penderita HIV-AIDS
normal Terapi toksoplasmosis Seumur hidup Terapi sesuai etiologi Dekompresi dan biopsi terbuka Lesi massa intrakranial Alert-lethargic stabil Steroid ? Stupor-koma Perburukan cepat, massa besar Dengan resiko herniasi Lesi multipel Lesi tunggal
Serologi toksoplasma Negatif Positif Obat antitoksoplasmosis Perbaikan Ya Tidak Biopsi stereotaktik Ancaman herniasi Skema-2. Algoritme Penatalaksanaan Lesi massa Intrakranial pada penderita HIV-AIDS
Toxoplasmosis Clinical Features Usually subacute over weeks
Headache 50% Fever 45% Behaviour changes 40% Confusion 15-52% Focal signs Seizures 24-29% TREATMENT Acute treatment : 3-6 weeks. Induction : pyrimethamine 200 mg First line : Pyrimethamin 75-100 mg/day + sulfadiazine + folinic acid or Pyrimethamin + clindamycin + folinic acid. Second line : Azithromycin, clarithromycin, or atovaquone can substitute for sulfadiazine. Glucocorticoid life threatening condition. TREATMENT Maintenance : Until the immune system has sufficiently reconstituted. Pyrimethamine and sulfadiazine or Pyrimethamine and clindamycin. Stop : Asymptomatik. CD4+ > 200/cmm until 6 months. Fase akut (3-6 minggu) Pemeliharaan/rum atan
Pyrimethamine + leucovorin (dosis di atas) + clindamycin oral 4 x 300 mg 450 mg
Pyrimethamine + leucovorin (dosis di atas) + salah satu antibiotika tersebut dosis sama. 107 CT - Multiple ring enhancing lesions Toxo more likely
Tuberculomas still possible
Differential Diagnosis Toxoplasmosis P CNS L Location Basal ganglia. Gray-white junction Periventricular Number of lesion Multiple Solitary>multiple Enhancement pattern Ring Heterogeneous or homogeneous. Edema Moderate to marked Variable T2-weighted image (lesion relative to white matter) Hyperintense Isointense to hyperintense. Diffusion-weighted image Usually hypointense Often hyperintense (positive) Differential Diagnosis Toxoplasmosis P CNS L MR perfusion Decreased Increased MR spectroscopy Markedly elevated lactate. Markedly elevated choline SPECT thallium (lesion relative to white matter) Cold-no thallium uptake Hot-increased thallium uptake. Other Toxoplasma IgG Ab (+) (90% of patients) EBV DNA amplified by PCR in CSF (most patients) Malaria Serebral (MS) MS adalah malaria dengan penurunan kesadaran ( dewasa GCS < 9 dan anak Blantyre coma score < 3) atau koma lebih dari 30 menit setelah serangan kejang yg tidak disebabkan oleh penyakit lain. MS komplikasi dari malaria falcifarum berat, dijumpai st ensefalopati difus dengan penurunan kesadaran dan berhubungan dengan sequestrasi mikrovaskuler serebral. Blantyre coma scale(0-7) Oculer response - Follow mothers facial reaction 1 - non reaction 0 Verbal response - Normal crying 2 - Whimpering 1 - no sound .. 0 Motoric response - Localize pain 2 - rettraction of limb ..1 - non reaction 0 Plasmodium falcifarum morphology in stained preparation Ring form: vary in shape; double chromatin, double infection, accole
Trophozoit: rare in peripheral blood after half grown Plasmodium falciparum Morphology of all stadiums Patogenese Ada 3 teori: 1. Teori mekanis : tjdnya penyumbatan pemb drh otak akibat tjdnya sitoadherens, sekuester, rosetting dan faktor rheologi. 2. Teori Toksik menghasilkan TNF 3. Teori Permeabilitas: tjdnya adhesi parasit pd endothel, vasculer serta banyak faktor toksik yg lepas serta radikal bebas terutama Nitric oxide (NO).
Diagnosa Malaria Serebral Gjl Klinik : Trias malaria ( demam, menggigil, dan berkeringat), Sakit kepala, ggn mental, nyeri tengkuk, kaku otot dan kejang umum Sering dijumpai splenomegali dan hepatomegali Ggn kesadaran atau koma ( biasanya 24-72 jam) Pemr darah (thin/thick smear) dijumpai bentuk aseksual P. Falcifarum Tidak ditemukan infeksi lain Lain-lain:hipoglicaemia, hiponatremia, hipofosfatemia, pleocytosis sampai 80 cel/ micron kubik, limfosit sampai 15 cel/ mikron kubik CT/ MRI: edema serebri. Laboratorium Pemeriksaan dengan mikroskop - sediaan darah tebal dan tipis Test diagnostik lain - Metode immunokromatografi - Analisa cairan Serebrospinal pd Malaria serebral didapti peningkatan limfosit > 15/ul. - CT dan MRI: edema serebral Comparison of diagnosis method Clinical diagnosis Microscopic RDTs Sensitivity 60-75% 60-95% 44-100% Specificity 30-40% 75-95% 95% (only for Pf or Pv or Pan) Infrastructure needed Minimal High Moderate Skill needed Minimal High Moderate Cost Cheap Moderate Expensive Pengobatan Malaria Tanpa Komplikasi Malaria Falsiparum Lini pertama = Artesunat + Amodiakuin + Primakuin Lini kedua = Kina + Doksisiklin atau Tetrasiklin + Primakuin Pengobatan lini kedua diberikan jika pengobatan lini pertama tidak efektif, dimana 28 hari setelah pemberian obat : Gejala klinis memburuk dan parasit aseksual positif, atau Gejala klinis tidak memburuk tetapi parasit aseksual tidak berkurang (persisten) atau timbul kembali (rekurensi) Neurocisticercosis (NCC) Def: cysticercosis cellulosa is the larval stage of development of the cestode Taenia solium (pork tapeworm). More than 60 million people are infected with T. saginata world wide and about 4 million are infected with T. solium
In Indonesia North Sumatra Lampung Jakarta Bali Flores East Timor Irian Jaya North Sulawesi West Kalimantan Fig. I. Geographic distribution of in Indonesia until 1995. Areas endemic with taeniasis are indicated in colour. ( Modified from the unpublished report CDC & EH. Ministry of Health, Indonesia, 1983 1996 ) Pathology :3 Form cysticercosis in CNS 1. A cystic form involving the ventricles and brain parenchyma 2. A racemose form involving the meninges 3. A miliary form that is common in children
PATOGENESIS Human NCC : ingest food contaminated with T.solium egg Parasite survive over period of year It secretes protease inhibitor, taeniastatin that inhibit complement activation, neutrophyl, lymphocyte and cytokine production. Minimal inflammation around viable cyst Inflammatory respons attacks the parasite, leads to degeneration and calcification
CLINICAL MANIFESTATION
Number of the cysts Location (parenchimal/spinal) Parasite activity Immune respons of the host
DIAGNOSIS Definitive Present of the scolex on histologic examination or on CT scan/MRI
MRI More sensitif for detect parenchymal cyst, intraventricular and subarachnoid cyst
MANAGEMENT NCC
Anti parasitic drug Symptomatic and anti- inflamatory Surgery
ANTI PARASITIC DRUG Praziquantel : 50mg/kg/day, two weeks. Albendazol : 15mg/kg/day, one month.
SYMPTOMATIC/ ANTIINFLAMMATION
Corticosteroid : Dexamethasone 4,5 12 mg/day, or Prednisone 1mg/kg/day. Decrease neurological symptoms due to the death of the parasite. Manitol 2g/kg/day, for acute intracranial hypertension. First line antiepileptic SURGERY For excision of large cysts or cyst in the ventricles