04 Neurologic


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04 Neurologic

  1. 1. Central Nervous System Infections
  2. 2.  Cerebrum  Frontal lobe  Parietal lobe  Temporal lobe  Occipital lobe  Cerebellum  Brain Stem
  3. 3. Pia mater, Arachnoid, Dura mater Subdural space, Subarachnoid space
  4. 4. The meninges of the spine cord is the continuation of the meninges of the brain
  5. 5. Acute Bacterial Meningitis Viral Meningoencephalitis General Introduction
  6. 6. <ul><li>Acute infection of the central nervous system(CNS) is the most common cause of fever associated with signs and symptoms of CNS disease in children </li></ul><ul><li>The specific pathogen is influenced by the age and immune status of the host and the epidemiology of the pathogen . </li></ul><ul><li> Viruses, bacteria, fungi, parasites, rickettsiae, mycoplasma </li></ul>General Introduction
  7. 7. <ul><li>3. Regardless of etiology, most patients with acute CNS infection have similar clinical syndromes. </li></ul><ul><li> Common symptoms and signs: </li></ul><ul><li>fever, headache, vomiting, photophobia, restlessness, irritability, stupor, coma, seizures </li></ul><ul><li>neck pain and rigidity, positive Kernig’s and Brudzinski’s signs, and focal neurologic deficits. </li></ul><ul><li> The severity and constellation of signs are determined by the specific pathogen, the host, and the anatomic distribution of the infection </li></ul>
  8. 8. 4. The anatomic distribution of infection may be diffuse or focal Meningitis: primary involvement of meninges Encephalitis: brain parenchymal involvement Meningoencephalitis: involvement of both Diffuse Focal Brain abscess: The neurologic expression of this infection is determined by the site and extent of the abscess(es)
  9. 9. 5. The diagnosis of diffuse CNS infections depends on careful examination of cerebrospinal fluid(CSF) obtained by lumbar puncture(LP). Production, circulation and function of CSF:  Produced by the choroid plexus in the cerebral ventricles  Circulates in the subarachnoid space surrounding the spinal cord and brain, protect them from injury
  10. 10. Acute Bacterial Meningitis  Most common CNS infection in children  One of the most potentially serious infections associated with a high rate of acute complications and risk of chronic morbidity  Prompt and reasonable treatment may improve the prognosis largely
  11. 11. Etiology Pathogenesis Pathology Clinical manifestations Laboratory examinations Diagnosis Complications Treatment Differential diagnosis Epidemiolgy Purulent meningitis Acute Bacterial Meningitis
  12. 12. <ul><li>Most common causes : </li></ul><ul><li>Neisseria meningitidis </li></ul><ul><li>Streptococcus pneumoniae </li></ul><ul><li>Haemophilus influenzae </li></ul><ul><li>Less common pathogens: P.aeruginosa, S.aureus, S.epidermidis, Salmonella, and L.monocytogenes </li></ul><ul><li>Individuals with alterations of host defense due to anatomic defects or immune deficits </li></ul><ul><li>Varies by age: </li></ul>Etiology
  13. 13. Neisseria meningitidis
  14. 14. Streptococcus pneumoniae
  15. 15. Haemophilus influenzae
  16. 16. Commonest Meningitis-Causing Bacteria according to Patient Age N. meningitidis, S. pneumoniae over 12 years H. influenzae, S.pneumoniae, N. meningitidis 2 months to 12 years Group B streptococcus,gram-negative enteric bacilli,Listeria monocytogenes Birth to two month of age Common bacteria causing meningitis Age
  17. 17. Epidemiology Meningitis can occur at any age, but the risk is greatest among infants between 1 and 12 mo of age ; 95% of cases occur between 1 mo and 5 yr of age  The lack of immunity to specific pathogens associated with young age. The mode of transmission is probably person to person contact through respiratory tract secretions or droplets. The predisposing season is the winter or spring
  18. 18. <ul><li>1. Bacteria reach the subarachnoid space </li></ul><ul><li>a. By hematogenous route(bacteremia) from a distant site of infection (nasopharynx) </li></ul><ul><li>b . By invasion directly from a contiguous focus of infection( paranasal sinusitis, otitis media, mastoiditis, orbital cellulitis, dermal sinus tracts, cranial or vertebral osteomyelitis, penetrating cranial trauma, or meningomyeloceles) </li></ul><ul><li>2. Bacteria cause inflammatory responses in CSF . </li></ul>Pathogenesis
  19. 19. Bacteria reach the subarachnoid space by hematogenous route <ul><li>Colonization of bacteria on nasophyrnx by pili </li></ul><ul><li>Bacteria locally invade tissue and gain access to the bloodstream </li></ul><ul><li>Bacterial virulence factors (outer polysaccharide capsule) overcome host defense mechanisms ( opsonophagocytosis ) </li></ul><ul><li>Bacteria survive and replicate in the blood stream </li></ul><ul><li>Bacteria cross the blood-brain barrier and invade the subarachnoid space </li></ul>
  20. 20. Large occipital encephalocele Small encephalocele high in the occipital region Posterior parietal encephalocele Lumbar myelomenigocele
  21. 21. Inflammatory responses in CSF caused by baterial invasion <ul><li>Bacterial replication and accumulation of WBCs </li></ul><ul><li>Production and release of inflammatory mediators: cytokine, interleukins, TNF, prostaglandins, leukotrienes </li></ul><ul><li> Vasculitis (increased capillary permeability, obstruction of blood flow), </li></ul><ul><li> Damage to CSF circulation system. </li></ul>
  22. 22. <ul><li>Meningeal exudates </li></ul><ul><li>Cerebral edema </li></ul><ul><li>Cerebral vascular inflammatory changes </li></ul><ul><li>Damage to the cerebral cortex( vasculitis, bacterial invasion, toxic encephalopathy, raised ICP) </li></ul><ul><li>Subdural effusion </li></ul><ul><li>Hydrocephalus(communicating, obstructive) </li></ul><ul><li>Changes of protein and glucose levels in CSF </li></ul>Pathology • Raised CSF protein levels, Hypoglycorrhachia
  23. 25. Cerebral edema <ul><li>Mechanism: </li></ul><ul><li>1.cytotoxic cerebral edema(cell death) </li></ul><ul><li>2.vasogenic cerebral edema(increased permeability) </li></ul><ul><li>3.interstitial cerebral edema(increased hydrostatic pressure) </li></ul><ul><li>4.ISADH(inappropriate secretion of anti-diuretic) </li></ul><ul><li>Cerebral edema </li></ul><ul><li>Increased intracranial pressure(ICP) </li></ul><ul><li>Brain herniation </li></ul>
  24. 26. Frontal subdural effusions
  25. 35. <ul><li>Raised CSF protein levels: </li></ul><ul><li> increased vascular permeability of the blood-brain barrier </li></ul><ul><li>Hypoglycorrhachia (reduced CSF glucose levels) : </li></ul><ul><li> decreased glucose transport by the inflamed meninges and </li></ul><ul><li> increased glucose utilization by the inflamed cerebral tissue and bacteria which may produce a local lactic acidosis. </li></ul>
  26. 36. <ul><li>Mode of onset </li></ul><ul><li>2. Symptoms and signs: </li></ul><ul><li>Systemic </li></ul><ul><li>Neurologic </li></ul><ul><li>Features of neonatal meningitis </li></ul>Clinical Manifestations
  27. 37. Mode of onset <ul><li>Sudden onset (fulminant type) </li></ul><ul><li> Most common in meningococcal sepsis with meningitis </li></ul><ul><li> Rapidly progressive manifestations of shock, purpura , DIC (disseminated intravascular coagulation), and reduced levels of consciousness , it may evolve to death within 24 hr </li></ul><ul><li>Subacute onset </li></ul><ul><li> Most common in H. Influenzae type b and pneumococcal meningitis </li></ul><ul><li> Often preceded by several days of upper respiratory tract or gastrointestinal symptoms </li></ul>
  28. 39. Systemic symptoms <ul><li>Fever 90% </li></ul><ul><li>Headache 90% </li></ul><ul><li>Photophobia </li></ul><ul><li>Lethargy </li></ul><ul><li>Anorexia, nausea, vomiting </li></ul><ul><li>Myalgia, arthralgia </li></ul><ul><li>Shock, rash, petechiae or purpura, DIC </li></ul><ul><li>Tache Cerebrale - stroke skin with a blunt instrument -> 30-60 sec ->raised red rash </li></ul>
  29. 40. Neurologic manifestation <ul><li>Signs of meningeal irritation(50%) </li></ul><ul><li> neck stiffness(nuchal rigidity) </li></ul><ul><li> Brudzinski’s sign </li></ul><ul><li> Kernig’ sign </li></ul><ul><li>Increased ICP </li></ul><ul><li>Generalized or focal seizures(30%) </li></ul><ul><li>Cranial nerve palsies and focal cerebral signs( hemiparesis, quadriparesis) (10-20%) </li></ul><ul><li>Papilledema (1%) </li></ul>
  30. 41. Definitions <ul><li>Nuchal rigidity </li></ul><ul><li> Passive or active flexion of the neck will usually result in an inability to touch the chin to the chest </li></ul><ul><li>Brudzinski’s sign </li></ul><ul><li> The Brudzinski sign refers to spontaneous flexion of the hips during attempted passive flexion of the neck </li></ul><ul><li>Kernig’ sign </li></ul><ul><li> The Kernig sign refers to the inability or reluctance to allow full extension of the knee when the hip is flexed 90 degrees </li></ul>
  31. 44. Symptoms and signs of increased ICP <ul><li>Headache </li></ul><ul><li>Emesis(projectile vomiting) </li></ul><ul><li>progressive decreased consciousness, may become coma,seizures </li></ul><ul><li>Bulging fontanel or diastasis(widening) of the sutures </li></ul><ul><li>In severe cases, the respiratory and circulatory functions may be damaged (a combination of hypertension and bradycardia with apnea or hyperventilation), even coma or herniation (anisocoria, respiratory and cardic arrest) occurs . </li></ul>
  32. 48. Normal papilla of optic nerve Papilledema
  33. 49. Clinical features of neonatal meningitis <ul><li>Symptoms and signs at onset can be variable and quite nonspecific ( Apnea and bradycardia, cyanosis, diarrhea, disinterest in feeding, jaundice, lethargy, respiratory distress, temperature instability (hypothermia or fever), vomiting ,high-pitched crying) </li></ul><ul><li>The maneuvers to test meningeal irritation are often not available .And the symptoms and signs of increased ICP are less common . </li></ul><ul><li>High index of suspicion : </li></ul><ul><li>Fever (50%) </li></ul><ul><li>Seizure (40%) </li></ul><ul><li>Bulging fontanelle (33%) </li></ul><ul><li>Irritable +/- change in consciousness & poor muscle tone (33%) </li></ul>
  34. 50. <ul><li>Subdural effusions and empyema </li></ul><ul><li>ISADH with hyponatremia </li></ul><ul><li>Ventriculitis and ependymitis </li></ul><ul><li>With bacteria and inflammatory cells in ventricular fluid </li></ul><ul><li>Hydrocephalus </li></ul><ul><li>Others : </li></ul><ul><li>Neurological deficits ( deaf, blindness, epilepsy or mental retardation,etc) </li></ul>Complications
  35. 51. Subdural effusions and empyema <ul><li>Accumulation of excess fluid or pus in the subdural space </li></ul><ul><li>Develop 30%; 85%-90% asymptomatic </li></ul><ul><li>Most common under 12 mo and H. Influenzae type b meningitis. </li></ul><ul><li>Clinical features: </li></ul><ul><li>Diagnosis of subdural effusion: </li></ul> History and associated symptoms and signs  Transillumination test  CT scan  Subdural aspirate Diagnostic
  36. 52. Clinical features of of subdural effusion <ul><li> Fever is persistent or reappears several days after the patient has become afebrile during the therapy for bacterial meningitis. </li></ul><ul><li> Progressive bulging fontanel, diastasis of sutures, enlarging head circumference , emesis ,seizures and abnormal consciousness develop during the course of bacterial meningitis </li></ul>
  37. 54. ISADH with hyponatremia <ul><li>Inflammatory changes in the hypothalamus and pituitary </li></ul><ul><li>30-50% of cases of meningitis </li></ul> Exacerbate cerebral edema  Produce hyponatremic seizures . hyponatremia reduced serum osmolarity
  38. 55. Hydrocephalus <ul><li> Communicating </li></ul><ul><li>adhesive thickening of the arachnoid villi lack of absoption of CSF </li></ul><ul><li> Obstructive </li></ul><ul><li>fibrosis and gliosis of the narrow outlets of the cerebral ventricular system after Ventriculitis and ependymitis an obstruction to flow of CSF </li></ul>
  39. 56. <ul><li>1. CSF Analysis </li></ul><ul><li> Can be diagnostic, and every patient with meningitis should have CSF obtained by lumbar puncture(LP)unless the procedure is contraindicated </li></ul><ul><li> Features of normal CSF </li></ul><ul><li> Typical CSF features of bacterial meningitis : </li></ul><ul><li>2. Other investigations </li></ul>Laboratory Findings
  40. 58.  Changes in the appearance, composition or the pressure of the  CSF indicates diseases of CNS  First drop appearance  First tube culture  Second biochemistry test  Third tube cell count, Gram stain Skin subcutaneous tissue yellow ligament(first feel of reduced resistance suddenly) dural mater and arachnoid(second feel)
  41. 59. Indication of LP:  LP should be performed when diffuse infection of CNS is suspected Contraindications for an immediate LP :  cardiorespiratory compromise  increased intracranial pressure (ICP)  infection in the area of needle insertion  bleeding diathesis (low platelet, hemophilia,DIC)
  42. 60. Features of normal CSF:  A clear colourless fluid,  contains little protein(<40mg/dl),  glucose(2.8~4.4mmol/L or 50~80mg/dl) and  some other components (chlorides:118~128mmol/L),  and few cells(0-8/mm 3 in infants and 0-5/mm 3 in adults, 0-30 mm 3 in neonates; lymphocytic or monocytic predominance)  Pressure of CSF is 25-70mmH 2 O in infants, 65-195mmH 2 O in adults
  43. 61. Typical CSF features of bacterial meningitis:  Appearance: cloudy (turbid), puric  Pressure: >200-300mmH 2 O  Cells: pleocytosis 1000- 10,000 WBC/mm 3 Neutrophilic predominance 75-95%  Protein: Elevated protein concentration ( 100-1000mg/dL)  Glucose: Hypoglycorrhachia (<1.1mmol/L) Glucose level Ratio of CSF to serum<0.4 (Continued)
  44. 62.  Gram stain  Bacterial cultrue Define the specific pathogen  Special test for CSF:  Countercurrent immunoelectroporesis  Latex particle agglutination antigens  Determination of CSF C-reactive protein and tumor necrosis factor levels
  45. 63. Other investigations :  Peripheral WBC: leukocytosis(20000-40000/mm 3 ), neutrophilic predominant( >80%) But in very severe cases, WBC may be low.  Blood culture:  Culture and staining of petechial lesions: meningcoccal meningitis.  Head CT scan:  brain abscesses  subdural effusions or empyemas  ventriculitis  hydrocephalus
  46. 64. review <ul><li>Most common causes for acute bacterial meningitis </li></ul><ul><li>Complications of acute bacterial meningitis </li></ul><ul><li>Typical CSF features of acute bacterial meningitis </li></ul>
  47. 65. <ul><li>History taking </li></ul><ul><li>suspected symptoms and signs </li></ul><ul><li>LP CSF analysis </li></ul><ul><li>confirm the diagnosis: </li></ul><ul><li>Head CT scan confirms the complications </li></ul>Diagnosis
  48. 66. <ul><li> Typical CSF features confirming the diagnosis of bacterial meningitis : </li></ul><ul><li> Turbid appearance </li></ul><ul><li> Increased pressure </li></ul><ul><li> Neutrophilic pleocytosis </li></ul><ul><li> Elevated protein </li></ul><ul><li> Reduced glucose content </li></ul><ul><li> Microorganisms on Gram stain and culture </li></ul><ul><li> Conditions in which CSF analysis shows normal or atypical: </li></ul><ul><li> Severe overwhelming sepsis and meningitis </li></ul><ul><li> The early stage (bacteremia stage) </li></ul><ul><li> Partial and short-term antibiotic treatment </li></ul>
  49. 67. <ul><li> Pyogenic meningitis must be distinguished from meningitis caused by other microorganisms ( viral, tuberculous and fungal) This differentiation is mainly dependent on a careful examination of CSF . </li></ul>Differential Diagnosis
  50. 68. *: Concurrently decreased glucose and chloride in CSF is a hallmark of TB-M CSF features in various infectious meningitis Fungal + Ink+    lymphocytes  ~   Fungal Viral + – normal  lymphocytes  Viral M.tuber-culosis+ Acid-fast+  *    lymphocytes   Tuberculous bacterial + Gram +     neutrophils    Bacterial predominance number culture stain glucose protein Pleocytosis
  51. 69. <ul><li>Antibiotic therapy </li></ul><ul><li>Supportive care </li></ul><ul><li>Symptomatic treatment </li></ul><ul><li>Dexamethasone treatment </li></ul><ul><li>Treatment of complications </li></ul>Treatment
  52. 70. Antibiotic therapy <ul><li> Principles </li></ul><ul><li> Initial(Empiric) therapy without defining the etiologic agent: </li></ul><ul><li> Subsequent antibiotic therapy after defining the etiologic agent </li></ul>
  53. 71. Principles of antibiotic therapy <ul><li>Early, intravenously </li></ul><ul><li>Administered immediately after LP in the absence of increased ICP </li></ul><ul><li>Administered immediately before LP in the presence of increased ICP which should be treated simultaneously. </li></ul><ul><li>Highly lipid soluble to cross the inflamed blood -brain barrier and achieve bactericidal levels in the CSF and, if given in combination, should not be antagonistic </li></ul>
  54. 72. Initial(Empiric) therapy without defining the etiologic agent: <ul><li>Ampicillin (300mg/kg.d) and Chloramphenicol (100mg/kg.d) ( less recommended) </li></ul><ul><li>Ampicillin and penicillin (400,000~800,000u/kg.d) </li></ul><ul><li>Third or fourth-generation cephalosprin: </li></ul><ul><li>Cefotaxime (200mg/kg.d) , Ceftriaxone (100mg/kg.d) </li></ul><ul><li>The treatment course: at least 10~14d. </li></ul>
  55. 73. Subsequent antibiotic therapy after defining the etiologic agent <ul><li>The choice of antibiotics should be based on the results of the bacterial susceptibility test. </li></ul><ul><li>H.influenza : ampicillin, cephalosprin(2~3w) </li></ul><ul><li>S. Pneumoniae: penicillin-G, cephalosprin(2~3w) </li></ul><ul><li>Meningococcus : penicillin-G(7~10d) </li></ul><ul><li>Gram-negative bacteria : aminoglycosides, cephalosporins </li></ul><ul><li>S.aureus: nafcillin, aminoglycosides, cephlosporins, vancomycin </li></ul>
  56. 74. Supportive care <ul><li> Reapted medical and neurological assessments </li></ul><ul><li>pulse rate, blood pressure, and respiratory rate </li></ul><ul><li>pupillary reflexes, level of consciousness, motor strength, cranial nerve signs and evaluation for seizures </li></ul><ul><li>important laboratory studies : BUN, serum sodium, chloride possium, and bicarbonate levels, urine output and specific gravity, complete blood and platelet counts, and coagulation factors in the presence of petechiae, purpura, or abnormal bleeding. </li></ul><ul><li> Maintenance of the fluid and electrolyte balance </li></ul>
  57. 75. Symptomatic treatment <ul><li> Control high fever </li></ul><ul><li> Control infectious shock </li></ul><ul><li> Control increased ICP to prevent herniation </li></ul><ul><li>20% Mannitol(0.5-1g/kg/dose) </li></ul><ul><li>furosemide(1mg/kg) </li></ul><ul><li>controlled ventilation to keep PCO 2 30~35mmHg </li></ul><ul><li> Control seizures </li></ul><ul><li>Intravenous diazepam(0.1-0.2mg/kg/dose) or lorazepam(0.05mg/kg/dose), phenytoin or phenobarbital(15-20mg/kg loading dose, 5mg/kg/24hr maintenance)for further control. </li></ul><ul><li> Specific therpay for hypoglycemia, hypocalcemia, or hyponatremia </li></ul>
  58. 76. Dexamethasone treatment <ul><li>Limit the overproduction of inflammatory mediators and may have a beneficial effect on the outcome of bacterial meningitis </li></ul><ul><li>Intravenous dexamethasone(0.15mg/kg/dose, given every 6 hr for 4 days) is suggested to be given at the same time as antibiotics </li></ul>
  59. 77. Treatment of complications <ul><li>Aspiration for subdural effusion, drainage for vasculitis and ependymitis </li></ul><ul><li>fluid restriction and supplement of sodium for hyponatremia due to ISADH </li></ul><ul><li>Surgical shunt for hydrocephalus </li></ul>
  60. 78. <ul><li>Neurodevelopmental sequelae(20%) include hearing deficit, seizures, language disorder, mental retardation, motor abnormalities, visual impairment, behavior disorders learning disorders, attention deficits, etc. </li></ul><ul><li>Hearing loss is the most common. All children should undergo hearing evaluation after meningitis </li></ul>Prognosis
  61. 79. Viral Meningoencephalitis  Relatively common  An acute inflammatory process involving the meninges and brain tissue  Caused by a number of different viral agents  Most cases are mild and self-limited, but in severe and progressive cases death or severe sequence may occur.
  62. 80. Etiology  Enteroviruses 80%  Arboviruses  Herpesviruses An important cause of severe encephalitis with a high mortality and severe sequence.  Mumps
  63. 81. Pathology  Meningeal congestion,  Mononuclear (lymphocytic) infiltration  Vascular and perivascular inflammatory changes  Demyelination and damaged neurons.  The involvement of brain tissues, spinal cord, nerve roots, and peripheral nerves is quite variable the clinical neurologic presentations are often variable.
  64. 82. Synapse Dendrites Axon(with myelin) Soma The structure of a neuron
  65. 83. Pathogenesis  Virus lymphatic system(first multiplication) bloodstream (extraneural phase, systemic symptoms) CNS(secondary multiplication, neurologic disease)  Neurologic damage is caused by:  A direct invasion and destruction of neural tissues by actively multiplying viruses Neuronal destruction  A reaction of the patient’s nervous tissue to antigens of the virus. Demyelination and vascular and perivascular destruction .
  66. 86. Normal conduction along a myelinated axon Effects of demyelination on impulse conduction
  67. 87. Clinical Manifestations  A wide range of severity, several patterns of onset:  Non-specific initial manifestations :fever, headache, nasopharyngitis, abdominal pain, nausea and vomiting, or in infants, screaming spells  Mildly affected initially, only to lapse into coma and die suddenly.  Ushered in by high fever, violent convulsions, bizarre movement, and hallucinations  Signs of meningeal irritation, increased ICP, local neurologic signs  Specific forms: acute transverse myelitis, Guillain-Barre syndrome, acute hemiplegia , and acute cerebellar ataxia.
  68. 88. Laboratory Findings 1. Analysis of CSF:  Pressure: normal~ elevated.  Appearance: generally clear  Leukocyte count: none~ several hundred/mm 3 , mononuclear or lymphocytic predominance(but during the first 8-12 hr of the onset may be polymorphonuclear predominance).  Protein concentration: normal~ slightly elevated( but may be very high if brain destruction is extensive HSV encephalitis.  Glucose level : usually normal(but may be depressed in mumps infection  Gram stain or bacterial culture: no bacteria recovered.
  69. 89. 2. Virological examinations 3. Electroencephalogram(EEG): typically shows diffuse slow wave activity 4. Neuroimaging studies(CT or MRI): may show swelling of the brain parenchyma or focal lesions.
  70. 90. Diagnosis 1. Clinical manifestations 2. Features of CSF 3. Virological findings 4. EEG 5. CT or MRI appearance
  71. 91. Differential Diagnosis which sometimes present acute onset, and has the similar CSF changes to that in viral meningoencephalitis. Cytological examination of CSF and neurological roentgenogram should be done . 1. Partial treated pyogenic meningitis The special antigen identification and gram stain of CSF may help the diagnose . 2. Other nonbacterial CNS infections Fungi, rickettsiae, Mycoplasma, protozoa and other parasites 3. Primary or secondary brain tumor,or brain abscess
  72. 92. Treatment 1.Antiviral agents: Acyclovir for herpes simplex Gancrclovir for CMV, EBV Virazole(ribavirin), interferon 2. Antibiotics: When bacterial cause cannot be excluded definitely. 3. General treament: Controlling fever, reducing intracranial pressure, maintenance of fluid and electrolyte balance, improving the cadiopulmonary function,etc.Supportive and rehabilitative efforts are very important after the patient recovers.
  73. 93. Prognosis  Depends on the severity of clinical illness, the specific cause, and the age of the child.  Most patients completely recover  Various, degree of neurologic sequence may be left in some cases( especially in those with infection caused by Herpes simplex virus
  74. 95. questions <ul><li>Causative organism of acute bacterial meningitis </li></ul><ul><li>Clinical manifestations of acute bacterial meningitis (definition) </li></ul><ul><li>Complications of acute bacterial meningitis </li></ul><ul><li>Analysis of cerebral spinal fluid(CSF findings in several infectious meningitis) </li></ul>
  75. 96. questions <ul><li>Principals of antimicrobial therapy for acute bacterial meningitis </li></ul>