1 / 61

Neuro 3…

Neuro 3…. Meningitis.. . Encephalitis. Trigeminal Neuralgia. Meningitis. Meningeal inflammation ...around brain and spinal cord. Cause: Viral vs Bacterial vs other…. Classic sx: HA, NV, neck stiffness, fever. epidemiology. WHO:infants <1yr & children 5 -10yr WHEN:

glain
Download Presentation

Neuro 3…

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Neuro 3… Meningitis.. Encephalitis Trigeminal Neuralgia

  2. Meningitis Meningeal inflammation ...around brain and spinal cord Cause: Viral vs Bacterial vs other….. Classic sx: HA, NV, neck stiffness, fever

  3. epidemiology WHO:infants <1yr & children 5 -10yr WHEN: highest incidence: late Spring to Fall reflecting peak activity of enteroviral and arthropod-borne infections Viral Meningitis: definition Viral (Aseptic) Meningitis: Meningeal inflammation w/ neg. bacterial cultures w/ No associated neurologic dysfunction

  4. VIRAL MENINGITIS: PATHOGENESIS Few viral particles replicate in the nasopharynx with spread/replication in resp. tract lymphatics. Most viral particles bind to specific receptors on enterocytes & traverse the intestinal lining cells to reach the Peyer's patches in the lamina propia, where they replicate on mucosal surfaces of the respiratory & GI tract • -->primary viremia (onset of illness) seeding of other organs (liver/spleen/heart) • second viremia(seedingof the CNS during first or second viremia) • s/sx of infx

  5. Viral meningitis: Causes • OTHER CAUSES • Mycobacteria • Fungi • Spirochetes • parameningeal infections • Medications • (Amox,. Bactrim, NSAIDS, zantac) • malignancy MOST COMMON: *Enterovirus (esp.Spring/Fall) Coxsackie Echovirus other non-poliovirus enteroviruses ?arbovirus • OTHER VIRUSES • HSV HIV West Nile virus (WNV) • varicella-zoster virus (VZV) Mumps • lymphocytic choriomeningitis virus (LCM)

  6. Most common cause: Enteroviruses EV: 85 -95 % viral meningitis Nonpolio-EV serotypes cycle from year to year however, certain serotypes have remained prevalent. Most common 2000-2005: Coxsackieviruses A9, B5, and B1 Echoviruses 6, 9, 13, 18, and 30 <3mo: usually group B coxsackie viruses and parecho viruses EV 71, closely related to coxsackie virus A16, the viral agent of hand-foot-mouth disease, has emerged as a significant cause of aseptic meningitis, encephalitis, myelitis. TRANSMISSION Humans: only known reservoir Transmission: fecal-oral route. (Rare:droplet inhalation) Possible Transplacental -> stillbirth, abortion, neonatal infx

  7. Risk factors for EV Seasonality In temperate climates: most EV infections outbreak during the warmest months; however, sporadic cases can develop throughout the year. In US: infections more frequent June - October In tropical and subtropical regions: consistent thru year • Host factors: • severe nonpolio EV infx if immunodeficient, age extremes • risk of chronic meningoencephalitis if child w/ deficient humoral immunodeficiency, especially X-linked agammaglobulinemia Incubation period for EV infection is approx. 3-6d

  8. Other viruses…Herpes viruses • All members of the Herpes viridae family can cause aseptic meningitis • USUALLY: HSV • INFREQUENTLY: CMV, VZV, human herpesvirus (HHV)-6, and Epstein-Barr virus (EBV) • Neonatal & CNSinfxs are the most devastating • Primary infection is followed by lifelong infection, w/ potential for reactivation • Humans are the only reservoir for transmission • Infections occur worldwide without seasonal prevalence • ? mechanisms of spread to the brain include: hematogenous dissemination, direct extension nasopharyngeal mucosa, or via neurogenic pathways

  9. VZV • Aseptic meningitis is a rare complication of chickenpox and herpes zoster • The syndrome known as zoster sine herpete is characterized by: • CSF pleocytosis • documented CNS infection with VZV by PCR • absence of typical skin lesions **Decreasedincidence since introduction of varicella vaccine CMV and EBV RARELY CAUSE Aseptic Meningitis however, aseptic meningitis is the most common neurologic complication seen in patients with primary EBV infection

  10. OTHER CAUSES: HHV-6 and HHV-7 • HHV-6, (roseola or exanthem subitum) • common cause of febrile sz & meningitis in infancy • HHV-7, (also exanthem subitum) • causes febrile seizures in infancy • causes meningitis in children

  11. Other causes: Arboviruses Highest incidence;: tropical, developing regions US: most common after EV The incubation period: 1 - 18 days Most important endemic US arboviruses : St. Louis encephalitis virus West Nile virus Eastern equine encephalitis virus Western equine encephalitis virus California encephalitis viruses Pathogenesis : Viruses are inoculated subcutaneously or intravenously per vecotor (mosquito) bite Replication in the skin or muscle -> primary viremia -> spreads to to the reticuloendothelial system or CNS.

  12. HISTORY..ask about exposure Ask about symptoms ?rodents (LCM) ?ticks (Lyme) ?mosquitos ?human contacts ?TB ?sexual activity (HSV-2, HIV, syphilis) Nonspecific sx: Fever HA Nausea & vomiting Photophobia Nuchal rigidity Altered mental status (Kernigs/Brudzinski’s usu. neg)

  13. MENINGEAL IRRITATION Physical Exam….look for

  14. PE: Signs of meningeal irritation

  15. PE: Examination for nuchal rigidity • Passive or active neck flexion: inability to touch the chin to chest • lateral motion less reliable finding • Kernig's & Brudzinski's signs were originally developed and tested in patients with severe, late stage meningitis • Brudzinski's sign: spontaneous flexion of the hips during attempted passive flexion of the neck. • Kernig's sign: inability or reluctance to allow full extension of the knee when the hip is flexed 90º. • When LP was performed w/ suspected meningitis : • sensitivity extremely low (5% for each sign; 30% for nuchal rigidity) • specificity :95% for each sign & 68% for nuchal rigidity. • Jolt accentuation of headache more sensitive for dx meningitis. • Sensitivity: 97 % & specificity of 60 % for dx of CSF pleocytosis

  16. PE.. look for rash DX: CSF • Diffuse maculopapular exanthem in mildly ill pt: • ?enteroviral infection, primary HIV, or syphilis. ?meningococcal infection & RMSF • Parotitis: mumps meningitis in unvaccinated pt. • Severe vesicular, ulcerative genital lesions: HSV-2 • Oral thrush & cervical lymphadenopathy: HIV • Asymmetric flaccid paralysis: West Nile Virus

  17. csf

  18. TREATMENT: Suspectedviral meningitis TREATMENT: if unclear etiology Usually self-limited (vs bact.meningitis) Resolves without specific therapy • Consider empiric therapy x 48hrs if Elderly, prior antibiotics, immunocompromised • Otherwise, consider observation • If suspect HIV: check HIV RNA and HIV antibody • If suspect HSV: acyclovir10 mg/kg IV q8hr • empiric antibiotics after blood / CSF cultures • OR observation with repeat LP in 6 - 24 hrs. • If symptomatically improved and culture negative: DC antibiotics w/o repeat LP • If persistent SX w/o clear dx: repeat LP

  19. HOSPITALIZE IF.. • Ill-appearance • Signs of encephalitis • altered mental status, behavior, or personality • motor or sensory deficits • speech or movement disorders; hemiparesis; flaccid paralysis; paresthesias; • seizures • Need for empiric antimicrobial therapy. • Need for IV hydration or aggressive pain control. • Immunocompromised host. • Age younger than one year.

  20. Bacterial Meningitis“purulent meningitis” • Meningitis is an inflammatory disease of the lepto-meninges, the tissues surrounding the brain and spinal cord, and is defined by an abnormal number of WBCs in CSF . • Meninges: • pia • arachnoid • dura maters • Bacterial meningitis: infx of arachnoid mater and CSF in both the subarachnoid space and cerebral ventricles.

  21. Bacterial Meningitis - Causes There are at least 50 causative bacteria Community Acquired: • Streptococcus pneumo (pneumococcus) • Neisseria meningitidis (meningococcus) • Listeria monocytogenes (50-60ys, immunideficient) • Haemophilus influenzae type b (Hib) • Healthcare-associated • (after neurosurgery, ventricular drains, w/trauma ) • usually staphylococci • aerobic gram-negative bacilli

  22. Symptoms Quite ill Rapid onset Classic Triad: *Fever (>38*) (95%x 4d) *Mental status changes (78%) *Nuchal rigidity (88% x7d) Also: Severe, generalized headache Photophobia Nausea/vomiting Rash 11-26% N. meningitidis, petechiae and palpable purpura Arthritis: 7% N. meningitidis, PHOTO

  23. Additional Symptoms Decreased consciousness Rapid breathing Agitation Opisthotonos Bulging fontanelles Poor feeding Irritability NEWBORN FUO

  24. Possible Complications Hearing loss Brain damage Loss of vision Hydrocephalus Waterhouse-Friderichsen syndrome (WFS) or hemorrhagic adrenalitis (Neisseria meningitidis )

  25. Differentials Viral meningitis Encephalitis Febrile viral syndromes Drug induced meningitis

  26. BACT. MENINGITIS :DX Tests LP Blood cx positive Other lab:CBC, chem Chest x-ray (r/o other sites of infx) Head CT scan (ICP ) (r/o hydrocephalus, abscess or deep swelling) CSF glucose: -<40 mg/dL or <1/2 serum CSF CELL count: - WBC’s >1000/microL with a predominance of neutrophils PROTEIN elevated >0.4g/dl POSITIVE gram stain/culture H. Influenzae b Gram Stain REFER!

  27. LABORATORY FEATURES FYI Routine blood work is often unrevealing. WBC: usually elevated, with left shift Leukopenia: possible w/ severe infection Platelet count: may be reduced. Leukopenia and thrombocytopenia = poor outcome Coagulation studies: may have DIC. Serum chemistry: may have metabolic acidosis or hyponatremia Blood cultures often positive (50- 90%) Obtain Two sets of blood cultures prior to the initiation of antimicrobial therapy Cultures obtained after antimicrobial therapy are much less likely to be positive, esp. meningococcus Tests of urine, mucosal surfaces for bacterial antigens are not generally helpful

  28. LUMBAR PUNCTURE FYI • Every patient w/suspected meningitis should have CSF obtained unless LP contraindicated. • PROs of CT then LP: • exclude a mass lesion or increased ICP, which rarely leads to cerebral herniation during LP • However, a screening CT scan is not usually necessary • Study: CT:24%had abnl finding, but only 5% had mass effect. • Abnl CT scan predicted by a suspicious hx/Exam : • -immunosuppression • -previous CNS disease • seizure within the previous week • reduced LOC • motor or cranial abnormalities, papilledema • CONS of CT then LP:2hr delay in dx, 1hr delay in rx.

  29. If LP is delayed… fyi Obtain blood cultures Start antibiotics empirically before the imaging study Also give dexamethasone (0.15mg/kg IV q6hr) shortly before or at the same time as the antibiotics ( rate of hearing loss & other neuro complications, & mortality) (Adjunctive dexamethasone should not be given after antimicrobial therapy b/c unlikely to improve pt outcome) Prior administration of antimicrobials tends to have minimal effects on the chemistry and cytology findings, but can reduce the yield of Gram stain and culture . However, a pathogen can still be cultured from the CSF in most patients up to several hours after the administration of antibiotics

  30. TREATMENT Antibiotics - depending on organism Extremes of age (<3m or >60 yrs) cover for listeria with ampicillin. Empiric therapy : rocephin (2grams Q12h) plus vancomycin Treatment of secondary symptoms including cerebral edema, shock, sz FYI • TRUE medical emergency • requires immediate admission Any form of bacterial meningitis that is untreated or treated very late in its course is almost uniformly fatal. Sequelae In-hospital mortality 27% Neurologic deficit at discharge 9 % independent predictors of adverse outcome: hypotension altered mental status seizures ADVERSE OUTCOME: no RF — 9 % 1 RF — 33 % 2-3 RF — 56 %

  31. Antibiotics FYI B/C uncertain effect of dexamethasone on the CSF penetration of vancomycin: Begin with vancomycin plus either ceftriaxone or cefotaxime. If susceptibility studies show intermediate susceptibility (MIC ≥2 mcg/mL) to ceftriaxone and cefotaxime, addrifampin B/C: vancomycin penetration into the CSF starts at a high level in the presence of bacterial meningitis.. impairment in penetration to a level that will reduce efficacy is not likely in the first few days before susceptibility studies are available.

  32. Patient Education Seek immediate medical attention if a child has any of the symptoms Early treatment is key to good outcome. Prevention of hflu: HiB vaccine Prevention of pneumococcal: Prevnar Prevention, high school students: Menactra Prophylaxis of household contacts w/ preventative antibiotics; highly recommended.

  33. Meningitis (bacterial vs viral) vs Encephalitis Bacterial Meningitis Very serious Meningeal irritation CSF Gram stain positive CSF WBC >1000/microL (neuts) CSF glucose <40 mg/dL Nl brain function • Viral Meningitis: • less severe • meningeal irritation • fever, HA, NV • seizures • hemiparesis • flaccid paralysis • paresthesias • resolves w/o specific Rx • CSF WBC<500/ microL • CSF protein <80 100mg/dL • CSF glucose: normal • Gram stain negative Encephalitis Viral, invades brain tissue altered mental status (confused.. obtunded) motor or sensory deficits (paresis,  DTRs) altered behavior & personality speech or movement d/o No meningeal irritation Abnl brain function:

  34. Encephalitis Viral Inflammation of the brain Rare disease (0.5 per 100,000) Most common in children elderly Immuno-compromised

  35. Encephalitis: PATHOGENESIS • Two viral mechanisms: • 1.directly invade brain tissue (acute viral encephalitis) • virus cultured from the brain • viremia from viral meningitis • spread from peripheral nerves (rabies, HSV) • 2.Post-infectious encephalitis (autoimmune response) • No virus detected • hx of illness or vaccination 2-4wk prior to S/S • Need neuroimaging to differentiate.

  36. Encephalitis…S/S subtle to profound… • Altered mental status: confused, agitated, obtunded • Behavior • Personality • Speech • movement.. Motor or sensory deficits : hemiparesis, cranial nerve palsies, exaggerated DTRs • Seizures are common NO S/S of meningeal irritation: photophobia, nuchal rigidity VS aseptic meningitis nonspecific, fever, headache, nausea, vomiting, photophobia, nuchal rigidity; nl cerebral function

  37. Neonates and young infants As with other infections in neonates (0-28d) and young infants, the presentation can be nonspecific. • Fever (variable ) • seizure • poor feeding • Irritability • Lethargy • In a series of 63 neonates with HSV1 CNS dz: • 49% lethargy • 57% seizure • 63% skin vesicles • 44% fever

  38. Children and adolescents SS at admission prospective series of 50 children (6wks-18yrs): 100%:Encephalopathy 80%: Fever 78% Seizure 56% Other Focal neuro signs 47%  LOC Complications status epilepticus cerebral edema inappropriate ADH cardiorespiratory failure DIC defined as depressed or altered LOC (lethargy, extreme irritability, significant change in personality or behavior) x ≥24hr

  39. Encephalitis - Causes measles Many different viruses Most cause meningitis or encephalitis Postinfectiousencephalitis: MMR, VZV, influenza Sporadicencephalitis:HSV1 Geographic location (eg, St. Louis encephalitis in North America, Japanese encephalitis in Asia) rmsf lyme • Tick Exposure: • Colorado tick fever (w. US) or • non-viral, ie: Lyme dz or RMSF

  40. Encephalitis-Causes Mosquito exposure: • Arboviruses (east.equine, west. equine, St. Louis (NA, Midwest/So.US) • Venezuelan equine encephalitis 2009 • WNV (multiple continents including Asia, Africa, Europe, NA) • weakness, rash • rare < 1999,now most commonly CNS arboviral infx 16

  41. Peds..causes *Enteroviruses—major cause. clear seasonality (78 % June - October) *HSV 1/11..5% all age groups but 75% neonatal infection Epstein-Barr virus—10 % Arbovirus La Crosse encephalitis: most common arbovirus in children Seasonal (July - September)usu 5-9yr\o Arbovirus West Nile virus .. rare Influenza virus:5 % usually< 5yo Other viruses MMR: rare b/c vaccinations

  42. physical examination IF Parotitis/mental status changes:Mumps encephalitis IF Flaccid paralysis: WNV infection Misdiagnosed as Guillain-Barre syn. Maculopapular rash 50% IF Tremors of eyelids, tongue, lips, extremities: St. Louis encephalitis or WN encephalitis IF Hydrophobia, aerophobia, pharyngeal spasms, hyperactivity: encephalitic rabies. Atypical : seizures, cranial nerve palsies, myoclonus IF Grouped vesicles in a dermatomal pattern: varicella-zoster virus

  43. Encephalitis - Differentials fyi noninfectious etiologies : intracranial tumors collagen vascular disorders vasculitis neoplastic diseases adverse effects of medications Other non-viral infectious etiologies Brain abscess Syphilis tuberculous meningitis fungal meningitis (eg, coccidioides REFER!!

  44. Encephalitis - Diagnostics Lumbar puncture: Serology test to detect the presence of antibodies EEG Brain imaging • Color: Clear • high pressure • WBC, usually < 250/mm3. • predominance of lymphocytes: • early infection -> Ý neuts • repeat @ 8 hr: shift to lymphs • protein < 150 mg/dL. • glucose nl (>50% of blood) • red cells : 0 • (presence suggests HSV-1 )

  45. DIAGNOSIS FYI Etiology in most cases remains undefined CSF: VS bacterial meningitis: higher WBC (>2000/mm3) w/ neuts predominantly higher protein concentration (>200 mg/dL) usually hypoglycorrhachia Culture— Viral culture of CSF routinely ordered but viruses recovered 6% polymerase chain reaction (PCR) tests for viruses PCR testing has replaced viral culture of CSF For HSV-1, HSV-2, and enteroviruses Most important viral etiology to r/o is HSV usually fatal if untreated

  46. Imaging fyi CT/MRI : may or may be abnormal CT: r/o space-occupying lesions or brain abscess. MRI:detects demyelination

  47. EMPIRIC THERAPY no specific therapies for most CNS viral infections. EXCEPT: HSV-1 / VZV :Acyclovir (10 mg/kg IV Q8h) initiated as soon as possible

  48. Prognosis IF diffuse cerebral edema or intractable seizures: poor neurologic recovery and increased risk of mortality IF self-limited seizure activity: rapid recovery IF HSV encephalitis :Even with prompt initiation of acyclovir, significant morbidity and mortality. one-year mortality:14 % epilepsy 24% neuropsychiatric sequelae 22 %

  49. Encephalitis – Pt Education Mosquito avoidance! Avoid being outside at dawn and dusk (when mosquitoes are most active) Wear protective clothing Use insect repellent Drain standing water (breeding grounds for mosquitoes) Vaccinate Animal against rabies Acute phase lasts up to one week Full recovery can take several wks - months

  50. An extremely painful inflammation of the largest nerve in the skull: Trigeminal Nerve Trigeminal Neuralgia SX: Sudden, severe spasms usually unilateral Brief 1-3 sec stabbing or lancinating recurrent episodes Facial muscle spasms continuous dull pain b/t no nite awakening … pain in the distribution of one or more branches of the fifth cranial (trigeminal) nerve

More Related