Bohomolets Neurology Infectious Dx of CNS

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Bohomolets Neurology Infectious Dx of CNS

  1. 1. INFECTIOUS DISEASES OF CENTRAL NERVOUS SYSTEM
  2. 2. INFECTIOUS INFLAMMATORY DISEASES OF CENTRAL NERVOUS SYSTEM Subacute sclerosing leukoencephalitis (demyelinating leuko- and panencephalitis) Arachnoiditis of brain Meningitis Encephalitis Poliomyelitis Myelitis
  3. 3. MENINGITIS
  4. 4. CLASSIFICATION OF MENINGITIS
  5. 5. By etiology Bacterial Viral Primary Secondary By pathogenesis
  6. 6. By the character of inflammatory process and changes in liquor Purulent Serous Serous-fibrinogenous Hemorrhagic
  7. 7. By clinical course Fulminant Acute Chronic Subacute
  8. 8. By localization of the process Basal Convexital light By degree of severity medium severe extremely severe
  9. 9. Clinical signs of meningitis
  10. 10. – fever – high body temperature – leucocytosis in blood with shift of the formula to the left, – erythrocyte sedimentation rate (EST) Syndrome of infectious disease I
  11. 11. Meningeal symptoms 1. General hyperesthesia and hyperesthesia of organs of senses 2. Reactive pain phenomena: – Bechterew’s zygomatic symptom – feeling of pain when you press on eyeballs, points of outlet of branches of trigeminal, occipital nerves 3. Muscular tonic tensions: – rigidity of occipital muscles, long muscles of the back – Kernig’s symptoms, Brudzinski’s upper , media, lower symptoms Meningeal syndrome II
  12. 12. – headache – vomiting – spasms – psychomotor excitement – impairment of consciousness Meningeal syndrome General brain symptoms II
  13. 13. Purulent meningitis Neutrophilic pleocytosis ( thousands of cells per 1 mm 3 ) Lymphocytic pleocytosis ( tens or hundreds of cells per 1 mm 3 ) Detection of pathogenic factor Syndrome of inflammatory changes in liquor Serous meningitis III
  14. 14. Pathogenesis of meningitis
  15. 15. Ways of infection of membrane Open craniocerebral trauma , which is combined with liquoria Perineural or lymphogenous spread of pathogenes in case of presence of purulent infection (sinusitis, otitis etc) Hematogenous spread from primary sources of infection
  16. 16. Pathogenesis Inflammation and edema of brain membranes (and adjacent brain tissue) Discirculation in brain and membranes vessels Hypersecretion of liquor and delay of its resorption High intracranial pressure and hydrocephalus Damage of membranes and roots of cranial and spinal nerves
  17. 17. <ul><li>In the shortest term possible it’s necessary to diagnose meningococcal infection only on the basis of clinical signs: acute beginning, fever, hemorrhagic rash. </li></ul><ul><li>For the patient’s life hyperdiagnostics is much better than not timely diagnosis </li></ul>Diagnostics
  18. 18. <ul><li>Liquor. Moderate pleocytosis (1-5 thousand or 10-12 thousand cells per 1 mm 3 ) with cellular-proteinous dissociation, minor decrease of glucose level. The colour of liquor is like water with milk. When pleocytosis is more than 5-6 thousand per 1 mm 3 , liquor gets a yellowish shade. </li></ul><ul><li>Express-diagnostics – bakterioscopy of thick drop of blood, blood smears and liquor . Colouring by gram already after 30 minutes allows to find out gram-negative diplococcuses. </li></ul><ul><li>Inflammatory changes in peripheral blood. </li></ul><ul><li>Clinical signs of meningitis </li></ul>
  19. 19. <ul><li>▪ meningococcal meningitis: cephalosporins of third generation, penicillin 300 000 units per 1 kilo of mass (18-24 mln units per 24 hours ) ≈ 8 days . To cancel when cytosis is less than 100 cells, when lymphocytes are less than 75 % </li></ul><ul><li> - А mpicillin (200-400 mg /1 kilo of mass ) </li></ul><ul><li> - sulfonamides </li></ul><ul><li> - dehydration </li></ul><ul><li>- antipyretics ( pirabutol, reoperin, ibubrophen ) </li></ul><ul><li> - seduxen ( in case of psychomotor excitement ) </li></ul>Treatment
  20. 20. PNEUMOCCOCAL MENINGITIS ( adults get this disease more often )
  21. 21. <ul><li>The beginning is very acute </li></ul><ul><li>Marked general-infectious symptoms. </li></ul><ul><li>High temperature. </li></ul><ul><li>Phenomena of meningoencephalitis are increasing very fast with involving of cranial nerves. </li></ul><ul><li>Phenomena of brain tumor are increasing fast. There is often observed wedging of brain stem into great occipital foramen . </li></ul><ul><li>On the third and fourth days hemorrhagic rash appears (face, mucous membrane of oral cavity). </li></ul><ul><li>In liquor – sharp decrease of glucose level </li></ul>
  22. 22. <ul><li>Antibiotics (penicillin, levomycetin, cephalosporins) </li></ul><ul><li>Antiinflammatory drugs </li></ul><ul><li>Antitumor drugs </li></ul>TREATMENT
  23. 23. STAPHYLO-, STREPTOCOCCAL MENINGITIS
  24. 24. <ul><li>They are aggravation of primary purulent diseases (otitis, sinusitis etc.) </li></ul><ul><li>Beginning is very acute </li></ul><ul><li>Marked meningeal symptoms. </li></ul><ul><li>High temperature up to 40 ° . </li></ul><ul><li>Impairment of consciousness </li></ul><ul><li>Sepsis </li></ul><ul><li>In liquor – neurophilic pleocytosis, sharp increase of protein. </li></ul>
  25. 25. <ul><li>Intravenously high doses of penicillin, cephalosporin </li></ul>Treatment
  26. 26. SEROUS MENINGITIS Acute lymphocytic choriomeningitis Parotitic Caused by Coxsackie viruses
  27. 27. <ul><li>Beginning is subacute </li></ul><ul><li>meningeal symptoms are not very marked </li></ul><ul><li>Cranial nerves ( ІІ, ІІІ, V, VIII) are involved </li></ul><ul><li>Meningeal posture </li></ul><ul><li>Conductive disorders (paresis) </li></ul><ul><li>Root pains </li></ul><ul><li>Liquor : xanthochromic, high pressure, moderate lymphocytic pleocytosis (200-400 in 1 mm 3 ), high level of protein, low level of glucose. In fibrinous film – microbacteria of tuberculosis </li></ul>Т uberculous (basal) meningitis
  28. 28. <ul><li>Not less than 4 antituberculous drugs </li></ul>TREATMENT
  29. 29. ARACHNOIDITIS
  30. 30. <ul><li>These are inflammatory or reactive local or spread changes of pia matters of brain as a result of endured or subacute neuroinfections </li></ul>
  31. 31. CLASSIFICATION OF ARACHNOIDITIS
  32. 32. By morphologic changes adhesive cystic
  33. 33. By localization of posterior cranial fossa of cerebellopontine angle cerebral spinal convexital basal optico-chiasmic
  34. 34. Clinical picture of arachnoiditis general cerebellar impairments (due to intracranial hypertension) focal impairments (depend on localization of the process) <ul><li>- headache </li></ul><ul><ul><li>vomiting, nausea </li></ul></ul><ul><ul><li>congestive disks of optic nerves or their atrophy </li></ul></ul><ul><ul><li>vertigo </li></ul></ul><ul><ul><li>epileptic attacks </li></ul></ul>
  35. 35. Clinical peculiarities of some cerebral arachnoiditis
  36. 36. Convexital arachnoiditis – jacksonian epileptic attacks – asymmetry of reflexes, more rarely paresis of limbs – conductive sensory impairments
  37. 37. Optico-chiasmic – headaches in forehead area, eye-sockets/orbits, bridge of nose – loss of eyesight – bitemporal hemianopsia or concentric narrowing of eyesight fields – bitemporal atrophy of discs of optic nerves ( more rarely congestive) – anosmia – sleep disorders, changes of carbohydrate-salt metabolism
  38. 38. Of posterior cranial fossa – general cranial symptoms prevail – pains in back of the head – vomiting – vertigo – anosmia – congestive disks of optic nerves
  39. 39. Of cerebellopontine angle – Tinnitus (ear noise) – loss of hearing – unsteadiness, vertigo – paresis of mimic muscles – trigeminal neuralgia – slight pyramidal lesions
  40. 40. <ul><li>Craniography </li></ul><ul><li>pneumoencelography </li></ul><ul><li>investigation of eye-ground </li></ul><ul><li>Perimetry </li></ul><ul><li>CT , MRI of brain </li></ul><ul><li>electroencephalography </li></ul><ul><li>echoelectroencephalography </li></ul>METHODS OF INVESTIGATION
  41. 41. <ul><li>Conservative: </li></ul><ul><li> antiinflammatory </li></ul><ul><li> dehydration </li></ul><ul><li> resolving drugs </li></ul><ul><li> Symptomatic treatment </li></ul><ul><li>Surgical: </li></ul><ul><li> - operation in case of cystic and adhesive arachnoiditis </li></ul>TREATMENT
  42. 42. ENCEPHALITIS
  43. 43. <ul><li>Encephalitis is an inflammation of brain parenchyma. Not only infectious, but also infectious-allergic and toxic diseases are considered to be encephalitis. That is why not only inflammation and swelling, but also hemorrhages, necrosis, demyelinization and degeneration are typical for pathomorphologic changes. </li></ul>
  44. 44. By clinical course Progressive-remitting acute chronic subacute By clinical picture <ul><li>Standard forms </li></ul><ul><li>asymptomatic </li></ul><ul><li>abortive </li></ul><ul><li>fulminant </li></ul>
  45. 45. Primary  With unknown virus (lethargic)  arboviral ( tick-borne/vernal, mosquito ) <ul><li>е nterovirus, in case of hydrophobia </li></ul> necrotic (herpetic, cytomegalovirus)
  46. 46. Secondary • parainfectious (in case of measles, rubella, epimic parotitis, chicken pox, flu) • postvaccinal, serum • caused by microbes, rickettsia, toxoplasma
  47. 47. <ul><li>If neurologic focal signs are absent, and general cerebral, asthenic or vegetative-distonic (after infectious disease) symptoms prevail in neorologic status – infectious encephalopathy, caused by discirculatory - dystrophic changes </li></ul>
  48. 48. General cerebral: Headache, vomiting, spasms, psychomotor disorders, impairment of consciousness General infectious : High temperature, inflammatory changes inj blood, catarrhal phenomena of upper respiratory tracts and gastrointestinal tract, focal : ( depend on localization of the process ) Clinical manifestations of encephalitis
  49. 49. Chronic stage : Parkinsonian syndrome Acute stage : High body temperature, pathologic sleepiness, oculomotor disorders, vegetative, vestibular, psychic impairments Epidemic encephalitis
  50. 50. Stage of recovering Stage of reconalescence Period of residual effects ( permanent atrophic paresises, Kojewnikoff’s epilepsy) Acute stage • The first period of fever: weakness, headache, pain in muscles, meningeal syndrome; • the second period of fever: peripheral paresises of muscles of arms and neck, bulbar syndrome Tick-borne(vernal) encephalitis
  51. 51. Ethiology . HSV of 1 and 2 type Pathogenesis . Central nervous system gets infected by virus through olfactory bulbs or ganglions of trigeminal nerve. Virus spreads hematogenicly or by perineural areas. Provocateurs of virus manifestation are: intercurrent diseases, prscription of cytostatics, HIV infection etc. It gets to central nervous sytem hematogenicly if hemaencephalitic barrier (HEB) is impaired (by perineural fissures – herpes zoster) Herpetic encephalitis
  52. 52. Herpetic encephalitis Pathomorphology - is characterized by hemorrhagic changes in nerval tissue with appearance of focuses of distruction, with further developing of cysts, mainly in grey sunstance (frontal, temporal, parietal lobes)
  53. 53. Clinical picture of herpetic encephalitis 1 . Early stage of clinical course Meningeal type – in 50 % • fever • general infectious effects • severe headache • impairment of consciousness Cortical type –in 20% of cases • non adequate behaviour • disorientation • elements of amnesia In 5-7 days - fever
  54. 54. Clinical picture of herpetic encephalitis 1. Early stage of clinical course Stroke-like type – in 10% of cases • sudden generalized spasms • loss of consciousness (up to coma) • fever Brainstem type – in 5% cases • diplopia • disarthria • dysphonia • alternating hemiaparesis
  55. 55. Clinical picture of herpetic encephalitis • general cranial and liquor-hypetensive symptoms • lesion of cranial nerves • paresis of limbs • huperkinesias, episyndrome • severe impairments of higher cortical functions (aphasia, apraxia, hallucinations, loss of intellect, bulbar syndrome)
  56. 56. <ul><li>CT of brain – signs of swelling </li></ul><ul><li>MRI of brain – signs of swelling+ nidi of hyperintensive signal </li></ul><ul><li>Electroencephalography (EEG) – increase of vascular readiness </li></ul><ul><li>Eye ground – swelling of DON ; in 1,5-2 months. Atrophy </li></ul>DIAGNOSTICS OF HSV
  57. 57. <ul><li> Resuscitation department (in acute stage) </li></ul><ul><li> antiviral </li></ul><ul><li> immunoglobulins </li></ul><ul><li> dehydration, desensitization </li></ul><ul><li> resolving </li></ul>TREATMENT
  58. 58. This is toxico-infectious lesion of nervous sytem, which is developping on peack of the flu Grippal enecephalitis (secondary) pathomorphology - ▪ swelling of brain ▪ small hemorrhages, diapedic hemorrhages ▪ perivascular infiltrations
  59. 59. Grippal encephalitis (secondary) Clinical picture – marked general cerebellar symptoms – meningeal symptom with domination of rigidity of occipital muscles – cerebral symptoms: aphasia. Oculomotor impairments, lesion of V ІІ, ІІІ, ІХ-ХІІ pairs of cranial nerves, pyramidal insufficiency – changes in eye ground: congestion, sometimes neuritis, loss of acuty of eye-sight – Liquor : bloody, xanthochromic, transparent
  60. 60. Grippal encephalitis (secondary Treatment – bed rest – calcium drugs – antihistaminic – antiviral – desintoxicating In case of absence of focal sisns, but with presence of asthenic, cephalgic, general cerebellar and hypertensive syndromes, grippal encephalopathy is diagnosed
  61. 61. Thank you for attention 

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