INFECTIOUS INFECTIOUS DISEASES OF DISEASES OF
CENTRAL NERVOUS CENTRAL NERVOUS SYSTEMSYSTEM
INFECTIOUS INFLAMMATORY DISEASES OF CENTRAL
NERVOUS SYSTEM
Subacute sclerosing
leukoencephalitis (demyelinating
leuko- and panencephalitis)
Arachnoiditis of brain
Meningitis Encephalitis
Poliomyelitis
Myelitis
MENINGITIS
CLASSIFICATION OF MENINGITIS
By etiology
Bacterial
Viral
Primary
Secondary
By pathogenesis
By the character of inflammatory process and changes in liquor
Purulent
Serous
Serous-fibrinogenous
Hemorrhagic
By clinical course
Fulminant
Acute
Chronic
Subacute
By localization of the process
Basal
Convexital
light
By degree of severity
medium
severe
extremely severe
Clinical signs of meningitis
– fever
– high body temperature
– leucocytosis in blood with shift of the formula to the left,
– erythrocyte sedimentation rate
(EST)
Syndrome of infectious disease
II
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 syndromeIIII
– headache – vomiting– spasms– psychomotor excitement– impairment of consciousness
Meningeal syndrome
General brain symptoms
IIII
Purulent meningitis
Neutrophilic pleocytosis (thousands of cells per 1 mm3)
Lymphocytic pleocytosis (tens or hundreds of cells per 1 mm3)
Detection of pathogenic factor
Syndrome of inflammatory changes in liquor
Serous meningitis
IIIIII
Pathogenesis of meningitis
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
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
In the shortest term possible it’s necessary to diagnose meningococcal infection only on the basis of clinical signs: acute beginning, fever, hemorrhagic rash.
For the patient’s life hyperdiagnostics is much better than not timely diagnosis
Diagnostics
• Liquor. Moderate pleocytosis (1-5 thousand or 10-12 thousand cells per 1 mm3) 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 mm3 , liquor gets a yellowish shade.
• 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.
• Inflammatory changes in peripheral blood.
• Clinical signs of meningitis
▪ 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 % - Аmpicillin (200-400 mg/1 kilo of mass) - sulfonamides - dehydration
- antipyretics (pirabutol, reoperin, ibubrophen) - seduxen (in case of psychomotor excitement)
Treatment
PNEUMOCCOCAL MENINGITIS
(adults get this disease more often)
• The beginning is very acute
• Marked general-infectious symptoms.
• High temperature.
• Phenomena of meningoencephalitis are increasing very fast with involving of cranial nerves.
• Phenomena of brain tumor are increasing fast. There is often observed wedging of brain stem into great occipital foramen.
• On the third and fourth days hemorrhagic rash appears (face, mucous membrane of oral cavity).
• In liquor – sharp decrease of glucose level
• Antibiotics (penicillin, levomycetin, cephalosporins)
• Antiinflammatory drugs• Antitumor drugs
TREATMENT
STAPHYLO-, STREPTOCOCCAL
MENINGITIS
They are aggravation of primary purulent diseases (otitis, sinusitis etc.)
• Beginning is very acute
• Marked meningeal symptoms.
• High temperature up to 40 °.
• Impairment of consciousness
• Sepsis
• In liquor – neurophilic pleocytosis, sharp increase of protein.
• Intravenously high doses of penicillin, cephalosporin
Treatment
SEROUS MENINGITIS
Acute lymphocytic
choriomeningitis
Parotitic
Caused by Coxsackie
viruses
• Beginning is subacute• meningeal symptoms are not very marked
• Cranial nerves (ІІ, ІІІ, V, VIII) are involved
• Meningeal posture• Conductive disorders (paresis)• Root pains• Liquor: xanthochromic, high pressure,
moderate lymphocytic pleocytosis (200-400 in 1mm3), high level of protein, low level of glucose. In fibrinous film – microbacteria of tuberculosis
Тuberculous (basal) meningitis
• Not less than 4 antituberculous drugs
TREATMENT
ARACHNOIDITIS
These are inflammatory or reactive local or spread changes of pia matters of brain as a result of endured or subacute neuroinfections
CLASSIFICATION
OF ARACHNOIDITIS
By morphologic changes
adhesive cystic
By localization
of posterior cranial fossa
of cerebellopontine angle
cerebral spinal
convexital basal
optico-chiasmic
Clinical picture of arachnoiditis
general cerebellar impairments (due to intracranial hypertension)
focal impairments (depend on localization of the process)
- headache–vomiting, nausea–congestive disks of optic nerves or their atrophy– vertigo– epileptic attacks
Clinical peculiarities of some cerebral arachnoiditis
Convexital arachnoiditis
– jacksonian epileptic attacks
– asymmetry of reflexes,
more rarely paresis of limbs
– conductive sensory impairments
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
Of posterior cranial fossa
– general cranial symptoms prevail
– pains in back of the head
– vomiting
– vertigo
– anosmia
– congestive disks of optic nerves
Of cerebellopontine angle
– Tinnitus (ear noise)
– loss of hearing
– unsteadiness, vertigo
– paresis of mimic muscles
– trigeminal neuralgia
– slight pyramidal lesions
Craniography pneumoencelography investigation of eye-ground Perimetry CT, MRI of brain electroencephalography echoelectroencephalography
METHODS OF INVESTIGATION
Conservative: antiinflammatory dehydration resolving drugs Symptomatic treatment
Surgical: - operation in case of cystic and adhesive arachnoiditis
TREATMENT
ENCEPHALITIS
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.
By clinical course
Progressive-remitting
acute
chronic
subacute
By clinical picture
−Standard forms
− asymptomatic
− abortive
− fulminant
Primary
With unknown virus (lethargic)
arboviral (tick-borne/vernal, mosquito)
еnterovirus, in case of hydrophobia
necrotic (herpetic, cytomegalovirus)
Secondary
• parainfectious (in case of measles, rubella, epimic parotitis, chicken pox, flu)
• postvaccinal, serum
• caused by microbes, rickettsia, toxoplasma
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
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
Chronic stage:Parkinsonian syndrome
Acute stage:High body temperature, pathologic sleepiness, oculomotor disorders, vegetative, vestibular, psychic impairments
Epidemic encephalitis
Stage of recoveringStage 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
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
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)
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
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
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)
CT of brain – signs of swelling MRI of brain – signs of swelling+ nidi of
hyperintensive signal Electroencephalography (EEG) –
increase of vascular readinessEye ground – swelling of DON; in 1,5-2
months. Atrophy
DIAGNOSTICS OF HSV
Resuscitation department (in acute stage)
antiviral immunoglobulins dehydration, desensitization resolving
TREATMENT
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
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 VІІ, 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
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
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