Neuroinfections

Written by the Head of Chair of neurology and

neurosurgery Prof. Natalia N. Maslova
Translated by Assist. Prof. Vladimir V. Sergeev
Neuroinfections

Infectious diseases
of the nervous system
1. Meningitises
2. Encephalitises
3. Meningoencephalitises
4. Cerebral arachnoiditis
5. Infectious lesions of the dura mater
 epidural abscess
 subdural empyema
6. Brain abscesses
Neuroinfections

Meningitis is an acute infectious disease that

affects the spider and soft membranes of the
brain

Pathogens: bacteria, viruses, fungi, protozoa

Entrance gate of infection (nasopharynx, bronchi, intestines)

Spread of the pathogenhematogenic or lymphogenic pathway

The meninges
Neuroinfections

Pathways of infection of the meninges

1. Contact distribution in opened and
penetrating brain and spinal trauma,
fractures of the skull bones accompanied
by liquorrhea
2. Perineural and lymphogenic distribution
with existing purulent infection of ENT
organs, eye sockets, oral cavity, etc.
3. Hematogenic spread with bacteremia
Neuroinfections

Classification of the meningitis

1. By the nature of the inflammatory process:
 purulent
 serouse

2. By pathogenesis:
 primary
 secondary

3. On localization:
 generalized
 limited
 basal
 convexital
Neuroinfections

Classification of the meningitis

4. According course
 Fulminant
 Acute
 Subacute
 Chronic

5. The severity of clinical manifestations:

 Mild
 Moderate
 Severe
 Extremely severe
6. According to the etiology:
 Bacterial
 Viral
Neuroinfections

Meningitises
PURULENT SEROUS

I. Acute I. Acute II. Chronic

Lymphocytic • Tubercular
1. Primary • Brucellar
 Epidemic (induced
by viruses • Syphilitic
meningococcal • at AIDS
 Pneumococcal Coxsackie and
ECHO and others) • for parasitic
 Caused by BPB diseases defeats

2. Secondary II. Chronic

• otogenic  Secondary
• rhinogenic  Recurrent
• odontogenic
Neuroinfections

Diagnostics

Making punctures
And taking CSF
Neuroinfections
Neuroinfections
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Modern methods of laboratory

diagnostics of the meningitis
 Polymerase chain reaction
 the reaction immunofluorescence (RIF)
 Complement binding reaction (CBR)
 Immunoblotting
 Co-agglutination reaction
 Latex agglutination
Neuroinfections

Meningeal syndrome
1. Common infectious symptoms
2. Brain-wide symptoms
3. Meningeal symptoms
stiff neck
Kernig’ sign
Brudzinsky’ signs (upper, middle, lower)
Zygomatic Bekchterev’ sign

4. CSF changes
increased liquor pressure
cell-protein dissociation
Neuroinfections

Meningeal symptoms

Nuchal rigidity

Kernig’s sign
Neuroinfections

Acute purulent meningitis

Most are caused by meningococci, pneumococci,

Haemophilus influenzae.

Meningococcal meningitis
• air-drop transmission
• path the source is sick or healthy
 carrier sporadic nature of the disease,rarely
 a small epidemic occurs at any age

Neisseria
meningitidis
Neuroinfections

BACTERIAL MENINGITIS
Pathogenesis
 Bacteria typically gain access to the central
nervous system by colonizing the mucous
membranes of the nasopharynx, leading to local
tissue invasion, bacteremia, and hematogenous
seeding of the subarachnoid space.
 Bacteria can also spread to the meninges directly,
through anatomic defects in the skull or from
parameningeal sites such as the paranasal
sinuses or middle ear.
Neuroinfections

BACTERIAL MENINGITIS
Pathogenesis
 Polysaccharide bacterial capsules,
lipopolysaccharides, and outer membrane
proteins may contribute to the bacterial invasion
and virulence.
 The low levels of antibody and complement
present in the subarachnoid space are inadequate
to contain the infection.
 The resulting inflammatory response is associated
with the release of inflammatory cytokines, that
promote blood-brain barrier permeability,
vasogenic cerebral edema, changes in cerebral
blood flow, and perhaps direct neuronal toxicity.
Neuroinfections

Meningococcal meningitis
Pathogenesis
entrance gate-upper respiratory tract

nasopharyngitis

penetration of the pathogen into the blood

meningococcemia (accompanied by a characteristic

hemorrhagic skin rash)

Hemorrhagic rashes
Neuroinfections

Meningococcal meningitis
Pathomorphology
The web and soft shells are hyperemic and
edematous. Accumulation of pus in the subarachnoid
space. Small hemorrhages in the brain substance
Neuroinfections

Meningococcal meningitis. Clinic.

The incubation period is 5-10 days
 Acute onset: headache, vomiting, photophobia, fever
(38-40°C)
 Consciousness is preserved, in severe forms -
confused
 Meningeal symptoms: rigidity of the nape of the neck,
symptoms of Kernig, Brudzinsky
 Focal disorders are usually absent
 In the blood-neutrophilic pleocytosis, accelerated ESR
 In CSF: pleocytosis up to 10,000 in 1 mm3 (mainly
neutrophils), presented meningococci
 protein 10-15 g / l, glucose reduction
 The duration of the disease is 2-6 weeks
In lightning-fast toxic forms-endotoxic shock,
coma with a fatal outcome
 With proper treatment, recovery is more likely
Neuroinfections

Treatment of the acute purulent meningitis

Antibioticotherapia
•Penicillin in a dose 200 000 - 300 000 UNITS / kg
•Ampicillin
at a dose(18 000 000 - 24 000 000 DB per day
and more) of 12-15g/day
•Route of administration-I / m or I / V
•The duration of treatment depends on the patient's
condition and the rate of CSF sanation (when the
temperature normalizes and the cytosis decreases to 100
lymphocytes in 1 mm3-cancellation)
Syndrome treatment
 (maintenance of water-electrolyte balance, prevention of
edema of the lungs, brain, and other complications)
 Neuroinfections

Antibacterial treatment
of the acute purulent meningitis
Start-therapy of the meningitis unknown etiology
•Aminoglycosides (Kanamycin, Gentamicin) 2-4 mg / kg / day
•Penicillin + Gentamicin + Kanamycin
•Ampicillin (50-100 mg / kg / day in 2 doses) + Gentamicin or
Kanamycin
•Cefotaxime (Ceftriaxone) + Ampicillin; Benzylpenicillin;
Chloramphenicol

In meningococcal, pneumococcal and

streptococcal etiology
Penicillin
24,000,000-32,000,000 U/day (300,000 units / kg) in 6-8
doses for 7-10 days
For severe forms: 48,000,000 U/day
At coma: 800 000-1 000 0000 U/kg + sodium salt of benzylpenicillin
4,000,000-12,000,000 U / day i/v
Cefotaxime (Ceftriaxone) 4 g/day
Neuroinfections

Antibacterial treatment
of the acute purulent meningitis

In meningitis caused by E. Coli

• Morfotsiklin
• Chloramphenicol hemisuccinate
• Kanamycin
• Cefotaxime (Ceftriaxone)

When PCB is infected

• Polymixin-M

For influenza meningitis

• Chloramphenicol hemisuccinate
• Cefotaxime (Ceftriaxone)
• Ampicillin
Neuroinfections
Antibacterial treatment
of the acute purulent meningitis
Use of semisynthetic penicillins:
 Ampicillin 200-300 mg/kg / day with 6-fold administration of
I/m or I/V
 Cefotaxime (Ceftriaxone) 4 g/day I/V (for children – 100-200
mg/kg/day)
 Levomycetin up to 100 mg / kg 3-4 times/day
 Prolonged-acting sulfanilamides (sulfamonometoxin,
sulfapiridazine, sulfadimetoxin) inside according to the
scheme:
1st day-2 g 2 times, then 2 g 1 time/day

When staphylococcal meningitis

endolumbal introduction:
•Tseporin(cephaloridine)
•Oleandomycin
•Olemorphocyclinum
Neuroinfections

Acute serous meningitis

• Caused by enteroviruses Coxsackie and ECHO
• Characterized by an epidemic distribution
Вирус Коксаки
• The incubation period is about 7 days
• The onset is acute: fever, severe headache, vomiting.
 Herpetic rashes on the lips, nose wings, herpetic
rashes
 Bright meningeal syndrome
 CSF: high CSF pressure, lymphocytic pleocytosis,
protein and glucose content does not change
 The course is quite favorable, but in 30% of cases there
is a tendency to relapse
 Symptomatic treatment (headache relief and prevention
of brain edema)
Neuroinfections

Chronic meningitis
They develop in chronic infections: tuberculosis,
brucellosis, syphilis, leptospirosis, AIDS, parasitic
lesions (cysticercosis), etc.

Tuberculous meningitis
• Develops in patients with hematogenically
disseminated forms of tuberculosis
Infection hematogenous route through the
choroid plexus of the ventricles

Mycobacterium
tuberculosis
Neuroinfections

Tuberculous meningitis

Pathomorphology
Tuberculous tubercles on the
base of the brain
 The shells are dim
Fibrous effusion in the sub-
spider space
The ventricles of the brain
are stretched
Neuroinfections

Tuberculous meningitis
Clinic and diagnostics
• The disease develops slowly
• First appear malaise, decreased appetite, daytime
drowsiness, subfebrility, headache, vomiting, m. b.
mental disorders
 Meningeal syndrome develops in 2-3 weeksLater,
there are symptoms of CHN damage: oculomotor,
facial, etc.
 CSF: transparent, pleocytosis 100-300cells in 1
mm3 (mainly lymphocytic), significantly increased
protein content –up to 1-5 g / l,
 Reduced glucose level
 Lethality 10%
Neuroinfections

Tuberculous meningitis. Treatment

It is performed with specific medications: isoniazid +

rifampicin + pyrazinamide 3 months then isoniazid +
rifampicin 7 monthsisoniazid-15 mg / kg /
daypyrazinamide-30 mg / kg / day rifampicin-600
mg/day

Pyridoxine 30 mg/day (isoniazid initiates pyridoxine

deficiency in the body)

For insufficient effectiveness: + streptomycin

Neuroinfections

Tuberculous meningitis. Treatment

Isoniazid 5-10 mg / kg
Streptomycin 0.75-1 g / day for the first 2 months
(ototoxicity!)
Ethambutol 15-30 mg / kg / day
The first schema + Rifampicin 600 mg 1 R / day

Isoniazid 5-10 mg / kg
Rifampicin 600 mg 1 R / day
Pyrazinamide 20-35 mg / kg

PASA up to 12 g /day (0.2 g / kg / day) in fractional doses 20-

30 minutes after meals, washed down with alkaline mineral
water
Streptomycin 0.75-1 g / day for the first 2 months
Ftivazid 40-50 mg / kg / day (0.5 g 3-4 R / day)

Use pyridoxine 30 mg/day (isoniazid initiates pyridoxine

insufficiency in the body)
Neuroinfections

Infectious lesions of the Dura mater of the brain

In most cases, TMO damage occurs due to the spread

of infection from the paranasal sinuses, the bones of
the skull, and the dental system.
When an infection occurs, an epidural abscess of
limited size forms between the TMO and the
periosteum.
When an infection enters the subdural space, the
spread of pus can take over the entire convexital
surface of the brain - the subdural empyema.
Neuroinfections

Brain abscess - a limited accumulation of pus

in the substance of the brain
• Intracerebral
• Epidural
• Subdural

Etiology: streptococci, meningococci, pneumococci,

Escherichia coli, Proteus, mixed flora

According to the etiology and pathogenesis of brain

abscesses are divided into:
1) contact (near the primary purulent focus)
2) metastatic
3) traumatic
Neuroinfections

Contact abscesses
Causes: mastoiditis, otitis, purulent processes in the
bones of the skull, paranasal sinuses, eye socket,
meninges, oral cavity (phlegmon of the bottom of
the mouth)

 Otogenic (50%)
 Rhinogenic
 Odontogenic
 Orbitalnye

Chronic purulent processes are more often

complicated by abscission than acute ones.
Neuroinfections

Otogenic abscesses
The infection penetrates from the temporal bone
through the roof of the tympanic cavity and cavernous

sinuses along the continuation of the SSC, causing an

abscess of the temporal lobe.
It can spread through the labyrinth and sigmoid sinus
in the PCA, leading to an abscess of the cerebellum.

• Otogenic and rhinogenic abscesses are more often

localized in the frontal lobes
• Develops local pachymeningitis, adhesive limited
meningitis, limited purulent encephalitis
• Less often, OTO - and rhinogenic abscesses occur
hematogenically due to venous thrombosis, sinuses,
septic arteritis (while localized deep in the brain and
Neuroinfections

Metastatic abscesses
Reasons:

Lung diseases: pneumonia, bronchiectasis,

abscess,
empyemaseptic
 Ulcerative endocarditis
 Osteomyelitis
 Abscesses of internal organs

The mechanism of penetration into the brain is

septic embolism.

In 25-30% of abscesses are multiple and localized

in the deep parts of the white matter.
Neuroinfections

Traumatic abscesses
• More often develop with open TBI
• When TMO is damaged, the infection enters the
perivascular slits in the brain tissue, which is
preceded by limited or diffuse inflammation of the
membranes
• If a foreign body gets in, the infection spreads with it
• The abscess spreads along the course of the wound
channel or around a foreign body
• Traumatic abscesses account for about 15% of all
brain abscesses
Neuroinfections

Abscess of the brain pathomorphology

The formation of an abscess goes through a number of
stages and takes 2-3 – 4-6 weeks.
The reaction to the introduction of infection is in the
form of limited inflammation of the brain tissue
(purulent encephalitis).
• Possible healing in the form of scarring.
• If there is a purulent meltdown of the brain, then a
cavity filled with pus is formed - the stage of dividing
the abscess.
• Then a dense connective tissue capsule is formed
around the abscess – the stage of an encapsulated
abscess.
• Sometimes everything remains at the stage of
purulent brain meltdown.
Neuroinfections

Abscess of the brain

Neuroinfections

Abscess of the brain. The clinical picture (1)

With contact abscesses, the disease develops gradually.

Against the background of subsiding symptoms of the
main disease, the body temperature rises again,
headache, vomiting, signs of irritation of the brain
membranes (meningism), there may be a violation of
consciousness up to a coma. In the future, the process
may involve the soft membranes and the substance of
the brain, which will be clinically manifested by focal
symptoms.
Otogenic abscesses sometimes develop on the opposite
side of the otitis media.
CSF: pleocytosis (lymphocytes and polynuclears),
increased protein to 0.75-3 g/l and pressure.
Neuroinfections

Abscess of the brain. The clinical picture (2)

Group 3 symptoms:
 General infectious diseases
 Brain-wide
 Brain-focal
Course:
• Acute
• Subacute
• Chronic

• An extremely severe complication is a breakthrough

of the abscess into the ventricles or subarachnoid
space.
• The mortality rate reaches 40-60%.
• 30% of survivors have persistent residual effects.
Neuroinfections

Abscess of the brain. Diagnostics.

• Clinical examination
• CSF research
• CT or radionuclide scintigraphy (formation of a
round
shape with a clear shape and a pronounced zone of

perifocal edema)

Differential diagnosis:
• Meningitis
• Neoplastic diseases of the brain
Neuroinfections

Abscess of the brain. Treatment.

It should be surgical (drainage) in combination with AB
therapy
• It is necessary to take into account the sensitivity of the
microflora to the drug (to carry out seeding of the
contents of the abscess with the determination of
sensitivity)
• Often wash the abscess capsule with kanamycin (but not
penicillin !!!)
• Penicillin 24,000,000 DB/day
• In complex mixed infections, the complex of antibiotics is
selected individually, and GC therapy and detoxification
therapy are performed
Neuroinfections

Encephalitis-inflammation
of the brain substance

• Primary
• Secondary post-or para-infectious
(about 50%)
 Caused by slow infections
Neuroinfections

Classification of encephalitis
I. Primary Encephalitis
1. Viral
 Arboviral
- tick-borne spring and summer
- mosquito Japanese
- American St. Louis
 Viral polyseasone
- enterovirus ECHO and Coxsackie
- herpetic
- with rabies
- retroviral (AIDS, HTLV-1 myelopathy, etc.)
 Caused by an unknown virus
- epidemic (Economo)

2. Microbial and rickettsial

- in neurosyphilis
- for typhoid fever
- neuroborreliosis (Lyme disease)
Neuroinfections

Classification of encephalitis
II. Encephalitis secondary
1. Viral
- for measles
- for chickenpox
- for rubella
- papovavirus (progressive multifocal leukoencephalopathy),
cytomegalovirus, encephalitis in neuro-AIDS
2. Post-vaccination
3. Microbial and rickettsial
- staphylococcal
- streptococcal
- malarial
- toxoplasmosis
III. Encephalitis caused by slow infections
1. Subacute sclerosing panencephalitis
2. Prion diseases (Creutzfeldt-Jakob disease, Kuru disease, etc.)
Neuroinfections

Encephalitic syndrome

1. Common infectious symptoms

2. General Brain symptoms
3. Local symptoms irritation or
insufficiency
4. Meningeal and liquor symptoms+/-
Neuroinfections

Herpetic encephalitis
• One of the most common encephalitis
• The causative agent is the herpes simplex virus type I
• It develops during primary infection or against the
background of reactivation of a persistent virus in the
body

Clinic
Develops acutely: fever, non-focal neurological
symptoms, epileptic seizures, meningeal signs,
olfactory hallucinations
• Within a few days a coma develops
• Death rate at 70%
Neuroinfections

Herpetic encephalitis
Pathomorphology
Morphological changes are found in the medial parts of
the temporal and frontal lobes, due to the spread of the
virus along the olfactory pathways (from the olfactory
bulbs) or perineurally along the branches of the trigeminal
nerve (from the Gasser node)
Detected by the acute hemorrhagic necrosis of the brain
tissue with lymphocytic infiltration
Neuroinfections

Herpetic encephalitis
Diagnostics
There are no absolute diagnostic criteria.
• Clinical examination
• CT (MRI)
• Serological examination of CSF and blood: increase in
the titer of antibodies to the virus by 10-12 days (which

is too late for the appointment of specific therapy)

Treatment
Start immediately in all cases suspected of herpetic
encephalitis.
• Acyclovir at a dose of 10 mg / kg in / in drip 3 R / day.
10-12 days
• To combat cerebral edema, treatment of epileptic
seizures
Neuroinfections

Herpetic encephalitis
Neuroinfections

Acute tick-borne (taiga)spring-summer

encephalitis
Caused by an arbovirus transmitted by a tick bite of the
species Ixodes persulcatus and ricinus
• The natural reservoir is small animals
• The virus when bitten from the blood of an animal
enters the saliva tick, and then into human blood
• When the virus enters the body, it actively multiplies at
the site of the bite, and by the 4th day it enters the
blood and brain
• Possible alimentary path of infection
through goat's milk containing the virus
• Endemic areas: far East, Ural, North-East Of
Europe
Neuroinfections

Acute tick-borne encephalitis

Pathomorphology
• Inflammatory changes in the brain stem and areas of
cervical enlargement
 Edema of the Meninges
 Microhemorrhages

Clinical forms
• Classic
• Meningeal
• Feverish
• Polyradiculoneuritis
Neuroinfections

Acute tick-borne encephalitis

Clinical picture
Acute onset: fever, chills, General brain symptoms
• After 2-3 days, meningeal symptoms and peripheral
paralysis of the upper extremities are added, the lower

ones often remain intact

• From 7-9 days – decrease in temperature
• From the 3rd week-reconvalescence
• Recovery can be complete or with a neurological
defect: "hanging head", kozhevnikovskaya epilepsy
(myoclonus-epilepsy), peripheral paralysis of the upper
extremities, atrophy of the shoulder girdle muscles
Neuroinfections

Acute tick-borne encephalitis

Treatment
• Gamma globulin titrated against the virus, 6 ml/m for 3

days
 Serum immunoglobulin from plasma of donors living in
endemic areas
 Ribonuclease 30 mg after 4 h / m 5 days
Detoxification, decongestant therapy
In the recovery period-medical and social rehabilitation

Prevention
• For endemic indications-tissue vaccination
by inactivated vaccine 1 ml n / a 3 times in autumn and

1 time in the spring with annual revaccination

• Persons who have been bitten by a tick - anti-tick
Neuroinfections

Chronic encephalitis
Currently, most researchers attribute chronic
inflammatory diseases of the brain to the slow
neuroinfections.

1)Viral infections:
• Subacute sclerosing panencephalitis
• Progressive multifocal leukoencephalopathy

2) Infections caused by virus-like particles:

• Kuru
• Subacute spongiform encephalopathy
Neuroinfections

Subacute sclerosing panencephalitis

Diagnostics
• The characteristic clinic
• High titer of antibodies to the measles virus
• CT - reducing the size of the ventricles, narrowing
the furrows and the longitudinal fissure of the large
brain

Treatment currently not developed.

Neuroinfections

Subacute sclerosing panencephalitis

It is caused by a cortex-like virus that accumulates in
the nuclei of neurons
Pathomorphology corresponds to chronic encephalitis:
lymphocytic infiltration, gliosis, neuronal degeneration
Clinic
The disease develops after 6-7 years after measles or
vaccination with a live measles vaccine
• Children and teenagers get sick
• There is a weakness, fatigue, change in personality
• After a few months, the myoclonia join, reduced
intelligence
• Six months later-dementia, tetraparesis,
blindness
• Death occurs in 1-2 years
• In adults, the disease can last up to 20 years
Neuroinfections

Arachnoiditis is an inflammation of the

soft membranes of the brain or spinal
cord with predominant suffering of the
arachnoid membrane
According to the localization of the pathological
process, there are:
 arachnoiditis of the convexital surface
• arachnoiditis of the base (basal)
• opto-chiasmal arachnoiditis
• cerebellar-pontine angle arachnoiditis
• arachnoiditis of the posterior cranial fossa
Depending on the current
• subacute
• chronic
Neuroinfections

Arachnoiditis. Etiology and pathogenesis

Causes: flu, rheumatism, chronic tonsillitis, rhinosinusitis,
otitis media, a common infection, head trauma.

• The main significance is autoimmune and autoallergic

reactions of the spider and soft membranes, vascular
plexuses and ventricular ependymes with proliferative
changes in them in response to damaging effects.
Clinic
Subacute beginning with the transition to a chronic form
• A combination of General brain symptoms (associated
with liquor hypertension or, less often, hypotension) and

local symptoms
• General brain symptoms: headache, nausea, vomiting,
non systemic dizziness, memory loss, irritability, fatigue,
Neuroinfections

Convexital arachnoiditis:
symptoms of irritation predominate
partial seizures of epilepsy are characteristic
Basal arachnoiditis:
• non-focal neurological symptoms

Optico-chiasmal arachnoiditis:
develops 2-3 weeks after the flu
• there is a "grid" in front of the eyes, vision decreases,
there is a scotoma, a concentric decrease in vision
• develops neuropathy of the optic nerves
• sometimes-hypothalamic disorders, reduced sense of
smell
Neuroinfections

Arachnoiditis of the of the brain peduncles:

• pyramid symptoms
• meningeal syndrome
Cerebellar-pontine angle arachnoiditis:
• headache of occipital localization
• cerebellar symptoms
• pyramid signs
• lesion of VIII, V, VI, VII cranial nerves
Neuroinfections

Arachnoiditis of the large (occipital) cistern:

• develops acutely: the temperature rises, vomiting
occurs, headache in the back of the head and neck
• lesion of IX, X, XII cranial nerves
• nystagmus
• pyramid symptoms
• meningeal syndrome

Posterior Cranial Fossa’ Arachnoiditis :

• defeat of V, VI, VII, VIII cranial nerves
• cerebellar symptoms
• minor conduction disorders
• the differential diagnosis of volumetric process
into posterior cranial fossa
• lumbar puncture only with normal ophthalmoscopy data
Neuroinfections

Arachnoiditis. Treatment.
A long-term course of treatment with the use of resorbing,
normalizing ICP, improving cerebral circulation and
metabolism of drugs is shown.

• Biogenic stimulants
• Iodide preparations (biyohinol, potassium iodide)
• Lydasum
• Pyrogenalum
• When increasing ICP-diacarb, glycerol
• For convulsive syndrome - anticonvulsants
• Nootropics, vasoactive drugs
• In the development of occlusive hydrocephalus-surgical
treatment (bypass surgery)
The life prognosis is favorable, for health - worse with
frequent relapses.
Neuroinfections

Neurosyphilis
Marvel at the different structures of the NS
• The damage is related to the implementation
Tr. pallidum and immune disorders
• Currently more often
there are vasculitis, meningitis,
less often-progressive paralysis
Tr. pallidum
Pathomorphology
In the early stages of the disease, meningitis often develops
with lymphoid infiltration of the membranes and damage to the
endothelium of the brain vessels
• In the chronic stages, similar changes occur occur in
the cortex: infiltration and atrophy in combination with
the proliferation of glial elements
• In the spinal cord in chronic courseneurosyphilis is
followed by the phase of inflammationdegeneration of
the posterior roots and posterior ropes
Neuroinfections

Neurosyphilis
Clinical forms

1) Asymptomatic neurosyphilis
 specific changes are found only in the CSF

2) Syphilitic meningitis
 develops within a year after infection
 acute or subacute serous meningitis
3) Endarteritis of the brain vessels
 secondary focal symptoms

4) Gumma of the brain or spinal cord

 it's leaking like a brain tumor
Neuroinfections

Neurosyphilis
Clinical forms
5) Dorsal drywall (Tabes dorsalis)
 it develops when the membranes of the spinal cord are
affected and proceeds with the spread of
inflammatory-dystrophic changes to the posterior
ropes and roots
 piercing pain in the legs, ataxia
6) Progressive paralysis
• develops as a result of chronic specific meningo
encephalitis's
• the clinic is diverse: dementia dominates with first the
critique, then the paralysis and epileptic attacks
Neuroinfections

Neurosyphilis. Diagnostics.
• CSF-lymphocytic pleocytosis (200-300 CL per1 mm3)

• Wassermann reaction
• RIF
• RIBT

Treatment
• Penicillin 200,000 DB every 3 hours V/m (course dose
40 000 000 Units)
• Within 2-4 weeks, potassium iodide is prescribed,
then the preparations of bismuth biyohinol,
bismoverol
 Courses of antibiotic therapy and heavy metal salts
spend with a break of 1-2 months
• Symptomatic therapy
Neuroinfections

Damage to the nervous system

in HIV infection

• HIV is classified as non-oncogenic

retroviruses, lentiviruses
(slow viruses),causing chronic
demyelination
HIV
• Routes of transmission: blood, sex
• The incubation period is long, viruses possess
tropism to certain cells-macrophages and
lymphocytes, persist in the NS, cause a
decrease in immunity
• Pandemic threat
Neuroinfections

AIDS: Clinical Picture

There are 3 stages:
 Latent period (incubation period)
 Generalized lymphadenopathy
 Detailed clinical picture

 CNS damage is observed in 60%

 In 10-20%, the lesion of NS may be the first
symptom
 The most common are "AIDS-dementia" and
sensory polyneuropathy
 Frequent lesions of V and VII pairs of cranial
nerves
Neuroinfections

"AIDS-dementia”
• The reason is multi-point giant cell encephalitis
and progressive diffuse leukoencephalopathy
• In the debut-complaints of drowsiness, impaired
attention, memory loss
• Then there is an increase in muscle tone,
sucking and grasping reflexes, adiadohokinesis,
apathy, indifference to the state, bradykinesia,
tremor
• In the advanced stage, against the background
of dementia, there is mutism, paraplegia,
violation of pelvic functions

Sensory polyneuropathy
• It is manifested by pain and paresthesia in the
legs, loss of knee reflexes
Neuroinfections
Neuroborreliosis
This is infectious multisystem disease, preeminentit
affects the skin, nervous system, joints and heart, causingmy
spirochete and transmitted to humans by the bite of Ixodes
ticks.
Incubationthe period is from 3 to 32 days.
The first stage is characterized by migrating ring
shaped erythema. Against the background of pathogen
dissemination increased headache, weakness, malaise,
muscle pain, sore throat, sometimes multiple
secondary
erythema and generalized lymphadenopathy.
• For the second stage of neuroborreliosis, a triad of
syndromes is typical: serous meningitis, cranial
neuropathy, multiple painful sciaticaTIA
(meningoradiculitis).
In the third stage, the defeat of the nervous system is
characterized by multiple encephalomyelitis syndrome,
Neuroinfections

Neuroborreliosis
Diagnostics
Diagnosis of neuroborreliosis is based on
anamnesis data, clinical picture, detection of
antibodies in blood serum and CSF sometimes-
determination of Borrelia in the CSF.

Treatment
It involves the administration of antibiotics
(penicillin, doxycycline, amoxicillin, cefuroxime,
cephalosporins of the third generation) for 2-4 weeks,
depending on the stage of the disease
When pain syndrome requires the appointment
of NSAID