Lecture meningitis of heuman brain .ppt

meningitis

1. Nervous system diseases Nervous system diseases
classificationclassification
CNS infections CNS infections
Prof. Natalya ShuleshovaProf. Natalya Shuleshova

2. Nervous system diseases Nervous system diseases
classificationsclassifications

International Classification of the International Classification of the
Diseases (1995) by 10Diseases (1995) by 10
thth
revision revision

Classification based on clinical picture Classification based on clinical picture
(Russia)(Russia)

NS infections, CNS slow infections, Multiple NS infections, CNS slow infections, Multiple
sclerosis and others myelinopathies, Periferal NS sclerosis and others myelinopathies, Periferal NS
diseases, Vascular NS diseases, CNS neoplasms, diseases, Vascular NS diseases, CNS neoplasms,
traumas, degenerative diseases, headache, sleep traumas, degenerative diseases, headache, sleep
disorders, ALS, Syringomyelia and othersdisorders, ALS, Syringomyelia and others

3. CNS infectionsCNS infections

MeningitisMeningitis

CerebritisCerebritis

EncephalitisEncephalitis

AbscessesAbscesses

Helmintic infectionsHelmintic infections

5. CSF circulation

6. CSF functionsCSF functions

Regulation of nervous osmotic balanceRegulation of nervous osmotic balance

Brain matter protection from traumasBrain matter protection from traumas

Transportation of nutrition substancesTransportation of nutrition substances

A role of intermediator in evacuation of A role of intermediator in evacuation of
products of metabolismproducts of metabolism

CSF possesses lytic and bactericidal CSF possesses lytic and bactericidal
featuresfeatures

It is a place of antibody’s concentrationIt is a place of antibody’s concentration

7. Acute bacterial menigitisAcute bacterial menigitis

Neusseria meningitisNeusseria meningitis (meningococcus) (meningococcus)

Streptococcus pneumoniaStreptococcus pneumonia
(pneumococcus) (pneumococcus)

Haemophilus influenzaeHaemophilus influenzae type b type b

Gram-negative meningitis (Gram-negative meningitis (Echerichia Echerichia
colicoli or or EnterobacterEnterobacter ) )

Staphylococcal meningitis Staphylococcal meningitis

8. Classic symptomsClassic symptoms

headacheheadache

stiff neck (nuchal rigidity) stiff neck (nuchal rigidity)

fever and chillsfever and chills

photophobiaphotophobia

vomitingvomiting

prodromal upper respiratory infection symptomsprodromal upper respiratory infection symptoms

seizures (30-40% in children, 20-30% in adults)seizures (30-40% in children, 20-30% in adults)

focal neurologic symptoms (including focal seizures)focal neurologic symptoms (including focal seizures)

altered sensoriumaltered sensorium
Symptoms in infantsSymptoms in infants ::

feverfever

lethargy and/or change in level of alertnesslethargy and/or change in level of alertness

poor feeding and/or vomitingpoor feeding and/or vomiting

respiratory distress, apnea, cyanosisrespiratory distress, apnea, cyanosis

10. Signs of meningeal irritationSigns of meningeal irritation

Nuchal rigidity or discomfort on Nuchal rigidity or discomfort on
passive neck flexionpassive neck flexion

Kerning sign: passive knee extension Kerning sign: passive knee extension
in supine patient elicits neck pain in supine patient elicits neck pain
and hamstring resistance.and hamstring resistance.

Brudzinski sign: passive neck or Brudzinski sign: passive neck or
single hip flexion is accompanied by single hip flexion is accompanied by
involuntary flexion of both hips.involuntary flexion of both hips.

11. Meningeal signs Meningeal signs

Neck stiffness Neck stiffness

Brudzinski’s Brudzinski’s
signs signs

Kernig’s sign Kernig’s sign

12. DiagnosisDiagnosis

Because acute bacterial meningitis, Because acute bacterial meningitis,
especially meningococcal, can be especially meningococcal, can be
lethal in hours, accurate diagnosis lethal in hours, accurate diagnosis
and speedy treatment are urgent. and speedy treatment are urgent.

NOTE!NOTE! When bacterial meningitis is When bacterial meningitis is
suspected, antibiotics should be suspected, antibiotics should be
given immediately, without waiting given immediately, without waiting
for diagnostic test result.for diagnostic test result.

13. Lumbar punctureLumbar puncture

should be performed promptly, but only after CT should be performed promptly, but only after CT
has excluded a mass lesion (lumbar puncture can has excluded a mass lesion (lumbar puncture can
precipitate acute neurological worsening if a brain precipitate acute neurological worsening if a brain
abscess or other mass lesion is present).abscess or other mass lesion is present).

elevated opening pressure correlates with a risk elevated opening pressure correlates with a risk
of high mortalityof high mortality

tube 1 to chemistry lab for glucose and proteintube 1 to chemistry lab for glucose and protein

tube 2 to hematology lab for cell count with cell’s tube 2 to hematology lab for cell count with cell’s
differentiationdifferentiation

tube 3 to microbiology and immunology lab for tube 3 to microbiology and immunology lab for
specific tests (Gram stain, bacterial culture stain, specific tests (Gram stain, bacterial culture stain,
TB, fungal cultures, cryptococcal antigen)TB, fungal cultures, cryptococcal antigen)

14. Between LBetween L
IIIIII-L-L
IV orIV or L L
IVIV-L-L
VV spinous processes spinous processes


Jackobi line Jackobi line –– between most prominent between most prominent
tops of cristae iliacatops of cristae iliaca

Novocaine Novocaine 0,5%0,5% anesthesia anesthesia

15. Tissues that are Tissues that are
passed: passed:

Skin Skin

Subcutaneus tissue Subcutaneus tissue

Interspinosum Interspinosum
ligament ligament

Yellow ligament Yellow ligament

Epidural cellulose Epidural cellulose

Dura materDura mater

16. Jackobi lineJackobi line

17. CSF SERUM

18. normal Bacterial meningitisViral meningitis Fungal meningitis
Pressure 5-15 cm
H
2
O
increased Normal or mildly
increased
Normal or mild
increased
Cell count
0-5 mononuclear
cells/mm
3
Typically thousands
of PMNs
Usually 500 cells
nearly 100%
mononuclaer
Hundreds of
mononuclears
Micro
No organisms
Gram stain 80%
effective
No organisms 
Glucose euglicemia:
50% serum
decreased normal Sometimes
decreased (lowest
level in TB)
Protein 0.2-0.4 g/l increased Mildly increased increased

19. DIAGNOSTICS OF VIRAL (INFLUENZAL) DIAGNOSTICS OF VIRAL (INFLUENZAL)
MENINGOENCEPHALITIS MENINGOENCEPHALITIS
Inside CSF: Inside CSF:
• Increased protein Increased protein
((1-1,5 1-1,5 gg//l)l)
• lymphocitic lymphocitic
pleocytosis pleocytosis
(0,02×10*9/(0,02×10*9/ll - -
0,7×10*9/0,7×10*9/ll))

20. Elevated protein with elevated cell Elevated protein with elevated cell
countcount

Acute and chronic meningitis Acute and chronic meningitis
and encephalitisand encephalitis

BacterialBacterial

ViralViral

FungalFungal

SpirochetalSpirochetal

ParasiticParasitic

NeoplasticNeoplastic

Chemical/physicalChemical/physical

poliomyelitispoliomyelitis

Protein elevationProtein elevation>cell count >cell count
elevationelevation

Gingullian-Barre syndromeGingullian-Barre syndrome

ССhronic inflammatory hronic inflammatory
demyelinating polyneuropathydemyelinating polyneuropathy

Tabes dorsalisTabes dorsalis

MyxedemaMyxedema

Diabetes mellitusDiabetes mellitus

SchwannomaSchwannoma

Chronic arachnoiditisChronic arachnoiditis

Brain tumorsBrain tumors

Cerebral venous thrombosisCerebral venous thrombosis

Status after subarachnoid Status after subarachnoid
hemorragehemorrage

Vit B12 deficiencyVit B12 deficiency

Mitochondrial Mitochondrial
encephalomyelopathyencephalomyelopathy

21. Elevated protein with Elevated protein with
or without elevated or without elevated
cell countcell count

CNS vasculitisCNS vasculitis

Gliomatosis cerebriGliomatosis cerebri

Epidural abscessEpidural abscess
Mildly elevated Mildly elevated
protein with or protein with or
without mildly without mildly
elevated cell countelevated cell count

MSMS

EpilepsyEpilepsy

Brain infarctBrain infarct

AbscessAbscess

UremiaUremia

22. Other studies:Other studies:

Lab studiesLab studies

complete blood countcomplete blood count

serum electrolytes to determine dehydratationserum electrolytes to determine dehydratation

serum glucoseserum glucose

creatinine and liver profilecreatinine and liver profile

coagulation profile and plateletscoagulation profile and platelets

serum test for syphilisserum test for syphilis

Imaging studiesImaging studies

CT scan or MRI with gadolinium (MRI detects CT scan or MRI with gadolinium (MRI detects
subarachnoid inflammation better)subarachnoid inflammation better)

23. Bacterial Bacterial
meningitis meningitis
Diagnosis: Diagnosis:
MRI – T1-WI and MRI – T1-WI and
FLAIR FLAIR
Lp – thousands of Lp – thousands of
cells cells

25. ММRI, FLAIR. Patient with RI, FLAIR. Patient with
H1N1 encephalitis in H1N1 encephalitis in
pandemics of pandemics of 20092009. . 9-9-th th
day from the onset of day from the onset of
symptoms and signssymptoms and signs (А). (А).
ААsymmetrical diffuse symmetrical diffuse
hyperintensive sygnals at hyperintensive sygnals at
putamenputamen area bilaterally area bilaterally
and right thalamus and right thalamus
opticus together with opticus together with
ventriculitis at the region ventriculitis at the region
of occipital horns of occipital horns
((arrowsarrows). ). At At 2424
thth
day of day of
illness foci resolved illness foci resolved (В). (В).

26. Differential DiagnosisDifferential Diagnosis

Bacterial meningitis must be distinguished from aseptic Bacterial meningitis must be distinguished from aseptic
meningitis (especially viral) and encephalitis. Diagnosis is meningitis (especially viral) and encephalitis. Diagnosis is
based on CSF findings, symptoms and signs.based on CSF findings, symptoms and signs.

Other diseases for differential diagnosis are:Other diseases for differential diagnosis are:

LeptospirosisLeptospirosis

Free-living amebae infection (swimmers)Free-living amebae infection (swimmers)

Subacute bacterial endocarditisSubacute bacterial endocarditis

Parameningeal infection or inflammation (mastoiditis, Parameningeal infection or inflammation (mastoiditis,
epidural abscess)epidural abscess)

Chemical meningitisChemical meningitis

Acute cerebellar hemorrhage or infarctionAcute cerebellar hemorrhage or infarction

Meningismus without CSF abnormalities may develop in Meningismus without CSF abnormalities may develop in
young children with pneumonia or Shigella infections. young children with pneumonia or Shigella infections.
Nonspecific infections in infants may cause nonspecific Nonspecific infections in infants may cause nonspecific
symptoms (eg. lethargy, irritability) with or without fever, symptoms (eg. lethargy, irritability) with or without fever,
requiring lumbar puncture to exclude meningitis.requiring lumbar puncture to exclude meningitis.

27. Prognosis and prophylaxisPrognosis and prophylaxis

Antibiotics and supportive care started early have reduced the Antibiotics and supportive care started early have reduced the
mortality rate of acute bacterial meningitis to mortality rate of acute bacterial meningitis to  10%. However, 10%. However,
meningitis treated late or occurring in neonates or the elderly is often meningitis treated late or occurring in neonates or the elderly is often
fatal. A low peripheral WBC count is a bad prognostic sign. Persistent fatal. A low peripheral WBC count is a bad prognostic sign. Persistent
leukopenia, delay therapy, and development of the Waterhouse-leukopenia, delay therapy, and development of the Waterhouse-
Fridericchen syndrome reduce the chances of survival. Fridericchen syndrome reduce the chances of survival. Waterhouse–Waterhouse–
Friderichsen syndromeFriderichsen syndrome 
(
 
(
WFSWFS) or
 
) or
 
hemorrhagic hemorrhagic
adrenalitisadrenalitis 
or 
 
or 
Fulminant meningococcemiaFulminant meningococcemia , is defined as
 adrenal
, is defined as
 adrenal
gland
 failure due to bleeding into the adrenal glands, caused by
gland
 failure due to bleeding into the adrenal glands, caused by
severe bacterial infection (most commonly the severe bacterial infection (most commonly the
meningococcusmeningococcusNeisseria meningitidisNeisseria meningitidis). The bacterial infection leads to ). The bacterial infection leads to
massive
 hemorrhage into one or (usually) both adrenal glands.
massive
 hemorrhage into one or (usually) both adrenal glands.
[2][2]
 
It is
 
It is
characterized by overwhelming bacterial characterized by overwhelming bacterial
infection
 meningococcemia leading to massive blood invasion, organ
infection
 meningococcemia leading to massive blood invasion, organ
failure,
 coma, low blood pressure and shock,disseminated
failure,
 coma, low blood pressure and shock,disseminated
intravascular coagulation
 (DIC) with widespread purpura, rapidly
intravascular coagulation
 (DIC) with widespread purpura, rapidly
developing
 adrenocortical insufficiency and death. Survivors
developing
 adrenocortical insufficiency and death. Survivors
occasionally have signs of cranial nerve damage or cerebral infarction, occasionally have signs of cranial nerve damage or cerebral infarction,
recurrent convulsions, or mental retardation.recurrent convulsions, or mental retardation.

28. Prognosis and prophylaxisPrognosis and prophylaxis

Meningococcal vaccine is used mainly during Meningococcal vaccine is used mainly during
epidemics and in close populations when epidemics and in close populations when
epidemic spread is actual. Family members, epidemic spread is actual. Family members,
medical personnel, and those in close medical personnel, and those in close
contact with an infected person should contact with an infected person should
receive prophylaxis with rifampin for 48 h.receive prophylaxis with rifampin for 48 h.

29. The duration of treatment is based on the findings of
serial clinical examination and CSF analysis.
Meningococci and H.Influenzae – 7-14 days
Pneumococci – 10-14 days
Listeria, Gram-negative aerobes - 3 weeks

31. Organism Age group antibiotic Dosage
Unknown Infants  1 moAmpicillin and
cefotaxim
(gentamycin)
100-200 mg/kg
100-150mg/kg
5mg/kg
Children  1
mo
Ampicillin and
cefotaxim
vancomycin
200-400 mg/kg
200 mg/kg
60 mg
Adults Ampicillin and
ceftriaxon
(cefotaxim)
vancomycin
12g
4-6g
12g
2g
Gram-
positive
organisms
Children and
adults
Vancomycin
and
Ceftriaxon
Cefatoxim and
ampicillin
Gram-
negative
rods
Children
adults
Ceftriaxon or
Cefatoxim and
gentamycin
Meningococ
cus
Children
(adults)
Penicillin G
(ampicillin)
300 000 U/kg (24
millionU)
Haemophil
us
influenzae
type b
Children
adults
Ceftriaxon
(Cefatoxim)

32. Streptococc
us
(pneumoco
ccus)
Children
adults
Vancomycin
and
Ceftriaxon
(cefotaxim)
With or
without
rifampin
20 mg/kg (600mg)
Staphyloco
ccus
Children
adults
Vancomycin or
Oxacillin
With or
without
rifampin
Listeria spChildren
adults
Penicillin G
ampicillin
gentamycin
Gram-
negative
enterics
(Echerichia
coli,
Klebsiella
sp, Proteus
sp)
Children
adults
Ceftriaxon or
Cefatoxim and
gentamycin
Pseudomon
as sp
Children
adults
Ceftazidime
and
gentamycin
150mg/kg (6g)

33. TherapyTherapy

Adjunctive therapy with Adjunctive therapy with
corticosteroids is helpful. Early corticosteroids is helpful. Early
use of dexamethasone (0.15 use of dexamethasone (0.15
mg/kg q 6 h for 2 days) or other mg/kg q 6 h for 2 days) or other
anti-inflammatory drugs may anti-inflammatory drugs may
avert major neurological sequel, avert major neurological sequel,
including hearing loss in children including hearing loss in children
with H. Influenzae meningitis. with H. Influenzae meningitis.
Some experts recommend Some experts recommend
corticisteroids for adults with corticisteroids for adults with
meningeal inflammation severe meningeal inflammation severe
enough to impair mental status, enough to impair mental status,
produce cranial nerve deficits, produce cranial nerve deficits,
cause cerebral edema on CT, cause cerebral edema on CT,
increase CSF pressure above 200 increase CSF pressure above 200
mm H2O, or produce many mm H2O, or produce many
neutrophils and organisms (seen neutrophils and organisms (seen
on CSF smear). If viral, TB or on CSF smear). If viral, TB or
fungal meningitis are suspected fungal meningitis are suspected
corticosteroid should be stopped.corticosteroid should be stopped.

Supportive therapySupportive therapy

Fever, dehydration, and electrolyte Fever, dehydration, and electrolyte
disorders require correction. disorders require correction.
Patients with cerebral edema must Patients with cerebral edema must
not be over hydrated. Convulsions not be over hydrated. Convulsions
and status epilepticus require and status epilepticus require
treatment. Vascular collapse and treatment. Vascular collapse and
shock may be due to adrenal shock may be due to adrenal
insufficiency (in the Waterhouse-insufficiency (in the Waterhouse-
Fridericchen syndrome), but loss of Fridericchen syndrome), but loss of
tissue fluid may be equally tissue fluid may be equally
important.important.

All patients with presumed All patients with presumed
bacterial meningitis must be bacterial meningitis must be
isolated for the first 24 h of isolated for the first 24 h of
therapy.therapy.

34. Acute viral encephalitis and Acute viral encephalitis and
««asepticaseptic»» meningitis meningitis

EncephalitisEncephalitis: An acute inflammatory disease of : An acute inflammatory disease of
the brain due to direct viral invasion or to the brain due to direct viral invasion or to
hypersensitivity initiated by a virus or other hypersensitivity initiated by a virus or other
foreign protein. foreign protein.

Aseptic meningitisAseptic meningitis: A febrile meningeal : A febrile meningeal
inflammation characterized by CSF mononuclear inflammation characterized by CSF mononuclear
pleocytosis, normal glucose, mild elevations in pleocytosis, normal glucose, mild elevations in
protein, and absence of bacteria on examination protein, and absence of bacteria on examination
and culture.and culture.

EncephalomyelitisEncephalomyelitis: Inflammatory disease of : Inflammatory disease of
the brain and spinal cord.the brain and spinal cord.

Encephalitis is distinguished from aseptic Encephalitis is distinguished from aseptic
meningitis by extent and severity of cerebral meningitis by extent and severity of cerebral
dysfunction, independent to the signs of dysfunction, independent to the signs of
meningeal inflammation.meningeal inflammation.

35. Etiology and pathologyEtiology and pathology

Viruses causing primary encephalitis may be epidemic (arbovirus, Viruses causing primary encephalitis may be epidemic (arbovirus,
poliovirus, echovirus, and coxackivirus) or sporadic (herpes simplex, poliovirus, echovirus, and coxackivirus) or sporadic (herpes simplex,
varicella-zoster).varicella-zoster).

Secondary encephalitis, usually a complication of viral infection, is Secondary encephalitis, usually a complication of viral infection, is
considered to have an immunologic mechanism. Examples are considered to have an immunologic mechanism. Examples are
encephalitides secondary to measles, chickenpox, rubella, smallpox encephalitides secondary to measles, chickenpox, rubella, smallpox
vaccination, vaccinia, and many other less well defined viral vaccination, vaccinia, and many other less well defined viral
infections. These parainfectious or postinfectious encephalitis infections. These parainfectious or postinfectious encephalitis
typically develop from 5 to 10 days after the onset of illness and are typically develop from 5 to 10 days after the onset of illness and are
characterized by perivascular demyelination seen at autopsy.characterized by perivascular demyelination seen at autopsy.

Cerebral edema is present, with numerous petechial hemorrhages Cerebral edema is present, with numerous petechial hemorrhages
scattered throughout the hemispheres, brain stem, cerebellum, and, scattered throughout the hemispheres, brain stem, cerebellum, and,
occasionally, in spinal cord. Direct viral invasion of the brain is likely occasionally, in spinal cord. Direct viral invasion of the brain is likely
to result in neuronal necrosis, frequently with visible inclusion to result in neuronal necrosis, frequently with visible inclusion
bodies. In parainfectious and postinfectious encephalomyelitis, bodies. In parainfectious and postinfectious encephalomyelitis,
perivenous demyelinating lesions are characteristic. perivenous demyelinating lesions are characteristic.

36. Symptoms, signs and diagnosisSymptoms, signs and diagnosis

Encephalitis may produce fever and malaise without Encephalitis may produce fever and malaise without
meningeal signs, or it may cause meningeal signs (fever, meningeal signs, or it may cause meningeal signs (fever,
headache, vomiting, malaise, and stiff neck and back) with headache, vomiting, malaise, and stiff neck and back) with
cerebral dysfunction (altered consciousness, personality cerebral dysfunction (altered consciousness, personality
changes, seizures, and paresis) and cranial nerve changes, seizures, and paresis) and cranial nerve
abnormalities.abnormalities.

Diagnosis is usually based on CSF characteristics, including Diagnosis is usually based on CSF characteristics, including
normal glucose and absence of bacteria in culture. Viruses (eg. normal glucose and absence of bacteria in culture. Viruses (eg.
enteroviruses) are occasionally isolated directly from CSF or enteroviruses) are occasionally isolated directly from CSF or
from other tissues but are identified in fewer than half of the from other tissues but are identified in fewer than half of the
cases. They can be precisely identified by polymerase chain cases. They can be precisely identified by polymerase chain
reaction techniques, which detects specific viral DNA in CSF. reaction techniques, which detects specific viral DNA in CSF.
Alternatively, an increase in specific antibodies in paired acute Alternatively, an increase in specific antibodies in paired acute
and convalescent sera can be detected, but this technique is not and convalescent sera can be detected, but this technique is not
practical for rapid diagnosis.practical for rapid diagnosis.

37. Prognosis and treatmentPrognosis and treatment

The mortality rate varies with The mortality rate varies with
etiology, and epidemics due to same etiology, and epidemics due to same
virus vary in severity in different virus vary in severity in different
years.years.

Acyclovir 10 mg/kg q 8 h – continued Acyclovir 10 mg/kg q 8 h – continued
at least 10 daysat least 10 days

Supportive therapy is as for acute Supportive therapy is as for acute
bacterial meningitis.bacterial meningitis.

39. Subacute and chronic meningitisSubacute and chronic meningitis

Meningeal inflammation that lasts Meningeal inflammation that lasts  2 wk 2 wk
(subacute) or (subacute) or  1 mo (chronic) 1 mo (chronic)

Subacute and chronic meningitis may develop with Subacute and chronic meningitis may develop with
fungal infections, TB, Lyme disease, AIDS, syphilis, fungal infections, TB, Lyme disease, AIDS, syphilis,
or noninfectious disorders, such as sarcoidosis, and or noninfectious disorders, such as sarcoidosis, and
neoplasms – eg. leukemia, lymphomas and other. neoplasms – eg. leukemia, lymphomas and other.
Subaccute meningitis may result from chemical Subaccute meningitis may result from chemical
reaction to certain intrathecal injections.reaction to certain intrathecal injections.

Neoplastic meningitis with diffuse leptomeningeal Neoplastic meningitis with diffuse leptomeningeal
involvement is a continuing problem in acute involvement is a continuing problem in acute
lymphoblastic leukemia, especially for children being lymphoblastic leukemia, especially for children being
treated with antileukemic drugs, which do not cross treated with antileukemic drugs, which do not cross
the blood-brain barrier. Rarely, the first sign of the blood-brain barrier. Rarely, the first sign of
malignant disease is a subacute meningeal malignant disease is a subacute meningeal
inflammation.inflammation.

41. Symptoms, signs and diagnosisSymptoms, signs and diagnosis

Manifestations are similar to those in acute Manifestations are similar to those in acute
meningitis but evolve more slowly – over meningitis but evolve more slowly – over
weeks rather than days. Fever may be weeks rather than days. Fever may be
minimal. In neoplastic meningitis, minimal. In neoplastic meningitis,
headache, dementia, backache, and cranial headache, dementia, backache, and cranial
and peripheral nerve palsies are common. and peripheral nerve palsies are common.
Chronic communicating hydrocephalus may Chronic communicating hydrocephalus may
be a complication. The course may be be a complication. The course may be
progressive and fatal within a few weeks or progressive and fatal within a few weeks or
months.months.

Diagnosis is based on specific tests, and on Diagnosis is based on specific tests, and on
CSF changes.CSF changes.

Most infections must be treated for a long Most infections must be treated for a long
time with time with hhighly specific drugs (antiTB, ighly specific drugs (antiTB,
antifungal and other). antifungal and other).

44. Herpetic encephalitis
• viruses
• protozoa
• fungi
• bacteriae
Diffuse and
focal lesion
Extensive Extensive
supratentorial supratentorial
infectious lesionsinfectious lesions

45. Viral encephalitis outcomeViral encephalitis outcome
PosthypoxialPosthypoxial scarring
and atrophic changes of
occipital lobes
DTIDTI::
Occipital lobes Occipital lobes
fractionating anisotropy fractionating anisotropy
data is data is 0,34 0,34
Depletion of tracts Depletion of tracts
inside occipital lobesinside occipital lobes

46. Wallerian degeneration
Viral encephalitis Viral encephalitis
outcomeoutcome

47. Thank you!Thank you!