1
Tuberculous Meningitis
CHCUMS
DIVISION OF INFECTIOUS DISEASE AND
GASTROENTEROLOGY
November 24th,2004
2
EPIDEMIOLOGY - TBM
Tuberculous Meningitis (TBM)
? The younger the children,the more
readily to develop TBM,
? 60% in Children aged 1-3 years
? Death rate,15-30%
3
TBM (Tuberculous meningitis)
? TBM is the most serious complication of
tuberculosis in children and is usually
fatal without treatment.
? TBM always be a part of systemic
disseminated tuberculosis.
? TBM often occurs within 1 year of initial
infection,especially in the first 2 to 6
months of infection.
4
Tuberculous
Bacilli
Primary
Complex
Bacteremia
Rich Foci
Subarachnoid
Space
Brain or Spinal
Cord PerenchymaTuberculomas
Meningitis
PATHOPHYSIOLOGY
Trauma/Diseases
measles,pertussis
Miliary
TB
5
PATHOLOGICAL EFFECTS
Meninges
? Diffuse Hyperemia
? Edema
? Inflammatory Exudates
? Conformation of Tubercles
6
PATHOLOGICAL EFFECTS
Subarachnoid Space
?A large amount of thick gelatinous
exudates concentrate to the pavimentum
cerebri,optic chiasma,bridge of varolius,
bulbus rhachidicus and Sylvian fissure,
? Basal meningitis accounts for the
frequent dysfunction of cranial nerves III,
VI,and VII.
7
PATHOLOGICAL EFFECTS
Cerebral Parenchyma
Tuberculous meningoencephalitis
?swelling and hyperemia of the parenchyma
contribute to the intracranial hypertension,then
ischemia of parenchyma occur,finally lead to
the foci of encephalomalacia and necrosis,
Hemiplegia may be present because of this
change,
?Meninges,spinal,and spinal nerve root also
involvement,The later always leads to
paraplegina.
8
PATHOLOGICAL EFFECTS
Cerebral Vessels
?The bacteria invade the adventitia directly in
the early stage and initiate the process of acute
vasculitis,
?Progressive destruction of adventitia,
disruption of elastic fibers,and finally intimal
destruction (endoarteritis),lead to the
obliterative vasculitis,which may facilitate the
ischemia,encephalomalacia and necrosis of
parenchyma,
9
Circulation
of CSF
Choroid plexus
Lateral ventricle
Interventricular foramen
the 3rd ventricle
Cerebral aqueduct
4th ventricle
2 Lateral foramina
1 Medial foramen
Subarachnoid space
Arachnoid granulations
Dural sinus
Venous drainage
10
PATHOLOGICAL EFFECTS
Hydrocephalus
Hyperemia of choroids overproduction of CSF
Inflammatory
adherence of
Meninge
defective absorption
of CSF
Communicating
hydrocephalus CSF flow is obstructed on the route before the cerebral aqueduct and the
4th ventricle
Noncommunicating
hydrocephalus
11
In tuberculous meningitis there is a tendency for the exudate to be primarily
located on the under surface of the brain,particularly over the ventral
surface of the brain stem.
12
CLINICAL MANIFESTIONS
A,Prodrome (1-2 week)
1,Fever,fatigue,malaise,myalgia,
drowsiness,headache,vomiting
2,Mental status changes
3,Focal neurologic signs are absent
4,CSF abnormity
13
CLINICAL MANIFESTIONS
B,Meningeal Irritation Stage (1-2 week)
1,More serious TB toxic symptoms
2,Intracranial hypertension,severe headache,irritation,
projectile vomiting,seizures;
Bulging of anterior fontanelle,widening of cranial
sutures in infant
3,Meningeal Irritation, nuchal rigidity,hypertonia
Kernig sign or Brudzinski sign
4,Cranial nerve abnormalities,3,6,7
5,Some children have no evidence of meningeal irritation
but may have signs of encephalitis,disorientation,
abnormal movements and speech impairment
14
CLINICAL MANIFESTIONS
C,Coma Stage (1-3 week)
1,Frequent convulsion,progressive altered
state of consciousness,lethargy,confusion,
semicoma,deep coma,decerebrate or
decorticate posturing
2,Depletion,extremely maransis,
constipation,urinary retention
3,progressive abnormalities of vital signs,
and eventual die from cerebral hernia
15
Characteristics of TBM in infants
and young children
1,A rapid onset with convulsion,
abruptly high fever
2,Atypical miningeal irritation
3,Intracranial hypertension
manifests as bulging of anterior
fontanelle and widening of
cranial sutures in infant
16
PROGNOSIS
? The prognosis of tuberculous meningitis correlates
most closely with the clinical stage of diagnosis and
treatment,
? Age,infants or younger children are generally
worse than that of older children
? Drug resistant strain
? Variation of host immunity
? Appropriate therapeutic regimen
? Completion of the antituberculor agent regimen
17
It is imperative that antituberculosis
treatment be considered for any child
who develops basilar meningitis and
hydrocephalus,cranial nerve palsy,or
stroke with no other apparent etiology.
18
DIAGNOSIS
? History
? Clinical Symptoms and Signs
? Auxiliary Examinations
19
DIAGNOSIS - History
Elucidate the following:
1,Medical and social history,including
recent contact with patients with TB
2,Negative history for Bacille
Calmette-Guerin (BCG) vaccination
3,History of immunosuppression from
a known disease or drug therapy
20
DIAGNOSIS – Symptoms and signs
? A gradual onset
? Fever,headache,alternant of irritability and
drowsiness,vomiting,constipation of
unknown origin
? Altered mental status
21
DIAGNOSIS – Tuberculin Skin Test
Purified protein derivative (PPD)
1,Injected intradermally on the volar
surface of the forearm
2,Reaction peaks at 48 to 72 hours
3,A nonreactive result does not
exclude M,tuberculosis infection or
disease,the tuberculin skin test is
nonreactive in up to 50% of cases
22
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
1,Gross appearance
Clear or slightly turbid
a fine clot resembling a pellicle or cobweb may form
2,Cell counts,differential count
50-500cells/mm3
Lymphocytic predominance
but Polymorphonuclear cells may predominate early
3,Glucose
Hypoglycorrhachia
4,Protein
High protein level with 1-3g/L
23
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
5,Chloridate,low
6,Acid-fast stain (+),Gram stain,India ink
7,Culture for M tuberculosis (+)
8,ELISA test for Specific PPD-IgM and
PPD-IgG in CSF
9,ELISA test for Specific TB-antigen in
CSF is a sensitive and rapid method
24
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
10,Total IgG,IgA and IgM
11,PCR, specific PCR to detect the gene of
M tuberculosis bacilli can provide a rapid
and reliable diagnosis of TBM,although
false-negative results potentially occur
25
DIAGNOSIS – Chest X-ray
Chest x-ray,Posteroanterior and
lateral views may reveal the following
? Hilar lymphadenopathy
? Simple pneumonia
? Infiltrate
? Pleural effusion/pleural scar
26
DIAGNOSIS – CT or MRI
? CT scan and MRI of the brain reveal
hydrocephalus,basilar meningeal thickening,
infarcts,edema,and tuberculomas,all these are
helpful clues,but nonspecific
? MRI and CT scan lack specificity,but help in
monitoring complications that require
neurosurgery,making the differentiations,and
knowing the prognosis
27
DIFFERENTIAL DIAGNOSIS
?Viral Meningocephalitis
? Pyogenic Meningitis
? CNS Cryptococcosis
28
DIFFERENTIAL DIAGNOSIS
Viral Meningocephalitis
Mumps,polio,enteroviruses,Measles,Herpes
viruses,EBV,and Japanese encephalitis virus,etc
CSF examination is the most important test
in differentiating the cause of meningitis:
?Clear appearance
?Cells,50 -200 cells/mm3,Mononuclear
cell predominance
?Protein,slightly elevated or normal
?Glucose and Chloridate, normal
29
DIFFERENTIAL DIAGNOSIS
Pyogenic Meningitis
Clinical manifestation
Acute onset of intense headache,fever,nausea,
vomiting,photophobia,and stiff neck
Group B streptococci,Neisseria meningitidis,
Streptococcus pneumoniae,Haemophilus influenzae,and Staph,aureus,etc.
? Pyogenic foci located other sites of the host
? Typical rash of meningococcal infection
? Examination of CSF
30
DIFFERENTIAL DIAGNOSIS
Pyogenic Meningitis
Typical CSF abnormalities in meningitis
include the following:
? Appearance is turbid
? Pleocytosis of PMN ( WBC counts always above
1000,even to a very high level as 10,000
cells/mm3,predominantly neutrophils)
? Decreased glucose concentration
? Increased protein concentration
? Gram stain and culture of CSF identify the
etiological organism
31
Brain surface (Pyogenic meningitis )
32
TBM
33
DIFFERENTIAL DIAGNOSIS
CNS Cryptococcosis
?Cryptococcosis is the most common fungal
infection of the central nervous system
?It is the fourth most common cause of
opportunistic infections in patients with AIDS
?Disease onset is usually insidious and has a
longer latent period
?Fever always be absent at beginning of disease
?Very notable intracranial hypertension,severe
headache
?Visual disturbances and papilledema are
common
34
DIFFERENTIAL DIAGNOSIS
CNS Cryptococcosis
CSF
? Appearance can be clear or turbid.
? Protein levels exceed
? Glucose and Chloridate
? Mononuclear pleocytosis,numbers vary from
50 to 500 mononuclear cells/mm3.
? It is easy to get the positive result for C
neoformans of CSF
? India ink stain is positive CSF or serum
cryptococcal antigen tests are positive
35
Cryptococcus is a cause of meningitis,a common complication in
AIDS,The organisms are usually easy to demonstrate histologically.
In this slide they are the circular-to-ovoid structures with thick
capsules.
36
TREATMENT
? Supportive treatment
? Antituberculous drugs
? Decreasing intracranial pressure
? Corticosteriods
? Symptomatic treatment
? Follow-up visit
37
TREATMENT
Supportive treatment
?Bed rest and close respiratory contacts
?Nutritional support are paramount
?Keep good hygiene for the coma children to
prevent of secondary infections,help them to
change position frequently to prevent decubital
? Management of electrolyte abnormalities
?Antipyretics
?Control of seizures,Diazepam (Valium)
38
TREATMENT
Antituberculous drugs
?isoniazid INH,rifampin RIF,pyrazinamide PZA,
streptomycin SM,and sometimes ethambutol
EMB.
?INH and RIF are bactericidal for all M,
tuberculosis population in any milieu.
?SM is most effective against rapidly multiplying
organisms.
?PZA is most effective against organisms found in
macrephages.
?enter CSF readily in the presence of meningeal
inflammation,
39
TREATMENT
Antituberculous drugs
? Any regimen must contain multiple
drugs
? In addition,the therapy must be taken
regularly and continued for a sufficient
period,
40
TREATMENT
Antituberculous drugs
1,intensification chemotherapy stage,3-4
months
INH (15-25mg/kg),RFP,PZA,SM
2,consolidation chemotherapy stage,with
total course 1 year at least
in order to prevent relapse,permit elimination
organisms persistent exist in the host
INH,RFP or EMB (ethambutol)
41
TREATMENT
Decreasing intracranial
pressure
? Dehydrant,Mannitol (MNT)
? Diuretic agent,Acetazolamide
Decreasing CSF secretion by the choroid plexus
? Ventricular tap or Open ventricular drainage
? Repeat LPs and intrathecal injection
? Shunting,to establish a communication between the CSF
(ventricular or lumbar) and a drainage cavity,Performed only
in cases of communicating hydrocephalus,
Ventricular shunt to cisterna magna
42
TREATMENT
Corticosteriods
? Children should be treated for 6-8 weeks
? More effective in early stage
? Decrease the immflamatory exudates,there fore
lower the intracranial pressure,Relieve the
meningeal irritation,Improve the CSF circulation
Reduce the adherence and prevent the
hydrocephalus.
? Dexamethasone
? pay attention to the side effects of corticosteriods
43
Criteria for Recovery
Follow-up visit
? Disappearance of all
clinical manifestations
? CSF examination is
normal
? No relapse within 2
years after completion
of antituberculosis
treatment
44
Which symptom should be excluded
in the early stage of TBM?
a) Drowsiness
b) Low fever,night sweat,poor
appetite,loss of weight
c) Personality changes
d) Headache
e) Recurrent convulsion
45
A baby who was definited as TBM when he was
1 years old and began to receive regular
treatment with antituberculosis drugs,How old
is he when he can be definited as full recovery?
a) 11/2 y
b) 2 y
c) 21/2 y
d) 3 y
e) 4 y
46
Which one is the typically cellular
characteristics of CSF in TBM?
a) 50-500 cells/mm3,with neutrophils predominance
b) 50-500 cells/mm3,with mononuclear
predominance
c) 0-50 cells/mm3,with mononuclear predominance
d) >1000,sometimes can above 10,000 with
neutrophil predominance
e) 0-50cells/mm3 with neutrophils predominance
47
THNAK YOU !
Tuberculous Meningitis
CHCUMS
DIVISION OF INFECTIOUS DISEASE AND
GASTROENTEROLOGY
November 24th,2004
2
EPIDEMIOLOGY - TBM
Tuberculous Meningitis (TBM)
? The younger the children,the more
readily to develop TBM,
? 60% in Children aged 1-3 years
? Death rate,15-30%
3
TBM (Tuberculous meningitis)
? TBM is the most serious complication of
tuberculosis in children and is usually
fatal without treatment.
? TBM always be a part of systemic
disseminated tuberculosis.
? TBM often occurs within 1 year of initial
infection,especially in the first 2 to 6
months of infection.
4
Tuberculous
Bacilli
Primary
Complex
Bacteremia
Rich Foci
Subarachnoid
Space
Brain or Spinal
Cord PerenchymaTuberculomas
Meningitis
PATHOPHYSIOLOGY
Trauma/Diseases
measles,pertussis
Miliary
TB
5
PATHOLOGICAL EFFECTS
Meninges
? Diffuse Hyperemia
? Edema
? Inflammatory Exudates
? Conformation of Tubercles
6
PATHOLOGICAL EFFECTS
Subarachnoid Space
?A large amount of thick gelatinous
exudates concentrate to the pavimentum
cerebri,optic chiasma,bridge of varolius,
bulbus rhachidicus and Sylvian fissure,
? Basal meningitis accounts for the
frequent dysfunction of cranial nerves III,
VI,and VII.
7
PATHOLOGICAL EFFECTS
Cerebral Parenchyma
Tuberculous meningoencephalitis
?swelling and hyperemia of the parenchyma
contribute to the intracranial hypertension,then
ischemia of parenchyma occur,finally lead to
the foci of encephalomalacia and necrosis,
Hemiplegia may be present because of this
change,
?Meninges,spinal,and spinal nerve root also
involvement,The later always leads to
paraplegina.
8
PATHOLOGICAL EFFECTS
Cerebral Vessels
?The bacteria invade the adventitia directly in
the early stage and initiate the process of acute
vasculitis,
?Progressive destruction of adventitia,
disruption of elastic fibers,and finally intimal
destruction (endoarteritis),lead to the
obliterative vasculitis,which may facilitate the
ischemia,encephalomalacia and necrosis of
parenchyma,
9
Circulation
of CSF
Choroid plexus
Lateral ventricle
Interventricular foramen
the 3rd ventricle
Cerebral aqueduct
4th ventricle
2 Lateral foramina
1 Medial foramen
Subarachnoid space
Arachnoid granulations
Dural sinus
Venous drainage
10
PATHOLOGICAL EFFECTS
Hydrocephalus
Hyperemia of choroids overproduction of CSF
Inflammatory
adherence of
Meninge
defective absorption
of CSF
Communicating
hydrocephalus CSF flow is obstructed on the route before the cerebral aqueduct and the
4th ventricle
Noncommunicating
hydrocephalus
11
In tuberculous meningitis there is a tendency for the exudate to be primarily
located on the under surface of the brain,particularly over the ventral
surface of the brain stem.
12
CLINICAL MANIFESTIONS
A,Prodrome (1-2 week)
1,Fever,fatigue,malaise,myalgia,
drowsiness,headache,vomiting
2,Mental status changes
3,Focal neurologic signs are absent
4,CSF abnormity
13
CLINICAL MANIFESTIONS
B,Meningeal Irritation Stage (1-2 week)
1,More serious TB toxic symptoms
2,Intracranial hypertension,severe headache,irritation,
projectile vomiting,seizures;
Bulging of anterior fontanelle,widening of cranial
sutures in infant
3,Meningeal Irritation, nuchal rigidity,hypertonia
Kernig sign or Brudzinski sign
4,Cranial nerve abnormalities,3,6,7
5,Some children have no evidence of meningeal irritation
but may have signs of encephalitis,disorientation,
abnormal movements and speech impairment
14
CLINICAL MANIFESTIONS
C,Coma Stage (1-3 week)
1,Frequent convulsion,progressive altered
state of consciousness,lethargy,confusion,
semicoma,deep coma,decerebrate or
decorticate posturing
2,Depletion,extremely maransis,
constipation,urinary retention
3,progressive abnormalities of vital signs,
and eventual die from cerebral hernia
15
Characteristics of TBM in infants
and young children
1,A rapid onset with convulsion,
abruptly high fever
2,Atypical miningeal irritation
3,Intracranial hypertension
manifests as bulging of anterior
fontanelle and widening of
cranial sutures in infant
16
PROGNOSIS
? The prognosis of tuberculous meningitis correlates
most closely with the clinical stage of diagnosis and
treatment,
? Age,infants or younger children are generally
worse than that of older children
? Drug resistant strain
? Variation of host immunity
? Appropriate therapeutic regimen
? Completion of the antituberculor agent regimen
17
It is imperative that antituberculosis
treatment be considered for any child
who develops basilar meningitis and
hydrocephalus,cranial nerve palsy,or
stroke with no other apparent etiology.
18
DIAGNOSIS
? History
? Clinical Symptoms and Signs
? Auxiliary Examinations
19
DIAGNOSIS - History
Elucidate the following:
1,Medical and social history,including
recent contact with patients with TB
2,Negative history for Bacille
Calmette-Guerin (BCG) vaccination
3,History of immunosuppression from
a known disease or drug therapy
20
DIAGNOSIS – Symptoms and signs
? A gradual onset
? Fever,headache,alternant of irritability and
drowsiness,vomiting,constipation of
unknown origin
? Altered mental status
21
DIAGNOSIS – Tuberculin Skin Test
Purified protein derivative (PPD)
1,Injected intradermally on the volar
surface of the forearm
2,Reaction peaks at 48 to 72 hours
3,A nonreactive result does not
exclude M,tuberculosis infection or
disease,the tuberculin skin test is
nonreactive in up to 50% of cases
22
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
1,Gross appearance
Clear or slightly turbid
a fine clot resembling a pellicle or cobweb may form
2,Cell counts,differential count
50-500cells/mm3
Lymphocytic predominance
but Polymorphonuclear cells may predominate early
3,Glucose
Hypoglycorrhachia
4,Protein
High protein level with 1-3g/L
23
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
5,Chloridate,low
6,Acid-fast stain (+),Gram stain,India ink
7,Culture for M tuberculosis (+)
8,ELISA test for Specific PPD-IgM and
PPD-IgG in CSF
9,ELISA test for Specific TB-antigen in
CSF is a sensitive and rapid method
24
DIAGNOSIS – Spinal Tap
Cerebrospinal Fluid
10,Total IgG,IgA and IgM
11,PCR, specific PCR to detect the gene of
M tuberculosis bacilli can provide a rapid
and reliable diagnosis of TBM,although
false-negative results potentially occur
25
DIAGNOSIS – Chest X-ray
Chest x-ray,Posteroanterior and
lateral views may reveal the following
? Hilar lymphadenopathy
? Simple pneumonia
? Infiltrate
? Pleural effusion/pleural scar
26
DIAGNOSIS – CT or MRI
? CT scan and MRI of the brain reveal
hydrocephalus,basilar meningeal thickening,
infarcts,edema,and tuberculomas,all these are
helpful clues,but nonspecific
? MRI and CT scan lack specificity,but help in
monitoring complications that require
neurosurgery,making the differentiations,and
knowing the prognosis
27
DIFFERENTIAL DIAGNOSIS
?Viral Meningocephalitis
? Pyogenic Meningitis
? CNS Cryptococcosis
28
DIFFERENTIAL DIAGNOSIS
Viral Meningocephalitis
Mumps,polio,enteroviruses,Measles,Herpes
viruses,EBV,and Japanese encephalitis virus,etc
CSF examination is the most important test
in differentiating the cause of meningitis:
?Clear appearance
?Cells,50 -200 cells/mm3,Mononuclear
cell predominance
?Protein,slightly elevated or normal
?Glucose and Chloridate, normal
29
DIFFERENTIAL DIAGNOSIS
Pyogenic Meningitis
Clinical manifestation
Acute onset of intense headache,fever,nausea,
vomiting,photophobia,and stiff neck
Group B streptococci,Neisseria meningitidis,
Streptococcus pneumoniae,Haemophilus influenzae,and Staph,aureus,etc.
? Pyogenic foci located other sites of the host
? Typical rash of meningococcal infection
? Examination of CSF
30
DIFFERENTIAL DIAGNOSIS
Pyogenic Meningitis
Typical CSF abnormalities in meningitis
include the following:
? Appearance is turbid
? Pleocytosis of PMN ( WBC counts always above
1000,even to a very high level as 10,000
cells/mm3,predominantly neutrophils)
? Decreased glucose concentration
? Increased protein concentration
? Gram stain and culture of CSF identify the
etiological organism
31
Brain surface (Pyogenic meningitis )
32
TBM
33
DIFFERENTIAL DIAGNOSIS
CNS Cryptococcosis
?Cryptococcosis is the most common fungal
infection of the central nervous system
?It is the fourth most common cause of
opportunistic infections in patients with AIDS
?Disease onset is usually insidious and has a
longer latent period
?Fever always be absent at beginning of disease
?Very notable intracranial hypertension,severe
headache
?Visual disturbances and papilledema are
common
34
DIFFERENTIAL DIAGNOSIS
CNS Cryptococcosis
CSF
? Appearance can be clear or turbid.
? Protein levels exceed
? Glucose and Chloridate
? Mononuclear pleocytosis,numbers vary from
50 to 500 mononuclear cells/mm3.
? It is easy to get the positive result for C
neoformans of CSF
? India ink stain is positive CSF or serum
cryptococcal antigen tests are positive
35
Cryptococcus is a cause of meningitis,a common complication in
AIDS,The organisms are usually easy to demonstrate histologically.
In this slide they are the circular-to-ovoid structures with thick
capsules.
36
TREATMENT
? Supportive treatment
? Antituberculous drugs
? Decreasing intracranial pressure
? Corticosteriods
? Symptomatic treatment
? Follow-up visit
37
TREATMENT
Supportive treatment
?Bed rest and close respiratory contacts
?Nutritional support are paramount
?Keep good hygiene for the coma children to
prevent of secondary infections,help them to
change position frequently to prevent decubital
? Management of electrolyte abnormalities
?Antipyretics
?Control of seizures,Diazepam (Valium)
38
TREATMENT
Antituberculous drugs
?isoniazid INH,rifampin RIF,pyrazinamide PZA,
streptomycin SM,and sometimes ethambutol
EMB.
?INH and RIF are bactericidal for all M,
tuberculosis population in any milieu.
?SM is most effective against rapidly multiplying
organisms.
?PZA is most effective against organisms found in
macrephages.
?enter CSF readily in the presence of meningeal
inflammation,
39
TREATMENT
Antituberculous drugs
? Any regimen must contain multiple
drugs
? In addition,the therapy must be taken
regularly and continued for a sufficient
period,
40
TREATMENT
Antituberculous drugs
1,intensification chemotherapy stage,3-4
months
INH (15-25mg/kg),RFP,PZA,SM
2,consolidation chemotherapy stage,with
total course 1 year at least
in order to prevent relapse,permit elimination
organisms persistent exist in the host
INH,RFP or EMB (ethambutol)
41
TREATMENT
Decreasing intracranial
pressure
? Dehydrant,Mannitol (MNT)
? Diuretic agent,Acetazolamide
Decreasing CSF secretion by the choroid plexus
? Ventricular tap or Open ventricular drainage
? Repeat LPs and intrathecal injection
? Shunting,to establish a communication between the CSF
(ventricular or lumbar) and a drainage cavity,Performed only
in cases of communicating hydrocephalus,
Ventricular shunt to cisterna magna
42
TREATMENT
Corticosteriods
? Children should be treated for 6-8 weeks
? More effective in early stage
? Decrease the immflamatory exudates,there fore
lower the intracranial pressure,Relieve the
meningeal irritation,Improve the CSF circulation
Reduce the adherence and prevent the
hydrocephalus.
? Dexamethasone
? pay attention to the side effects of corticosteriods
43
Criteria for Recovery
Follow-up visit
? Disappearance of all
clinical manifestations
? CSF examination is
normal
? No relapse within 2
years after completion
of antituberculosis
treatment
44
Which symptom should be excluded
in the early stage of TBM?
a) Drowsiness
b) Low fever,night sweat,poor
appetite,loss of weight
c) Personality changes
d) Headache
e) Recurrent convulsion
45
A baby who was definited as TBM when he was
1 years old and began to receive regular
treatment with antituberculosis drugs,How old
is he when he can be definited as full recovery?
a) 11/2 y
b) 2 y
c) 21/2 y
d) 3 y
e) 4 y
46
Which one is the typically cellular
characteristics of CSF in TBM?
a) 50-500 cells/mm3,with neutrophils predominance
b) 50-500 cells/mm3,with mononuclear
predominance
c) 0-50 cells/mm3,with mononuclear predominance
d) >1000,sometimes can above 10,000 with
neutrophil predominance
e) 0-50cells/mm3 with neutrophils predominance
47
THNAK YOU !
