结核性脑膜炎(英文)PPT课件
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4th ventricle
Communicating hydrocephalus
Noncommunicating hydrocephalus
10
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.
Cord Perenchyma Rich Foci 4
PATHOLOGICAL EFFECTS
Meninges
Diffuse Hyperemia Edema Inflammatory Exudates Conformation of Tubercles
5
PATHOLOGICAL EFFECTS
readily to develop TBM. 60% in Children aged 1-3 years Death rate: 15-30%
2
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.
3
PATHOPHYSIOLOGY
Tuberculous Bacilli
Primary Complex
Bacteremia
Miliary TB
Meningitis
Trauma/Diseases
measles, pertussis
Tuberculomas
Subarachnoid Space
Brain or Spinal
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.
7
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.
Tuberculous Meningitis
CHCUMS
DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGY
November 24th, 2004
1
EPIDEMIOLOGY - TBM
Tuberculous Meningitis (TBM) The younger the children, the more
Basal meningitis accounts for the frequent dysfunction of cranial nerves III, VI, and VII.
6
PATHOLOGICAL EFFECTS
Cerebral Parenchyma
Tuberculous meningoencephalitis swelling and hyperemia of the parenchyma
Subarachnoid Space
A large amount of thick gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius, bulbus rhachidicus and Sylvian fissure.
8
Hale Waihona Puke Baidu
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
9
PATHOLOGICAL EFFECTS
Hydrocephalus
Hyperemia of choroids
overproduction of CSF
Inflammatory adherence of
Meninge
defective absorption of CSF
CSF flow is obstructed on the route before the cerebral aqueduct and the
Communicating hydrocephalus
Noncommunicating hydrocephalus
10
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.
Cord Perenchyma Rich Foci 4
PATHOLOGICAL EFFECTS
Meninges
Diffuse Hyperemia Edema Inflammatory Exudates Conformation of Tubercles
5
PATHOLOGICAL EFFECTS
readily to develop TBM. 60% in Children aged 1-3 years Death rate: 15-30%
2
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.
3
PATHOPHYSIOLOGY
Tuberculous Bacilli
Primary Complex
Bacteremia
Miliary TB
Meningitis
Trauma/Diseases
measles, pertussis
Tuberculomas
Subarachnoid Space
Brain or Spinal
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.
7
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.
Tuberculous Meningitis
CHCUMS
DIVISION OF INFECTIOUS DISEASE AND GASTROENTEROLOGY
November 24th, 2004
1
EPIDEMIOLOGY - TBM
Tuberculous Meningitis (TBM) The younger the children, the more
Basal meningitis accounts for the frequent dysfunction of cranial nerves III, VI, and VII.
6
PATHOLOGICAL EFFECTS
Cerebral Parenchyma
Tuberculous meningoencephalitis swelling and hyperemia of the parenchyma
Subarachnoid Space
A large amount of thick gelatinous exudates concentrate to the pavimentum cerebri, optic chiasma, bridge of varolius, bulbus rhachidicus and Sylvian fissure.
8
Hale Waihona Puke Baidu
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
9
PATHOLOGICAL EFFECTS
Hydrocephalus
Hyperemia of choroids
overproduction of CSF
Inflammatory adherence of
Meninge
defective absorption of CSF
CSF flow is obstructed on the route before the cerebral aqueduct and the