Transcript Document

Dr. Amitabha Basu. MD
CNS
Topic
Edema of brain
 Herniation
 Hydrocephalous
 Vascular diseases

Edema
1.
Vasogenic edema : Seen in case of
abscess and Neoplasm.

2.

Fluid accumulate in the interstitial space.
Cytotoxic Edema:
intracellular fluid accumulation due to
Hypoxic Cell Injury.
Edema: complication
Herniation of brain matter in severe case.
Herniation
Herniation

Etiology:

Due to mass effect.
 Tumor,
Trauma( blood clot),
 Infection induced edema.
Types
1.
Transtentorial Herniation (uncal gyral )
2.
Subfalcine herniation (cingulate gyrus )
3.
Tonsillar Herniation
Transtentorial Herniation [Uncus]
Involved Brain : Uncus: medial
portion of the temporal lobe
Cause : A Mass in the temporal
area.
Clinical effects:
1. Posterior cerebral artery
compression : Occipital infarct.
2. Ipsilateral dilated pupil [
stretching of CN III
Subfalcine Herniation
(involve Cingulate gyrus )
Subfalcine herniation
Involved Brain : cingulate gyrus
Cause : A Mass in temporal/fontal(?)
R
lobe
Clinical effect:
Anterior Cerebral Artery compression :
Weakness and Sensory abnormality of
the leg typically occur with a
Meningioma.
Tonsillar Herniation

Herniation of the cerebellar tonsil
through foramen Magnum.

It is life threatening : causes
compression of the vital
respiratory center.

Complication: Secondary Brain
stem or Duret hemorrhage.
Duret hemorrhage

Kinking of the penetrating median and
paramedian pontine arteries – a branch off
the basilar artery.
Pons
Spinal cord
Secondary Brain stem or Duret hemorrhage

Causes:
 Tonsillar
 Gliomas
Herniation
Hydrocephalus
The Thinker
Hydrocephalus:

Def: Accumulation of excessive CSF
within the Ventricular System.
Etiology:
1. Decreased resorption of the CSF.
2. Overproduction of CSF (in a choroid
plexus tumor-a papillary tumor in ventricle).

2 Types

1. Non communicating
Hydrocephalous. Obstruction within
the ventricular system.

2. Communicating Hydrocephalous.
the obstruction is in the subarachnoid
space or venous sinuses.
Non communicating Hydrocephalous
(0bstructive) ; Cause
Medulloblastoma,
2. Ependymoma
1.
No communication
between ventricles
and subarachonoid
space.
Communicating Hydrocephalous.
Meningitis- adult.
2. Subarachnoid
hemorrhageobstruction in
subarachnoid space
(SAP)- adult
1.
Hydrocephalous by meningitis

Early acute phage: obstruction of the SAP
by exudates.

Late chronic phage: obstruction of the SAP
by fibrosis.
Morphology of hydrocephalous

Infant : Dilated ventricles, enlarged
cranium (increase Head circumference),
atrophy of cortex of brain.
Adult:
 Dilated ventricle, Atrophy of cortex,
enlargement of cranium does not take
place- dementia.

Child and adult
Sunset sign
Clinical features

Infants & young children:
 Signs
symptoms of increased ICP- irritability,
impaired conscious level, and vomiting.

Adult:
 Early:
Signs symptoms of increased ICPheadache, vomiting, papilledema and
deteriorating conscious level.
 Late: Dementia.
Vascular Diseases
Persistence of the
memory : Salvador Dali
Vascular Diseases





GENERAL FEATURES
TYPES
ETIOPATHOLOGY
MORPHOLGY
CLINICAL FEARYRES WITH INVESTIGATIONS.
RISK FACTORS OF ISCHEMIC BRAIN
INJURY::
1.
2.
3.
AGE
DURATION OF THE HYPOXIA
TEMPERATURE [HYPOTHERMIA
PROTECT HYPOXIC BRAIN DAMAGE]
Three categories'
A.
Global Hypoxic Ischemic
Encephalopathy.
B.
Local infarct [ 80 % of the total]
C.
Hemorrhage.
A. Global Hypoxic Ischemic Encephalopathy.
It occur when the systolic blood pressure goes
below 50mmHg.
Cause:
Cardiac arrest (due to myocardial infarct,
cardiac arrhythmias),
Aspiration of foreign objects, drowning.
Early feature: border zone infract
Late features: Laminar cortical necrosis
Border zone infarct: Watershed infarct : May follows a
Hypotensive episode.
Lesion lies at the boundary between the
anterior and middle cerebral artery
territories.
Morphology: Global Hypoxic Ischemic Encephalopathy.
Laminar cortical necrosis : A LINEAR ZONE OF
SOFTENING DISCOLORATION IN THE CORTICAL
MANTLE.
B. Infarct

Caused by Local obstruction in blood vessels.
Thromboembolism and other embolisms
HAEMORRHAGE, Atheroma
Hypertension
Risk: hypertension, smoking, diabetes mellitus.
 Most common form called “Strokes”.
 Age : 7th Decades
 Sex : Male > Female.

Thrombo-embolism


Most common in Middle cerebral Artery.
Source of emboli:
 Mural thrombus in the left ventricle of the
heart,
 Atherosclerotic plaques involving more
proximal arteries (especially the carotid
arteries).
Description of Morphological Changes of brain
infarct.
Microscopical changes
1. After 12 hours : Red neuron and neutrophils
infiltration.
2. 36 to 48 hours : Non-hemorrhagic or
hemorrhagic infarct (due to reperfusion).
3. By 10 days : liquefaction occur : presence of
macrophages and surrounding reactive gliosis.
4. 1– 6 months: a cystic cavity will form (remote
infarct).
Red neuron
Normal
Hemorrhagic infarct
Liquefactive necrosis
Tissue shows macrophage and microglial proliferation in this
time. CT shows enhancing lesion.
Remote infarct ( cavity )
Remote infarct ( cavity )
In the wall of the
cavity= shows reactive
astrocytes with
reactive gliosis.
 An CT would show
enhancing shadow.

Shower embolization
Multiple small hemorrhage: fat embolism,
amniotic fluid embolism
Hypertension induced infarct
Lacunar infarcts
Site: The pons.
Clinical features
What are the signs infarction?
1)
TIA: transient ischemic attack:
persists < 24 hours.
2)
Stroke: >24 hours
Sudden numbness or weakness
on one side of the face, arm or leg
.
2) Sudden trouble speaking or
understanding.
3) Sudden trouble seeing.
1)
Clinical Features: If middle cerebral Artery is effected.



Contralateral hemiparesis and spasticity.
Visual Field abnormality
In some case speech aphasia.
End of Stroke
Guernica