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