Title: CNS
1CNS
2(No Transcript)
3Topic
- Edema of brain
- Herniation
- Hydrocephalous
- Vascular diseases
4Edema
- Vasogenic edema Seen in case of abscess and
Neoplasm. - Fluid accumulate in the interstitial space.
- Cytotoxic Edema
- intracellular fluid accumulation due to Hypoxic
Cell Injury.
5Edema complication
- Herniation of brain matter in severe case.
6 7Herniation
- Etiology
- Due to mass effect.
- Tumor, Trauma( blood clot),
- Infection induced edema.
8Types
- Transtentorial Herniation (uncal gyral )
- Subfalcine herniation (cingulate gyrus )
- Tonsillar Herniation
9- Transtentorial Herniation Uncus
- Involved Brain Uncus medial portion of the
temporal lobe - Cause A Mass in the temporal area.
- Clinical effects
- Posterior cerebral artery compression Occipital
infarct. - Ipsilateral dilated pupil stretching of CN III
10- Subfalcine Herniation
- (involve Cingulate gyrus )
11Subfalcine herniation
Involved Brain cingulate gyrus Cause A Mass
in temporal/fontal(?) lobe Clinical effect
Anterior Cerebral Artery compression Weakness
and Sensory abnormality of the leg typically
occur with a Meningioma.
R
12Tonsillar 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.
13Duret hemorrhage
- Kinking of the penetrating median and paramedian
pontine arteries a branch off the basilar
artery.
Pons
Spinal cord
14Secondary Brain stem or Duret hemorrhage
- Causes
- Tonsillar Herniation
- Gliomas
15The Thinker
16Hydrocephalus
- Def Accumulation of excessive CSF within the
Ventricular System. - Etiology
- Decreased resorption of the CSF.
- Overproduction of CSF (in a choroid plexus
tumor-a papillary tumor in ventricle).
17 2 Types
- 1. Non communicating Hydrocephalous. Obstruction
within the ventricular system. - 2. Communicating Hydrocephalous. the obstruction
is in the subarachnoid space or venous sinuses.
18Non communicating Hydrocephalous (0bstructive)
Cause
- Medulloblastoma,
- Ependymoma
No communication between ventricles and
subarachonoid space.
19Communicating Hydrocephalous.
- Meningitis- adult.
- Subarachnoid hemorrhage- obstruction in
subarachnoid space (SAP)- adult
20Hydrocephalous by meningitis
- Early acute phage obstruction of the SAP by
exudates. - Late chronic phage obstruction of the SAP by
fibrosis.
21Morphology 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.
22Child and adult
Sunset sign
23Clinical features
- Infants young children
- Signs symptoms of increased ICP- irritability,
impaired conscious level, and vomiting. - Adult
- Early Signs symptoms of increased ICP- headache,
vomiting, papilledema and deteriorating conscious
level. - Late Dementia.
24Persistence of the memory Salvador Dali
25Vascular Diseases
- GENERAL FEATURES
- TYPES
- ETIOPATHOLOGY
- MORPHOLGY
- CLINICAL FEARYRES WITH INVESTIGATIONS.
26RISK FACTORS OF ISCHEMIC BRAIN INJURY
- AGE
- DURATION OF THE HYPOXIA
- TEMPERATURE HYPOTHERMIA PROTECT HYPOXIC BRAIN
DAMAGE
27Three categories'
- Global Hypoxic Ischemic Encephalopathy.
- Local infarct 80 of the total
- Hemorrhage.
28A. 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
29Border zone infarct Watershed infarct May
follows a Hypotensive episode.
Lesion lies at the boundary between the anterior
and middle cerebral artery territories.
30Morphology Global Hypoxic Ischemic
Encephalopathy.
- Laminar cortical necrosis A LINEAR ZONE OF
SOFTENING DISCOLORATION IN THE CORTICAL MANTLE. -
31B. 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 gt Female.
32Thrombo-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).
33Description of Morphological Changes of brain
infarct.
- Microscopical changes
- After 12 hours Red neuron and neutrophils
infiltration. - 36 to 48 hours Non-hemorrhagic or hemorrhagic
infarct (due to reperfusion). - By 10 days liquefaction occur presence of
macrophages and surrounding reactive gliosis. - 1 6 months a cystic cavity will form (remote
infarct).
34Red neuron
Normal
Hemorrhagic infarct
35Liquefactive necrosis
Tissue shows macrophage and microglial
proliferation in this time. CT shows enhancing
lesion.
36Remote infarct ( cavity )
37Remote infarct ( cavity )
- In the wall of the cavity shows reactive
astrocytes with reactive gliosis. - An CT would show enhancing shadow.
38Shower embolizationMultiple small hemorrhage
fat embolism, amniotic fluid embolism
39Lacunar infarcts
Hypertension induced infarct
Site The pons.
40What are the signs infarction?
Clinical features
- TIA transient ischemic attack persists lt 24
hours. - Stroke gt24 hours
- Sudden numbness or weakness on one side of the
face, arm or leg . - Sudden trouble speaking or understanding.
- Sudden trouble seeing.
41Clinical Features If middle cerebral Artery is
effected.
- Contralateral hemiparesis and spasticity.
- Visual Field abnormality
- In some case speech aphasia.
42End of Stroke
Guernica