CNS

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CNS

• Dr. Amitabha Basu. MD

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(No Transcript)
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Topic

• Edema of brain
• Herniation
• Hydrocephalous
• Vascular diseases

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Edema

• 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.

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Edema complication

• Herniation of brain matter in severe case.

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• Herniation

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Herniation

• Etiology
• Due to mass effect.
• Tumor, Trauma( blood clot),
• Infection induced edema.

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Types

1. Transtentorial Herniation (uncal gyral )
2. Subfalcine herniation (cingulate gyrus )
3. Tonsillar Herniation

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• 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

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• Subfalcine Herniation
• (involve Cingulate gyrus )

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Subfalcine 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
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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.

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Duret hemorrhage

• Kinking of the penetrating median and paramedian
  pontine arteries a branch off the basilar
  artery.

Pons
Spinal cord
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Secondary Brain stem or Duret hemorrhage

• Causes
• Tonsillar Herniation
• Gliomas

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• Hydrocephalus

The Thinker
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Hydrocephalus

• 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).

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2 Types

• 1. Non communicating Hydrocephalous. Obstruction
  within the ventricular system.
• 2. Communicating Hydrocephalous. the obstruction
  is in the subarachnoid space or venous sinuses.

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Non communicating Hydrocephalous (0bstructive)
Cause

• Medulloblastoma,
• Ependymoma

No communication between ventricles and
subarachonoid space.
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Communicating Hydrocephalous.

• Meningitis- adult.
• Subarachnoid hemorrhage- obstruction in
  subarachnoid space (SAP)- adult

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Hydrocephalous by meningitis

• Early acute phage obstruction of the SAP by
  exudates.
• Late chronic phage obstruction of the SAP by
  fibrosis.

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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.

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Child and adult
Sunset sign
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Clinical 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.

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• Vascular Diseases

Persistence of the memory Salvador Dali
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Vascular Diseases

• GENERAL FEATURES
• TYPES
• ETIOPATHOLOGY
• MORPHOLGY
• CLINICAL FEARYRES WITH INVESTIGATIONS.

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RISK FACTORS OF ISCHEMIC BRAIN INJURY

• AGE
• DURATION OF THE HYPOXIA
• TEMPERATURE HYPOTHERMIA PROTECT HYPOXIC BRAIN
  DAMAGE

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Three categories'

1. Global Hypoxic Ischemic Encephalopathy.
2. Local infarct 80 of the total
3. Hemorrhage.

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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

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Border zone infarct Watershed infarct May
follows a Hypotensive episode.
Lesion lies at the boundary between the anterior
and middle cerebral artery territories.
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Morphology Global Hypoxic Ischemic
Encephalopathy.

• Laminar cortical necrosis A LINEAR ZONE OF
  SOFTENING DISCOLORATION IN THE CORTICAL MANTLE.

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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 gt Female.

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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).

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Description 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).

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Red neuron
Normal
Hemorrhagic infarct
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Liquefactive necrosis
Tissue shows macrophage and microglial
proliferation in this time. CT shows enhancing
lesion.
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Remote infarct ( cavity )
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Remote infarct ( cavity )

• In the wall of the cavity shows reactive
  astrocytes with reactive gliosis.
• An CT would show enhancing shadow.

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Shower embolizationMultiple small hemorrhage
fat embolism, amniotic fluid embolism
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Lacunar infarcts
Hypertension induced infarct
Site The pons.
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What are the signs infarction?
Clinical features

1. TIA transient ischemic attack persists lt 24
   hours.
2. Stroke gt24 hours
3. Sudden numbness or weakness on one side of the
   face, arm or leg .
4. Sudden trouble speaking or understanding.
5. Sudden trouble seeing.

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Clinical Features If middle cerebral Artery is
effected.

• Contralateral hemiparesis and spasticity.
• Visual Field abnormality
• In some case speech aphasia.

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End of Stroke
Guernica