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What is Vasogenic Cerebral Oedema

Cerebral Oedema

The term cerebral edema denotes an increase in the water content of brain and it will leads to brain volume expansion. 

Cerebral edema can occur either focally or diffusely and this can be seen after any type of primary injury to the brain and  in some systemic medical conditions, example acute or acute-on-chronic liver failure.

Vasogenic Oedema

Vasogenic cerebral edema is due to the dysfunction of the blood-brain barrier, 

There is a physical and metabolic barrier between the systemic circulation  and brain and it is formed by endothelial cells, the tight junctions between endothelial cells, astrocytes, and pericytes.

Blood-brain barrier dysfunction leads to extravasation of ions and macromolecules from the plasma; these ions and macromolecules generate an osmotic pressure, which, combined with vascular hydrostatic pressure, results in net movement of water into the brain.

The resulting water expands the extracellular space and it is collected mainly in the subcortical white matter, and this will spare  the cortical and deep gray matter. 

What are the conditions you get Vasogenic cerebral oedema?

Vasogenic edema is typically seen with brain tumors, cerebral abscesses, and posterior reversible encephalopathy syndrome (PRES).

Recent literature have shown that for producing vasogenic edema frank blood-brain barrier disruption visible on microscopy is not necessary. As this can be contributed by abnormal transcellular transport across endothelial cells and degradation of endothelial tight junctions by proteolytic enzymes, such as matrix metalloproteinase-9.

Thyroid and cardiac abnormalities

Thyroid examination is done for evidence of hypo  and hyperthyroidism  which can lead to heart disease.
Signs of thyroid dysfunction
Hands
  • Tachycardla/bradycardia, tremor, warmth
Eyes
  • Exophthalmos and eye signs
Neck
  • Goitre


Blood supply of internal capsule

Blood supply of internal capsule comes from 3 main arteries they are
Lateral striate branches of middle cerebral artery.
Medial striate branches of anterior cerebral artery.
Anterior choroidal branches of internal carotid artery.

Lateral striate branches of middle cerebral artery supply
  1. Anterior limb.
  2. Genu.
  3. Posterior limb.
  4. Basal ganglia.
Medial striate branches of anterior cerebral artery supply
  1. Anterior limb.
  2. Genu.
  3. Basal ganglia.
Anterior choroidal branches of internal carotid supply
  1. Posterior limb.
  2. Retrolenticular part.
Anterior limb is supplied by the following arteries
  1. Ant cerebral artery through medial striate branch.
  2. Middle cerebral artery through lateralstriate and lenticulostriate branches.
Genu is supplied by
  1. Anterior cerebral artery through medial striate branch.
  2. Middle cerebral artery through lateral striate and lenticulostriate branch.
  3. Branches of internal carotid artery.
Posterior limb is supplied by
  1. Middle cerebral artery through lateral striate and lenticulostriate branch. It is called Charcot’s artery of cerebral haemorrhage.
  2. Anterior choroidal artery, direct branch of internal carotid artery As it is long and slender it has tendency to get thrombosis.

Mechanism of continuous murmur

1.High pressure system communicating with low pressure system
Intracardiac
  • RSOV to RV, RA ,Pulmonary artery.
  • Coronary artery fistula to cardiac chamber.
Extracardiac
  • PDA.
  • Aorto pulmonary septal defect.
  • Pulmonary AVF.
  • Systemic AVF.
  • Anomalous left coronary artery from pulmonary artery.
2.Narrowing of vessel
  • Coarctation of aorta.
  • Peripheral pulmonary artery stenosis.
  • Carotid stenosis.
3.Increased blood flow through vessels
  • Venous hum - Devil’s murmur - root of neck.
  • Venous hum (Cruveilhier – Baumgarten murmur) - umbilicus - in portal hypertension.
  • Intercostal arteries - Coarctation of aorta.
  • Bronchopulmonary anastomoses.
  • Pulmonary atresia and TOF.
  • Internal mammary artery - Mammary Souffle in pregnancy.

Vascular theories of Migraine

It is the most common Migraine is the most common disabling primary headache globally.

12 percent of migraine are Episodic and 1 - 2 percentage is Chronic.Migraine Attacks are typically present with unilateral throbbing headache and it is associated with following  symptoms 

  1. Nausea
  2. Multisensory Hypersensitivity
  3. Marked fatigue.

The diverse symptomatology highlights the complexity of migraine as a whole nervous system disorder involving somatosensory, autonomic, endocrine, and arousal networks

Vascular Theory of Aura in Migrane

In Migraine  there is Hereditary Susceptibility of Brain. There is Abnormal Intracranial and extra-cranial  vascular reactivity to triggers. Aura is followed by Vasoconstriction, ischemia and focal neurological symptoms. Headache is due to Vasodilation and leads to pulsatile headache

What are the Pitfalls in Vascular theory

MRI perfusion study has showed that there is focal hyperemia precedes oligemia during Migraine aura. Perfusion abnormalities need not always match with symptoms of migraine. Oligemia may spread at 3mm/min beyond vascular territory. Headache can occur as that of migraine aura. Vascular theory cannot explain the premonitory phase. There wont be any Diffusion restriction in  MRI doesn’t show  

Normal Second heart sound (Identify the abnormalities of S2)

The most difficult thing in auscultation is to identify the abnormalities of S2.

Physiology of Second heartsound
Two components for 2nd heart sound are- aortic and pulmonary

Aortic component it is the 1st component and loud one heard in all areas.

Pulmonary component - 2nd component and soft, heard only over pulmonary area.

Normal second heart sound
It is a high pitched sound with normal split - 2 components are separately heard during inspiration and as single component during expiration over the pulmonary area.
Distance between the 2 components during inspiration is 0.04 sec, during expiration is 0.02 sec. Human ear can appreciate, when the distance between the 2 components is 0.03 or more. Normal second heart sound is expressed as - normal in intensity and normal split with respiration.

Things to look for in S2:
Intensity
Splitting
A2 heard over aortic area and pulmonary area and the apex.
P2 heard over pulmonary area and 2-4 LICS only and not at the apex.
P2 heard over the apex only in pulmonary artery hypertension and in young.
Best site for S2 in COPD - epigastrium.

NINDS (National Institute of Neurological Disorders and Stroke ) criteria for possible PSP

NINDS criteria for possible PSP

  • Gradually progressive disorder with onset aged 40 years or older.
  • Either vertical supra nuclear palsy or both slowing of vertical saccades and prominent postural instability with falls in the first year of onset.
  • No evidence of other diseases that can explain the clinical features.

Criteria for probable PSP

Vertical supranuclear palsy with prominent postural instability, falls in the first year of onset, and other features of possible PSP, as follows:

  • Symmetric proximal greater than distal akinesia or rigidity.
  • Abnormal neck posture, especially retrocollis.
  • Poor or absent response of parkinsonism to levodopa therapy.
  • Early dysphagia and dysarthria.
  • Early cognitive impairment with at least 2 of the following: apathy, abstract thought impairment, decreased verbal fluency, imitation behavior, or frontal release signs.

Criteria for definite PSP are as follows:

  • History of probable or possible PSP.
  • Histopathologic evidence that is typical of the disease.