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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.

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  

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

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.