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Cerebral Ischemia and Infarction

Majid Ali, M.D.

The common term stroke refers to loss of neurologic function caused by death of brain cells due to hemorrhagic infarction (cerebral hemorrhage) or ischemic infarction (cerebral thrombosis). The term TIA (transient ischemic attacks) refers to temporary loss of some brain functions due to reversible ischemia, often caused by a spasm of cerebral arteries.

Causes of Brain Hypoxia and Anoxia

1. Functional hypoxia due to diminished partial pressure of oxygen (pO 2) in the inspired air.

2. Severe hypoxia due to generalized cardiovascular failure, such as in cardiac arrest.

3. Impaired oxygen carrying capacity due to anemia.

4. Impaired oxygen carrying capacity due to toxins, such as carbon monoxide.

5. Temporary perfusion deficits caused by vasospasm.

6. Long-lasting perfusion deficits caused by vascular occlusion.

7. Inhibition of oxygen metabolism by poisons, such as arsenic.

8. Dysoxygenosis (inhibition of oxygen metabolism by impaired function of oxygen metabolism due to cumulative burden of environmental and microbial toxins as well as toxic organic acids produced in excess due to acidosis and oxidosis).

Two important molecular pathways in anoxic and dysoxygenetic brain injury are noteworthy. In the first, initial oxygen deficiency leads to overproduction of certain excitatory amino acid neurotransmitters (including glutamate and aspartate). That, in turn, seriously threatens the neuronal metabolism by further reducing oxygen supply. The putative mechanism of such injury involves persistent opening of such specific membrane channels as NMDA (N-methyl-D-aspartate receptor) that maintains uncontrolled and dangerous influx of calcium ions. Increased intracellular calcium promotes cell apoptosis in addition to exert other cytotoxic effects.

The second mechanism of incremental neuronal injury involves activation of nitric oxygenase, an enzyme that plays crucial regulatory roles in health by carefully controlling the production of nitric acid, another important neurotransmitter and a highly potent toxin when present in excess.

Ischemic Encephalopathy

Very mild forms of ischemic encephalopathy may cause short periods of mental confusion with full recovery. In moderate cases, there is progressive impairment of mentation which, unless expeditiously reversed, leads to permanent functional loss. In severe cases, extensive necrosis of brain parenchyma leads to diffuse softening of the brain parenchyma so that brain tissue becomes diffluent and freely flows through fingers when the brain is pulled out of the skull at autopsy.

Cerebral Infarction

Discrete areas of brain necrosis (infarction) usually result from:

1. Thrombotic occlusion due to arteriosclerosis developing within the brain.

2. Embolic occlusion due to emboli formed outside the brain and carried in there (as in atrial fibrillation).

3. Cerebral hemorrhage due to leaking or rupture of blood vessels, as in malignant hypertension (lacunar state) and aneurysm blow-outs.

4. Trauma.

5. Hemorrhage in neoplasia.

6. Septicemia.

About 15% of cases of cerebral hemorrhage die with or without treatment. Regrettably, such statistics represent the fate of individuals who were not treated with robust intravenous oxystatic and nutrient therapies, bowel and liver detox, and nondrug spice and herbal anti-inflammatory agents.

 

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