This type of brain injury (encephalopathy) is caused by partial (hypoxia) or total (anoxia) deprivation of the brain’s oxygen supply for longer than the compensatory mechanisms designed to prevent neuronal death can cope.

Oxygen is vital for the normal functioning of the brain, as the following figures illustrate:
“The brain represents 2% of our total body weight, but it consumes 20% of all the oxygen in our body.”

This fact is especially relevant given the following:
“The brain has limited capacity to store nutrients, which is why it demands a constant high level of oxygen supply.”

This is why brain tissue is widely accepted as being capable of surviving for up to four or five minutes of sustained anoxia. Once this time has elapsed, the anoxia will begin to cause damage to the brain tissue, and this damage will become more and more severe the longer the anoxia lasts. After 15 minutes of oxygen deprivation, more than 95% of the brain tissue will have been damaged.


In general, a drop in oxygen supply may be due to many causes, although the common trigger in all these causes is cardiocirculatory or respiratory failure. The distinction between circulatory failure and hypoxia is important. Although they tend to occur together, they generally cause different injuries in the brain that may manifest themselves differently:

ISQUEMIA refers to a reduction in blood supply to the brain, leading to a reduction in the oxygen supply (hypoxia). In these cases, in addition to the lack of oxygen supply, circulation failure limits or deactivates the mechanisms that eliminate toxic cellular substances (metabolites), which can aggravate the brain injury caused by the ischemia.

HIPOXIA refers to a reduction in the supply or use of oxygen. In cases of isolated hypoxia, a temporary compensatory mechanism is put in place to increase oxygen circulation in the brain. This mechanism makes it possible to continue supplying glucose to the brain and continue eliminating toxic substances for a short time.

There are different types of cerebral hypoxic injury:


Caused by an insufficient supply of oxygen in the environment. A famous example of this aetiology is altitude sickness, which typically occurs during holidays to locations where high altitude means that the quantity or concentration of oxygen in the environment is low. Other causes include strangulation or near strangulation whether due to immersion or choking, attempted strangulation by an assailant, obstructions in the respiratory tract, or severe asthma (anaphylaxis).


Caused by an insufficient oxygen supply to the brain because of a drop or irregularity in the oxygen­binding capacity of the haemoglobin.

ISCHEMIC Anoxia/Hipoxia

Caused by an insufficient supply of oxygen to the brain due to a drop in cerebral blood flow or arterial pressure. This mechanism is the most common cause of anoxic encephalopathy, and it includes strokes, brain haemorrhages, prolonged severe hypotension, and cardiac arrests.


Cardiac arrest is the most common cause of brain hypoxia and is usually due to cardiac arrhythmia.

Ischemic anoxia/hypoxia is most commonly caused by the following problems in newborns: problems with blood flow between the mother and foetus, placental abruption, umbilical cord compression, or uterine rupture.

TOXIC Anoxia caused by toxins or substances that interfere with the use of oxygen. Causes include intoxication by carbon monoxide, cyanide, narcotics, alcohol, formaldehyde, acetone, toluene, and some anaesthetics.


The sequelae of oxygen deprivation in the brain depend on several factors including the following:

From a clinical perspective, the symptoms of this disease reflect how certain areas of the brain are especially vulnerable to the consequences of a lack of oxygen. These especially vulnerable areas include the following:

  • The CA1 and CA 4­6 regions of the hippocampus: Responsible for acquiring new information.
  • The basal ganglia (caudate nucleus and putamen): Responsible for controlling movement.
  • Purkinje cells in the cerebellum: Responsible for coordinating movement.
  • Border zones of the vascular territory system: Responsible for processing information flowing between different territories in the brain.
  • Some layers (III, V, and VI) of the cerebral cortex: Responsible for cognitive function.

The most common symptoms presented by these patients include the following:

  • Epileptic seizures: As many as one in three patients who have suffered brain injury of this type may experience epileptic seizures, which instead of producing convulsive symptoms, usually present themselves in the form of episodes of disconnection (complex partial seizures) or muscle tremors (myoclonus).
  • Movement disorders: including mainly kinetic–rigid Parkinsonism, associated with dystonic postures. Other types of common movements are muscle tremors, choreic movements, slower yet uncontrollable abnormal movements (athetosis), and trembling.
  • Sensorimotor disorders: often including symptoms of generalized weakness (tetraparesis) or weakness in lower members (paraparesis), etc.
  • Visual impairment: including visual fixation problems and cortical blindness.
  • Altered levels of consciousness: including symptoms of prolonged periods of low interaction or response to surroundings (unresponsive wakefulness syndrome or minimally conscious state).
  • Cognitive problems: fundamentally associated with attention and learning.

The clinical spectrum of this disease is highly variable, ranging from isolated cognitive disorders to symptoms compatible with brain death. This disease, especially when compared with other aetiologies, generally leads to a high rate of disability and dependence among survivors. It has been reported that 65% of patients are dependent after being discharged from hospital. In general, the prognosis is among the worst of all causes of acquired brain injury, and the aforementioned motor and cognitive sequelae are common.

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