Hypoxia

Globally decreased cerebral perfusion causes generalized nonfocal brain dysfunction. Dizziness, lightheadedness, confusion, and mental concentration difficulty are common. Focal symptoms and signs, such as hemiplegia, hemianopia, and aphasia, are rarely present. At times, prior strokes or vascular occlusions may contribute to asymmetric signs. Patients with globally decreased cerebral perfusion often appear ill with sweating, tachycardia, and hypotension. Prolonged severe hypotension causes coma; initially, the patients often have no remaining brainstem reflexes (pupillary, corneal, oculovestibular).

When and if coma clears, or hypotension is less severe, abnormalities of cortical function-memory, vision, and behavior predominate.

The hippocampi are particularly vulnerable to ischemia; therefore memory loss is particularly common. The border zone cerebral cortex located between the middle cerebral arteries and the anterior and posterior cerebral arteries are often rendered ischemic. The posterior border zone between the middle cerebral artery and the posterior cerebral arteries territories are most often involved, possibly because these regions are farthest from the heart.

Lesions in the posterior border zones can disconnect the preserved calcarine visual cortex in the occipital lobe from the more anterior centers that control eye movements. A visual problem called Balint syndrome, often results. Patients act as if they cannot see but sometimes surprisingly notice small objects. The features of Balint syndrome are (1) asimultagnosia: patients see things piecemeal that is, do not see all the objects in their field of vision at one time and may notice only parts of objects, (2) optical ataxia: patients cannot coordinate hand and eye movements and point erratically at objects; and (3) gaze apraxia: patients cannot direct their gaze where desired.

When hypotension is more severe, lesions can spread to the anterior border zones between the anterior cerebral artery and the middle cerebral artery. The areas of the motor homunculus most affected are those related to the shoulder, arm, and thigh. The face territory in the central portion of the middle cerebral artery territory and the foot region in the center of the anterior cerebral artery supply are spared. The distribution of weakness has been likened to a “man in a barrel.” The frontal eye fields are also affected so that roving eye movements and hyperactive passive head movements (doll’s eye reflexes) result. Stupor results from extensive bilateral border-zone ischemia.

When hypoperfusion is severe and prolonged, diffuse anoxic damage to cerebral, brainstem, and cerebellar neurons occurs. The most severe damage may occur in the large cell regions of the cerebral cortex, producing a laminar necrosis pattern. Severe hypoxic-ischemic damage causes coma and brain death. In some patients, partial recovery leaves the patients in a minimally conscious state or a persistent vegetative state in which there is no or minimal communication.

Although hypoxic-ischemic cerebellar damage is often found at necropsy, clinical signs of cerebellar dysfunction are rare and are usually overshadowed by cerebral abnormalities. After cardiac arrest, some patients have spontaneous arrhythmic fine or coarse muscle jerking, markedly exaggerated when the limbs are used. This disorder of limb movements is usually referred to as action myoclonus or the Lance-Adams syndrome and is often accompanied by gait ataxia.

Very occasionally, a delayed progressive deterioration develops after a single hypoxic insult. In other rare instances, patients recover from coma without obvious cerebral damage but instead have paraplegia related to hypoxic-ischemic damage to the spinal cord. The most vulnerable spinal regions are the upper and lower thoracic and lumbar spinal cord segments. The cervical cord is usually not involved so that the arms are normal despite severe weakness of the lower limbs.

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