The effects of traumatic head injuries

PATHOLOGY OF THE NERVOUS SYSTEM

 

Explanation for working with teaching material.

Examine the lecture information and guide.

Give answers to the tests.

Give the answers to one of the proposed variant of the final control.

 

 

LECTURE

Anatomically and functionally the brain is the most complex structure in the body. It controls our ability to think, our consciousness of things around us, and our interactions with the outside world. Signals to and from various parts of the body are controlled by very specific areas within the brain. This renders the brain much more defenceless to focal lesions than other organs in the body.

Mechanisms of brain Injury

The causes of brain damage include hypoxia or ischemia, accumulation of excitatory neurotransmitters, increased ICP, and cerebral edema. Deprivation of oxygen (i.e., hypoxia) or of blood flow (i.e., ischemia) can have harmful effects on the brain structures.

Hypoxia of brainusually is seen in conditions such as reduced atmospheric pressure, carbon monoxide poisoning, severe anemia, and failure to oxygenate the blood.

Neurons are capable of anaerobic metabolism and are tolerant of pure and chronic hypoxia; it commonly produces euphoria, listlessness, drowsiness, and impaired problem solving.

Unconsciousness and convulsions may occur when hypoxia is sudden and severe.

Ischemia can be focal, as in stroke, or global. Global ischemia occurs when blood flow is inadequate to the metabolic needs of the brain.

The brain makes up only 2% of the body weight, but receives one sixth of the cardiac output and 20% of the oxygen consumption.

Focal ischemia involves a single area of the brain, as in stroke. Collateral circulation may provide low levels of blood flow during focal ischemia. The residual perfusion may provide sufficient substrates to maintain a low level of metabolic activity, preserving neuronal integrity.

Global ischemia occurs when blood flow is inadequate to provide the metabolic needs of the brain. In contrast to persons with focal ischemia, global ischemia have no collateral circulation. Unconsciousness occurs within seconds of severe global ischemia, that results from complete cessation of blood flow, as in cardiac arrest. If circulation is restored immediately, consciousness is regained quickly. However, if blood flow is not promptly restored, severe pathologic changes take place. Energy sources (i.e., glucose and glycogen) are exhausted in 2 to 4 minutes, and cellular ATP stores are depleted in 4 to 5 minutes.

Excitatory Amino Acid Injury

Glutamate is the principal excitatory neurotransmitter in the brain, and its interaction with specific receptors is responsible for many higher-order functions, including memory, cognition, movement, and sensation. Normally, extracellular concentrations of glutamate are regulated, with excess amounts removed

and actively transported into astrocytes and neurons.

During prolonged ischemia, these transport mechanisms become immobilized, causing extracellular glutamate to accumulate.

In the case of cell injury and death, intracellular glutamate is released from the damaged cells.

Many of the glutamate actions are coupled with receptor-operated ion channels. One type of glutamate receptor, called - the glutamate N-methyl-D-aspartate receptor (NMDA), has been implicated in causing central nervous system (CNS) injury. The uncontrolled opening of NMDA receptor-operated channels produces an increase in intracellular calcium and leads to a series of calcium-mediated processes called the calcium cascade.

Activation of the calcium cascade leads to the release of intracellular enzymes that cause protein breakdown, free radical formation, lipid peroxidation, fragmentation of DNA, and nuclear breakdown. Drugs called neuroprotectants are being developed to interfere with the glutamate-NMDA pathway and thus reduce brain cell injury.

Increased intracranial pressure

Intracranial pressure (ICP) is the pressure exerted by the brain tissue, CSF, and cerebral blood (intracranial components) against the skull.

Initially the body uses its compensatory mechanisms to attempt to maintain homeostasis and lower ICP in the following ways:

- limiting blood flow to the head

- displacing CSF into the spinal canal

- increasing absorption or decreasing production of CSF — withdrawing water from brain tissue and excreting it through the kidneys.

But if these mechanisms become overwhelmed and are no longer effective, ICP continues to rise. Cerebral blood flow diminishes and perfusion pressure falls. Ischemia leads to cellular hypoxia, which initiates vasodilation of cerebral blood vessels in an attempt to increase cerebral blood flow. This only causes the ICP to increase further. As the pressure continues to rise, compression of brain tissue and cerebral vessels further impairs cerebral blood flow.

If ICP continues to rise, the brain begins to shift under the extreme pressure and may herniate to an area of lesser pressure. When the herniating brain tissue's blood supply is compromised, cerebral ischemia and hypoxia worsen. The herniation increases pressure in the area where the pressure was lower, thus impairing its blood supply. As ICP approaches systemic blood pressure, cerebral perfusion slows even more, ceasing when ICP equals systemic blood pressure.

 

Cerebral Edema

Cerebral edema, or brain swelling, is an increase in tissue volume secondary to abnormal fluid accumulation. There are 4 types of brain edema.

Vasogenic Edema. Vasogenic edema results from an increase in the extracellular fluid that surrounds brain cells. It occurs with conditions such as tumors, prolonged ischemia, hemorrhage, brain injury, and infectious processes (e.g., meningitis) that impair the function of the blood-brain barrier and allow water and plasma proteins to leave the capillary and move into the interstitium.

Cytotoxic Edema. Cytotoxic edema involves the swelling of brain cells. It involves an increase in fluid in the intracellular space, chiefly the gray matter, although the white matter may be involved. Cytotoxic edema can result from hypoosmotic states, such as water intoxication or severe ischemia, that impair the function of the sodium-potassium membrane pump. Changes in cerebral function, such as stupor and coma, occur with cytotoxic edema. The edema associated with ischemia may produce cerebral infarction with necrosis of brain tissue.

Ischemic: Due to cerebral infarction and initially confined to intracellular compartment; after several days, released lysosomes from necrosed cells disrupt blood brain barrier.

Interstitial: Movement of CSF from ventricles to extracellular spaces increases brain volume.

Hydrocephalus

Enlargement of the CSF compartment occurs with hydrocephalus, which is defined as an abnormal increase in CSF volume in any part or all of the ventricular system. There are two types of hydrocephalus: noncommunicating and communicating. Hydrocephalus refers to dilation of the ventricular system and a compensatory increase in CSF volume, secondary to a loss of brain tissue.

Noncommunicating or obstructive hydrocephalus occurs when obstruction in the ventricular system prevents the CSF from reaching the arachnoid villi. CSF flow can be obstructed by congenital malformations, tumors, inflammation, or hemorrhage.

Communicating hydrocephalus results from impaired reabsorption of CSF from the arachnoid villi into the venous system. The cerebral hemispheres become enlarged, and the ventricular system is dilated behind the point of obstruction. Acute-onset hydrocephalus is usually marked by symptoms of increased ICP, including headache vomiting, and by edema of the optic disk (papilla edema). If the

obstruction is not relieved, mental deterioration eventually occurs. Slowly developing hydrocephalus is less likely to produce an increase in ICP, but it may produce deficits such as progressive dementia and gait changes.

The effects of traumatic head injuries

The effects of traumatic head injuries can be divided into two categories: primary or direct injuries, in which damage is caused by impact, and secondary injuries, in which damage results from the subsequent brain swelling, an intracranial hematoma, infection, or cerebral ischemia. Ischemia is the most common cause of secondary brain injury. It can cause the hypoxia and hypotension or the impairment of regulatory mechanisms that maintain cerebral blood flow and oxygen supply. Even if there is no break in the skull, a blow to the head can cause severe and diffuse brain damage. Such closed injuries can be classified as focal or diffuse. Diffuse injuries include concussion and diffuse axonal injury.

  Foca l injuries include contusion, laceration, and hemorrhage. Brain injury is manifested by alterations in sensory and motor function and by changes in the level of consciousness.

Global brain injury, caused by head trauma, stroke, or other pathologies, is manifested by alterations in sensory and motor function, by changes in the level of consciousness and brain death.

Stroke, or “brain attack,” is an acute focal neurologic deficit caused by a vascular disorder, that injures brain tissue. There are two main types of stroke: ischemic and hemorrhagic. Ischemic stroke, which is the most common type, is caused by cerebrovascular obstruction by a thrombus or emboli. Hemorrhagic stroke, which is associated with greater morbidity and mortality, is caused by the rupture of a blood vessel and bleeding into the brain. The acute manifestations of stroke depend on the location of the blood vessel that is involved and can include motor, sensory, language, speech, and cognitive disorders.

 Most subarachnoid hemorrhages are the result of a ruptured cerebral aneurysm. Presenting symptoms include headache, nuchal rigidity, photophobia, and nausea. Complications include rebleeding, vasospasm, and hydrocephalus. Arteriovenous malformations are congenital abnormal communications between arterial and venous channels that result from failure in the development of the capillary network in the embryonic brain. The vessels in the arteriovenous malformations may enlarge to form a spaceoccupying lesion, become weak and predispose to bleeding, and divert blood away from other parts of the brain; they can cause brain hemorrhage, seizures, headache, and other neurologic deficits.

Cognitive disorders

Cognitive disorders can be caused by any disorder that permanently damages large cortical or subcortical areas of the hemispheres. The most common cause of dementia is Alzheimer’s disease, which is a major health problem among the elderly. It is characterized by cortical atrophy and loss of neurons, the presence of neuritic plaques, granulovacuolar degeneration, and cerebrovascular deposits of amyloid. The disease follows an insidious and progressive course that begins with memory impairment and terminates in an inability to recognize family or friends and the loss of control over bodily functions.

Multi-infarct dementia is associated with vascular disease and Pick’s disease with atrophy of the frontal and temporal lobes.

Creutzfeldt-Jakob disease is a rare transmissible form of dementia. Wernicke-Korsakoff syndrome results from chronic alcoholism. Huntington’s disease is a rare hereditary disorder characterized by chronic and progressive chorea, psychological change, and dementia.