What if any are the stages of brain damage due to lack of oxygen? ?!
Question: What if any are the stages of brain damage due to lack of oxygen!? !?
such as after a serious heart attack!?Www@Answer-Health@Com
Answers:
Glasgow Coma Scale
The GLASGOW COMA SCALE (GCS) is a tool to assist doctors to describe the level of consciousness, especially in the early acute stage of brain damage!.
This table shows the criteria for the Glasgow Coma Scale!. A total score of 8 or less usually means that the person is in the vegetative state
Eye opening
Spontaneously 4
To verbal command 3
To pain 2
No response 1
Best motor response
Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Abnormal flexion 3
Abnormal extension 2
No response 1
Best verbal response
Oriented converses 5
Disoriented 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
The worst score obtainable is not 0, but 3!. Note that score for the motor response is based on
the best response so that a hemiplegia on one side with a normal contralateral side receives a
motor score of 6!. A patient with quadriplegia from a spinal cord injury receives a motor score of 1!. The Glasgow Coma Scale provides a useful standard for comparison to help determine if
there is deterioration, improve ment, or no change in the patient's level of consciousness
A survivor's degree of consciousness is often used to determine the severity of his/her brain injury!. Instruments such as the Glasgow Coma Scale (GCS) use the survivor's visual, motor, and verbal responsiveness to measure level of consciousness!. Scores of 8 or below are considered to represent a true coma (no eye opening, no response to simple commands, and unable to communicate) and to indicate a severe brain injury!. Scores from 9 - 12 on the GCS are suggestive of a moderate brain injury!. GCS scores of 13 and above are thought to indicate that the brain injury is mild!.
The duration or length of coma (LOC) is also used to measure severity of injury and to predict outcome!. The longer the LOC, the more severe the brain injury!. LOC greater than 6 hours post-admission is considered to be a severe brain injury!. LOC between 20 minutes and 6 hours post-admission is considered to be moderate brain injury!. LOC of less than 20 minutes is considered to be indicative of a mild brain injury!.
A head injury( traumatic brain injuries e!.g!. fr car accidents) will frequently impact on the survivor's initial level of consciousness!. Level of consciousness is a continuum ranging from full alertness, drowsiness, lethargy, daze-like symptoms, to loss of consciousness or coma!. Loss of consciousness typically involves injuries to the brain stem, the oldest part of the brain, which is responsible for basic fife functions such as alertness, arousal, heartbeat, and breathing!.
It is rare for true coma to last more than several weeks, and in fact, almost all survivors will eventually awaken from a coma!. The length of time before someone wakes up depends on the severity of the injury!. It is important to understand that emergence from a coma is a gradual process in which the brain injured survivor may go through several stages including periods of disorientation, post-traumatic or anterograde amnesia (survivor has no memory of recent events), agitation!. Some of these survivors may require medication or even physical restraints to prevent them from harming themselves or others!.
Now let's discuss about heart attack ( myocardial infarction )!.
Greater than 5 minutes of CPR without assisted ventilation can lead to decreased arterial oxygenation and coronary artery obstruction further compromises the myocardium!. We evaluated the need for assisted ventilation during 10 minutes of CPR in a swine cardiac arrest model with coronary artery obstruction!.
Therefore, a person who suffered a heart attack (myocardial infarction) and had no assisted ventilation( breathing center is in the brain stem ) for 5 minutes will most likely go into cardiac arrest and death would ensue!. If they survive, even with proper CPR- but 5 minutes have elapsed, brain damage would occur rendering them to go into an irreversible coma!. The heart has to beat in order to provide oxygen to the brain!.Www@Answer-Health@Com
The GLASGOW COMA SCALE (GCS) is a tool to assist doctors to describe the level of consciousness, especially in the early acute stage of brain damage!.
This table shows the criteria for the Glasgow Coma Scale!. A total score of 8 or less usually means that the person is in the vegetative state
Eye opening
Spontaneously 4
To verbal command 3
To pain 2
No response 1
Best motor response
Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Abnormal flexion 3
Abnormal extension 2
No response 1
Best verbal response
Oriented converses 5
Disoriented 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
The worst score obtainable is not 0, but 3!. Note that score for the motor response is based on
the best response so that a hemiplegia on one side with a normal contralateral side receives a
motor score of 6!. A patient with quadriplegia from a spinal cord injury receives a motor score of 1!. The Glasgow Coma Scale provides a useful standard for comparison to help determine if
there is deterioration, improve ment, or no change in the patient's level of consciousness
A survivor's degree of consciousness is often used to determine the severity of his/her brain injury!. Instruments such as the Glasgow Coma Scale (GCS) use the survivor's visual, motor, and verbal responsiveness to measure level of consciousness!. Scores of 8 or below are considered to represent a true coma (no eye opening, no response to simple commands, and unable to communicate) and to indicate a severe brain injury!. Scores from 9 - 12 on the GCS are suggestive of a moderate brain injury!. GCS scores of 13 and above are thought to indicate that the brain injury is mild!.
The duration or length of coma (LOC) is also used to measure severity of injury and to predict outcome!. The longer the LOC, the more severe the brain injury!. LOC greater than 6 hours post-admission is considered to be a severe brain injury!. LOC between 20 minutes and 6 hours post-admission is considered to be moderate brain injury!. LOC of less than 20 minutes is considered to be indicative of a mild brain injury!.
A head injury( traumatic brain injuries e!.g!. fr car accidents) will frequently impact on the survivor's initial level of consciousness!. Level of consciousness is a continuum ranging from full alertness, drowsiness, lethargy, daze-like symptoms, to loss of consciousness or coma!. Loss of consciousness typically involves injuries to the brain stem, the oldest part of the brain, which is responsible for basic fife functions such as alertness, arousal, heartbeat, and breathing!.
It is rare for true coma to last more than several weeks, and in fact, almost all survivors will eventually awaken from a coma!. The length of time before someone wakes up depends on the severity of the injury!. It is important to understand that emergence from a coma is a gradual process in which the brain injured survivor may go through several stages including periods of disorientation, post-traumatic or anterograde amnesia (survivor has no memory of recent events), agitation!. Some of these survivors may require medication or even physical restraints to prevent them from harming themselves or others!.
Now let's discuss about heart attack ( myocardial infarction )!.
Greater than 5 minutes of CPR without assisted ventilation can lead to decreased arterial oxygenation and coronary artery obstruction further compromises the myocardium!. We evaluated the need for assisted ventilation during 10 minutes of CPR in a swine cardiac arrest model with coronary artery obstruction!.
Therefore, a person who suffered a heart attack (myocardial infarction) and had no assisted ventilation( breathing center is in the brain stem ) for 5 minutes will most likely go into cardiac arrest and death would ensue!. If they survive, even with proper CPR- but 5 minutes have elapsed, brain damage would occur rendering them to go into an irreversible coma!. The heart has to beat in order to provide oxygen to the brain!.Www@Answer-Health@Com
Carbon monoxide is a potentially lethal --- yet colorless and odorless --- gas that can cause devastating and permanent injuries due to the multiple mechanisms by which it damages brain, cardiac, and other vital structures!. For decades, it has been known that carbon monoxide causes hypoxic (lack of oxygen) damage to brain structures as a consequence of elevated carboxyhemoglobin levels in the blood stream!. But medical research undertaken in the past fifteen (15) years has demonstrated the even greater pervasiveness of carbon monoxide's damage potential!.
While hypoxic injury is clearly an element of the systemic damage, scientists have found that carbon monoxide is a neurotoxin and---due to a cascade of complex biochemical events---it creates a marked increase in oxidative injury that can directly damage perivascular (the area surrounding a blood vessel or lymphatic vessel) and neuronal (relating to a nerve cell or neuron) structures!. Those same biochemical cascades can also result in injury to the cardiovascular and pulmonary systems!.
Victims of carbon monoxide poisoning, then, are at risk for a range of injuries, including to the brain, the central nervous system, the cardiovascular system, and the pulmonary system!. The manifestations of those injuries can be devastating, including cognitive damage, impairment of executive functioning, memory loss, damage to learning processes, headaches, reduced capacity to multi-task or to contend with multiple environmental inputs, impaired emotional control, irritability and frustration and confusion, tinnitus (ear ringing) and hearing loss, vision disturbances, anxiety and depression, fatigue, reduced stamina and pulmonary functioning, motor weakness, peripheral neuropathies including tics and movement disorders, cardiac damage with possible increased risk of cardiac-related death, and accelerated development of dementia, premature cognitive decline, and Parkinson's-like syndromes!.
A!. Damage Mechanism: Hypoxia!. Carbon monoxide's destructive potential arises---in part---because it prevents oxygen from being delivered to brain cells and other vital organs of the body!. If the cells do not have a rich supply of oxygen, delivered by the hemoglobin that is a constituent part of our red blood cells, the cells will die!. Carbon monoxide molecules are 200 times more likely to bind to hemoglobin than are oxygen molecules!. Thus, when carbon monoxide is inhaled, it enters the bloodstream, binds to hemoglobin, and crowds out the oxygen molecules, thus depriving the cells of the oxygen needed to maintain their vitality!. Moreover, the iron atoms which are embedded in the hemoglobin molecule (and which normally bind oxygen to the hemoglobin) will hold onto any residual oxygen more tightly if carbon monoxide is present---resulting in even less oxygen being delivered to the cells and tissue!. The cells die, and, for the brain, the cells cannot regenerate!.
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The brain is extraordinarily dependent upon a constant supply of oxygen and is, accordingly, extraordinarily vulnerable to permanent damage when deprived of oxygen!. Areas of the brain that can be damaged by carbon monoxide poisoning include the deep white matter structures (particularly in the periventricular white matter regions) and deep gray matter structures such as the basal ganglia (particularly the globus pallidus and putamen, which are located within the basal ganglia)!. These structures are found at the "end" of the vascular "watershed" --- the intricate elaboration of arterial vessels through which hemoglobin transports oxygen to the cells --- and are especially susceptible to damage from a lack of oxygen!. The hippocampus --- another "watershed" structure of the brain --- can atrophy as a result of carbon monoxide exposure, and this damage may not develop for weeks or longer following the exposure!. Those areas of the brain --- the white matter, the basal ganglia (including the globus pallidus and the putamen), and the hippocampus --- are critical structures for the regulation of learning, memory, cognitive functioning, emotional functioning, and movement!.
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B!. Damage Mechanism: Cardiac Injury!. The hypoxic insult resulting from the increase of carboxyhemoglobin levels in the blood stream can damage structures in addition to the brain, including the heart!. It also is composed of cells that require oxygen for survival---and that will die when deprived!. But cardiac injury can then magnify the hypoxic injury to the brain in that reduced cardiac efficiency will reduce perfusion of the blood to the brain, thereby exacerbating the hypoxic impact of the increased carboxyhemoglobin levels!. Less oxygen is delivered by the hemoglobin molecule---but less blood is also being delivered!.
C!. Damage Mechanism: Oxidative Destruction!. The injury potential of carbon monoxide also arises from oxidative damage, and ***Www@Answer-Health@Com
While hypoxic injury is clearly an element of the systemic damage, scientists have found that carbon monoxide is a neurotoxin and---due to a cascade of complex biochemical events---it creates a marked increase in oxidative injury that can directly damage perivascular (the area surrounding a blood vessel or lymphatic vessel) and neuronal (relating to a nerve cell or neuron) structures!. Those same biochemical cascades can also result in injury to the cardiovascular and pulmonary systems!.
Victims of carbon monoxide poisoning, then, are at risk for a range of injuries, including to the brain, the central nervous system, the cardiovascular system, and the pulmonary system!. The manifestations of those injuries can be devastating, including cognitive damage, impairment of executive functioning, memory loss, damage to learning processes, headaches, reduced capacity to multi-task or to contend with multiple environmental inputs, impaired emotional control, irritability and frustration and confusion, tinnitus (ear ringing) and hearing loss, vision disturbances, anxiety and depression, fatigue, reduced stamina and pulmonary functioning, motor weakness, peripheral neuropathies including tics and movement disorders, cardiac damage with possible increased risk of cardiac-related death, and accelerated development of dementia, premature cognitive decline, and Parkinson's-like syndromes!.
A!. Damage Mechanism: Hypoxia!. Carbon monoxide's destructive potential arises---in part---because it prevents oxygen from being delivered to brain cells and other vital organs of the body!. If the cells do not have a rich supply of oxygen, delivered by the hemoglobin that is a constituent part of our red blood cells, the cells will die!. Carbon monoxide molecules are 200 times more likely to bind to hemoglobin than are oxygen molecules!. Thus, when carbon monoxide is inhaled, it enters the bloodstream, binds to hemoglobin, and crowds out the oxygen molecules, thus depriving the cells of the oxygen needed to maintain their vitality!. Moreover, the iron atoms which are embedded in the hemoglobin molecule (and which normally bind oxygen to the hemoglobin) will hold onto any residual oxygen more tightly if carbon monoxide is present---resulting in even less oxygen being delivered to the cells and tissue!. The cells die, and, for the brain, the cells cannot regenerate!.
Click To Enlarge
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The brain is extraordinarily dependent upon a constant supply of oxygen and is, accordingly, extraordinarily vulnerable to permanent damage when deprived of oxygen!. Areas of the brain that can be damaged by carbon monoxide poisoning include the deep white matter structures (particularly in the periventricular white matter regions) and deep gray matter structures such as the basal ganglia (particularly the globus pallidus and putamen, which are located within the basal ganglia)!. These structures are found at the "end" of the vascular "watershed" --- the intricate elaboration of arterial vessels through which hemoglobin transports oxygen to the cells --- and are especially susceptible to damage from a lack of oxygen!. The hippocampus --- another "watershed" structure of the brain --- can atrophy as a result of carbon monoxide exposure, and this damage may not develop for weeks or longer following the exposure!. Those areas of the brain --- the white matter, the basal ganglia (including the globus pallidus and the putamen), and the hippocampus --- are critical structures for the regulation of learning, memory, cognitive functioning, emotional functioning, and movement!.
Click To Enlarge
B!. Damage Mechanism: Cardiac Injury!. The hypoxic insult resulting from the increase of carboxyhemoglobin levels in the blood stream can damage structures in addition to the brain, including the heart!. It also is composed of cells that require oxygen for survival---and that will die when deprived!. But cardiac injury can then magnify the hypoxic injury to the brain in that reduced cardiac efficiency will reduce perfusion of the blood to the brain, thereby exacerbating the hypoxic impact of the increased carboxyhemoglobin levels!. Less oxygen is delivered by the hemoglobin molecule---but less blood is also being delivered!.
C!. Damage Mechanism: Oxidative Destruction!. The injury potential of carbon monoxide also arises from oxidative damage, and ***Www@Answer-Health@Com