OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

OD is often the first and arguably the most debilitating form of AD [11,12]. The ANS, including its two branches, is a very dynamic system and never actually “rests.” In fact, when the body is at rest, as in sleeping, it may be argued that the P&S systems are most active. This is important because most ADs are not well documented when the patient is at rest. In fact, the primary ADs documented at rest are much later stage dysfunctions [4], such as Diabetic Autonomic Neuropathy or Advanced Autonomic Dysfunction and Cardiovascular Autonomic Neuropathy. These are conditions indicating that patients are already at increased morbidity [11] and mortality [12] risk, respectively. This may be a reason why EDSh symptoms have failed to be associated with AD, because these tend to be younger patients, tested at rest, before most would consider AD. As expected, EDSh seems to affect morbidity and thereby quality of life and productivity, even though common physiologic measures (i.e., HR & BP) are well within normal ranges.

To compound the problem that most ADs are not well documented when the patient is at rest, is the fact that Heart Rate Variability (HRV), a standard measure of autonomic activity, is a mixed measure of P&S responses. Given that the P&S branches work synergistically and attempt to remain in balance, the total responses measured tend to look normal in younger patients.

Standard HRV measures from spectral analysis include Low Frequency (LF) and the ratio of low to high frequency (LF/HF). LF is a mixed measure of P&S activity; however, it is assumed to be primarily a measure of Sympathetic activity. Although, the standards articles [5,6] state that the ratio of LF/HF is found to be a better measure of the change in Sympathetic activity with standing than LF alone. Perhaps the thinking is that HF is assumed to measure Parasympathetic activity, and therefore will yield a more pure measure of Sympathetic activity from the ratio, LF/HF, by dividing out some of the Parasympathetic activity. In fact, HF is a mixed measure of Parasympathetic activity and noise, when the respiratory frequency is high enough; otherwise, it is just noise. [4]

P&S Monitoring enables a direct measure of SW. Some of the symptoms of the typical EDSh patient are: 1) diffuse pain, especially in the shoulders, upper back, and inter-scapular area; 2) shortness of breath and palpitations; 3) inability to stand for long periods of time without lightheadedness or dizziness, often with a history of fainting or near-fainting, and oftentimes needing to lie down when trying to stand for periods of time; 4) extreme tiredness or persistent fatigue (that does not necessarily qualify as chronic fatigue syndrome); 5) sleep difficulties and difficulty getting going in the morning; 6) brain fog or memory and cognitive difficulties; 7) frequent headache or migraine; 8) edema of the legs, ankles, and feet; and 9) sensitivity to bright light or sound. All of these may be explained by poor cerebral perfusion due to OD, caused or contributed to by SW.

The diffuse pain in areas above the heart may be a result of poor perfusion of any structure above the heart. Shortness of breath and palpitations may be a result of poor cardiac perfusion or poor cerebral perfusion leading to the brain releasing adrenaline to stimulate the heart, or both. Of course, lightheadedness is caused by poor cerebral perfusion (including Cranial Nerves), and so dizziness may be due to either or both central vestibular degradation due to poor cerebral perfusion or peripheral vestibular degradation due to poor perfusion above the heart. The inability to stand for long periods of time may be a combination of edema and associated pain in the lower extremities and lightheadedness.

The extreme tiredness or fatigue symptoms, which mimic depression-like symptoms is a direct result of poor cerebral perfusion. In fact, many patients also report bouts of anxiety-like symptoms with the feelings of fatigue and depression. This may be explained by the “adrenaline storms” [13]. The sleep difficulties may be a result of abnormal changes in cerebral perfusion due to SW. For example, while upright (e.g., sitting or standing all day) and due to SW, the brain is only marginally perfused and marginally functional (causing among the others the fatigue). As soon as a supine position is assumed, cerebral perfusion is restored (like falling down after fainting). Now the brain is fully perfused and fully functional. In fact, many patients report being more alert during this time (immediately after lying down in bed) than they were during the day. In effect, the patient’s day and night have been reversed. This leads to difficulty falling asleep, waking frequently during the night (more than twice even to go to the bathroom; the brain is still alert and active), or both. Ultimately, the poor sleep leads to the difficulty getting going in the morning, and compounds the fatigue (and any depression). [14]

Of course, brain fog or memory and cognitive difficulties are a direct result of poor cerebral perfusion, as well as some types of headaches and migraines, and these may also involve sensitivity to bright light or sound. Also, edema of the lower extremities is an obvious result of OH due to SW. Relieving SW helps to relieve the OD, poor cardiac perfusion, and poor cerebral perfusion symptoms associated with SW, in the majority of the cases. [14]