It’s about clarity. It’s about knowledge. It’s about peace. It’s about reducing suffering by understanding your nervous system.
I will be breaking down research articles, medical exams, and medications into bite size information. These research articles will be focused around the autonomic nervous system. The autonomic nervous system (ANS) is the system in your body that takes care of unconscious functions such as your cardiovascular system, digestion, sweating etc. The ANS is involved with many co-morbidities because of its integral nature in the functions of the body and its involvement with the immune system. It’s a field that few specialize in and leads to the patients being referred to numerous specialties. It is a source of confusion for patients and doctors.
My hope is through this reduction in confusion will help you navigate your own medical journey. I want you to become your best advocate in the medical industry. I also look forward to learning about new research areas and expanding my own understanding of the nervous system from my readers.
In our previous post, we discussed the overall structure of the autonomic nervous system and how it interacts with the endocrine system to stimulate the cardiovascular system. In this post, we will be discussing what sensors or receptors are present in the peripheral nervous system and how this contributes to the variation in symptoms of dysautonomia.
In the above diagram, we have discussed, in previous posts, the distinctions of the central nervous system, somatic (motor) nervous system, and the autonomic nervous system. In this post, we will be discussing the sensory nervous system, or afferent. The red arrows above show how the signal exits the central nervous system and the blue arrows indicate how sensory and autonomic nerves arrive back to the central nervous system.
Both the sensory and autonomic nerves are categorized under the same type of fiber – the group C fiber or small fiber nerves. The group C fibers sensations are burning (like a sunburn), warmth, itching (like bug bites), light touch (like a feather brushed against your skin), and muscle cramping or burning. The group C fibers also are responsible for gut (or gastrointestinal function), heart rate, blood pressure, and sweating.
The symptoms of dysautonomia do not seem random nor exaggerated when you understand the nerve endings involved with the autonomic nervous system. Let’s take a look.
C-Fiber Nerves of the Peripheral Nervous System
If these C-fiber nerves malfunction, this results in painful sensations without painful stimuli
C fiber nociceptors
Responsible for the burning pain (like sunburn, or placing your finger on a hot item)
C fiber warming receptors
Responsible for warmth (like detecting the warmth of water)
C fiber for ultra-slow histamine-selective receptors
Responsible for itch (like itching sensation after a bug bite)
C fibers tactile receptors
Responsible for tactile sensations (like a feather being rubbed against you or a pet rubbing up against your leg)
C mechano- and metabo- receptors in muscles or joints
Responsible for muscle exercise, burn and cramp
Aδ Nerves of the Peripheral Nervous System
Group A-delta nociceptor
For acute cold, pressure and pain signals
The nerve fiber is myelinated or “insulated” to transmit messages quicker than C fibers for the main purpose of recoiling from sharp pain such as placing a finger on a hot item. This is called the withdrawal reflex and is not actively thought about during the action.
The autonomic nerves that extend from the central nervous system in the spinal cord are the C group fibers and extend all the way down into the skin. Please take note of the free nerve endings labelled with an A and the group C sensory cell as these are the unencapsulated nerve fibers.
UNENCAPSULATED NEVE ENDINGS are sensory dendrites that are not wrapped in connective tissue. For instance, hair recptors, merkel receptors and free nerve endings. These are group A-delta and group C fibers.
ENCAPSULATED NERVE ENDINGS are nerve fibres wrapped in connective tissue. They insulated for transmission speed. These are not either A-delta fibers or group C fibers.
Now that we have a better understanding of the structure and where these small fiber nerves / Group C fibers originate and reside, we can now discuss what the implications of a dysfunction in these nerve fibers looks like. Let’s here what a clinician and neurologist in this speciality is looking for, Dr. Oaklander.
What about small fibers? “Physicians are only now learning the wide range of symptoms that small-fiber polyneuropathy can cause. Sensory symptoms include everything from severe burning pain to chronic itch,” Dr. Oaklander says. Symptoms of autonomic small-fiber neuropathy are less likely to be recognized, notes Dr. Oaklander, so they are often chalked up to other conditions. “For example,” she says, “neuropathy of the autonomic nerves to the heart or blood vessels can cause low blood pressure, perceived as chronic fatigue and faintness or dizziness. Damage to nerve fibers serving the gastrointestinal tract may cause bloating, nausea, digestion problems, constipation, or diarrhea; these are often labeled as irritable bowel syndrome.
In our previous post, we talked about the prevalent attitude in the medical community to dismiss patients suffering from invisible illnesses and in particular those with dysautonomia or POTS. We’ve shown that it is not a problem to dismiss and is a valid, serious condition. In our last post, we explained the structure of the autonomic nervous system in relation to other nervous systems in the human body. In this post we’d like to discuss the interconnection between the endocrine system and the autonomic nervous system and how that results in communication with the neurotransmitters. Neurotransmitters are particularly helpful in regulating blood or perfusion to the extremities.
The autonomic nervous system stimulating the adrenal gland atop the kidney. The hormones stimulated from the adrenal gland are circulated in the blood vessels to later be picked back up by the autonomic nerves attached to the vascular smooth muscles.
We know from the previous post, What is the ANS?, we know that the vagus nerve that runs along the spinal cord either directly reaches out to the organ or passes through it. This is how the sympathetic nervous system of the ANS directly stimulates the adrenal gland or other endocrine glands.
The complex part of the autonomic system occurs at the peripheral nervous system receptors. The key management between the autonomic nervous system and the endocrine system is from the hypothalamus. It receives information from the vagus nerve and peripheral nervous system and secretes the necessary hormones to keep the body in balance or homeostasis.
The nor-epinephrine, or noradrenalin, is a reaction to a stimulus (e.g. standing up) and is created and released from the receptors as a result of the stimulation. The nor-epinephrine is released at the axon via enzyme conversion process of tyrosine in the cytoplasm to nor-epinephrine. This uptake of nor-epinephrine at the axon creates the vasoconstriction of the vascular smooth muscle. The vasoconstriction results in blood pressure regulation.
” The cardiovascular system is controlled and influenced by not only a unique intrinsic conduction system, but is also heavily influenced by the autonomic nervous system as well as the endocrine system. “
Autonomic and endocrine control of cardiovascular function World J Cardiol. 2015 Apr 26; 7(4): 204–214.
This interconnection between the autonomic and endocrine system and the resulting feedback loop has a large part to play in the dysfunction of the autonomic nervous system or dysautonomia. In the below diagram for the “autonomic efferent pathway”, we have the spinal cord, the peripheral autonomic nervous system (with “insulated” / myelinated and “noninsulated” nerves) and the receptor transmitting to the vascular smooth muscle. The axon highlighted in the top right-hand corner shows the release of nor-epinephrine to the vascular smooth muscle to cause vasodilation at low levels and at high levels causes vasoconstriction. What is unknown about dysautonomia, is why blood levels of nor-epinephrine are quite high but vasoconstriction does not occur.
“In addition to the ANS, cardiovascular function is also influenced by numerous endocrine hormones. Released from the adrenal gland, epinephrine and dopamine (and ultimately, norepinephrine) are all involved in the initiation of the “fight-or-flight” response, while vasopressin, renin, angiotensin, aldosterone, and atrial-natriuretic peptide are all involved in water reabsorption for the purpose of blood pressure regulation.”
Autonomic and endocrine control of cardiovascular function World J Cardiol. 2015 Apr 26; 7(4): 204–214.
Also take note, that adrenaline is circulated through the cardiovascular system from the excretion from the adrenal gland. The adrenal gland is stimulated as a secondary effect from the autonomic nervous system as well. Once the body is stimulated by a “flight or fight” stimulus (such as a bear or other terrifying scenario), the autonomic nervous system relays signals to the hypothalamus, which signals the adrenal gland to release stress hormones.
The central nervous system and muscular system are far simpler, than the multiple systemic reactions occurring in the autonomic nervous system.
In our last post, we talked about the prevalent attitude in the medical community to dismiss patients suffering from invisible illnesses and in particular those with dysautonomia or POTS. We’ve shown that it is not a problem to dismiss and is a valid and serious condition. Before we go into the specifics of what dysautonomia is we need to understand the complex and integrate structure of the autonomic nervous system (ANS). So what is the ANS?
To understand what the autonomic nervous system is, we must first distinguish it from the central nervous system (CNS). The distinction between the CNS and peripheral nervous system is human categorization based on differing functionality between the CNS and peripheral. The only physical separation is where the vagus nerve and the spinal cord are connected at the base of the brain stem. The peripheral nervous system, functions differently in comparison to the CNS, is connected directly to the spinal cord.
The CNS is the spinal cord and brain highlighted in gold in the above image. The vagus nerve is highlighted in green. The peripheral nervous system is highlighted in blue which is the somatic nervous system and the autonomic peripheral nervous system. Somatic is the peripheral nerves in the extremities that send messages to the voluntary muscles as well senses (such as temperature, touch, pain, vibration, and spatial reference).The vagus sends messages to and from all of the involuntary functions of the body (such as the organs and glands).
“Most of the ganglia for the sympathetic division are located just outside the spinal cord on both sides of it. The ganglia for the parasympathetic division are located near or in the organs they connect with.”
Ever heard a doctor say to you, “It’s all in your head”, “You’re just anxious”, or “You’re just stressed from family life.”
Thinking back on these comments it makes me feel isolated and hopeless. Who is going to help me? Who is going to help me if not one of the heads of neurology in a leading university?
The aloneness and despair are a lie. I am not alone. There are many who have come before me and many who came after me that had legitimate health issues. They too were not respected or believed. I have met many well educated, respected and empathetic autonomic specialists. There is no need for despair.
We can not talk about the autonomic nervous system without talking about the Great Dismissiveness in the medical community for invisible illnesses.
Dr. Satish Raj, an autonomic specialist who diagnosed me, partners with Vanderbilt and developed his own autonomic clinic in Calgary, CA, completed a small study of 21 POTS patients in 2010. He analyzed this small cohort against a control and showed that POTS patients are less anxious than the general population. He also noted that POTS patients “do not have excess cognitive anxiety” (DOI: 10.1136). POTS patient test high in anxiety with the Beck Anxiety Inventory [BAI] but reported low anxiety with Anxiety Sensitivity Index [ASI] there was no significant correlation between length of illness and BAI score” (DOI: 10.1136)
The author theorizes that the differences in the final results from the psychological exams are to do measuring of somatic symptoms. “A major difference between the BAI and ASI is that the former measures both somatic symptoms and subjective anxiety and panic symptoms on factor analysis, while the latter measures sensitivity to anxiety-provoking stimuli but not somatic symptoms.” (DOI: 10.1136)
Dr. Khurana also completed a study of POTS patients showing that, “Individual symptoms analysis revealed that significant increase in scores was limited to the somatic symptoms of palpitations, dyspnea, and twitching or trembling. In conclusion, the symptoms of POTS are phenomenologically different and clinically distinguishable from panic disorder symptoms.” (DOI: 10.1007)
Dr. also states, “These results suggest that the HR response to orthostatic stress in POTS patients is not caused by anxiety but that it is a physiological response that maintains arterial pressure during venous pooling.” (DOI: 10.1152)
References:
Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome.
Nervana 