If you experience rapid heart rate when standing, dizziness that makes daily activities difficult, crashes after minimal exertion, or temperature regulation problems—and your doctors have told you it is anxiety, panic disorder, or deconditioning—you may be experiencing autonomic dysfunction in Lyme disease.
The autonomic nervous system controls the unconscious functions that keep your body stable: heart rate, blood pressure, digestion, temperature regulation, and breathing. When Lyme disease affects the autonomic nervous system, patients develop genuine physiological dysfunction—not psychological symptoms.
This is one of the most commonly dismissed manifestations of Lyme disease. Patients are told they are anxious, deconditioned, or imagining their symptoms. They are prescribed antidepressants or referred to psychiatry when what they need is recognition that their autonomic nervous system is not functioning properly.
In my practice, I have seen autonomic dysfunction in hundreds of patients. It is not rare. It is not psychiatric. And it deserves investigation and treatment—not dismissal.
What Is Autonomic Dysfunction?
The autonomic nervous system has two main divisions: the sympathetic nervous system (which activates the “fight or flight” response) and the parasympathetic nervous system (which promotes “rest and digest” functions). These systems work together to maintain balance in heart rate, blood pressure, digestion, temperature, and other unconscious processes.
When the autonomic nervous system is disrupted, this balance is lost. Patients may experience inappropriate heart rate increases, blood pressure instability, temperature dysregulation, digestive dysfunction, or difficulty maintaining consciousness when upright.
In Lyme disease, autonomic dysfunction can result from direct infection of autonomic nerve fibers, neuroinflammation affecting autonomic pathways, immune-mediated damage to autonomic ganglia, or disruption of signaling between the brain and autonomic centers.
The result is a constellation of symptoms that are physiological—not psychological—but are frequently misattributed to anxiety because they involve heart rate, breathing, and dizziness.
POTS: Postural Orthostatic Tachycardia Syndrome
One of the most common forms of autonomic dysfunction in Lyme disease is postural orthostatic tachycardia syndrome, or POTS. POTS is defined by an excessive increase in heart rate when moving from lying down to standing—typically an increase of 30 beats per minute or more within 10 minutes of standing.
Patients with POTS describe feeling lightheaded, dizzy, or faint when standing. Some experience palpitations, chest discomfort, or difficulty concentrating. Many find that prolonged standing—such as waiting in line or standing to cook a meal—becomes intolerable.
POTS is not caused by anxiety, even though anxiety can worsen the symptoms. It is caused by failure of the autonomic nervous system to properly regulate blood flow and heart rate when the body changes position.
In Lyme disease, POTS may develop during active infection or persist after antibiotic treatment. It can be one of the most disabling symptoms patients experience, yet it is frequently dismissed as deconditioning or panic disorder.
Proper diagnosis requires measuring heart rate and blood pressure changes during a standing test or tilt table test. Treatment may include increased fluid and salt intake, compression garments, medications to support blood pressure or heart rate control, and addressing the underlying infection or inflammation.
Temperature Dysregulation and Sweating Abnormalities
Another manifestation of autonomic dysfunction in Lyme disease is difficulty regulating body temperature. Patients describe feeling too hot or too cold regardless of the environment, sudden episodes of drenching sweats (especially at night), or inability to tolerate temperature changes.
The autonomic nervous system controls sweating, shivering, and blood vessel dilation or constriction to maintain stable body temperature. When these mechanisms fail, patients experience temperature instability that can be profoundly uncomfortable.
Night sweats are particularly common in Lyme disease and may be related to autonomic dysfunction, immune activation, or co-infections such as Babesia. Patients often soak through sheets and clothing, disrupting sleep and contributing to fatigue.
Temperature dysregulation is rarely recognized as a sign of autonomic dysfunction. Instead, patients are told it is related to hormones, anxiety, or normal aging—when in fact it reflects genuine neurologic dysfunction.
Crashes After Activity: Post-Exertional Malaise
Many patients with autonomic dysfunction experience what is sometimes called post-exertional malaise—a worsening of symptoms after physical or cognitive activity that is disproportionate to the level of exertion.
This is not simple fatigue. It is a physiological crash that can include worsening brain fog, increased pain, profound exhaustion, dizziness, nausea, and difficulty functioning. The crash may occur hours or even a day after the triggering activity, making the connection less obvious.
Post-exertional malaise reflects autonomic dysfunction, mitochondrial impairment, or immune activation triggered by activity. It is not deconditioning—in fact, pushing through the symptoms typically makes them worse rather than better.
Patients are often told that exercise will help them regain function, but standard exercise recommendations can be harmful when autonomic dysfunction is present. Instead, activity must be carefully paced and gradually increased based on the patient’s tolerance.
Why Autonomic Dysfunction Is Dismissed as Anxiety
Autonomic dysfunction produces symptoms that overlap with anxiety: rapid heart rate, shortness of breath, dizziness, chest discomfort, and difficulty concentrating. When physicians see these symptoms—especially in the absence of obvious cardiac or pulmonary disease—the default explanation is often anxiety or panic disorder.
The problem is that the cause-and-effect relationship is backward. Patients are not anxious because they have a psychiatric condition—they feel anxious because their autonomic nervous system is malfunctioning, producing physical sensations that the brain interprets as distress.
This misattribution leads to inappropriate treatment. Patients are prescribed antidepressants or anti-anxiety medications when what they need is evaluation and treatment of the underlying autonomic dysfunction and infection.
I have seen many patients whose symptoms were attributed to anxiety for years before autonomic dysfunction was recognized. Once the correct diagnosis is made and treatment is directed at the autonomic and infectious components, symptoms improve—sometimes dramatically.
The Role of Neuroinflammation
One of the mechanisms by which Lyme disease causes autonomic dysfunction is through neuroinflammation—inflammation affecting the nervous system. Borrelia burgdorferi can invade the central and peripheral nervous systems, triggering immune responses that damage nerve fibers and disrupt signaling.
Autonomic nerve fibers are particularly vulnerable to this process. When inflammation affects the autonomic ganglia (clusters of autonomic nerve cells) or the pathways connecting the brain to autonomic centers, the result is dysregulation of heart rate, blood pressure, digestion, and temperature control.
Neuroinflammation can persist even after antibiotics have reduced bacterial load, contributing to ongoing autonomic symptoms. This is one reason why some patients continue to experience autonomic dysfunction after treatment—the inflammatory process may outlast the active infection.
Addressing neuroinflammation may require extended antimicrobial therapy, immune modulation, or supportive treatments targeting the autonomic nervous system.
Clinical Takeaways
Autonomic dysfunction in Lyme disease reflects genuine physiological malfunction of the autonomic nervous system caused by infection, neuroinflammation, or immune dysregulation. Common manifestations include POTS with excessive heart rate increases when standing, temperature dysregulation with night sweats or heat intolerance, crashes after minimal activity, and dizziness often dismissed as anxiety. These symptoms overlap with anxiety disorders—rapid heart rate, shortness of breath, chest discomfort—leading physicians to misattribute physiological symptoms to panic disorder when patients feel anxious because their autonomic nervous system is malfunctioning, not the reverse.
Frequently Asked Questions
What is autonomic dysfunction in Lyme disease?
Autonomic dysfunction disrupts heart rate, blood pressure, digestion, and temperature regulation, causing POTS, dizziness, crashes after activity, and temperature problems—often dismissed as anxiety.
How is POTS related to Lyme disease?
POTS (postural orthostatic tachycardia syndrome) causes excessive heart rate increases when standing. Lyme can damage autonomic pathways through direct infection, neuroinflammation, or immune-mediated mechanisms.
Can autonomic dysfunction persist after Lyme treatment?
Yes. Autonomic dysfunction can persist due to ongoing neuroinflammation, immune dysregulation, or inadequately treated infection. Some patients require extended therapy or specific treatments targeting autonomic symptoms.
References
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- Kanjwal K, Saeed B, Karabin B, Kanjwal Y, Grubb BP. Comparative clinical profile of postural orthostatic tachycardia patients with and without joint hypermobility syndrome. Indian Pacing Electrophysiol J. 2010;10(4):173-178.
- Novak P, Felsenstein D, Mao C, Octavien NR, Zubcevik N. Association of small fiber neuropathy and post treatment Lyme disease syndrome. PLoS One. 2019;14(2):e0212222.
- Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease. N Engl J Med. 1990;323(21):1438-1444.
