24×7 Emergency Care

1-8-31/1, Minister Road, Secunderabad, Telangana 500003

EMERGENCY:Severe fainting with injury, autonomic dysreflexia, or suspected autonomic crisis —call040-46324365immediately — 24 hours, 7 days— 24/7

AUTONOMIC NERVOUS SYSTEM DISORDERS

Dysautonomia — Autonomic Nervous System Specialist in Hyderabad at KIMS

Q: I am a 28-year-old woman and have been dizzy and exhausted every time I stand up for the past 6 months. My heart races and I feel like I am going to faint. Multiple doctors have told me it is anxiety. Could this be POTS?

Yes — POTS is frequently misdiagnosed as anxiety, panic disorder, or psychosomatic illness, particularly in young women. The symptoms of POTS (palpitations, dizziness, sweating, breathlessness, and a sense of impending doom on standing) can closely mimic anxiety. The key distinction: POTS symptoms are consistently triggered by standing and relieved by lying down — anxiety symptoms are not consistently postural. A simple bedside test: measure your heart rate lying down, then measure it again after 10 minutes of standing. If it rises by 30 beats per minute or more, POTS is likely. The gold standard is a tilt table test at KIMS. POTS is a real physiological disorder of autonomic function — not anxiety — and it responds to specific treatments. On average, patients with POTS wait 4–6 years for a diagnosis in many countries — please do not wait that long. Call 040-44885000 and ask for an autonomic function assessment.

Q: My father with Parkinson's disease gets very dizzy and almost faints when he stands up from his chair every morning. His blood pressure drops significantly on standing. What is causing this and how can it be managed?

Orthostatic hypotension (OH) — a significant fall in blood pressure on standing — is one of the most disabling autonomic complications of Parkinson's disease, and one of the most common causes of falls in PD patients. It results from autonomic failure (Lewy body deposition in sympathetic ganglia impairing the normal reflex vasoconstriction that maintains blood pressure on standing). It is often worsened by anti-Parkinson medications (levodopa, dopamine agonists) and antihypertensives. The management at KIMS: (1) Review all medications for those worsening OH (reduce antihypertensives, adjust PD medications if possible) · (2) Non-pharmacological: 2–3 litres fluid + 6–10g salt/day, head-of-bed elevation 30°, compression stockings, avoiding big meals and hot environments · (3) Midodrine 2.5–5 mg TDS (alpha-agonist) · (4) Droxidopa (a noradrenaline precursor, where available) for neurogenic OH in PD. 24-hour ambulatory BP monitoring at KIMS characterises the OH pattern and guides treatment. Call 040-44885000.

Q: I had COVID-19 four months ago and since then have been unable to stand for more than a few minutes without feeling dizzy, my heart racing, and my brain feeling completely foggy. Could this be related to COVID?

Yes — what you are describing is consistent with post-COVID POTS, which is now one of the most common neurological sequelae of COVID-19. The combination of palpitations, dizziness, and cognitive fog ("brain fog") that is triggered or worsened by standing, in someone who was previously well and has not recovered 4+ months after acute COVID, is a recognised post-COVID autonomic syndrome. The mechanism appears to involve autoimmune-mediated small fibre neuropathy + autonomic dysfunction, possibly triggered by the immune response to SARS-CoV-2 spike protein. The tilt table test at KIMS will confirm the POTS diagnosis. Treatment is the same as for POTS from other causes: structured exercise rehabilitation (the most important), increased salt and fluid intake, compression garments, and medications if needed. Most patients with post-COVID POTS improve significantly over 6–18 months with appropriate management. Call 040-44885000.

Q: My husband has had diabetes for 20 years. He has started getting dizzy when he stands and has been having stomach problems — feeling full quickly and feeling sick after meals. Could these both be from the diabetes?

Yes — both of these problems — orthostatic hypotension (dizziness on standing) and gastroparesis (early satiety and nausea from delayed stomach emptying) — are classic features of diabetic autonomic neuropathy, which affects 30–50% of people with long-duration diabetes. After 20 years of diabetes, the small autonomic nerve fibres that control the cardiovascular system, the gut, the bladder, and the sweat glands are significantly damaged by chronic hyperglycaemia. The autonomic function battery at KIMS will characterise the full extent of the autonomic damage. For the orthostatic hypotension: midodrine + fluids + compression stockings. For the gastroparesis: domperidone or metoclopramide before meals · small, low-fat, low-fibre, frequent meals · liquid or semi-solid meals when symptoms are worst · optimise glucose control (gastroparesis makes glucose management very difficult and erratic). Most importantly: the best intervention is now optimising his glucose control to prevent further autonomic nerve damage. Call 040-44885000.

Dysautonomia is a broad term referring to any dysfunction of the autonomic nervous system — the system that controls automatic body functions including heart rate, blood pressure, sweating, digestion, bladder control, and temperature regulation. Because the autonomic nervous system governs so many body functions simultaneously, dysautonomia produces a constellation of symptoms that span multiple organ systems and that often seem unrelated: dizziness on standing, palpitations, fainting, abnormal sweating (too much or too little), nausea, constipation or diarrhoea, urinary urgency or retention, sexual dysfunction, and temperature intolerance.

View Our Specialists

Dysautonomia is any dysfunction of the autonomic nervous system (ANS) — the involuntary control of heart rate, blood pressure, sweating, digestion, bladder, and temperature. Because the ANS governs many organ systems simultaneously, dysautonomia produces multi-system symptoms that often seem unrelated. POTS (Postural Orthostatic Tachycardia Syndrome): defined by a heart rate rise of ≥30 bpm (≥40 bpm in under-19s) within 10 minutes of standing, without significant orthostatic hypotension. Predominantly affects young women (4–5:1 female:male ratio). Four subtypes: hypovolaemic, neuropathic (small fibre autonomic neuropathy), hyperadrenergic, secondary (EDS, MCAS, autoimmune). Post-COVID POTS increasingly recognised. Orthostatic hypotension (OH): sustained BP fall ≥20/10 mmHg within 3 minutes of standing; coat hanger neck/trapezius pain is OH-specific. Diabetic autonomic neuropathy: 30–50% of long-duration diabetics; erectile dysfunction earliest symptom (5+ years before others). Treatment: fluid + salt loading, compression, exercise, fludrocortisone, midodrine, ivabradine (hyperadrenergic POTS), pyridostigmine (neuropathic POTS). Diagnosis at KIMS: tilt table test + full autonomic battery + QSART + skin biopsy for small fibre neuropathy.

POTS vs OH — the defining distinction: POTS: HR rises ≥30 bpm (teens: ≥40 bpm) within 10 minutes of standing, WITHOUT a significant BP fall (≥20/10 mmHg). The heart compensates for inadequate leg venous return by racing, but BP is maintained. OH: BP FALLS ≥20/10 mmHg within 3 minutes of standing, with or without compensatory HR rise. In neurogenic OH (autonomic failure), the HR does not rise appropriately despite the BP fall. This distinction determines treatment (ivabradine for POTS tachycardia; midodrine for OH vasoconstriction).
Four POTS subtypes — mechanism determines medication: Hypovolaemic: low blood volume; salt/fluid loading + fludrocortisone. Neuropathic: small fibre autonomic neuropathy; pyridostigmine (AChE inhibitor). Hyperadrenergic: elevated noradrenaline on standing; ivabradine (HCN4 inhibitor reduces HR without reducing BP) or low-dose propranolol — low-dose beta-blockers can improve tachycardia and symptoms in selected patients; ivabradine preferred when HR reduction without BP reduction is needed. Secondary: underlying cause (EDS, mast cell activation syndrome, autoimmune); treat the underlying cause.
Ivabradine — preferred in hyperadrenergic POTS: Ivabradine inhibits the HCN4 (funny current) channel in the sinoatrial node, reducing heart rate without affecting blood pressure — unlike beta-blockers, which reduce both HR and BP. In hyperadrenergic POTS, ivabradine is preferred as it selectively reduces HR without lowering BP — unlike beta-blockers, which also reduce BP. Low-dose propranolol is a valid alternative in selected patients and can improve symptoms and tachycardia; the choice depends on individual BP response and tolerance. Dose: 5–10 mg BD, titrated to effect.
Diabetic autonomic neuropathy — the India-first presentation: With 101 million diabetics in India, diabetic autonomic neuropathy is the most common cause of autonomic dysfunction in Hyderabad. Cardiovascular (resting tachycardia, silent MI), GI (gastroparesis), genitourinary (neurogenic bladder; erectile dysfunction the EARLIEST autonomic symptom in diabetic males, preceding other features by 5+ years), sudomotor (gustatory sweating pathognomonic for diabetic AN, distal anhidrosis with compensatory proximal hyperhidrosis).
QSART — pattern of sweat loss diagnoses the cause: Quantitative sudomotor axon reflex test measures sweat output at 4 standard sites in response to acetylcholine. Length-dependent loss (feet most affected) = diabetic or length-dependent peripheral neuropathy. Patchy, non-length-dependent loss = autoimmune autonomic neuropathy or paraneoplastic process. Absent output = severe sudomotor failure (MSA, pure autonomic failure).
Midodrine at night — the supine hypertension risk: Midodrine (alpha-1 agonist) should NEVER be taken within 4 hours of bedtime or lying down. Midodrine taken at night in a supine patient causes supine hypertension. Take the morning dose immediately before getting up, take the afternoon dose by 4–6pm at the latest, never take it at night.
Post-COVID POTS — the post-pandemic dysautonomia: Post-COVID POTS is now one of the most common post-COVID neurological sequelae. Mechanism: autoimmune-mediated small fibre neuropathy + venous pooling from physical deconditioning during prolonged bedrest. Tilt table test confirms POTS. Skin biopsy for small fibre neuropathy. Treatment follows the standard POTS protocol with emphasis on graded exercise rehabilitation (most important).

Fact	Details
POTS definition	HR ≥30 bpm (≥40 bpm <19 years) within 10 min of standing · WITHOUT BP fall ≥20/10 mmHg · Symptoms: palpitations, dizziness, fatigue, fog
POTS: 4:1 female:male ratio	Average diagnosis delay 4–6 years · Frequently misdiagnosed as anxiety · Postural triggers distinguish from pure anxiety
OH definition	BP fall ≥20/10 mmHg within 3 min of standing · Coat hanger pain (neck/trapezius) = OH-specific · Neurogenic OH: HR fails to rise appropriately
Diabetic AN	30–50% of long-duration diabetics · Erectile dysfunction EARLIEST symptom (5+ years before others) · Gustatory sweating pathognomonic · Silent MI
Key medications	Ivabradine: HCN4 inhibitor, for hyperadrenergic POTS · Pyridostigmine: neuropathic POTS + neurogenic OH · Midodrine: NOT at night (supine hypertension) · Fludrocortisone: expands plasma volume
Testing at KIMS	Tilt table test (POTS + OH) · Autonomic battery (HRV, Valsalva, 30:15 ratio) · QSART (sweat pattern) · Skin biopsy for small fibre neuropathy · 24-hour ABPM
Emergency	Severe fainting with injury · Autonomic dysreflexia · Suspected autonomic crisis · 040-46324365 (24/7)

About This Condition

Dysautonomia at a Glance

POTS definition

Heart rate rise ≥30 bpm (≥40 bpm in under 19 years) within 10 minutes of standing, without orthostatic hypotension · Symptoms: palpitations, dizziness, lightheadedness, fatigue, cognitive fog.

Orthostatic hypotension (OH)

Sustained fall in systolic BP ≥20 mmHg or diastolic BP ≥10 mmHg within 3 minutes of standing · Causes: dehydration, medications, Parkinson's, MSA, diabetes, amyloidosis.

Pure autonomic failure (PAF)

Isolated progressive autonomic failure without parkinsonism or cerebellar features · Lewy body pathology · May evolve to PD or MSA over years.

Autonomic neuropathy causes (India)

Diabetes (most common: affects 30–50% of long-duration diabetics) · Amyloidosis · Sjögren's · Autoimmune (anti-ganglionic AChR antibodies) · Paraneoplastic (anti-Hu) · Hereditary (ATTR amyloidosis · Fabry disease).

Sweat dysfunction

Anhidrosis (no sweating) + compensatory hyperhidrosis elsewhere = a clue to autonomic neuropathy distribution · Tested by QSART + thermoregulatory sweat test at KIMS.

Post-COVID dysautonomia

POTS is one of the most common long COVID neurological sequelae · Mechanism: autoimmune + small fibre neuropathy + venous pooling from deconditioning.

Diagnosis at KIMS

Tilt table test · Autonomic function battery (Valsalva ratio, deep breathing HR variability, cold pressor, sustained handgrip) · QSART · 24-hour ABPM · Skin biopsy for small fibre neuropathy.

India note

Diabetic autonomic neuropathy most common cause · Post-COVID POTS increasing · Hyderabad heat: dysautonomia worsens in summer · Autonomic testing underutilised.

About This Condition

Dysautonomia — The Multi-System Disorder of Automatic Body Function

Dysautonomia is far more common than is generally recognised. POTS (Postural Orthostatic Tachycardia Syndrome) alone affects an estimated 1–3 million people in the USA and is one of the leading causes of chronic disability in young women. Orthostatic hypotension affects up to 30% of adults over 70 and is a major risk factor for falls, syncope, and cardiovascular events. Diabetic autonomic neuropathy — the most common cause of dysautonomia in India given the country's 101 million diabetics — is a leading cause of silent cardiac ischaemia, gastroparesis, and neurogenic bladder.

Autonomic Clinic / Consultation

Speak directly with the KIMS autonomic neurology team — coordinated tilt table testing, autonomic function battery, QSART, skin biopsy for small fibre neuropathy, and individualised pharmacological and rehabilitation planning.

040-44885000Autonomic function assessment line

POTS, Orthostatic Hypotension, and Diabetic Autonomic Neuropathy

The Most Important Forms of Dysautonomia

POTS — the most common dysautonomia in young adults

POTS is defined by a heart rate rise of 30+ bpm (40+ bpm in adolescents) within 10 minutes of standing, in the absence of significant orthostatic hypotension. The symptoms — palpitations, dizziness, lightheadedness, pre-syncope, fatigue, and cognitive fog ("brain fog") — arise because the autonomic nervous system fails to adequately constrict leg veins on standing, causing blood to pool in the legs. The heart compensates with a tachycardia, but cerebral perfusion still falls enough to produce symptoms. POTS predominantly affects young women (female:male ratio 4–5:1) and often follows a viral illness, pregnancy, or prolonged bedrest. Post-COVID POTS has become increasingly recognised since 2020. Four main subtypes reflect different underlying mechanisms: hypovolaemic POTS (low blood volume) · Neuropathic POTS (small fibre autonomic neuropathy reducing leg vasoconstriction) · Hyperadrenergic POTS (elevated noradrenaline on standing) · Secondary POTS (from an identified underlying cause: EDS, mast cell activation syndrome, autoimmune).

Orthostatic hypotension — the blood pressure that falls when you stand

Orthostatic hypotension (OH) is defined as a sustained fall in systolic blood pressure of 20 mmHg or more (or diastolic 10 mmHg or more) within 3 minutes of standing. Unlike POTS, the heart rate does not necessarily rise significantly (in neurogenic OH from autonomic failure, the baroreceptor reflex is impaired and the heart rate fails to compensate appropriately for the BP fall). Symptoms: dizziness, visual greying or blackening, neck pain (coat hanger pattern from trapezius muscle ischaemia), near-fainting or fainting on standing, worsened by morning, by meals, by exercise, and by hot environments. Causes in India: dehydration (common in summer) · Antihypertensives, diuretics, alpha-blockers, antidepressants · Diabetic autonomic neuropathy · Parkinson's disease · Multiple system atrophy · Amyloidosis.

Diabetic autonomic neuropathy — the most prevalent form in India

Diabetic autonomic neuropathy (DAN) affects 30–50% of people with long-duration diabetes and is the most common cause of autonomic dysfunction in India. It results from chronic hyperglycaemia damaging the small unmyelinated autonomic nerve fibres. Clinical manifestations across body systems: cardiovascular — resting tachycardia (HR >100 at rest), orthostatic hypotension, painless (silent) myocardial infarction (autonomic denervation eliminates chest pain), sudden cardiac death · GI — gastroparesis (delayed stomach emptying: early satiety, nausea, vomiting, erratic glucose control), oesophageal dysmotility, constipation alternating with diarrhoea · Genitourinary — neurogenic bladder (failure to empty, recurrent UTIs), erectile dysfunction (earliest autonomic symptom in diabetic males, preceding other manifestations by 5+ years) · Sudomotor — gustatory sweating (sweating triggered by eating) + distal anhidrosis with compensatory proximal hyperhidrosis.

Diagnosis at KIMS

Autonomic Function Testing at KIMS

Tilt table test — the primary test for POTS and OH

The patient lies flat on a motorised table for 20 minutes, then the table tilts to 70–80 degrees from horizontal while continuous ECG (heart rate) and beat-to-beat blood pressure are monitored. POTS: HR rise ≥30 bpm (without significant BP fall) · OH: BP fall ≥20/10 mmHg. Provocation with GTN spray can unmask vasovagal syncope. Duration 45–60 minutes. At KIMS, tilt table testing is performed in the autonomic laboratory with a nurse and neurologist present.

Cardiovascular autonomic function battery

Heart rate variability (HRV) during deep breathing (6 breaths/min): the expiration:inspiration HR ratio (E:I ratio) — reduced in parasympathetic failure · Valsalva ratio: HR response to straining — tests sympathetic and parasympathetic integrity · 30:15 ratio: immediate HR response to standing · Blood pressure response to sustained handgrip (sympathetic adrenergic) · Cold pressor test.

QSART — quantitative sudomotor axon reflex test

Measures sweat output in response to iontophoretically applied acetylcholine at four sites (forearm, proximal and distal leg, foot). Reduced or absent sweat output = sudomotor neuropathy. The pattern of loss (length-dependent: feet most affected = diabetic · Patchy or non-length-dependent = autoimmune or paraneoplastic) guides diagnosis.

Skin punch biopsy for small fibre neuropathy

3 mm skin punch biopsy at the distal leg (10 cm above the lateral malleolus) counts intraepidermal nerve fibre (IENF) density. Reduced IENF density = small fibre neuropathy (SFN) — which affects the small autonomic and pain fibres that are not detected on standard nerve conduction studies. SFN is common in POTS, diabetic autonomic neuropathy, and post-COVID dysautonomia.

Treatment

Management at KIMS

Non-Pharmacological Foundation + Targeted Drug Therapy

Lifestyle Measures, Subtype-Specific Pharmacotherapy, and Diabetic Autonomic Neuropathy Care

Fluid and salt — first-line for POTS and OH: 2–3 litres water + 6–10 g salt per day to expand plasma volume · 300–500 mL cold water bolus before standing reduces OH.

Compression garments: Waist-high graduated compression stockings (30–40 mmHg) + abdominal binder for OH · Reduce venous pooling.

Exercise rehabilitation: Recumbent exercise first (rowing machine, recumbent cycling, swimming) · Gradual progression to upright · 3–5 sessions/week · Exercise is one of the most effective long-term POTS treatments.

Postural manoeuvres: For vasovagal syncope: isometric counter-pressure manoeuvres (hand-clasping, leg-crossing, squatting) at onset of presyncope · Timed water ingestion before situations that provoke OH.

Fludrocortisone: Fludrocortisone 0.05–0.2 mg/day: Mineralocorticoid · Expands plasma volume · First-line for POTS + hypovolaemic OH.

Midodrine: Midodrine 2.5–10 mg TDS: Alpha-1 agonist · Constricts venous capacitance · First-line for neurogenic OH · Do not take at night (supine hypertension).

Ivabradine: Ivabradine 5–10 mg BD: If pacemaker current (HCN4) inhibitor · Reduces HR without reducing BP · Preferred in hyperadrenergic POTS as it reduces HR without lowering BP; low-dose propranolol is an alternative in selected patients.

Propranolol: Propranolol 10–20 mg: Low-dose non-selective beta-blocker · Can be used for POTS with tachycardia including hyperadrenergic subtype in selected patients · Evidence-based at low dose (Raj et al. JACC 2009) · Preferred over atenolol (non-selective β1/β2 blockade) · Avoid in hypovolaemic POTS · Monitor BP response.

Pyridostigmine: Pyridostigmine 30–60 mg TDS: AChE inhibitor · Enhances ganglionic transmission · Particularly useful for neuropathic POTS + neurogenic OH.

Diabetic Autonomic Neuropathy: Tight glucose control (HbA1c <7%) to prevent progression · Gastroparesis: domperidone, metoclopramide, low-fat/low-fibre diet, small frequent meals · Erectile dysfunction: PDE5 inhibitors (sildenafil) · Neurogenic bladder: intermittent self-catheterisation + oxybutynin.

Related Conditions

Dysautonomia belongs to the family of autonomic nervous system disorders evaluated and managed at KIMS Neuroscience. Explore related conditions or return to the hub.

Autonomic Nervous System Disorders Diabetes — Neurological Complications

FAQs

Frequently Asked Questions

Yes — POTS is frequently misdiagnosed as anxiety, panic disorder, or psychosomatic illness, particularly in young women. The symptoms of POTS (palpitations, dizziness, sweating, breathlessness, and a sense of impending doom on standing) can closely mimic anxiety. The key distinction: POTS symptoms are consistently triggered by standing and relieved by lying down — anxiety symptoms are not consistently postural. A simple bedside test: measure your heart rate lying down, then measure it again after 10 minutes of standing. If it rises by 30 beats per minute or more, POTS is likely. The gold standard is a tilt table test at KIMS. POTS is a real physiological disorder of autonomic function — not anxiety — and it responds to specific treatments. On average, patients with POTS wait 4–6 years for a diagnosis in many countries — please do not wait that long. Call 040-44885000 and ask for an autonomic function assessment.

Orthostatic hypotension (OH) — a significant fall in blood pressure on standing — is one of the most disabling autonomic complications of Parkinson's disease, and one of the most common causes of falls in PD patients. It results from autonomic failure (Lewy body deposition in sympathetic ganglia impairing the normal reflex vasoconstriction that maintains blood pressure on standing). It is often worsened by anti-Parkinson medications (levodopa, dopamine agonists) and antihypertensives. The management at KIMS: (1) Review all medications for those worsening OH (reduce antihypertensives, adjust PD medications if possible) · (2) Non-pharmacological: 2–3 litres fluid + 6–10g salt/day, head-of-bed elevation 30°, compression stockings, avoiding big meals and hot environments · (3) Midodrine 2.5–5 mg TDS (alpha-agonist) · (4) Droxidopa (a noradrenaline precursor, where available) for neurogenic OH in PD. 24-hour ambulatory BP monitoring at KIMS characterises the OH pattern and guides treatment. Call 040-44885000.

Yes — what you are describing is consistent with post-COVID POTS, which is now one of the most common neurological sequelae of COVID-19. The combination of palpitations, dizziness, and cognitive fog ("brain fog") that is triggered or worsened by standing, in someone who was previously well and has not recovered 4+ months after acute COVID, is a recognised post-COVID autonomic syndrome. The mechanism appears to involve autoimmune-mediated small fibre neuropathy + autonomic dysfunction, possibly triggered by the immune response to SARS-CoV-2 spike protein. The tilt table test at KIMS will confirm the POTS diagnosis. Treatment is the same as for POTS from other causes: structured exercise rehabilitation (the most important), increased salt and fluid intake, compression garments, and medications if needed. Most patients with post-COVID POTS improve significantly over 6–18 months with appropriate management. Call 040-44885000.

Yes — both of these problems — orthostatic hypotension (dizziness on standing) and gastroparesis (early satiety and nausea from delayed stomach emptying) — are classic features of diabetic autonomic neuropathy, which affects 30–50% of people with long-duration diabetes. After 20 years of diabetes, the small autonomic nerve fibres that control the cardiovascular system, the gut, the bladder, and the sweat glands are significantly damaged by chronic hyperglycaemia. The autonomic function battery at KIMS will characterise the full extent of the autonomic damage. For the orthostatic hypotension: midodrine + fluids + compression stockings. For the gastroparesis: domperidone or metoclopramide before meals · small, low-fat, low-fibre, frequent meals · liquid or semi-solid meals when symptoms are worst · optimise glucose control (gastroparesis makes glucose management very difficult and erratic). Most importantly: the best intervention is now optimising his glucose control to prevent further autonomic nerve damage. Call 040-44885000.

Dizziness every time you stand. A racing heart that is called anxiety. A stomach that will not empty. A diabetic who faints in the Hyderabad heat. Dysautonomia has a name, a test, and a treatment.

At KIMS Hyderabad, the autonomic neurology clinic provides tilt table testing, the full autonomic function battery, and individualised management for every form of dysautonomia. Call 040-44885000.

040-44885000

International enquiries: info@kimsneurosciences.com