Demystifying Common Culprits of "Dizziness"

Lightheadedness. Fatigue. “My vision is spotty.” These symptoms are common issues for patients, especially in the rehab setting. As physical therapists, we often hear these complaints but struggle to pinpoint the physiological cause. When orthostatic intolerance is suspected, three conditions should be on your differential: orthostatic hypotension (OH), neurogenic orthostatic hypotension (nOH), and postural orthostatic tachycardia syndrome (POTS). Understanding their mechanisms and how to differentiate them is critical to ensure safe, effective treatment.

Defining the Big Three: OH, nOH, and POTS

Diagnosing with Tilt Table Testing

TTT is the gold standard for differentiating these disorders in a safe, reproducible environment.

Tilt Table Protocol:

1. Supine rest for 10–20 minutes: Record baseline BP and HR every 1–2 minutes.

2. Tilt to 60–70° for 10–45 minutes: Monitor BP/HR at 1, 3, 5 minutes, then every 5 minutes.

3. Watch for symptoms: Dizziness, nausea, fainting, pallor, or palpitations.

Diagnostic Criteria:

A Closer Look at nOH

nOH is particularly common in individuals with Parkinson’s Disease, Multiple System Atrophy (MSA), spinal cord injuries, diabetic autonomic neuropathy, and pure autonomic failure. It arises from failure of the autonomic nervous system to release enough norepinephrine in response to upright posture, which prevents the normal vasoconstriction needed to maintain blood pressure.

This leads to a dangerous combination of upright hypotension and supine hypertension, which can severely disrupt daily function and therapy participation. Patients often report:

• Fatigue

• Lightheadedness

• “Coat-hanger pain” – aching in the neck and shoulders from poor perfusion of postural muscles

• Syncope or near-syncope

• Falls

Several factors can make nOH s/s worse:

1. Morning Orthostasis: After a night of lying down, fluid redistributes to the central compartment. Upon standing in the morning, gravity pulls that fluid into the lower extremities and splanchnic circulation. In patients with autonomic failure, there’s inadequate vasoconstriction to maintain cerebral perfusion causing sharp BP drops, dizziness, and even collapse shortly after getting out of bed.

2. Postprandial Hypotension: After eating, blood is naturally diverted to the gut (splanchnic vasodilation) to aid digestion. In healthy individuals, systemic vasoconstriction compensates for this shift. In nOH, this compensatory response is blunted or absent, leading to a 30–60 minute drop in blood pressure post-meal, often accompanied by fatigue, dizziness, or even fainting. Patients may describe feeling “wiped out” after eating or may avoid meals before therapy.

3. Heat and Prolonged Standing: Heat causes vasodilation in the skin to cool the body. In patients with nOH, this further reduces vascular resistance and exacerbates orthostatic symptoms. Prolonged standing similarly increases pooling in the lower extremities. Without appropriate autonomic responses, patients can experience progressive hypotension over time, leading to a delayed but severe drop in BP, especially in warm environments or during endurance tasks.

Recognizing and addressing these patterns is key to keeping patients safe and active in therapy.

Non-Pharmacological Treatments

Non-pharmacological management should always be the first-line approach for neurogenic orthostatic hypotension (nOH). It empowers patients to manage symptoms through simple, structured interventions often without the side effects associated with medications. Below are the main strategies, including updated guidance on appropriate exercise intensity for this population:

1. Hydration & Salt Intake

   Goal: Expand plasma volume and improve circulatory stability.

   Target: ≥2–2.5L fluid per day and 2.3–4.6g sodium per day.

   Tips: Use electrolyte drinks or salt tablets. Always consult MD for patients with CHF or renal impairments.

2. Water Bolus

   Protocol: 500 mL cold water consumed rapidly within 5 minutes.

   Effect: Triggers sympathetic activation, raising SBP by ~30 mmHg.

   Use Case: Great just before therapy or ADLs to reduce symptom onset.

3. Compression Garments

   Type: Waist-high compression or abdominal binders (30–40 mmHg).

   Rationale: Helps prevent venous pooling in the splanchnic and lower extremity vessels, improving venous return.

   Note: Knee-high socks are ineffective due to poor adherence and minimal impact on core blood volume.

4. Positional & Movement Strategies

   Head of bed elevation: When sleeping raise HOB 4 inches or ~30° to reduce nocturnal central pooling and supine hypertension.

   Slow transitions: Encourage seated pause before standing, especially after lying down, to reduce orthostatic burden.

5. Therapeutic Exercise: Intensity Matters

   Exercise is a powerful tool for managing nOH, but intensity and modality must be carefully selected. Here's what works best:

Recommended Activities:

• Recumbent cycling or seated rowing: Promotes cardiovascular conditioning without upright stress.

• Mat-based strength training: Core, glutes, and quads.

• Active lower limb exercises (e.g., ankle pumps, leg cross, squats, step-ups): Mimic muscle-pump effects and directly counteract venous pooling.

Pharmacological Management: When Exercise Isn’t Enough

When lifestyle adjustments don’t suffice, medication may be required. Knowing drug peaks, valleys, and side effects helps therapists identify when it’s time to refer back to the MD.

Clinical Red Flags: excessive supine hypertension, new headaches, severe fatigue, or worsening dizziness may indicate overmedication or poor response. If this occurs, then it’s time to refer back.

Parting Thoughts

Dizziness, lightheadedness, and fatigue aren’t just annoying symptoms, they’re clinical clues. Misinterpreting them can delay recovery, cause falls, or lead to poor adherence. Accurate diagnosis and tailored management can transform therapy outcomes.

• Know the difference between OH, nOH, and POTS

• Monitor for subtle cues during mobility and endurance testing

• Titrate exercise based on symptom stability, not just vitals

References:

1. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011;21(2):69-72. doi:10.1007/s10286-011-0119-5

2. Raj SR. Postural tachycardia syndrome (POTS). Circulation. 2013;127(23):2336-2342. doi:10.1161/CIRCULATIONAHA.112.144501

3. Kalra DK, Raina A, Sohal S. Neurogenic Orthostatic Hypotension: State of the Art and Therapeutic Strategies. Clin Med Insights Cardiol. 2020;14:1179546820953415. Published 2020 Aug 30. doi:10.1177/1179546820953415

4. Akiba T, Terayama K, Ogawa A, Teramoto H, Nakajima A. Ankle plantar-dorsal flexion exercises mitigate orthostatic hypotension in patients with neurodegenerative diseases. Int J Rehabil Res. Published online May 6, 2025. doi:10.1097/MRR.0000000000000671

5. Hoxhaj P, Shah S, Muyolema Arce VE, et al. Ampreloxetine Versus Droxidopa in Neurogenic Orthostatic Hypotension: A Comparative Review. Cureus. 2023;15(5):e38907. Published 2023 May 11. doi:10.7759/cureus.38907

6. Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol. 2017;264(8):1567-1582. doi:10.1007/s00415-016-8375-x

7. Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008;7(5):451-458. doi:10.1016/S1474-4422(08)70088-7

8. Isaacson SH, Skettini J. Neurogenic orthostatic hypotension in Parkinson's disease: evaluation, management, and emerging role of droxidopa. Vasc Health Risk Manag. 2014;10:169-176. Published 2014 Apr 3. doi:10.2147/VHRM.S53983

Disclaimer:

I am a current Doctor of Physical Therapy (DPT) student sharing information based on my formal education and independent studies. The content presented in this newsletter is intended for informational and educational purposes only and should not be considered professional medical advice. While I strive to provide accurate and up-to-date information, my knowledge is based on my current academic and clinical rotations and ongoing learning, not extensive clinical practice.