A 70-year-old man with a 10-year history of well-controlled Parkinson disease is brought to the clinic for evaluation of dizziness. He was able to walk 1 mile daily until he developed occasional episodes of dizziness and syncope when standing. His medications include levodopa, carbidopa, and a multivitamin. Seated blood pressure is 120/70 mm Hg with a heart rate of 66/min; standing blood pressure is 89/60 mm Hg with a heart rate of 68/min. Cardiopulmonary examination is normal. Neurologic examination shows mild tremor and bradykinesia. A complete blood count, basic metabolic panel, and ECG are normal. Which of the following is the most likely cause of this patient's dizziness?
Clues to etiology of syncope | ||
Reflex syncope | Vasovagal |
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Situational |
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Carotid hypersensitivity |
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Orthostatic syncope | Medications |
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Hypovolemia |
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Autonomic dysfunction |
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Cardiac syncope | LV outflow obstruction |
|
Ventricular tachycardia |
| |
Conduction impairment* |
| |
*Sick sinus syndrome or advanced atrioventricular block. DM = diabetes mellitus; HD = heart disease; LV = left ventricular. |
Neurogenic orthostatic hypotension (NOH) is a common complication of Parkinson disease and other related neurodegenerative diseases (eg, Lewy body disease, multisystem atrophy), manifesting with lightheadedness or syncope on standing. In the normal state, standing from a seated or supine position triggers arterial baroreceptors to increase sympathetic drive, causing vasoconstriction (which mobilizes pooled venous blood from the legs) and an increase in heart rate (to aid cardiac output). NOH occurs due to autonomic dysfunction that may result from degenerative changes to autonomic ganglia or CNS nuclei; there is impaired release of norepinephrine and consequent failure of vasoconstriction and increased heart rate.
Therefore, like orthostatic hypotension from other causes, NOH leads to a drop in systolic blood pressure ≥20 mm Hg with standing (orthostasis); however, unlike other causes of orthostatic hypotension that occur with an intact autonomic nervous system (eg, hypovolemia), the expected increase in heart rate is absent.
Notably, dopamine agonists used to treat Parkinson disease (eg, levodopa) may further contribute to orthostatic hypotension, possibly due to undesired peripheral activity of dopamine that stimulates vasodilation.
(Choices A and D) Intravascular volume depletion due to primary adrenal insufficiency (PAI) or other causes (eg, reduced oral intake) can cause orthostatic hypotension and syncope. However, PAI is not an expected complication of Parkinson disease and is usually accompanied by electrolyte abnormalities (eg, hyperkalemia, hyponatremia). In addition, an increase in heart rate is expected with orthostasis that is due to hypovolemia.
(Choice C) Carotid sinus hypersensitivity involves an exaggerated vagal response triggered by tactile stimulus of the carotid sinus. Patients often experience syncope with activities such as shaving or putting on a necktie.
(Choice E) Sinus node dysfunction commonly manifests as sick sinus syndrome, a potential cause of syncope. Although the heart rate response is often impaired, vascular autonomic innervation and vasoconstriction are intact, making orthostatic symptoms less prominent with sick sinus syndrome. In addition, suggestive ECG abnormalities (eg, sinus pauses) are commonly present.
Educational objective:
Autonomic dysfunction is common with Parkinson disease and can lead to neurogenic orthostatic hypotension, with patients experiencing lightheadedness or syncope on standing. The disorder is typically recognized by a ≥20 mm Hg drop in systolic blood pressure with standing and an absence of the expected increase in heart rate.