CAUSE DISTINGUISHES nOH FROM NON-NEUROGENIC ORTHOSTATIC HYPOTENSION

Neurogenic orthostatic hypotension (nOH) is characterized by cause. While patients with nOH may experience symptoms similar to those associated with non-neurogenic orthostatic hypotension, patients with nOH have a neurologic component of the disorder unique to nOH.1-4 Neurodegenerative disorders, such as Parkinson’s disease, may affect the neurologic functions that control the release of norepinephrine.2-6 Norepinephrine is the major neurotransmitter responsible for blood pressure maintenance.5 Symptoms of nOH may manifest as a result of this norepinephrine deficiency.2,5,7

 

Graphic adapted with permission from Horacio Kaufmann.

nOH MAY OCCUR WHEN THE AUTONOMIC NERVOUS SYSTEM RELEASES AN INSUFFICIENT LEVEL OF NOREPINEPHRINE

When a healthy individual stands, approximately 500-1000 mL of blood pools in the lower extremities. The resulting hemodynamic changes trigger a compensatory reflex response of the autonomic nervous system and the release of norepinephrine.5,8,9

In nOH patients, the autonomic nervous system is unable to release an adequate amount of norepinephrine to balance blood pressure upon standing.2,3,5,6 This may lead patients to feel symptomatic when standing up and explains why symptoms improve upon sitting down.2,5,9

A NEURODEGENERATIVE DISORDER CAN DISRUPT BLOOD PRESSURE REGULATION

Neurodegenerative disorders tend to disrupt the autonomic nervous system, resulting in many patients with Parkinson’s disease, multiple system atrophy, and pure autonomic failure to also experience symptoms of nOH.2,3,6,10,11  While the morning may be especially problematic for patients experiencing symptoms of nOH, patients may experience blood pressure drops throughout the day.2,6,9,12 Symptoms associated with nOH may appear when a patient’s blood pressure falls below the lower limit of cerebral autoregulation.2,5,12

nOH patients may experience a drop in blood pressure upon standing, but the compensatory increase in heart rate is inadequate. If a symptomatic patient experiences an increase in heart rate less than 15 bpm within 3 minutes, he or she could have nOH. However, an increase of more than 15 bpm within 3 minutes may suggest non-neurogenic orthostatic hypotension.1,2,5,6,14

Orthostatic measurements of blood pressure and heart rate while a patient is supine as well as standing may help identify nOH in at-risk patients.2,14

MEDICAL HISTORY MAY REVEAL WHICH PATIENTS ARE AT RISK FOR nOH

A patient's medical history may help determine if he or she could be at risk for nOH. The following patient groups are at increased risk for nOH1,6,7,9:

  • Patients with unexplained syncope
  • Patients experiencing postural dizziness or nonspecific symptoms that only occur upon standing and diminish upon sitting or lying down
  • Patients with a pre-existing neurodegenerative disorder such as Parkinson’s disease, multiple system atrophy, and pure autonomic failure
  • Elderly patients

MANY nOH PATIENTS MAY ALSO EXPERIENCE SUPINE HYPERTENSION

Up to 70% of patients with nOH will also experience supine hypertension.2,15 The association of supine hypertension with nOH stems from the autonomic deficiency in patients with a neurodegenerative disorder. Patients with autonomic failure lack the normal blood pressure buffering mechanisms that offset both hypo- and hypertension.1,12,16

References: 1. 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. 2. Kaufmann H, Norcliffe-Kaufmann L, Palma JA. Droxidopa in neurogenic orthostatic hypotension. Expert Rev Cardiovasc Ther. 2015;13(8):875-891. 3. 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. 4. Goldstein DS, Sharabi Y. Neurogenic orthostatic hypotension: a pathophysiological approach. Circulation. 2009;119(1):139-146. 5. 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. 6. Low PA. Neurogenic orthostatic hypotension: pathophysiology and diagnosis. Am J Manag Care. 2015;21(suppl 13):s248-s257. 7. Kaufmann H, Malamut R, Norcliffe-Kaufmann L, et al. The Orthostatic Hypotension Questionnaire (OHQ): validation of a novel symptom assessment scale. Clin Auton Res. 2012;22(2):79-90. 8. Robertson D. The pathophysiology and diagnosis of orthostatic hypotension. Clin Auton Res. 2008;18(suppl 1):s2-s7. 9. Freeman R. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358(6):615-624. 10. Ha AD, Brown CH, York MK, et al. The prevalence of symptomatic orthostatic hypotension in patients with Parkinson’s disease and atypical parkinsonism. Parkinsonism Relat Disord. 2011;17(8):625-628. 11. Kaufmann H. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure and multiple system atrophy. Clin Auton Res. 1996;6(2):125-126. 12. Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008;7(5):451-458. 13. Naschitz JE, Rosner I. Orthostatic hypotension: framework of the syndrome. Postgrad Med J. 2007;83(983):568-574. 14. Shibao C, Lipsitz LA, Biaggioni I. Evaluation and treatment of orthostatic hypotension. J Am Soc Hypertens. 2013;7(4):317-324. 15. Berganzo K, Diez-Arrola B, Tijero B, et al. Nocturnal hypertension and dysautonomia in patients with Parkinson’s disease: are they related? J Neurol. 2013;260(7):1752-1756. 16. Naschitz JE, Slobodin G, Elias N, et al. The patient with supine hypertension and orthostatic hypotension: a clinical dilemma. Postgrad Med J. 2006;82(966):246-253.