Orthostatic dizziness is feeling dizzy or lightheaded when standing up. Hemodynamic orthostatic dizziness can be caused by autonomic dysfunction such as orthostatic hypotension or postural tachycardia syndrome. The interpretation of the autonomic function test results in patients with orthostatic dizziness is crucial for diagnosing and managing the underlying condition. The head-up tilt and Valsalva tests are especially important for evaluating adrenergic function in patients with hemodynamic orthostatic dizziness. However, it is important to note that autonomic function tests do not cover the entire diagnostic process, since their findings need to be considered along with the detailed history and physical examination results of the patient because various differential diagnoses exist for orthostatic dizziness. Ensuring appropriate treatment by interpreting the autonomic function test results can help to determine the improvement of and prevents falls from orthostatic dizziness.

This paper introduces new diagnostic criteria and differential diagnosis of orthostatic dizziness to help clinicians to diagnose hemodynamic orthostatic dizziness. Clinicians need to be able to discriminate hemodynamic orthostatic dizziness from other types of dizziness that are induced or aggravated when standing or walking. Measurements of the orthostatic blood pressure and heart rate are important when screening hemodynamic orthostatic dizziness. Detailed history-taking, a physical examination, and laboratory tests are essential for finding the cause of hemodynamic orthostatic dizziness. The differential diagnosis of hemodynamic orthostatic dizziness is crucial because it can be caused by various autonomic neuropathies.

Citations

• Mareo y vértigo ortostático, funcional y cinetosis
  Liliana F. Invencio-Da-Costa, Carmen Sánchez-Blanco, Raquel Yáñez-González, Hortensia Sánchez-Gómez, Paula Peña-Navarro, Sofía Pacheco-López, Susana Marcos-Alonso, Cristina Nicole Almeida-Ayerve, Luis Cabrera-Pérez, Victoria Díaz-Sánchez
  Revista ORL.2023; 15(3): e31540.     CrossRef

Background
: Syncope was defined as transient loss of consciousness and postural tone. The mechanisms of changes in cerebral hemodynamics during syncope have not been fully evaluated. Transcranial Doppler Ultrasonography can continuously monitor the changes in cerebral hemodynamics during head-up tilt (HUT). TCD could reveal the different patterns of changes in cerebral hemodynamics during syncope. Syncope without hypotension or bradycardia could be detected by TCD. We investigated the changes in cerebral blood flow velocity during HUT using TCD in 33 patients with a history of recurrent syncope or presyncope of unknown origin. Methods & Results : The positive responses were defined as presyncope or syncope with hypotension, bradycardia, or both. During HUT without isoproterenol infusion, there were a 86?3% drop in DV and a 41?4% drop in SV in 5 patients with positive reponses, and mean changes in those were less than 10% in patients with negative reponses ( p=.00, p=.00). During HUT with isoproterenol infusion, TCD showed a 80?8% drop in diastolic velocity in 14 patients with positive reponses, and a 47?0% drop in that in patients with negative reponses (p=.00), however the change in systolic velocity did not differ. TCD showed three patterns during positive responses; loss of all flow, loss of end diastolic flow, and a decrease in diastolic velocity. Loss of consciousness occurred in the patients with loss of all flow or end-diastolic flow during positive reponses. Conclusions : TCD shows different patterns of changes in cerebral hemodynamics during HUT. TCD can be used to investigate the pathophysiology of neurocardiogenic syncope

The most significant factor in pathogenesis of vascular headaches like migraine and cluster headache is dynamic changes of diameters of the cerebral arteries. TCD is a valuable noninvasive tool to assess the cerebral hemodynamic status by measuring the flow velocities of the intracranial cerebral arteries around the circle of Willis. TCD can evaluate flow velocities and vasoreactivity of the patients with a vascular headache during the ictal phase as well as during intericatal phase. Distribution of the changes recorded differ between types of headaches nd also between the major ictal symptoms. The Changes suggest the presence of prolonged vasospasm interictally and more marked relaxation of the cerebral arteries. TCD can be used to monitor the long-term clinical course of patients with vascular headache by correlation the symptomatic improvement and TCD data before and after long-term pharmacological prophylactic treatments. During the ictal phases large intervention. The results may be used in selecting and evaluating the agents for abortive therapy for acute attacks. In conclusion TCD can quantitatively evaluate vascular headaches when making diagnosis and classification and can provide guidelines to choose more individualized therapeutic options for both acute and long-term treatment