Orthostatic hypotension, cerebral hypoperfusion, and visuospatial deficits in Lewy body disorders

2016 ◽  
Vol 22 ◽  
pp. 80-86 ◽  
Author(s):  
Andrew D. Robertson ◽  
Michelle A. Messner ◽  
Zahra Shirzadi ◽  
Galit Kleiner-Fisman ◽  
Joyce Lee ◽  
...  
Keyword(s):  
Orthostatic Hypotension ◽  
Lewy Body ◽  
Cerebral Hypoperfusion ◽  
Visuospatial Deficits

Case 24: Orthostatic Cerebral Hypoperfusion Syndrome with Vision Loss

2019 ◽  
pp. 157-162
Author(s):  
Peter Novak
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Orthostatic Hypotension ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Vision Loss ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Hypoperfusion ◽  
Tilt Test

The tilt test showed orthostatic cerebral hypoperfusion syndrome (OCHOS) with intermittent reduction in cerebral blood flow velocity and vision loss. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.

Case 23: Orthostatic Cerebral Hypoperfusion Syndrome, Severe

2019 ◽  
pp. 153-156
Author(s):  
Peter Novak
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Orthostatic Hypotension ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Hypoperfusion ◽  
Tilt Test

The tilt test showed severe orthostatic cerebral hypoperfusion syndrome (OCHOS) with reduced cerebral blood flow velocity. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.

Syncope

2019 ◽  
pp. 251-258
Author(s):  
Ricardo Ruiz-Granell
Keyword(s):  
Patient Education ◽  
Orthostatic Hypotension ◽  
Pharmacological Treatment ◽  
Cerebral Hypoperfusion ◽  
Cardiac Syncope ◽  
Neurally Mediated Syncope

Syncope results from sudden, transient, global cerebral hypoperfusion. Neurally mediated syncope, orthostatic hypotension, arrhythmic and cardiac syncope, and steal syndromes are the main pathophysiological forms of syncope. This chapter focuses on the treatment of neurally mediated syncope and orthostatic syncope, since other forms of syncope are reviewed elsewhere. In neurally mediated and orthostatic syncope, patient education and non-pharmacological measures are the mainstay of treatment, although benefits of pharmacological treatment are not so evident.

scholarly journals Neurogenic Orthostatic Hypotension. Lessons From Synucleinopathies

2020 ◽  
Author(s):  
Juan Francisco Idiaquez ◽  
Juan Idiaquez ◽  
Juan Carlos Casar ◽  
Italo Biaggioni
Keyword(s):  
Blood Pressure ◽  
Orthostatic Hypotension ◽  
Treatment Options ◽  
Lewy Body Dementia ◽  
Cerebral Hypoperfusion ◽  
Neurogenic Orthostatic Hypotension ◽  
Compression Garments ◽  
Novel Treatments ◽  
Mild Disease ◽  
Noradrenergic Fibers

Abstract Maintenance of upright blood pressure critically depends on the autonomic nervous system and its failure leads to neurogenic orthostatic hypotension (NOH). The most severe cases are seen in neurodegenerative disorders caused by abnormal α-synuclein deposits: multiple system atrophy (MSA), Parkinson’s disease, Lewy body dementia, and pure autonomic failure (PAF). The development of novel treatments for NOH derives from research in these disorders. We provide a brief review of their underlying pathophysiology relevant to understand the rationale behind treatment options for NOH. The goal of treatment is not to normalize blood pressure but rather to improve quality of life and prevent syncope and falls by reducing symptoms of cerebral hypoperfusion. Patients not able to recognize NOH symptoms are at a higher risk for falls. The first step in the management of NOH is to educate patients on how to avoid high-risk situations and providers to identify medications that trigger or worsen NOH. Conservative countermeasures, including diet and compression garments, should always precede pharmacologic therapies. Volume expanders (fludrocortisone and desmopressin) should be used with caution. Drugs that enhance residual sympathetic tone (pyridostigmine and atomoxetine) are more effective in patients with mild disease and in MSA patients with spared postganglionic fibers. Norepinephrine replacement therapy (midodrine and droxidopa) is more effective in patients with neurodegeneration of peripheral noradrenergic fibers like PAF. NOH is often associated with other cardiovascular diseases, most notably supine hypertension, and treatment should be adapted to their presence.

scholarly journals Altered Amyloid-β and Tau Proteins in Neural-Derived Plasma Exosomes in Patients with Type 2 Diabetes and Orthostatic Hypotension

2020 ◽  
Author(s):  
Jinbiao Zhang ◽  
Haiyan Chi ◽  
Tong Wang ◽  
Shukun Zhang ◽  
Tengqun Shen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Orthostatic Hypotension ◽  
Cerebral Blood Flow Velocity ◽  
Linear Regression Analysis ◽  
Amyloid Β ◽  
Tau Proteins ◽  
Cerebral Hypoperfusion ◽  
Clinical Trial Registry ◽  
T Tau

Abstract BackgroundEmerging evidence suggests a role for orthostatic hypotension (OH) in contributing to the progression of Alzheimer disease (AD). The aim of the study was to investigate whether neural-derived plasma exosomal amyloid-β and tau protein levels are associated with OH in diabetes mellitus (DM) patients.MethodsThere were 274 subjects without dementia included in the study: 81 control participants (controls), 101 normotensive patients with DM without OH, and 92 patients with DM and neurogenic OH (DMOH). Neuronal-derived exosomal proteins were measured by ELISA kits for amyloid-β and tau.ResultsThe neuronal-derived exosome levels of Aβ42, T-tau, and P-T181-tau in the DM with OH group were higher than those in the DM and control groups. Multivariable linear regression analysis showed that the presence of OH in patients with DM was associated with elevated exosomal Aβ42 (β = 0.172, P = 0.018), T-tau(β = 0.159, P = 0.030), and P-T181-tau (β = 0.220, P = 0.003) levels after adjustment for age, sex, APOE ε4, duration of type 2 diabetes, HbA1c and cardiovascular risk factors. Furthermore, the levels of Aβ42, T-tau, and P-T181-tau in neuronal-derived exosomes were correlated with HIF-1α levels and the drop in mean cerebral blood flow velocity from the supine to upright position.ConclusionsThe presence of OH in DM patients was independently associated with elevated the Aβ42, T-tau, and PT181-tau levels in neural-derived plasma exosomes. Cerebral hypoperfusion from DM with OH are likely candidate mechanisms.Trial registrationChinese Clinical Trial Registry (Identifier: ChiCTR1900021544 ). Registered 27 February 2019.

scholarly journals Orthostatic arterial hypotension

2017 ◽  
Vol 12 (2) ◽  
pp. 12-15
Author(s):  
Camelia C. DIACONU ◽  
◽  
Denisa BUCUR ◽  
Daniel BERCEANU ◽  
Ovidiu Gabriel BRATU ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Elderly Patients ◽  
Orthostatic Hypotension ◽  
Pharmacological Treatment ◽  
Elderly Population ◽  
Autonomic Failure ◽  
Clinical Manifestations ◽  
The Elderly ◽  
Cerebral Hypoperfusion ◽  
Blurred Vision

Orthostatic hypotension is a persistent decrease of systolic blood pressure by at least 20 mm Hg and/or diastolic blood pressure by at least 10 mm Hg in the first 3 minutes upon standing. Orthostatic hypotension is more common in the elderly patients, being one of relatively frequent causes of hospitalization in the elderly population. Orthostatic hypotension may be primary or secondary, acute or chronic. Its etiology is represented in most cases by the primary or secondary autonomic failure. Clinical manifestations of orthostatic hypotension occur after the transition from supine to standing, and are due to cerebral hypoperfusion. These consist of nausea, dizziness, generalized weakness, postural instability, fatigue, blurred vision. Cardiological and neurological consult are necessary for diagnosis. Pharmacological treatment of orthostatic hypotension is often unsatisfactory, imposing combination with non-pharmacological measures.

Syncope

2019 ◽  
pp. 251-258
Author(s):  
Ricardo Ruiz-Granell
Keyword(s):  
Patient Education ◽  
Orthostatic Hypotension ◽  
Pharmacological Treatment ◽  
Cerebral Hypoperfusion ◽  
Cardiac Syncope ◽  
Neurally Mediated Syncope

Syncope results from sudden, transient, global cerebral hypoperfusion. Neurally mediated syncope, orthostatic hypotension, arrhythmic and cardiac syncope, and steal syndromes are the main pathophysiological forms of syncope. This chapter focuses on the treatment of neurally mediated syncope and orthostatic syncope, since other forms of syncope are reviewed elsewhere. In neurally mediated and orthostatic syncope, patient education and non-pharmacological measures are the mainstay of treatment, although benefits of pharmacological treatment are not so evident.

Case 77: Painful Small Fiber Neuropathy in Posttreatment Lyme Disease Syndrome

2019 ◽  
pp. 390-393
Author(s):  
Peter Novak
Keyword(s):  
Lyme Disease ◽  
Orthostatic Hypotension ◽  
Autonomic Failure ◽  
Small Fiber Neuropathy ◽  
Cerebral Hypoperfusion ◽  
Supine Hypertension ◽  
Autonomic Testing ◽  
Small Fiber ◽  
Immune Globulins ◽  
Sensory Fibers

This case illustrates autonomic failure in painful post-Lyme disease syndrome. Autonomic testing has shown supine hypertension, orthostatic hypotension, and hypocapnic cerebral hypoperfusion (HYCH). Small fiber neuropathy was painful, affecting sensory fibers. Patient noted improvement in the pain by about 40% after 12 month of intravenous immune globulins.

Syncope and palpitation

2020 ◽  
pp. 3284-3293
Author(s):  
K. Rajappan ◽  
A.C. Rankin ◽  
A.D. McGavigan ◽  
S.M. Cobbe
Keyword(s):  
Orthostatic Hypotension ◽  
Cardiac Rhythm ◽  
Cerebral Hypoperfusion ◽  
Loss Of Consciousness ◽  
Neurocardiogenic Syncope ◽  
Cardiac Syncope ◽  
Appropriate Treatment ◽  
Heart Beating ◽  
Transient Episode ◽  
Premature Beats

Syncope is a transient episode of loss of consciousness due to cerebral hypoperfusion. Its causes can be subdivided on the basis of pathophysiology, including neurally mediated—or reflex—syncope; orthostatic hypotension; cardiac causes; and cerebrovascular or psychogenic causes. Neurocardiogenic syncope, or simple faint, is the commonest cause and is benign, but it is always important to exclude or establish the diagnosis of cardiac syncope, because this has an adverse prognosis that may be improved with appropriate treatment. Meanwhile, palpitation is the awareness of one’s heart beating—it may be due to an awareness of an abnormal cardiac rhythm, or an abnormal awareness of normal rhythm. It is most commonly due to premature beats (ectopics) and is benign. Correlation between symptoms and cardiac rhythm is the initial aim of investigations in patients presenting with palpitations.

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