Data submitted needs to have distinguished hypertension from hypotension, which does cause giddiness. Drug effects also need to be taken into account, as antihypertensives can cause overshoot, lowering blood pressure too much and hence causing dizziness from inner ear hypotension.
Hypertension never give rise from hypotension diziness but it stands person in action, hypotension give rise diziness and a prevail day sleep all the time in patients.But any person taking a complete course to control hypertension, post hypertension relax provides diziness, and same is found unifromly in hypotension patient. Physiological rhythm and awakening and sleeping become slow and lead to an increase in diziness.
Dizziness is common symptom in decompensated hypertension disease - typical sign of Hypertensive encephgalopathy. Acute increase of blood pressure is acompanied by diffuse headache, lightheaddeness and mallaise.
Acute hypertension can cause hypoperfusion of the labyrint with acute onset of vertigo, vomiting and instability. Or Vertebro-basilar ischemia with central type of vertigo, typicaly with other focal symptoms from brainstem (double vision, swallowing dificulties etc.)
The common underlying causes of hypertension (atherosclerotic plaquing, stress, and inflammation) do indeed contribute mightily to vestibular dysfunction. However, all of the studies going back to Northwestern University (1978) demonstrated correlation not causation. So, I see your point, Anthony. When I get some time I will come back to answer more thoroughly. But I believe that many of the same factors (not all) that cause hypertenstion cause similar (mostly vascular) effects on vestibular and hearing function. Prescribed drugs for hypertension do indeed become over-prescribed, in my opinion, because they are not looking to address an underlying issue, but instead striving to reach a number on a piece of paper and calling it a day. Consequently, hearing acuity takes a beating, as well turning a chronic cardiovascular situation into an acute event in the end. Great question and worthy of discussion.
Ali's mention of the hypotension connection is an excellent one. We usually find this when people are taking multiple hypertension meds and/or are chronically dehydrated. Both dehyrdration and polypharmacy can co-occur, especially when ADH is secreted in response to such an egregious treatment combination.
Dear Anthony,
I have asked the same question many times in the clinical setting. There has been no satisfactory answer to date. The converse is true(dizziness leading to elevations of blood pressure), from clinical observations and following up patients over many months and years in the ambulatory setting of elderly patients.
However, I can understand how we may have gotten lost amongst the trees in the woods as severe chronic hypertension has a strong correlation with severe postural hypotension. The proposed pathophysiology is that as an end result of the damage from the chronic over-stimulation of the baroreceptors from chronic hypertension, the baroreceptors are no longer able to detect and compensate for changes in BP due to postural changes.
This leads to the entity of severe postural hypotension with co-existing severe supine or sitting hypertension (Naschitz Je et al. "The patient with supine hypertension and orthostatic hypotension: a clinical dilemma". Postgrad Med J 2006;82:246–253.) Not only is this very difficult to manage and is an often unseen precipitating factor of recurrent falls in the elderly, they often have both symptoms of dizziness and hypertension at the same time.
This leads to the conclusion that the dizziness is a result of the hypertension, whereas repeatedly we have found that it is the ever escalating doses and multitudes of antihypertensive agents used to treat the ever rising blood pressure that is the culprit, leading to worsening of the symptoms of the dizziness until a point where the patient is unable to even stand.
Hence, it is no longer possible to assess for or diagnose postural hypotension.
Gradual reduction and withdrawal with close observations of the blood pressure in an in-patient setting have resulted in resolution of the symptoms of dizziness and secondary hypertension.
And ironically, when these patients are well enough to stand, often we have found significant postural hypotension without any anti-hypertensives. In a few cases, these patients required further non-pharmacological and pharmacological treatment of the severe underlying postural hypotension.
The best analogy I can think of to explain this phenomenon is "Medication Overuse Headache", a phenomenon described in 1951 by Peters and Horton. The underlying mechanisms are not well elucidated but the clinical pictures is that the headaches gets worst with increasing use of analgesia. Gradual phased withdrawal of the analgesic agents leads to the resolution of the headaches (Butt TF, Evans B. "Drug-induced headache". Adverse Drug Reaction Bulletin, October 2006, p 919–922 ).
This seems to selectively affect the very elderly as the baroreceptors are less able to buffer changes in BP as compared to young patients with advancing age (Monahan KD. "Effect of aging on baroreflex function in humans". Am J Physiol Regul Integr Comp Physiol 293: R3–R12, 2007.) However, baroreflex control of sympathetic outflow is not thought to be impaired with aging, hence a possible underlying aetiology for this phenomenon.
Perhaps this is the beginning of the recognition of a similar phenomenon that one day may be recognized as "Anti-hypertensive Overuse Hypertension" or AOH.
Excessive antihypertensive use, leading to dizziness from the over-stimulation of the vestibular system via endolymphatic hydrops, is also the likely driver for the secondary severe refractory hypertension, as a result of the anti-hypertensive induced one-sided baroreflex sympathetic over-activity.
I wonder also If there is a known positive activation from the vestibular apparatus (dizziness) to the sympathetic nervous system and baroreflexes? I seem to notice dizziness due to non-haemodynamic causes (i.e. motion sickness) may sometimes lead to a rise in blood pressure as well.
Best regards,
Samuel Chew
http://journals.lww.com/adversedrugreactbull/toc/2006/10000
http://www.ncbi.nlm.nih.gov/pubmed/17442786
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2579630/
"Acute increase of blood pressure is acompanied by diffuse headache, lightheaddeness and mallaise. Acute hypertension can cause hypoperfusion of the labyrint with acute onset of vertigo, vomiting and instability. "
Could someone please supply convincing reference(s) for this (preferably after reading Samuel Chew's last post on the complexities of the matter)?
"I wonder also If there is a known positive activation from the vestibular apparatus (dizziness) to the sympathetic nervous system and baroreflexes? I seem to notice dizziness due to non-haemodynamic causes (i.e. motion sickness) may sometimes lead to a rise in blood pressure as well."
C Pellarin has an excellent discussion of these matters in his "Memoire sur le mal de mer" in Annales d'hygiene publique 1847;37:307, but comes to the opposite conclusion. This was before the vestibular system was discovered, but he clearly pinpoints the role of movement /motion detectors. I am hoping to summarise his article in my RG question on Morning Sickness, meanwhile some of his conclusions:
1. Le mal de mer, le mal de voiture, celui que produit chez quelques personnes la balancoire, sont tous des phenomenes de la meme nature, essentiellement determines par l'influence exercee sur la marche circulatoire du sang par les mouvemens que le corps subit dans ces diverses circonstances;
2. Cette influence a pour principal effet de diminuer la force ascendante du liquide excitateur dans l'aorte et dans les arteres qui naissent de sa crosse: de la resulte un etat hyposthenique du cerveau par anemie ou hypohemie;
3. L'insuffisante excitation de l'organe cerebral determine sur-le-champ, par voie sympathique, des contractions spasmodic du diaphragme, des vomissements...
From PLOS:
Orthostatic Hypotension and the Long-Term Risk of Dementia: A Population-Based Study
Frank J. Wolters,
Francesco U. S. Mattace-Raso,
Peter J. Koudstaal,
Albert Hofman,
M. Arfan Ikram, …
Published: October 11, 2016
http://dx.doi.org/10.1371/journal.pmed.1002143..
Abstract
Background
Orthostatic hypotension (OH) is a common cause of transient cerebral hypoperfusion in the population. Cerebral hypoperfusion is widely implicated in cognitive impairment, but whether OH contributes to cognitive decline and dementia is uncertain. We aimed to determine the association between OH and the risk of developing dementia in the general population.
Methods and Findings
Between 4 October 1989 and 17 June 1993, we assessed OH in non-demented, stroke-free participants of the population-based Rotterdam Study. OH was defined as a ≥20 mm Hg drop in systolic blood pressure (SBP) or ≥10 mm Hg drop in diastolic blood pressure (DBP) within 3 min from postural change. We furthermore calculated within participant variability in SBP related to postural change, expressed as coefficient of variation. Follow-up for dementia was conducted until 1 January 2014. We determined the risk of dementia in relation to OH and SBP variability, using a Cox regression model, adjusted for age; sex; smoking status; alcohol intake; SBP; DBP; cholesterol:high-density lipoprotein ratio; diabetes; body mass index; use of antihypertensive, lipid-lowering, or anticholinergic medication; and apolipoprotein E genotype. Finally, we explored whether associations varied according to compensatory increase in heart rate. Among 6,204 participants (mean ± standard deviation [SD] age 68.5 ± 8.6 y, 59.7% female) with a median follow-up of 15.3 y, 1,176 developed dementia, of whom 935 (79.5%) had Alzheimer disease and 95 (8.1%) had vascular dementia. OH was associated with an increased risk of dementia (adjusted hazard ratio [aHR] 1.15, 95% CI 1.00–1.34, p = 0.05), which was similar for Alzheimer disease and vascular dementia. Similarly, greater SBP variability with postural change was associated with an increased risk of dementia (aHR per SD increase 1.08, 95% CI 1.01–1.16, p = 0.02), which was similar when excluding those who fulfilled the formal criteria for OH (aHR 1.08, 95% CI 1.00–1.17, p = 0.06). The risk of dementia was particularly increased in those with OH who lacked a compensatory increase in heart rate (within lowest quartile of heart rate response: aHR 1.39, 95% CI 1.04–1.85, p-interaction = 0.05). Limitations of this study include potential residual confounding despite rigorous adjustments, and potentially limited generalisability to populations not of European descent.
Conclusions
In this population predominantly of European descent, OH was associated with an increase in long-term risk of dementia."
As we see hundreds of patients heading into various stages of dementia and balance disorders, we note that one of the common denominators is they are all taking multiple hypertensive medications that have as one of their most pronounced side/interaction effects orthostatic hypotension. We note that while the macro reading of their systolic/diastolic numbers appear within the range of normality that they consistently complain of freezing feet and cold hands, indicating to us that they are over medicated in the quest for achieving normality in blood pressure. We also note elevated ADH levels when taking multiple hypertensive meds, which in turn can adversely affect the sodium/potassium electrolyte balance of the cochleovestibular function. When we report these effects to the prescribing clinic (such as the VA) we rarely see any changes made to medications and the patients too often continue their downward trek in mental and vestibular status. These are our observations, keeping in mind that medication per capita use in the US is reportedly at least three times as high in the geriatric population as it is in the UK.
"As we see hundreds of patients heading into various stages of dementia and balance disorders, we note that one of the common denominators is they are all taking multiple hypertensive medications that have as one of their most pronounced side/interaction effects orthostatic hypotension."
With the advent of personal BP monitors, it should be possible nowadays to clarify whether side effects or symptoms are associated with surges of high BP, or with overcorrected episodes of low BP.
"Acute hypertension can cause hypoperfusion of the labyrint with acute onset of vertigo, vomiting and instability. Or Vertebro-basilar ischemia with central type of vertigo, typicaly with other focal symptoms from brainstem" (Rudolf)
I don't understand how hypertension can cause labyrinthine hypoperfusion. Why not hyperperfusion or bleeds?
What is the evidence that VBI vertigo cannot be of peripheral origin? VBI can directly affect the brain-stem and cause neurological signs/symptoms. But it can also reduce blood supply to the cochlea, which is a much more statistically likely mechanism for vertigo. What brainstem substrate or locus is there for isolated vertigo?
That is a most insightful observation and question, Anthony. I suspect that lowering of blood volume (either by the body's increase of anti-diuretic hormone [ADH] secretions or too much diuretic action of the medication--both resulting from too much hypertension medication) may also contribute to layrinthine hypofusion. We see this all the time with our veterans who go to the VA for their healthcare. They are easily, in our estimation, the most over-medicated group on planet earth.
"I suspect that lowering of blood volume .. may also contribute to layrinthine hypofusion."
The cochlea works by fluid pressure differentials, so in the first instance inner ear disorders would be expected to be due to abnormal pressures, eg hydrops. Are you proposing that volume changes without pressure changes are involved? If pressure changes are implicit, then I don't see the relevance of thinking about volume changes. Does it not complicate thinking about the situation?
Well, when blood volume drops (as a result of dehydration or too much diuretic medication, for instance) the pituitary gland secretes anti-diuretic hormone (ADH) to raise sodium levels and to thicken the blood. From this, electrolyte balances change enough to create vertigo and other labyrinthine anomalies. The delicate balance between the potassium-rich endolymph and sodium-rich perilymph will be at least secondarily effected by the body's secretion of ADH and resulting electrolyte imbalances.
Max, I don't know enough to comment on your model, but it does contain at least six stages, any which one could be wrong or of limited generality. My head and heart is in Ancient Greece, so I will stick with the very simple hydrostatic model, which is also resistant to specific differences in the metabolic environment..
Yes, you're model is correct, but in the US where millions of people with simple hypertension are given extraordinary amounts of diuretics by prescription, where they are typically semi-dehydrated and consume several times the caffeine quantity in their daily diet as other countries, we see elevated levels of ADH in the general population. Hence, the incidence of Meniere's and Meniere's-like disorders are much higher than we see in other countries. This complicates matters a great deal in trying to explain llabyrinthine disorders. A lack of recognition of these trends also hampers developing a consensus in the professional community. Our healthcare system is too incentivized toward over-medication of symptoms and typically disregards dietary influences in health states at the macro level of consideration.
"This complicates matters a great deal in trying to explain llabyrinthine disorders"
One thing my model cannot be accused of is complicating matters -- oversimplifying maybe. I maintain that anything that reduces inner pressure leads to Meniere Spectrum Disorder. This is a totally non-specific process.
I agree, I'm just referring to one of the often overlooked causal factors in Meniere's that we see often.
From Krafft-Ebing on Dementia Senilis summarised in London Medical Record 1874;2:827-8:
"The proximate cause is disturbed nutrition of the brain from insufficient blood-supply, owing to fatty degeneration of the heart and atheroma of the carotids and cerebral -arteries."
"The conditions depend chiefly on cerebral anaemia"..
"The first signs of approaching failure of intellect are in the memory. Whilst that for past events remains, that for recent ones is destroyed.."
See London Evening Standard Nov 14 p 7 for evidence that blood loss causes vertigo:
"The boy didn't know what to do because he was dizzy and losing too much blood. I told him to come inside and sit down and he tried but couldn't sit because he was so dizzy"
I maintain that here as in the vast majority of non-traumatic cases the vertigo comes from the ear. If from the brain, which part? And why was he evidently not obviously neurologically impaired if the brain was blood-deprived?
"Middle-aged people who experience temporary blood pressure drops that often cause dizziness upon standing up may be at an increased risk of developing cognitive decline and dementia 20 years later, new Johns Hopkins Bloomberg School of Public Health research suggests.
The findings, being presented March 10 at the American Heart Association’s EPI|LIFESTYLE 2017 Scientific Sessions in Portland, Ore., suggest that these temporary episodes – known as orthostatic hypotension – may cause lasting damage, possibly because they reduce needed blood flow to the brain. Previous research has suggested a connection between orthostatic hypotension and cognitive decline in older people, but this appears to be the first to look at long-term associations.
“Even though these episodes are fleeting, they may have impacts that are long lasting,” says study leader Andrea Rawlings, PhD, MS, a post-doctoral researcher in the Department of Epidemiology at the Bloomberg School. “We found that those people who suffered from orthostatic hypotension in middle age were 40 percent more likely to develop dementia than those who did not. It’s a significant finding and we need to better understand just what is happening.”
jhsph.edu/news
