still dizzy.
 

after a week or so. i have been getting extremely dizzy each time i stand up. has anybody else experienced that? some of you mentioned it could be blood pressure, but i took mine, multi times and it always seems fine. does anybody else have any ideas.? my mom is remembering that a few years ago ( when i was in my wheelchair) i was extremly dizzy.
thank you everyone.
keep your chins up :)

That could be *anything*. I'd go see a doctor asap.

I absolutely agree, go see your doctor...:D

I get dizzy a lot, also. It's so bad that at times, I actually feel like I am going to pass out and think I actually have a few times!

When we mentioned it to my Dr, he said that my blood pressure was a bit low and that it was probably from the pain and was sort of my bodies way of 'coping' with the pain. For example, when my pain gets too much, I go dizzy and pass out in order for my body to recover. I guess it makes sense as I always feel worse when my pain is really high.

I agree with what the others said, please go and see your Dr again just to rule out any other possibilities. When you go to stand, stand really slowly too - don't rush up otherwise that will make you go even dizzier!

Take care and keep us posted!:hug:

I agree with everyone. Call and make an appt. with your doctor.

When my pain is at it's worst is when I have the most problem with dizzy spells. When my pain is flaired I also can have balance issues. Today is an awful day for my pain. I was walking to my car and if anyone was looking they would have thought me to be drunk. Truth is today was a day I should have had someone drive me. I stayed alert and took extra care to be careful.

I have trouble with the neck area of my spine (cervical) and when I see my chiropractor and complaine of balance issues. He will adjust the very top of my spine at the base of my head. He uses and activator not a his hands and then I am fine. I see him 3 times a week when I'm not flaired and 5 days a week when I am flaired. So my dizzy spells don't happen very often.

As we all know our medications can cause dizziness. If we take some of them on empty stomachs they can cause problems. As well as just being hungry can cause us to be dizzy.

Be sure to call you doctor for an appointment.

Take care,
Sherrie

Once again from the chorus, “I agree with everyone else, you should see your doctor.” That said, it sounds a lot like "orthostatic hypotension," which as defined by the online mondofacto is:

A drop in blood pressure that is precipitated by changes in body position. May be related to hydration status, drug side effect or be caused by a dysfunction in the autonomic nervous systems ability to maintain blood pressure with positional changes (for example autonomic neuropathy secondary to diabetes).

http://www.mondofacto.com/facts/dict...ion=look+it+up

And just because there are many causes of orthostatic hypotension, is why it has to be checked out with a doctor. That said, some common patterns emerge, where it is often a function of autonomic dysfunction. (Ring any bells?) See, “A sympathetic view of the sympathetic nervous system and human blood pressure regulation,” Joyner MJ, Charkoudian N, Wallin BG, Experimental Physiology 2008 Jun;93(6):715-24, free full text at http://ep.physoc.org/content/93/6/715.full.pdf:

Abstract
New ideas about the relative importance of the autonomic nervous system (and especially its sympathetic arm) in long-term blood pressure regulation are emerging. It is well known that mean arterial blood pressure is normally regulated in a fairly narrow range at rest and that blood pressure is also able to rise and fall 'appropriately' to meet the demands of various forms of mental, emotional and physical stress. By contrast, blood pressure varies widely when the autonomic nervous system is absent or when key mechanisms that govern it are destroyed. However, 24 h mean arterial pressure is still surprisingly normal under these conditions. Thus, the dominant idea has been that the kidney is the main long-term regulator of blood pressure and the autonomic nervous system is important in short-term regulation. However, this 'renocentric' scheme can be challenged by observations in humans showing that there is a high degree of individual variability in elements of the autonomic nervous system. Along these lines, the level of sympathetic outflow, the adrenergic responsiveness of blood vessels and individual haemodynamic patterns appear to exist in a complex, but appropriate, balance in normotension. Furthermore, evidence from animals and humans has now clearly shown that the sympathetic nervous system can play an important role in longer term blood pressure regulation in both normotension and hypertension. Finally, humans with high baseline sympathetic traffic might be at increased risk for hypertension if the 'balance' among factors deteriorates or is lost. In this context, the goal of this review is to encourage a comprehensive rethinking of the complexities related to long-term blood pressure regulation in humans and promote finer appreciation of physiological relationships among the autonomic nervous system, vascular function, ageing, metabolism and blood pressure.

PMID: 18326553 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

That and many drugs or drug interactions can apparently trigger it. See, “Autonomic control of the venous system in health and disease: effects of drugs,” Pang CC, Pharmacol Ther. 2001 May-Jun;90(2-3):179-230:

Abstract
The venous system contains approximately 70% of the blood volume. The sympathetic nervous system is by far the most important vasopressor system in the control of venous capacitance. The baroreflex system responds to acute hypotension by concurrently increasing sympathetic tone to resistance, as well as capacitance vessels, to increase blood pressure and venous return, respectively. Studies in experimental animals have shown that interference of sympathetic activity by an alpha1- or alpha2-adrenoceptor antagonist or a ganglionic blocker reduces mean circulatory filling pressure and venous resistance and increases unstressed volume. An alpha1- or alpha2-adrenoceptor agonist, on the other hand, increases mean circulatory filling pressure and venous resistance and reduces unstressed volume. In humans, drugs that interfere with sympathetic tone can cause the pooling of blood in limb as well as splanchnic veins; the reduction of cardiac output; and orthostatic intolerance. Other perturbations that can cause postural hypotension include autonomic failure, as in dysautonomia, diabetes mellitus, and vasovagal syncope; increased venous compliance, as in hemodialysis; and reduced blood volume, as with space flight and prolonged bed rest. Several alpha-adrenoceptor agonists are used to increase venous return in orthostatic intolerance; however, there is insufficient data to show that these drugs are more efficacious than placebo. Clearly, more basic science and clinical studies are needed to increase our knowledge and understanding of the venous system. [Emphasis added.]

PMID: 11578657 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

These include diuretics to relieve edema, when taken along with opioid analgesics, which is of course where I live. See, “Metabolic and adverse effects of diuretics,” Wilcox CS, Seminars in Nephrology 1999 Nov;19(6):557-68:

Abstract
Diuretics are among the most frequently prescribed drugs. They enjoy a very high clinical reputation for safety and efficacy. However, more than 3 decades of clinical investigation have disclosed a number of abnormalities in fluid electrolyte handling, metabolism, and other adverse effects that can complicate therapy with diuretic drugs. Some of these complications are a direct extension of the wanted action of the drug. These include extracellular fluid volume depletion, associated orthostatic hypotension, and prerenal azotemia. Others are not a direct action of the diuretic, but can be explained as an intranephronal compensation to the diuretic action. These include hypokalemia, in part to increased potassium secretion secondary to the enhanced tubular fluid flow and aldosterone secretion induced by diuretic administration. Metabolic abnormalities are usually mild. Hyperglycemia and carbohydrate intolerance have been related to diuretic-induced hypokalemia, which inhibits insulin secretion by the beta cells, and reductions in extracellular fluid volume and cardiac output. This is compounded by increases in catecholamines from sympathetic nerve activity which decrease peripheral glucose utilization. A mild increase in serum cholesterol concentration is seen frequently during initiation of diuretic therapy, but during steady state therapy after 6 to 12 months, values usually return to baseline. Knowledge of the more common adverse effects induced by diuretics helps the physician in predicting patients at risk and taking effective steps to anticipate or treat adverse responses. [Emphasis added.]

PMID: 10598543 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

And of course, if one is on diuretics, drinking lots of water, while possibly controlling the orthostatic hypotension, will defeat the entire purpose of the diuretics . . . .

Not to worry,
Mike

Not sure how that happened, but I hit "Submit Reply" on my last post, without including the citations I had spent quite a while putting together. Something about being called to dinner. That error has now been corrected and the authorities are offered for whatever they are worth. Sorry about that.

Separately, for a nice article on neurogenic orthostatic hypertension in general, check out, “Management of neurogenic orthostatic hypotension: an update,” Low PA, Singer W, The Lancet Neurology 2008 May;7(5):451-8, NIH Author Manuscript at http://www.ncbi.nlm.nih.gov/pmc/arti...ihms-86024.pdf:

Abstract
Orthostatic hypotension (OH) is common in elderly people and in patients with disorders such as diabetes and Parkinson's disease. Grading of the severity of OH and its effect on the patient's quality of life are important. The symptoms vary with orthostatic stress, and subtle symptoms such as tiredness and cognitive impairment should be recognised. Standard drug treatment for OH is effective but worsens supine hypertension, whereas pyridostigmine can improve OH slightly but significantly without worsening of supine hypertension. Because orthostatic stress varies from moment to moment and drug treatment is suboptimal, drug treatment of OH needs to be combined with non-pharmacological approaches, such as compression of venous capacitance beds, use of physical counter-manoeuvres, and intermittent water-bolus treatment.

PMID: 18420158 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

thank you everybody for all the info. i'm planning on going to see my doctor today. i will keep you all posted. hope your all having a great hopefully low pain day. :grouphug: