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I know a number of us have SPECT scans showing characteristic hypoperfusion (i.e. decreased blood flow to specific portions of the brain). But, can anyone explain to me the mechanism why this would occur? And, if we are to increase our blood pressure with medications or increased salt intake, would the perfusion to these portions of the brain increase?
Posts: 99 | From Bucks County, PA | Registered: Aug 2008
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Keebler
Honored Contributor (25K+ posts)
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This would just be a start to the research. You might check out the library to the left of this page - and at the LDA site, link on the left, as well.
You will also find more information about this at the CFIDS Chronicle site.
I would get further advice from an ILADS' specialist, not an IDSA doctor.
For certain, if hypoperfusion is a player, aerobic exercise should be avoided so as to not further stress a brain that has decreased circulation. Gentle movement, of course, is still good.
While slight to moderate increases with sea salt may be helpful, it is vital that you talk first to your LLMD about this.
Increased salt can put serious stress on kidneys and the heart and is not advised for anyone with diabetes (and many patients with chronic infections do develop diabetes).
A drug, Florinef, has been used for POTS or NMDH, types of low blood pressure often affected lyme patients. I don't know if that would be good with hypoperfusion or not. It can be a strain on some patients' kidneys but, for some, it works well.
The low blood pressure and hypoperfusion may occur in the same patient and may have some connections but they are not the same thing.
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From Wiki, basic info. below.
While much of what they say at this site is good, some is not so accurate, especially about treatment as it does not consider the vast amount of research by ILADS' doctors.
However, this part about hypoperfusion does help as an introduction about hypoperfusion with lyme patients.
Single photon emission computed tomography (SPECT) imaging has been used to look for cerebral hypoperfusion indicative of Lyme encephalitis in the patient.[62] Although SPECT is not a diagnostic tool itself, it may be a useful method of determining brain function.
In Lyme disease patients, cerebral hypoperfusion of frontal subcortical and cortical structures has been reported.[63] In about 70% of chronic Lyme disease patients with cognitive symptoms, brain SPECT scans typically reveal a pattern of global hypoperfusion in a heterogeneous distribution through the white matter.[64]
This pattern is not specific for Lyme disease, since it can also be seen in other central nervous system (CNS) syndromes such as HIV encephalopathy, viral encephalopathy, chronic cocaine use, and vasculitides. However, most of these syndromes can be ruled out easily through standard serologic testing and careful patient history taking.
The presence of global cerebral hypoperfusion deficits on SPECT in the presence of characteristic neuropsychiatric features should dramatically raise suspicion for Lyme encephalopathy among patients who inhabit or have traveled to endemic areas, regardless of patient recall of tick bites.[citation needed]
Late disease can occur many years after initial infection. The average time from symptom onset to diagnosis in these patients is about 4 years.
Because seronegative disease can occur, and because CSF testing is often normal, Lyme encephalopathy often becomes a diagnosis of exclusion: once all other possibilities are ruled out, Lyme encephalopathy becomes ruled in.
Although the aberrant SPECT patterns are caused by cerebral vasculitis, a vasculitide, brain biopsy is not commonly performed for these cases as opposed to other types of cerebral vasculitis.
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