Brain spect

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18
I get the results of my brain spect (without stimulation) and it says slight bilateral hypoperfusion. Anyone get this test done? What were their results and what they mean?
 

linusbert

Senior Member
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1,723
what does the doctor say?

ai defines it like this:
Definition of "Bilateral Hypoperfusion":


Bilateral hypoperfusion
refers to insufficient blood flow (hypoperfusion) affecting both sides (bilateral) of the brain. It is typically used in the context of cerebral (brain) circulation.




Medical Context:


  1. Pathophysiology:
    • The brain receives blood through the internal carotid and vertebral arteries on both sides.
    • In bilateral hypoperfusion, blood flow is reduced in both cerebral hemispheres, often due to systemic causes such as low blood pressure, heart failure, or bilateral arterial narrowing.
  2. Possible Causes:
    • Global circulatory shock (e.g., cardiac arrest, severe sepsis)
    • Hypotension in elderly patients with pre-existing cerebrovascular disease
    • Bilateral carotid artery stenosis or occlusion
    • Postoperative state (e.g., after cardiac surgery), or generalized hypoxia
  3. Clinical Significance:
    • Can lead to bilateral ischemic damage, especially in "watershed" areas (border zones between major cerebral arteries)
    • Symptoms: confusion, altered consciousness, bilateral neurological deficits, possibly coma
    • Diagnosed using brain imaging (e.g., MRI or CT perfusion scans) to detect areas of reduced perfusion
  4. Treatment:
    • Stabilization of blood circulation and optimization of blood pressure
    • Management of underlying causes (e.g., vascular surgery for stenosis)
    • Monitoring for and managing potential ischemic brain injury



Summary:


Bilateral hypoperfusion indicates reduced blood supply to both sides of the brain, usually due to a systemic circulatory problem. It is a serious condition that can result in significant neurological impairment if not promptly addressed.


Non-Traumatic Causes of Bilateral Cerebral Hypoperfusion:


If trauma is excluded, bilateral hypoperfusion of the brain typically results from systemic or vascular pathologies that impair global or symmetrical cerebral blood flow. These causes include:




1. Systemic Hypotension


  • Severe dehydration
  • Cardiogenic shock (e.g., from myocardial infarction or heart failure)
  • Septic shock (due to infection and systemic vasodilation)
  • Overmedication with antihypertensives or sedatives
  • Perioperative hypotension (especially during cardiac or vascular surgery)



2. Cardiac Causes


  • Low cardiac output states
    • Congestive heart failure (CHF)
    • Arrhythmias (e.g., atrial fibrillation with rapid ventricular response, bradycardia)
  • Aortic stenosis or cardiomyopathies reducing cerebral perfusion pressure



3. Vascular Pathologies


  • Bilateral carotid artery stenosis or occlusion
  • Large vessel vasculitis (e.g., Takayasu arteritis)
  • Aortic arch syndrome affecting flow to both hemispheres



4. Global Hypoxia / Hypoxemia


  • Respiratory failure
  • Severe anemia
  • Carbon monoxide poisoning



5. Autoregulatory Failure


  • Impaired cerebral autoregulation (e.g., in elderly or hypertensive patients)
  • Conditions like posterior reversible encephalopathy syndrome (PRES) in rare cases



6. Metabolic or Toxic Causes


  • Hypoglycemia or hypoxia reducing neuronal activity and perfusion
  • Drug overdose (e.g., opioids, sedatives, barbiturates) causing hypotension or hypoventilation



7. Post-Cardiac Arrest (Global Cerebral Ischemia)


  • Even without trauma, resuscitated cardiac arrest patients may exhibit bilateral hypoperfusion on imaging due to global ischemic injury



Summary:


In the absence of trauma, bilateral cerebral hypoperfusion is most commonly due to systemic hypotension, cardiac dysfunction, vascular narrowing, or global hypoxic conditions. Identifying and treating the underlying systemic or vascular cause is critical to prevent irreversible brain injury.

not sure what it means. but doctor actually should say something about this. they shouldnt give you the diagnose and not do anything... well "shouldnt" ...


the above ai info was in general cases. for cfs patients, i asked it differently and it also gave a somewhat more pleasing answer:
Cerebral Hypoperfusion in Chronic Fatigue Syndrome (CFS/ME): Causes and Treatment




1. Pathophysiological Causes in CFS/ME


In patients with Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME), studies have consistently reported reduced cerebral blood flow (CBF), sometimes bilaterally. The underlying mechanisms are multifactorial:


A. Autonomic Nervous System Dysfunction


  • Orthostatic intolerance (OI) and Postural Orthostatic Tachycardia Syndrome (POTS) are common in CFS/ME.
  • Dysregulated sympathetic and parasympathetic tone impairs cerebral autoregulation, reducing perfusion when upright.

B. Hypovolemia


  • Many CFS/ME patients have low circulating blood volume.
  • Leads to inadequate cerebral perfusion, especially during orthostatic stress.

C. Endothelial Dysfunction


  • Impaired vasodilation due to endothelial cell abnormalities may restrict cerebrovascular reactivity.

D. Neuroinflammation


  • Evidence of microglial activation and low-grade inflammation in the CNS may alter vascular tone and reduce flow.

E. Impaired Mitochondrial Function


  • Energy metabolism dysfunction may contribute to vascular dysregulation.



2. Clinical Consequences


  • Cognitive dysfunction (“brain fog”)
  • Lightheadedness, dizziness, especially when standing
  • Exacerbation of fatigue due to reduced cerebral oxygen and glucose delivery



3. Diagnostic Tools


  • Tilt table testing: to identify orthostatic intolerance/POTS
  • SPECT, PET, or Doppler ultrasonography: to measure cerebral perfusion
  • MRI with perfusion imaging (in research settings)



4. Treatment Strategies


Treatment is supportive and symptom-targeted. There is no cure, but several approaches may help:


A. Non-Pharmacological:


  • Increased salt and fluid intake: to expand blood volume
  • Compression garments: to reduce venous pooling
  • Supine rest periods and avoidance of prolonged standing
  • Tilt training or graded recumbent exercise (only in selected patients)

B. Pharmacological:


  • Fludrocortisone: to expand plasma volume
  • Midodrine or droxidopa: to increase vascular tone and blood pressure
  • Beta-blockers (e.g., propranolol): to control heart rate in POTS
  • Ivabradine: used off-label for heart rate control in some cases

C. Experimental / Investigational Approaches:


  • Rintatolimod (Ampligen): immune modulator studied in CFS/ME
  • Immunotherapy or anti-inflammatory agents (under investigation)
  • Mitochondrial support (e.g., CoQ10, L-carnitine): variable evidence



Summary


In CFS/ME, cerebral hypoperfusion is primarily linked to autonomic dysfunction, low blood volume, and vascular dysregulation. Treatment focuses on managing orthostatic intolerance, expanding blood volume, and improving cerebral perfusion through both lifestyle adjustments and pharmacologic agents. Regular monitoring and individualized management are essential due to high variability in response.

in addition to what ai suggested i would also consider Sulbutiamine.
in any POTS-like and hypovolemic situation i would suggest thiamine as its related in this kind of body physiology. Sulbutiamine is a B1/thiamine derivate which is more readily available in the brain then other forms.
 
Last edited:

Zebra

Senior Member
Messages
1,101
Location
Northern California
I get the results of my brain spect (without stimulation) and it says slight bilateral hypoperfusion. Anyone get this test done? What were their results and what they mean?

I am following this thread because I am also interested in getting this test, and I'm also interested in your test results.

I would discuss this finding with your doctor, and not pay too much attention to what AI has to say about it. The AI we all have access to now is, literally, just a tossed word salad.
 

kushami

Senior Member
Messages
741
Hypoperfusion means that there is a reduction in blood flow, but the degree of reduction would be important to know. I am not sure exactly what bilateral means in this context. Obviously it means "on both sides of the brain" but whether that equates to overall hypoperfusion or not, I'm not sure.

One common cause for low blood flow to the brain that often gets overlooked is orthostatic intolerance. This can be investigated by an autonomic specialist.

Some do use SPECT scans, but the more-common method for diagnosing orthostatic intolerance is a NASA lean test, although it has some limitations in the types it can detect.

https://batemanhornecenter.org/nasa-10-minute-lean-test-2/

A carotid/vertebral or transcranial Doppler scan is more comprehensive. This is usually done in conjunction with a tilt table test.

https://www.brighamhealthonamission...o-pinpoint-causes-of-orthostatic-intolerance/

SPECT scans are done lying down, so they may not always detect the degree of hypoperfusion the person would be experiencing when sitting or standing if orthostatic intolerance is playing a role in the person's fatigue and cognitive symptoms.

As @andyguitar says, there are quite a few things that cause low blood flow to the brain, so this is just my two cents' worth.
 

Dan_USAAZ

Senior Member
Messages
175
Location
Phoenix, AZ
I get the results of my brain spect (without stimulation) and it says slight bilateral hypoperfusion. Anyone get this test done? What were their results and what they mean?
I had a spect scan done a few years ago. Excerpts of my results are below. I believe when they say "decreased tracer activity" in my study, it might mean the same as "hypoperfusion" cited in your study.


Brain SPECT Findings and Conclusions:
The most significant findings are moderately to severely decreased tracer activity in the bilateral temporal lobes and dorsomedial prefrontal cortex and mildly to moderately decreased activity in the inferior orbital prefrontal cortex accompanied by scalloping, more notably in the concentration study. Combined with the decreased activity in the prefrontal pole, dorsal parietal cortex, internal cerebellum and occipital lobe, these findings may be consistent with past brain injury and possibly an encephalopathic process.
Additionally, there is severely increased tracer activity in the thalamus in both studies and mildly
increased activity in the basal ganglia in the baseline study.

1: Decreased left and right temporal lobe tracer activity seen on both studies.

2: Decreased tracer activity in the left and right inferior orbital prefrontal cortex seen on both studies, more severe with concentration, and decreased prefrontal cortex pole tracer activity seen on both studies, more severe at rest.

3: Decreased medial prefrontal cortex tracer activity seen on both studies, and decreased left and right lateral prefrontal cortex tracer activity seen on both studies, more severe with concentration.

4: Increased diffuse and focal thalamic tracer activity seen on both studies, and Limbic steal phenomenon seen with concentration.

5: Brain injury. A combination of findings suggests past brain injury. These findings include:
- Decreased prefrontal pole activity
- Decreased cerebellar activity
- Decreased temporal lobe activity
- Decreased parietal lobe activity
- Decreased occipital lobe activity
- Decreased dorsal prefrontal cortex activity.

6: Mild scalloping seen on both studies.

7: Decreased left and right occipital lobe tracer activity seen on both studies, more severe with concentration, and decreased internal cerebellar tracer activity seen on both studies, more severe with concentration.

8: Decreased left and right parietal lobe tracer activity seen on both studies, more severe with concentration, and decreased medial parietal lobe tracer activity seen with concentration.
 
Messages
18
Hi. Thank you all for your answers.

My doctor told me that he was waiting these results or similar, because he had seen similar results in people with cfs. He said that reduced blood flow (even only left or right brain blood flow) it is a patron in people with cfs, that there were studies showing this and it would be an objetive proof.
 

kushami

Senior Member
Messages
741
This thread reminds me that I had attempted to get my autonomic specialist here in Australia to order a SPECT scan, but he wasn't very keen on the idea. (I later found out he had overstated his experience and knowledge a lot, and apparently didn't know how to order scans like this.)

I am going to be seeing a neurologist soon about a different condition (muscle problem), and if he seems helpful and sympathetic I will ask whether he can take on my brain blood flow problems as well, at least in terms of ordering scans, even if he can't treat me.

@waitingyet, was the SPECT scan hard to do?
 
Messages
18
This thread reminds me that I had attempted to get my autonomic specialist here in Australia to order a SPECT scan, but he wasn't very keen on the idea. (I later found out he had overstated his experience and knowledge a lot, and apparently didn't know how to order scans like this.)

I am going to be seeing a neurologist soon about a different condition (muscle problem), and if he seems helpful and sympathetic I will ask whether he can take on my brain blood flow problems as well, at least in terms of ordering scans, even if he can't treat me.

@waitingyet, was the SPECT scan hard to do?
No it was not. They injected me a tracer and I wait for some minutes lying. Then they put the scan to work (taking images around your head) for maybe 30 or 40 minutes. Not painful at all. The risk is that the tracer has a very low radiation, but it so low that you need to take thousands of spects to be dangerous
 
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