Chronic Cerebro-Spinal Venous Insufficiency and Parkinson’s Disease: The Presence of Abnormal Flow and White Matter Hyperintensities
E. Mark Haacke, Ph.D.1,2, Manju Liu1, Haibo Xu3, David Utriainen2 1 Department of Biomedical Engineering, Wayne State University, Detroit MI 48201, USA. 2 Magnetic Resonance Innovations, Inc., Detroit, MI 48202, USA. 3 Department of Radiology, Union Hospital,Wuhan, China
Background and Objective: Idiopathic Parkinson's disease (IPD) is one of those neurodegenerative diseases where the cause remains unknown. Many clinically diagnosed cases of IPD are associated with cerebrovascular disease and white matter hyperintensities (WMH). The presence of high iron content in the basal ganglia and midbrain in multiple sclerosis (MS) and the potential role of extracranial flow abnormalities in the venous system stimulated us to consider the possibility that patients with IPD might also have similar venous abnormalities. Therefore, the purpose of this study was to investigate the presence of transverse sinus and extracranial venous flow abnormalities in IPD patients and their relationship with brain WMH.
Methods: Twenty-three IPD patients and 23 age-matched normal controls were recruited from the same site in Wuhan, China. Each patient and subject had conventional MR structural and angiographic brain scans. In addition, blood flow in the extracranial vessels was quantified at C6/C7 with 2D phase- contrast (PC) imaging. The cross sections and flow were measured using SPIN (signal processing in NMR). The internal jugular vein (IJV) flow was normalized by the total arterial flow. Venous structures were evaluated with 2D-time-of-flight (TOF). WMH volume was quantified with T2 weighted fluid attenuated inversion recovery (FLAIR). The ratio of the flow in the dominant IJV and the sub-dominant IJV (Fd/Fsd) was calculated for each case. The IPD and normal subjects were classified using both the MR TOF and PC images into four categories: 1) missing transverse sinus and partially missing IJVs on the TOF images with high Fd/Fsd; 2) missing transverse sinus and stenotic IJVs with high Fd/Fsd; 3) reduced flow in the sub-dominant IJV with high Fd/Fsd; and 4) normal flow and no stenosis.
Results: When broken into the above 4 categories with categories 1 through 3 combined, a significant difference in the distribution of the IPD patients and normal controls (χ2=7.7, p<0.01) was observed. Venous abnormalities (categories 1, 2 and 3) were seen in 57% of IPD subjects and only in 30% of controls. Patients with venous abnormalities tended to show higher volume WMH. In IPD subjects, category type correlated with both flow abnormalities and WMH.
Discussion and Conclusion: A major fraction of IPD patients appear to have abnormal venous anatomy and flow on the left side of the brain and neck and the flow abnormalities in particular appear to correlate with WMH volume. Although having WMH is not a standard clinical diagnostic criterion for IPD, in this study cohort, 21 patients showed WMH, 5 had very high WMH volume (more than 10,000mm3) and of these 4 had a high visual Schelten’s score (greater than 9). According to many in vivo imaging studies, 30% to 55% of PD patients show WMHs. An MRI-pathological correlation study by Gao et al. (Alzheimer's and Dementia. 2008;4(4):T368-T9) demonstrated that focal and periventricular hyperintensities (PVH) often relate to venules. They proposed that venous collagenosis dilates the veins, making them macroscopic and causing venous insufficiency with consequent vessel leakage and vasogenic edema. Despite this evidence, a larger study is needed to validate these findings at other sites.
- See more at: http://www.wpahs.org/news/9-8-2011/mri- ... QS54T.dpufBased on this case, Dr. Jannetta and his colleagues at AGH conducted a blinded MRI study analyzing the brains of 20 patients with Parkinson’s and 20 healthy control subjects. The study showed that 78 percent of the Parkinson’s Disease patients had visible arterial compression/distortion of one or both cerebral penduncles. Of the study’s 20 control subjects, just two had low grade compression of the cerebral penduncle and one of those was subsequently diagnosed with Parkinson’s.
Beginning in 1966, a growing number of cranial nerve and brainstem syndromes have been reported to be caused by pulsatile vascular compression, arterial or venous or both. These include such apparently disparate problems as trigeminal neuralgia3–5 (both typical and atypical), hemifacial spasm,6,7 Meniere’s disease,8 disabling positional vertigo,9 glossopharyngeal neuralgia,10–12 Bell’s palsy,13 essential hypertension14–17 and type 2 diabetes.18,19 This knowledge of the above entities, although known and accepted in the neurosurgical community, have not penetrated into the general medicine literature. Beginning in the same year (1966), treatment of the pulsatile compression (microvascular decompression) was developed. These findings and treatments were possible because of the use of then new technology, and the magnification, lighting and recording capabilities of the surgical binocular microscope.13–19
A member of the ISNVD and founding President, Dr. Mark Haacke, presented research at the 2nd Annual ISNVD conference. His paper, which has been submitted for publication , looked at 21 patients with Parkinson’s. These participants were imaged by MRV, and 15 of them (71%) had abnormal venous structures and/or blood flow. All participants with CCSVI exhibited the same pattern: reduced flow on the left side and abnormal left transverse sinus and jugular vein, with the right internal jugular carrying most of the flow out of the brain.
pulsatile compression is part of an overall edemic situation, due to restricted extracranial venous flow?
"Following the vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery The patient's Parkinson's signs disappeared over a 48-hour period. "
My question, which is way over my head is the quote from Peter J Jannetta and Donald Whiting's paper…"Following the vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery The patient's Parkinson's signs disappeared over a 48-hour period. "
What the hell is "vascular decompression of the trigeminal nerve, the midbrain was decompressed by mobilizing and repositioning the posterior cerebral artery"
Are they moving things around in the brain through surgery? Do these actions help venous flow?
Is this stuff safe?
Thank god for brave surgeons, may they heal us all. Just amazing stuff….
From this link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3207233/
Neurol Int. 2011 July 5; 3(2): e7.
Parkinson’s disease: an inquiry into the etiology and treatment
Peter J. Jannetta, Donald M. Whiting, Lynn H. Fletcher, Joseph K. Hobbs, Jon Brillman, Matthew Quigley, Melanie Fukui, and Robert Williams
From this link http://radiopaedia.org/articles/vascular-compression-disorders
Vascular compression disorders are numerous and can be divided into those cases where a vascular structure is the "compress-er" or the "compress-ee" . Some conditions fall into both categories, where one vessel compresses another
A multi-center clinical trial to further explore the AGH team's premise has already been organized and is slated to begin later this year.
SOURCE Allegheny General Hospital
From the kind Dr. Okun on that site
Other scientists, reviewing these findings, have pointed out that the blood vessels image only very small diameters. The MRI protocol that they used may not be optimal to examine such small blood vessels, and especially their compressive effects. It would definitely be very difficult to see straining artery walls using this MRI technique. The authors may however be inferring that there is pressure by seeing that the blood vessels are located closer to regions of interest in the brainstem in people with PD. One problem with that observation is that reduced brain volume in this region is an established aspect of PD, and when the brain moves, so too can the blood vessels. When the structures shift in PD it is not because of pressure-- it is because of slow neurodegeneration and consequent shrinking. Finally, one must remember the anatomy and that those blood vessels normally course by the brainstem and provide blood and nutrition to those areas of the brain--being close to the areas of the brain does not prove compression---and when we do see compression there are usually unilateral motoric neurological examination findings evident on exam. The argument for compression and symptoms based on the MRI findings is speculative. There are several well-established biological explanations that offer attractive alternatives to Jannetta's findings.
Is it just me or does this discovery seem to put into question the long-standing belief that dopamine-producing cells are dead? if the cells are dead (as opposed to dormant, disabled, etc) than how does one explain the (rather instantaneous - 48 hrs) elimination of PD symptoms? if the dopamine cells ARE in fact dead and (assuming) the body CAN regenerate enough cells to eliminate symptoms, this would take presumably longer than 48 hrs to accomplish. So how does removing the toxic condition (the compression in the mid-brain) cause dopamine levels to spike back to normal? Maybe those cells that we thought were dead, were actually only disabled.....does anyone else find this interesting?
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