This Is MS Multiple Sclerosis Community: Knowledge & Support

Multiple sclerosis (MS) is a disease with multiple etiologies. The most recent theory of the vascular etiology of MS, Chronic Cerebrospinal Venous Insufficiency (CCSVI), suggests that cerebral venous obstruction could lead to cerebral venous reflux, promoting local inflammatory processes.

This review article offers strong evidence that the route of the observed narrowing of cerebral veins arises from autonomic nervous system dysfunction, particularly cardiovascular autonomic dysfunction.

A unifying theory for MS which does not explain the influence of genes in the etiology of MS. Not the whole puzzle, so incomplete.
MarkW

Ann Biomed Eng. 1985;13(3-4):311-20.
Cerebrovascular transmural pressure and autoregulation.
Wagner EM, Traystman RJ.
Abstract
The cerebral blood flow (CBF) response to changes in perfusion pressure mediated through decreases in arterial pressure, increases in cerebrospinal fluid (CSF) pressure and increases in jugular venous pressure was studied in anesthetized dogs. A preparation was developed in which each of the three relevant pressures could be controlled and manipulated independently of each other. In this preparation, the superior vena cava and femoral vein were cannulated and drained into a reservoir. Blood was pumped from the reservoir into the right atrium. With this system, mean arterial pressure and jugular venous pressure could be independently controlled. CSF pressure (measured in the lateral ventricle) could be manipulated via a cisternal puncture. Total and regional CBF responses to alterations in perfusion pressure were studied with the radiolabelled microsphere technique. Each hemisphere was sectioned into 13 regions: spinal cord, cerebellum, medulla, pons, midbrain, diencephalon, caudate, hippocampus, parahippocampal gyrus, and occipital, temporal, parietal and frontal lobes. Despite 30 mm Hg reductions in arterial pressure or increases in jugular venous pressure or CSF pressure, little change in CBF was observed provided the perfusion pressure (arterial pressure minus jugular venous pressure or CSF pressure depending on which pressure was of greater magnitude) was greater than the lower limit for cerebral autoregulation (approximately 60 mm Hg). However, when the perfusion pressure was reduced by any of the three different methods to levels less than 60 mm Hg (average of 48 mm Hg), a comparable reduction (25-35%) in both total and regional CBF was obtained. Thus comparable changes in the perfusion pressure gradient established by decreasing arterial pressure, increasing jugular venous pressure and increasing CSF pressure resulted in similar total and regional blood flow responses. Independent alterations of arterial and CSF pressures, and jugular venous pressure produce opposite changes in vascular transmural pressure yet result in similar CBF responses. These results show that cerebral autoregulation is a function of the perfusion pressure gradient and cannot be accounted for predominantly by myogenic mechanisms.
PMID: 4037460 [PubMed - indexed for MEDLINE]

Am J Physiol. 1988 Dec;255(6 Pt 2):H1516-24.
Effect of jugular venous pressure on cerebral autoregulation in dogs.
McPherson RW, Koehler RC, Traystman RJ.
Source
Department of Anesthesiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Abstract
We determined the importance of a myogenic sensor of cerebral autoregulation by assessing the effect of vascular transmural pressure on cerebral blood flow (CBF) as cerebral perfusion pressure (CPP) was decreased. Decreasing CPP by decreased arterial pressure (Pa) or increased intracranial pressure (Pcsf) decreases transmural pressure, whereas increased jugular venous pressure (Pjv) increases transmural pressure. Regional CBF was measured in barbiturate-anesthetized dogs using radiolabeled microspheres. In group 1 (n = 5), CPP was decreased by decreasing Pa; in group 2 (n = 5), CPP was decreased by increasing Pcsf (Pa = 80 mmHg); and in group 3 (n = 5) CPP was decreased by increasing Pjv (Pa = 80 mmHg). CPP was reduced from 80 to 30 mmHg in 10-mm increments in each group. In groups 1 and 2 regional CBF was maintained as CPP was decreased to 40 mmHg; however, at CPP of 30 mmHg, blood flow to cerebrum, caudate, and periventricular white matter decreased, whereas flow to cerebellum and medulla remained unchanged. In group 3 regional CBF was unchanged as CPP decreased from 80 to 50 mmHg but decreased in all regions as CPP decreased further. In all three groups, cerebrovascular resistance continuously declined as CPP was decreased. In all groups, cerebral O2 uptake was unaltered. Autoregulation fails at a higher CPP with increased Pjv than with decreased Pa or increased Pcsf, particularly in brain stem. We conclude that metabolic autoregulation predominates over the myogenic mechanism until CPP is low.
PMID: 3144187 [PubMed - indexed for MEDLINE]

J Neurosurg. 1998 Jul;89(1):118-24.
Local cerebral blood flow autoregulation following "asymptomatic" cerebral venous occlusion in the rat.
Nakase H, Nagata K, Otsuka H, Sakaki T, Kempski O.
Source
Department of Neurosurgery, Nara Medical University, Kashihara, Japan.
Abstract
OBJECT:
Maintenance of cerebral blood flow (CBF) autoregulation in the brain is of major importance for patient outcome in various clinical conditions. The authors assessed local autoregulation after "asymptomatic" cortical vein occlusion.
METHODS:
In Wistar rats, a single cortical vein was occluded photochemically by using rose bengal and fiberoptic illumination. In rats with bilateral carotid artery occlusion, mean arterial blood pressure (MABP) was lowered in 5-mm Hg increments down to 40 mm Hg by using hypobaric hypotension. Local CBF at each pressure level was assessed by performing laser Doppler (LD) scanning at 25 (5 x 5) locations within bilateral cranial windows. In this manner, the lower limit of autoregulation (LLA) was detected. The LLA was 60 mm Hg in both right and left hemispheres in Group A (five rats), in which the animals received illumination without rose bengal and had no venous occlusion. Of the 11 rats that underwent vein occlusion, three developed severe reductions in local CBF and/or a growing venous thrombus and were distinguished as Group C (symptomatic; three rats); from previous work we know that those animals are bound to experience venous infarction. The remaining rats formed Group B (asymptomatic; eight rats). In this group the LLA remained at 60 mm Hg in the left hemisphere without occlusion, whereas, in the right cortex with the occluded vein, the LLA was found to be 65 mm Hg. Below a carotid stump pressure of 25 mm Hg regional CBF in the affected hemisphere dropped more abruptly to a possibly ischemic range than that in the opposite normal hemisphere.
CONCLUSIONS:
The results of the present study suggest that cerebral venous circulation disorders are manifested via additional pathways, that is, from a partially impaired local autoregulation in the vicinity of the occluded vein, even under conditions in which the vein occlusion itself does not cause brain damage. Care should be taken in the control of blood pressure in patients with this pathological condition.
PMID: 9647182 [PubMed - indexed for MEDLINE]