ISNVD FEB 9,2014

ISNVD Feb 9,2014
Day 2
Nitric Oxide and Vascular Hypothesis in MS
Dr Yulin Ge
Diffuse Inflammatory activities
NO
inhibit mitochondria aerobic respiration and neurovascular coupling tiring out leas to decrease of oxygen consumption
leading to hypoxia
 leading to hypo-perfusion  an d to neuronal/axonal dysfunction and neurodegeneration

apoptotic cell death of oligodendrocytes at later stages of lesion development
measuring NO effects using MRI
effects on oxygen metabolism
effects on oxygen delivery
Facts of oxygen metabolism in brain
brain uses 20% of total oxygen
oxygen delivery..
oxygen consumption in MS is decreased
oxygen metabolic abnormalities in MS measured with TRUST MRI
why is there is less oxygen consumption in MS
it's not only atrophy but it's because of the mitochondria has high levels of NO
BOLD...
CO2 like NO is a  potent vasodilator and can cause increase of CBF
compared to controls MS showed significantly decreased CVR
The CVR defect inMS...impaired vasculaar regulation of blood flow supply or defective neurocoupling mechanism may affect effective oxygen delivery
decreased CMRO2 in MS and decreased CVR inMS
recent accumulating evidence of mitochondrial of/NO hypotheses in neuronal axonal tissure damage
both O2 delivery and O2 uptake impairment can lead to chronic hypoxic condition
NO is not the only mechanism that is responsible to neurodegeneration
the increase in NO may be from the endothelium or microglia( as a result of infection) but either is due to inflammation

Perfusion imaging in stroke
Its current clinical status and its role in treating patients
Dr Larry Latour

there is insufficient evidence to support or refute the value of PWI in diagnosing acute ischemic stroke
what is a mini stroke and being treated with tPA?
15 minutes makes a difference in the treatment of an acute ischemic stroke. It is safe to reat even if it's a mimic of a stroke...as the treatment can prevent a stroke




Hemodynamic impairment in MS...Imaging techniques and perspectives
Yulin Ge
vascular hypotheses has been around for numerous years
pathology in MS...vascular
perivascular inflammation...Dawson's finger...new lesions start around abnormal vessels
first imaging sign of lesion formation
 BBB breakdown and increased permeability
with effective anti inflammatory drugs
first sign is prominent perivenular space using 7T MRI
perfusion MRI
detect abnormality before lesion
increased perfusion in NAWN just before lesion formation
venous dilation in initial inflammatory stage... priminet venules companied with increased perfusion
enhancing lesion with increased perfuion
new or recurred lesion activity that are not seen on conventional MRI
the is hemodynamic impairment in MS
fibrin deposition, small venous thrombosis, intimal hyperplasia
there are lesions with different type of perfusion patterns
significantly reduction of perfusion in deep GM in MS
vascular component is critical in neurological disease
MS patients with cardiovascular problems have increased MS problems




SPECT and PECT perfusion changes after CCSVI restoration
Paolo Zamboni

diffuse hypo-perfusion in MS is a FACT. It cant be explained with autoimmunity but CCSVI is a valuable hypothesis
hypo-perfusion precedes plaque formation approx 2 weeks earlier
chronic plaques were more prevalent in WM regions with lower relative perfusion.  can ccsvi be a strong contributor to hypoperfusion. may outflow restoration restore brain perfusion
the data support a role of ccsvi in cerebral hemodynamic changes, such as a decreases of CBV and CBF regardless of diagnosis of MS
theres is a relationship between brain perfusion and jugular flow
flow reduction in and significant flow increase in collaterals
the collateral veins drain blood respect to ED inflow to the head
are the collateral veins filled by premature intra extra cranial anastomosis?
hypo-perfusion may be consequence of  blood shunting through meningeal arteries
pilot study with 5 ccsvi cases...not only MS
used PET scan.
3 patients who improved with venoplasty ...one of them had Huntington disease had improvement of perfusion
pilot study 2 using SPECT using open angioplasty
8 ccsvi cases
vast majority of patients improved flow
PET and spect both reliably detect change in perfusion in ccsvi
spect demonstrate hypoperfusion in ccsvi
the procedure seems to cause significant improvement


The rest of the morning session was devoted to traumatic brain injury:

Abstract...cerebral hemodynamic changes in mild traumatic brain injury at the acute stage

Abstract...altered IJV hemodynamics and impaired cerebral auto-regulation in patients with panic disorder
PD patients have decreased IJV lumen

Traumatic brain injury and vascular consequences
state of the art understanding the fundamental physiology of TBI...from research to treatment

Dr Ramon Diaz Arrastia
single most common cause of death and permanent disability in young people under 45
10%-15% of pts with TBI have micro blood vessel injuries
there is also diffuse meningeal injury
 chronic mild tB of retired professional boxers
cerebral blood flow is normal but the reactivity of the blood vessels is impaired
Treatment:
Sildenafil,erythropoietin, statins, G-CSF, VEGF, pioglitazone, exercise , enriched endothelia progenitor cells, from cord blood or bone marrow, low level laser light therapy, Infrared can penetrate the skull.
It has anti inflammatory properties and promotes angiogenesis and releases NO
people who have had TBI in early life have an increased risk of dementia in later life.


Typical vascular lesions of TBI and their evolution
Dr Gunjan Parikh
brain micro vascular tree
the first thing hit is the dura and cortex
prospective study of acute TBI in the ED with blood on clinical CT or on MR
256 subjects had indications of hemorrhage
all were considered mild TBI



The clinical spectrum and natural history of TBI Sequelae
Dr Karen Tung

role of perfusion and SWI in TBI
how TBI and how it relates to the micro vasculature of the brain
neurovascular unit NVU
TBI damages the vessel wall or causes impaired perfusion and cause tissue ischemia
BBB dysfunction results in edema and may affect protein clearance and accelerate brain aging or disease pathology


State of the Art...the role of imaging and venous abnormalities in TBI
Dr Zhifeng Kou

Abstract...Hemorrhagic lesions based on venous and arterial damage and its clinical correlation in Traumatic Brain Injury
Hardik Doshi


Abstract...Thalamic Shape and Cognitive performance in amnesic mild cognitive impairment
Hyun-kook Lim

It is my understanding that the ISNVD will provide summaries of each of the presentations in a few weeks.