Mountain man proves CCSVI theory
Posted: Tue Jan 26, 2010 8:05 pm
I stumbled upon this article while dredging up material for the blood flow and altitude thread. I believe it to be a fairly significant find, so I am making a new thread of it. If I have transgressed a thread-making policy, please forgive.
While scaling the Himalayas, this otherwise healthy bloke developed MS-like symptoms from a complete left JV thrombosis. The symptoms consisted of "neurological dysfunction in the form of loss of equilibrium, progressive motor weakness, slurring of speech and diarrhea and later on day 12 at 4500 meters height he developed left sided hemiparesis and right sided facial nerve palsy."
While the mechanism of injury would be different in such an acute case, the elicited symptoms support a blood reflux flow hypothesis in CCSVI. Instead of a sudden onset like this, imagine CCSVI of a much minor degree over a longer time causing lesions in the same blood flow channels in the brain due to chronic exposure. This is why CCSVI might be difficult to detect without sensitive equipment and proper training.
Click on the link to view the MRI and Doppler images.
http://medind.nic.in/ibn/t06/i3/ibnt06i3p313.pdf
While scaling the Himalayas, this otherwise healthy bloke developed MS-like symptoms from a complete left JV thrombosis. The symptoms consisted of "neurological dysfunction in the form of loss of equilibrium, progressive motor weakness, slurring of speech and diarrhea and later on day 12 at 4500 meters height he developed left sided hemiparesis and right sided facial nerve palsy."
While the mechanism of injury would be different in such an acute case, the elicited symptoms support a blood reflux flow hypothesis in CCSVI. Instead of a sudden onset like this, imagine CCSVI of a much minor degree over a longer time causing lesions in the same blood flow channels in the brain due to chronic exposure. This is why CCSVI might be difficult to detect without sensitive equipment and proper training.
Click on the link to view the MRI and Doppler images.
http://medind.nic.in/ibn/t06/i3/ibnt06i3p313.pdf
Rare Case of Cerebral Stroke & Venous Thrombosis
Developed During High Altitude Expedition.
A PRABHAKAR, M AGGARWAL, P KHURANA, N TREHAN
Ind J Radiol Imag 2006 16:3:313-314
Key words : Cerebral venous thrombosis, stroke, high attitude
INTRODUCTION :
High Altitude pulmonary edema and cerebral edema are
well known entities related to high altitude climbing.
Cerebral sinus thrombosis and hemorrhage also develop
as a consequence of dehydration. We present a case in
which a mountaineer developed cerebral stroke and
venous thrombosis at an altitude of about 5000 meters
during an expedition to the Himalayas.
CASE REPORT:
A 56 year old male, with no known previous health problem
went on an expedition to scale a place at 5500 meters in
the Himalayas. On day 6 of his expedition at about 5000
meters he developed neurological dysfunction in the form
of loss of equilibrium, progressive motor weakness,
slurring of speech and diarrhea and later on day 12 at
4500 meters height he developed left sided hemiparesis
and right sided facial nerve palsy. On day 15, he was
airlifted to the nearest hospital given emergency medical
care in the form of hyperbaric oxygen and then brought
to our hospital.
...
A small thrombus in left sigmoid sinus and complete
thrombosis of left jugular vein was noted (Fig 3,4).
MR angiography for the Cerebral vessels showed mild
pinching of right Middle Cerebral Artery, secondary to mass
effect due to hemorrhage and edema.
Doppler also showed complete thrombosis of Internal
Jugular Vein on left side. Follow up CT scan was done
after 2 days, which confirmed the findings.
DISCUSSION:
Altitude illness refers to a constellation of syndromes that
result from hypoxic injury alone or in combination with
various maladaptive physiological changes. Cerebral
syndromes develop at a altitude of 2500 metres and
everyone is at risk, regardless of the level of physical
fitness or previous altitude experience.(1)
Rapid ascent to high altitude overtaxes the body's ability
to tolerate decreasing availability of oxygen that causes
changes in blood brain barrier permeability and results in
vasogenic edema.
In rare cases focal neurological signs and deficits like
IIIrd nerve palsy, VIth nerve palsy, stroke, and sinus venous
thrombosis may develop. Pulmonary odema, DVT,
pulmonary thromboembolism are also known to occur.
HACE may present with altered mental status, progressive
ataxia, coma & death.
HACE is characterized in MRI with reversible vasogenic
white matter edema with a predilection for splenium of
corpus callosum (2).
Hemorrhagic cerebral infarction can be induced by venous
thrombosis a consequence of high altitude dehydration
polycythaemia (3,4).
SK Jha et al (5) reported that long term stay at high altitude
was also associated with higher risk of stroke. Ischemic
strokes were the commonest although all types of strokes
were seen.
In our study the site of hemorrhage in right basal ganglia
was indicative of an ischemic etiology. The filling defect
in the sigmoid sinus and complete occlusion of the jugular
vein was on the opposite side, could be a result of
heamoconcentration leading to polycythemia.
