When I began my fellowship training in diagnostic neuroradiology and interventional neuroradiology at Stanford University Medical Center in 2010, both the medical world and the lay press were abuzz with the possibility that both MS and idiopathic intracranial hypertension could be, in part, vascular diseases secondary to insufficient venous drainage of the head and neck. Given the far greater prevalence of MS, and Stanford University’s early experience (both positive and negative) with angioplasty and stenting for CCSVI, I chose to further explore the CCSVI hypothesis of MS.
Fully expecting to contribute another “no difference” paper to the accumulating MS vs. healthy control literature, I was surprised when my well-blinded expert readers (Drs. Nancy Fischbein and Greg Zaharchuk) discovered anatomic differences between our study groups. In our paper published in the September 2012 issue of AJNR, we reported anatomic differences between patients with MS and healthy subjects—notably, patients with MS had greater internal jugular vein (IJV) flattening and a trend toward more non-IJV collaterals than healthy subjects.
Furthermore, at present there is no convincing evidence that endovascular therapy provides any benefit to patients with MS, and it may in fact pose unnecessary risk. Conversely, endovascular therapy does seem to benefit some patients with idiopathic intracranial hypertension.
The importance of venous sinus disease as a cause of idiopathic intracranial hypertension is probably underestimated. Patients with idiopathic intracranial hypertension should be evaluated with direct retrograde cerebral venography and manometry. In patients with venous sinus lesions, treatment by an endoluminal venous sinus stent is a safe and effective alternative for amenable lesions.
The pathophysiological mechanism in IIH requires further elucidation, but venous sinus stenosis with subsequent intracranial hypertension appears to be an important mechanism in at least a subgroup of patients with IIH. Among these patients, 78% had complete relief or improvement of their main presenting symptoms after endovascular stenting. Resolution or improvement in papilledema was seen in 85.1% of patients. Endovascular stenting should be considered whenever venous sinus stenosis is diagnosed in patients with IIH.
Boo22 wrote:I also wanted to say that I have two shunts in place bc when they did my lumbar puncture the CSF was so built up it squirted out my back and hit the hospital room ceiling! They couldn't get an accurate opening pressure bc the pressure from the CSF made attaching the manometer impossible. They charted it as 55+ immeasurable. This happened again during my shunt surgery two weeks later. When the neurosurgeon drilled the burr hole in my skull, he was hit in the face mask with CSF squirting out.
CSF production, flow and drainage from the brain is inexorably linked to venous drainage from the brain.CSF pressure in the ventricles is normally slightly higher than venous pressure so that it’s flow is toward the veins.
The CSF pressure gradiant is very small so that venous drainage issues, such as back pressure in the veins in the basement of the skull, can affect intracranial compliance. It can also affect cranial hydrodynamics resulting in either too much CSF in the brain, called normal pressure hydrocephalus in adults
In the 1960s, a neurosurgeon in Bogota, Columbia made the controversial claim that he could reverse neurodegeneration by surgically diverting an excess of cerebrospinal fluid (CSF) by placing a shunt in his patients.
Professor Salomon Hakim first published his thesis in 1964 and then published 6 case reports of "normal pressure hydrocephalus" in The New England Journal of Medicine and the Journal of the Neurological Sciences in 1965. Hakim rose to the forefront of academic medicine as he described a newfound ability to reverse symptoms of “neurodegeneration” that had long been considered irreversible.
http://journals.lww.com/neurosurgery/Ab ... re.21.aspx
It is important to understand that today, 60 years after Hakim's discovery, treating normal pressure hydrocephalus is an accepted practice, even though diagnosing NPH is an inexact science. There were never any double blinded clinical trials for this surgery. Hakim claimed he could reverse gait impairment, cognitive problems and urinary incontinence by diverting CSF flow. And the proof was in his patients' recovery. No one cries "placebo effect!" after a patient recovers mobility, cognition or bladder control once treated for NPH.
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