CCSVI PTA treats IIH? Other options...

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

CCSVI PTA treats IIH? Other options...

Postby Anonymoose » Wed Feb 13, 2013 9:15 am

I know a lot of us suspect improved CSF drainage/IIH correction causes many of the post-PTA improvements. That means PTA is not the only treatment option available for symptoms caused by cranial nerve/medulla compression. We know chiropractic/atlas treatment is also a viable option for treating IIH. There are more alternative methods (which happen to be more mainstream than PTA or AO treatments), "surgeries" and medications...some of which are currently being trialed for use with MS.

CCSVI PTA and atlas adjustment work for some, but not all. And, especially for PTA, we can't expect the treatment to last forever. We need backup. These two treatments have given us priceless clues as to how we can alleviate some of the worst MS symptoms. We need to focus on those clues.

Don't stop exploring just because PTA/atlas work didn't help you or stopped helping you. The doctors and researchers have all the time in the world to figure this out. We don't. This is your health and your isn't about banging the drum for one treatment. It's about saving ourselves. WE need to keep looking and trying new things.

IIH symptoms from wiki ... pertension
The most common symptom of IIH is headache, which occurs in almost all (92–94%) cases. It is characteristically worse in the morning, generalized in character and throbbing in nature. It may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. The pain may also be experienced in the neck and shoulders.[1] Many have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse.[1][2] Various other symptoms, such as numbness of the extremities, generalized weakness, loss of smell, and loss of coordination, are reported more rarely; none are specific for IIH.[1] In children, numerous nonspecific signs and symptoms may be present.[3]
The increased pressure leads to compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck. Most commonly, the abducens nerve (sixth nerve) is involved. This nerve supplies the muscle that pulls the eye outward. Those with sixth nerve palsy therefore experience horizontal double vision which is worse when looking towards the affected side. More rarely, the oculomotor nerve and trochlear nerve (third and fourth nerve palsy, respectively) are affected; both play a role in eye movements.[3][4] The facial nerve (seventh cranial nerve) is affected occasionally –- the result is total or partial weakness of the muscles of facial expression on one or both sides of the face.[1]
The increased pressure leads to papilledema, which is swelling of the optic disc, the spot where the optic nerve enters the eyeball. This occurs in practically all cases of IIH, but not everyone experiences symptoms from this. Those who do experience symptoms typically report "transient visual obscurations", episodes of difficulty seeing that occur in both eyes but not necessarily at the same time. Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision.[1][5]

MORE OPTIONS: ... 99172.aspx
Idiopathic Intracranial Hypertension Associated with Either Primary Or Secondary Aldosteronism
Khan, M. Usman MD; Khalid, Heena MD; Salpietro, Vincenzo MD; Weber, Karl T. MD
Published Ahead-of-Print
Background: Idiopathic intracranial hypertension (IIH) is a syndrome consisting of headache, visual field defects and papilledema of uncertain etiology. The prospect was raised previously as to an association between aldosteronism and increased intracranial pressure in 2 middle-aged women with IIH and primary aldosteronism (PAL). Since then, 2 additional adults were identified and 2 other cases were reported from the United Kingdom, whereas 6 cases of IIH and secondary aldosteronism (SAL) in children have been reported in the English literature worldwide.

Methods: A retrospective analysis of cases from author institutions and published literature comparing clinical features, laboratory findings and therapeutic interventions in these 12 cases.

Results: The female-to-male ratio was 10:2. The mean age of the PAL patients was 49 +/- 3 years-all hypertensive, with adrenal pathology in most. The mean age of the SAL patients was 11 +/- 2 years-mostly normotensive, with 3 having Bartter's and 2 Gitelman syndromes, and 1 renal congenital hypoplasia. Plasma aldosterone levels were elevated (31 +/- 5 ng/dL) in PAL and SAL, whereas plasma renin activity was suppressed in PAL. Hypokalemia (3.2 +/- 0.2 mmol/L), hypomagnesemia (1.6 +/- 0.3 mg/dL) and a putative metabolic alkalosis (serum HCO3 30 +/- 1 mmol/L) were observed. IIH symptoms were controlled by spironolactone in 5, amiloride in 1, correction of hypokalemia and hypomagnesemia in 2, discontinuation of nonsteroidal anti-inflammatory drugs in 2, and reduction of body weight in 1. One patient required serial lumbar punctures, 2 a ventriculoperitoneal shunt, whereas all 3 patients with adrenal adenoma underwent surgical resection.

Conclusions: An association between IIH and PAL occurs in hypertensive middle-aged women, whereas normotensive girls having an inherited renal tubular defect may have IIH with SAL. Patients with IIH should be evaluated for aldosteronism and considered for spironolactone therapy.

(C) Copyright 2013 Southern Society for Clinical Investigation
Idiopathic intracranial hypertension.
Binder DK, Horton JC, Lawton MT, McDermott MW.
Department of Neurological Surgery, University of California, San Francisco, San Francisco, California 94143-0112, USA.
The history, diagnosis, and therapy of idiopathic intracranial hypertension (IIH) (pseudotumor cerebri) are reviewed. Theories of pathogenesis are considered, the clinical presentation is described, and potential diagnostic and therapeutic challenges are explored.
An extensive literature review of IIH and related conditions (secondary pseudotumor syndromes) was performed. The history of and rationale for the diagnosis and medical and surgical approaches to treatment are reviewed. Available outcome studies are presented.
Diagnosis of IIH requires that the modified Dandy criteria be satisfied. Multiple potential contributing causes of intracranial hypertension must be identified or excluded. The clinical presentation most often includes headaches and papilledema, but many other findings have been described. The most important goal of therapy is to prevent or arrest progressive visual loss. Medical therapies include alleviation of associated systemic diseases, discontinuation of contributing medications, provision of carbonic anhydrase inhibitors, and weight loss. Surgical therapies include lumboperitoneal shunting, ventriculoperitoneal shunting, and optic nerve sheath fenestration. On the basis of the advantages and disadvantages of these treatment modalities, a suggested treatment paradigm is presented.
Idiopathic intracranial hypertension is the term to be adopted instead of pseudotumor cerebri. IIH remains an enigmatic diagnosis of exclusion. However, prompt diagnosis and thorough evaluation and treatment are crucial for preventing visual loss and improving associated symptoms.

Sitting back, feeling hopeless/helpless, and endlessly tossing about theories will get us nowhere. Research, post your ideas, discuss, choose a treatment option and share the results. *WE* can move things forward. :smiley cracks a whip:
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