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Just clutchIng at straws obviously! I think I improved a good deal after stopping enoxaparin after my recent pregnancies but that might just be the vasculature returning to normal after pregnancy. I can't quite believe that I have restenosed so soon after treatment (within 24hours). I have had such odd up and down symptoms in the last 3 weeks...

... with a near constant ache where the skull meets the spine that I have no idea what is going on. I will need rescanning if the symptoms remain like this.

Int J Clin Pract. 2009 Mar;63(3):457-61.
Hyponatraemia in patients with normal pressure hydrocephalus.
Chou CY, Liu JH, Wang SM, Yang YF, Lin HH, Liu YL, Huang CC.
Source
Division of Nephrology, Department of Internal Medicine, China Medical University Hospital, North District, Taichung, Taiwan.
Abstract
BACKGROUND:
In clinical practice, hyponatraemia was frequently found in patients with hydrocephalus. We conducted this study to determine the prevalence and risk factors for hyponatraemia in patients with normal pressure hydrocephalus (NPH).
METHODS:
We retrospectively reviewed all patients with NPH who were admitted to China Medical University Hospital between 1998 and 2006. Hyponatraemia was defined as a plasma sodium concentration < 135 mEq/l on admission. Possible risk factors between patients with and without hyponatraemia were analysed using Student's t-test or chi2 test. The association between hyponatraemia and possible factors was analysed using multivariate logistic regression. The odds ratio was calculated to determine the effect of possible risk factors.
RESULTS:
A total of 146 patients (84 men and 62 women) who had NPH with a mean age of 66.1 +/- 15.9 years old were reviewed and 33 (22.6%) patients were found having hyponatraemia. Patients who developed hyponatraemia had a significantly higher prevalence of hypertension, use of nasogastric tube (NG), bed-ridden status and fever. In multivariate logistic regression, the presence of hypertension and the use of NG were two important risk factors for hyponatraemia. The odds ratio (95% CI) for hypertension and NG were 2.604 (95% CI: 1.136-5.967, p = 0.024) and 7.179 (95% CI: 2.3-22.409, p = 0.001) respectively.
CONCLUSION:
Hyponatraemia is not uncommon in patients with NPH. Physicians should be aware of this complication and obtain necessary laboratory examination for early detection of hyponatraemia.

South Med J. 1991 Feb;84(2):279-80.
Cerebrospinal fluid losses through ventricular catheters leading to hyponatremia in two children.
Tobias JD.
Source
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Hospital, Baltimore, MD.
Abstract
I have presented two cases of patients with hyponatremia due to excessive cerebrospinal fluid losses from ventricular drains. The possibility of such losses exists whether the drain is used to treat hydrocephalus or to monitor intracranial pressure. I find normal saline (sodium concentration = 154 mEq/L) to be an appropriate fluid to replace ongoing losses of cerebrospinal fluid from a ventricular drain and currently start such replacement therapy (mL for mL) when the drain is placed.
PMID: 1990472 [PubMed - indexed for MEDLINE]

Neurol Neurochir Pol. 1980 Jul-Aug;14(4):411-7.
[Studies on the cerebrospinal fluid pressure changes in patients treated for hydrocephalus by the so-called ventricular filling test. Preliminary report].
[Article in Polish]
Muszyński A, Koźniewska H, Moszyński K, Stocka-Muszyńska Z.
Abstract
The curves of cerebrospinal fluid pressure (CFP) in the lateral cerebral ventricle during the so called ventricular filling-up test are presented in 6 patients with high-pressure and medium-pressure hydrocephalus as compared with CFP curves obtained in 2 patients with low-pressure hydrocephalus. The method of filling-up test (infusion test) is described. In this method portions of normal saline 2 ml each are administered rapidly into a lateral ventricle every 30 seconds. The obtained results demonstrated a difference in the shape of the CFP curves in patients with low-pressure open hydrocephalus as compared with patients with closed hydrocephalus. This could help in qualifying patients with hydrocephalus for treatment with ventriculo-atrial shunt.
PMID: 7412996 [PubMed - indexed for MEDLINE]

Ann Neurol. 2012 Feb;71(2):186-94. doi: 10.1002/ana.22665.
A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.
Shields SD, Cheng X, Gasser A, Saab CY, Tyrrell L, Eastman EM, Iwata M, Zwinger PJ, Black JA, Dib-Hajj SD, Waxman SG.
Source
Department of Neurology, Yale University School of Medicine, New Haven, CT, USA.
Abstract
OBJECTIVE:
Cerebellar dysfunction in multiple sclerosis (MS) contributes significantly to disability, is relatively refractory to symptomatic therapy, and often progresses despite treatment with disease-modifying agents. We previously observed that sodium channel Nav1.8, whose expression is normally restricted to the peripheral nervous system, is present in cerebellar Purkinje neurons in a mouse model of MS (experimental autoimmune encephalomyelitis [EAE]) and in humans with MS. Here, we tested the hypothesis that upregulation of Nav1.8 in cerebellum in MS and EAE has functional consequences contributing to symptom burden.
METHODS:
Electrophysiology and behavioral assessment were performed in a new transgenic mouse model overexpressing Nav1.8 in Purkinje neurons. We also measured EAE symptom progression in mice lacking Nav1.8 compared to wild-type littermates. Finally, we administered the Nav1.8-selective blocker A803467 in the context of previously established EAE to determine reversibility of MS-like deficits.
RESULTS:
We report that, in the context of an otherwise healthy nervous system, ectopic expression of Nav1.8 in Purkinje neurons alters their electrophysiological properties, and disrupts coordinated motor behaviors. Additionally, we show that Nav1.8 expression contributes to symptom development in EAE. Finally, we demonstrate that abnormal patterns of Purkinje neuron firing and MS-like deficits in EAE can be partially reversed by pharmacotherapy using a Nav1.8-selective blocker.
INTERPRETATION:
Our results add to the evidence that a channelopathy contributes to cerebellar dysfunction in MS. Our data suggest that Nav1.8-specific blockers, when available for humans, merit study in MS.
Copyright © 2012 American Neurological Association.

Despite the deterioration in my leg and foot since the surgery I would like to note that one striking thing which HAS definitely improved is my appetite! I used to feel totally apathetic about eating, especially after a coffee at breakfast but now I am eating proper manly adult portions! .... After each pregnancy my appetite dramatically dropped as would my weight but now I think I stand a chance of gaining weight. Weird.

Nutcracker syndrome: symptoms of syncope and hypotension improved following endovascular stenting.
Daily R, Matteo J, Loper T, Northup M.
Source
University of Florida, Shands Jacksonville, Jacksonville, FL 32209, USA.
Abstract
'Nutcracker syndrome' encompasses classical symptoms of hematuria and flank pain resulting from the compression of the left renal vein between the aorta and the superior mesenteric artery. In patients with unexplained left-sided hematuria, flank pain or non-specific abdominal pain, careful interrogation of diagnostic abdominal imaging should be performed to exclude the possibility of external compression on the left renal vein. The patient discussed in this case report is a 19-year-old woman with unilateral hematuria. Her symptoms started 13 months prior with nausea, lower abdominal pain and weight loss. Six months after the nausea began, she started having syncope, sometimes multiple episodes in one day. Syncope is one of the more rarely reported symptoms associated with nutcracker syndrome. As more cases are reported, endovascular repair is becoming an alternative treatment for nutcracker syndrome. The patient was treated with stenting of her left renal vein. At the three-week follow-up, she reported near resolution of nausea and abdominal pain. She had gained four pounds, no longer had gross hematuria and had had no episodes of syncope and her blood pressure had normalized. Endovascular specialists should be aware of the variety of symptoms that can occur with nutcracker syndrome, including syncope. The severity of these symptoms should guide the recommendation for intervention.

NCS is associated with hematuria (which can lead to anemia)[3] and abdominal pain (classically left flank pain).[4]
Since the left gonad drains via the left renal vein it can also result in left testicular pain[5] in men or left lower quadrant pain in women. Nausea and vomiting can result due to compression of the splanchnic veins.[5] An unusual manifestation of NCS includes varicocele formation and varicose veins in the lower limbs.[6] Another clinical study has shown that that nutcracker syndrome is a frequent finding in varicocele-affected patients and possibly, nutcracker syndrome should be routinely excluded as a possible cause of varicocele.[7]