Int J Clin Pract. 2009 Mar;63(3):457-61.http://www.ncbi.nlm.nih.gov/pubmed/19222630
Hyponatraemia in patients with normal pressure hydrocephalus.
Chou CY, Liu JH, Wang SM, Yang YF, Lin HH, Liu YL, Huang CC.
Division of Nephrology, Department of Internal Medicine, China Medical University Hospital, North District, Taichung, Taiwan.
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).
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.
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.
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.
In normal pressure hydrocephalus patients have too little sodium. Patients with MS have sodium in their brains...Sodium seems to be quite important for cerebrospinal disease.
South Med J. 1991 Feb;84(2):279-80.http://www.ncbi.nlm.nih.gov/pubmed/1990472
Cerebrospinal fluid losses through ventricular catheters leading to hyponatremia in two children.
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Hospital, Baltimore, MD.
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]
When the brain's ventricles are drained mechanically for hydrocephalus, patients lose a lot of sodium which the above author replaces with salty water into the CSF.
Is the CSF being displaced into the MS brain and leaving salt in there because it isn't draining properly into the dural sinuses?
Neurol Neurochir Pol. 1980 Jul-Aug;14(4):411-7.http://www.ncbi.nlm.nih.gov/pubmed/7412996
[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.
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]
Saline administration affects (i think) the cerebrospinal pressure differently depending on whether you have open hydrocephalus or closed hydrocephalus.
Ann Neurol. 2012 Feb;71(2):186-94. doi: 10.1002/ana.22665.http://www.ncbi.nlm.nih.gov/pubmed/22367990
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.
Department of Neurology, Yale University School of Medicine, New Haven, CT, USA.
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.
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.
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.
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.