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Hydrocephalus Medication

  • Author: Stephen L Nelson, Jr, MD, PhD, FAAP; Chief Editor: Jasvinder Chawla, MD, MBA  more...
 
Updated: Apr 13, 2016
 

Medication Summary

Acetazolamide (ACZ) and furosemide (FUR) treat posthemorrhagic hydrocephalus in neonates. Both are diuretics that also appear to decrease secretion of CSF at the level of the choroid plexus. ACZ can be used alone or in conjunction with FUR. The combination enhances efficacy of ACZ in decreasing CSF secretion by the choroid plexus. If ACZ is used alone, it appears to lower risk of nephrocalcinosis significantly.

Medication as treatment for hydrocephalus is controversial. It should be used only as a temporary measure for posthemorrhagic hydrocephalus in neonates.

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Carbonic anhydrase inhibitors

Class Summary

These agents inhibit an enzyme found in many tissues of the body that catalyzes a reversible reaction in which carbon dioxide becomes hydrated and carbonic acid dehydrated. These changes may result in a decrease in CSF production by the choroid plexus.

Acetazolamide (Diamox)

 

Noncompetitive reversible inhibitor of enzyme carbonic anhydrase, which catalyzes the reaction between water and carbon dioxide, resulting in protons and carbonate. This contributes to decreasing CSF secretion by choroid plexus.

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Loop diuretics

Class Summary

These agents increase excretion of water by interfering with the chloride-binding cotransport system, which results from inhibition of reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule.

Furosemide (Lasix)

 

Mechanisms proposed for lowering ICP include lowering cerebral sodium uptake, affecting water transport into astroglial cells by inhibiting cellular membrane cation-chloride pump, and decreasing CSF production by inhibiting carbonic anhydrase. Used as adjunctive therapy with ACZ in temporary treatment of posthemorrhagic hydrocephalus in neonates.

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Contributor Information and Disclosures
Author

Stephen L Nelson, Jr, MD, PhD, FAAP Section Head of Pediatric Neurology, Associate Professor of Pediatrics, Neurology, and Psychiatry, Tulane University School of Medicine

Stephen L Nelson, Jr, MD, PhD, FAAP is a member of the following medical societies: Academic Pediatric Association, American Academy of Neurology, American Academy of Pediatrics, American Medical Association, Association of Military Surgeons of the US, Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Anthony M Murro, MD Professor, Laboratory Director, Department of Neurology, Medical College of Georgia, Georgia Regents University

Anthony M Murro, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Nothing to disclose.

Acknowledgements

Alberto J Espay, MD, MSc Associate Professor, Director of Clinical Research, Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati College of Medicine

Alberto J Espay, MD, MSc is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Abbott Consulting fee Consulting; Chelsea therapeutics Consulting fee Consulting; Novartis Honoraria Speaking and teaching; TEVA Consulting fee Consulting; NIH Grant/research funds K23 Career Development Award; Eli Lilly Consulting fee Consulting; Great Lakes Neurotechnologies Other; Michael J Fox Foundation Grant/research funds Other; Lippincott Williams & Wilkins Royalty Book; American Academy of Neurology Honoraria Speaking and teaching

Eugenia-Daniela Hord, MD Instructor, Departments of Anesthesia and Neurology, Massachusetts General Hospital Pain Center, Harvard Medical School

Eugenia-Daniela Hord, MD is a member of the following medical societies: American Academy of Neurology and American Pain Society

Disclosure: Nothing to disclose.

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Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.
Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.
Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.
Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recovery (FLAIR) sequences. Note that apical cuts (lower row) do not show enlargement of the sulci, as is expected in generalized atrophy. Pathological evaluation of this brain demonstrated hydrocephalus with no microvascular pathology corresponding with the signal abnormality (which likely reflects transependymal exudate) and normal brain weight (indicating that the sulci enlargement was due to increased subarachnoid cerebrospinal fluid [CSF] conveying a pseudoatrophic brain pattern).
 
 
 
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