Spina Bifida Medication

  • Author: Mark R Foster, MD, PhD, FACS; Chief Editor: Consuelo T Lorenzo, MD   more...
 
Updated: Aug 25, 2011
 

Medication Summary

The medications used most frequently in myelomeningocele are for treatment of neurogenic bladder dysfunction. These medications are used in conjunction with some form of bladder emptying technique to prevent upper urinary tract complications and to facilitate social continence.

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Anticholinergics

Class Summary

Anticholinergics are employed to suppress detrusor overactivity.

Oxybutynin chloride (Ditropan, XL, Gelnique, Oxytrol)

 

Oxybutynin exerts direct antispasmodic effect on smooth muscle and inhibits muscarinic action of acetylcholine on smooth muscle. It is used to decrease bladder contractility and reduce detrusor-sphincter dyssynergia. Intravesical instillation of oxybutynin is associated with fewer side effects. A long-acting oral form is also available for once-daily dosing.

Hyoscyamine sulfate (Levsin, Levbid, Symax, Anaspaz, HyoMax)

 

Through parasympatholytic action, hyoscyamine relaxes smooth muscle spasm. It is indicated in management of lower urinary tract disorder associated with hypermotility.

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Tricyclic Antidepressants

Class Summary

Tricyclic antidepressants may act through anticholinergic effects

Imipramine hydrochloride (Tofranil)

 

Imipramine has significant anticholinergic activity, as well as some alpha-adrenergic activity. These combined effects may improve bladder-urethral storage function.

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Alpha-Adrenergic Antagonists

Class Summary

Alpha-adrenergic receptors are found in the bladder neck and urethra. Alpha-adrenergic antagonists decrease bladder outlet resistance, increase urinary flow rate, and improve bladder emptying.

Terazosin

 

Terazosin is an alpha 1-adrenergic blocking agent that decreases smooth muscle tone in the bladder neck, leading to reduction of bladder outlet obstruction without affecting bladder contractility. Its major side effects are postural hypotension and syncope, which can be avoided by starting at lowest dose and increasing slowly. If terazosin therapy is discontinued for several days, restart using the initial dosing regimen.

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Contributor Information and Disclosures
Author

Mark R Foster, MD, PhD, FACS  President and Orthopedic Surgeon, Orthopedic Spine Specialists of Western Pennsylvania, PC

Mark R Foster, MD, PhD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Physical Society, Christian Medical & Dental Society, Eastern Orthopaedic Association, North American Spine Society, Orthopaedic Research Society, and Pennsylvania Orthopaedic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Kat Kolaski, MD  Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Lee H Riley III, MD  Chief, Division of Orthopedic Spine Surgery, Associate Professor, Departments of Orthopedic Surgery and Neurosurgery, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Teresa L Massagli, MD  Professor of Rehabilitation Medicine and Pediatrics, University of Washington School of Medicine

Teresa L Massagli, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Kat Kolaski, MD  Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Mary Ann E Keenan, MD  Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania

Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health, Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

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The lumbar region of a newborn baby with myelomeningocele. The skin is intact, and the placode-containing remnants of nervous tissue can be observed in the center of the lesion, which is filled with cerebrospinal fluid.
Myelomeningocele in a newborn.
T1-weighted, coronal magnetic resonance imaging (MRI) scans of the brain show a Chiari II malformation. Note the stretching of the brainstem, aqueduct, and fourth ventricle.
Neonate with a lumbar myelomeningocele with an L5 neurologic level. Note the diaphanous sac filled with cerebrospinal fluid and containing fragile vessels in its membrane. Also, note the neural placode plastered to the dorsal surface of the sac. This patient underwent closure of his back and an untethering of his neural placode. The neural placode was circumnavigated and placed in the neural canal. A dural sleeve was fashioned in a way that reconstructed neural tube geometry.
Sagittal, T1-weighted magnetic resonance imaging (MRI) scan of a child after closure of his myelomeningocele. Child is aged 7 years. Note the spinal cord ends in the sacral region far below the normal level of T12-L1. It is tethered at the point at which the neural placode was attached to the skin defect during gestation. The MRI scan showed dorsal tethering, and the child complained of back pain and had a new foot deformity on examination. By definition, all children with a myelomeningocele have a tethered cord on MRI, but only about 20% of children require an operation to untether the spinal cord during their first decade of life, during their rapid growth spurts. Thus, the MRI scan must be placed in context of a history and examination consistent with mechanical tethering and a resultant neurologic deterioration.
Axial T1-weighted MRI scan of a 15-year-old girl who was born with thoracic myelomeningocele, hydrocephalus, and Arnold-Chiari II syndrome. She was treated with a ventriculoperitoneal shunt. The ventricular system has a characteristic shape, with small frontal and large occipital horns, which are typical in patients with spina bifida. The shunt tube is shown in the right parietal region.
 
 
 
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