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Normal Pressure Hydrocephalus Follow-up

  • Author: Michael J Schneck, MD, MBA; Chief Editor: Selim R Benbadis, MD  more...
Updated: Jul 12, 2016


The overall prognosis of NPH remains poor both due to a lack of improvement in some patients following surgery as well as a significant complication rate. In a study by Vanneste et al, one of the more comprehensive studies described above, marked improvement was noted in only 21% of patients following shunt surgery. Complication rate was approximately 28% with death or severe residual morbidity in 7% of patients, further emphasizing the importance of careful patient selection.[24] Concomitant cerebrovascular disease is a recognized negative prognostic factor.[25]

In a small prospective study, Hamilton et al measured the impact of cortical Alzheimer disease pathology on shunt responsiveness in 37 individuals treated for idiopathic NPH. Clinical measures, including neuropsychometrics and gait, were correlated with amyloid β (Aβ) plaques, neuritic plaques, and neurofibrillary tangles observed in cortical biopsies obtained during shunt insertion. Patients with no tau and Aβ pathology and mild tau and Aβ pathology improved on the neuropsychometric and gait evaluations. In contrast, patients with moderate-to-severe pathology did not show improvement on any study measure. However, the relatively small numbers in the study, presence of contradictory studies, and absence of a widely accepted biomarker for Alzheimer disease make it difficult to use this finding while evaluating patients with NPH.[26]

In patients who develop recurrent symptoms after initial improvement, shunt malfunction should be suspected and an evaluation for mechanical failure should be pursued. In some of these cases, catheter migration may have occurred, which is a correctable cause of shunt malfunction. In one case series, shunt revision was required in more than half of treated patients over a 6-year period, with improvement in most of these patients.[27]

The incidence of shunt complications is estimated in 30-40% of patients.[21] These include anesthetic complications, intracranial hemorrhage from placement of the ventricular catheter, infection, CSF hypotensive headaches, subdural hematomas, shunt occlusion, and catheter breakage. Rapid reduction in ventricular size following the shunt favors complications such as subdural hematoma, which may occur in 2-17% of patients.[21] Dual-switch valves and programmable valves may reduce the incidence of this complication.[28]


Patient Education

For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education article Normal Pressure Hydrocephalus.

Contributor Information and Disclosures

Michael J Schneck, MD, MBA Vice Chair and Professor, Departments of Neurology and Neurosurgery, Loyola University, Chicago Stritch School of Medicine; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center

Michael J Schneck, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, Stroke Council of the American Heart Association, Neurocritical Care Society

Disclosure: Received honoraria from Boehringer-Ingelheim for speaking and teaching; Received honoraria from Sanofi/BMS for speaking and teaching; Received honoraria from Pfizer for speaking and teaching; Received honoraria from UCB Pharma for speaking and teaching; Received consulting fee from Talecris for other; Received grant/research funds from NMT Medical for independent contractor; Received grant/research funds from NIH for independent contractor; Received grant/research funds from Sanofi for independe.

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.

Nestor Galvez-Jimenez, MD, MSc, MHA The Pauline M Braathen Endowed Chair in Neurology, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, International Parkinson and Movement Disorder Society

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

Additional Contributors

Arif I Dalvi, MD Director, Movement Disorders Center, NorthShore University Health System; Clinical Associate Professor of Neurology, University of Chicago Pritzker Medical School

Arif I Dalvi, MD is a member of the following medical societies: International Parkinson and Movement Disorder Society, European Neurological Society

Disclosure: Nothing to disclose.

Ashvini P Premkumar, MD Associate Director, Movement Disorders Center, NorthShore University HealthSystem, Clinical Instructor of Neurology, University of Chicago Pritzker Medical School

Ashvini P Premkumar, MD is a member of the following medical societies: American Academy of Neurology, International Parkinson and Movement Disorder Society

Disclosure: Nothing to disclose.

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T2-weighted MRI showing dilatation of ventricles out of proportion to sulcal atrophy in a patient with normal pressure hydrocephalus. The arrow points to transependymal flow.
CT head scan of a patient with normal pressure hydrocephalus showing dilated ventricles. The arrow points to a rounded frontal horn.
This image shows ventriculomegaly, which is typical in hydrocephalus ex vacuo.
This image shows cortical atrophy, which is the defining feature of hydrocephalus ex vacuo.
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