AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

First described by Hakim and Adams in 1965, normal pressure hydrocephalus (NPH) refers to a clinical entity consisting of the triad of gait disturbance, dementia, and incontinence, coupled with the laboratory findings of normal cerebrospinal fluid (CSF) pressures and radiographic findings of ventriculomegaly.¹ Although NPH is a relatively rare cause of dementia, identifying NPH is important because it is one of the few treatable entities.

See Normal Pressure Hydrocephalus in eMedicine's Neurology journal for an in-depth description of NPH as a clinical entity.

Pathophysiology

Although the pathophysiology of NPH has been under debate for decades, aberrations in CSF flow dynamics generally are considered to be central to the condition's development. One proposed mechanism involves a transmantle pressure gradient wherein CSF pressure in the ventricles is greater than CSF pressure in the subarachnoid space. Short-lasting CSF pulsations (B waves) periodically apply pressure to the ventricular walls and have a water-hammer effect that enlarges the ventricles. Abnormalities of ventricular wall compliance may contribute to ventricular dilatation.

Another mechanism involved in increasing transmantle pressure is impaired CSF flow, which may be at the level of the aqueduct (noncommunicating NPH) or distal to it (communicating NPH). In either case, flow is impaired enough to increase the transmantle CSF pressure gradient but not enough to raise intracranial pressure.

With respect to etiology of NPH, approximately 50% of cases generally are accepted to be idiopathic. In the other 50% of patients, there exists a history of events that can alter CSF flow dynamics, such as subarachnoid hemorrhage, trauma, meningitis, or surgery.

Frequency

United States

NPH is relatively rare, and the exact incidence and prevalence in the United States is not known.  However, some experts believe that NPH may cause up to 5% of cases of dementia. Thus, an estimated 750,000 Americans may have NPH, but this is probably an overestimation. Hospital discharge data suggest that annually around 11,500 patients in the United States are diagnosed with NPH.

International

Estimates have placed the frequency of NPH at approximately 1 case per 25,000 cases of dementia or as high as 6% of patients with dementia.^{2, 3, 4} Vanneste and colleagues suggest that the incidence of shunt-responsive NPH represents approximately 0.4% of patients with dementia.⁵ These estimates have been derived from US and European data.

Mortality/Morbidity

The natural course of NPH appears to be a continual cognitive and motor decline, akinetic mutism, and eventual death, although this prognosis has been clouded by the tendency towards surgical intervention since the first description of NPH in the mid-1960s.

• To the authors' knowledge, no trials have utilized control subjects in studying the treatment of patients with NPH. Thus, morbidity and mortality information for NPH must largely be derived through analysis of the success and complications of surgical treatment. Further, due to the age group afflicted, other complicating medical issues often affect morbidity and mortality.
• Traditionally, the success of CSF shunting in NPH is reported as follows^{6, 7, 8}:
  
  
  • One third of patients improve
  • One third of patients experience arrested symptom progression
  • One third of patients continue to deteriorate
  • Approximately one third of patients experience complications
• A further breakdown of treatment success by Vanneste and colleagues suggests that a 50-70% improvement may be seen in select patients with NPH with a known etiology.⁵ Postoperative complications still occurred in approximately one third, although only 5-15% of cases involved death or severe, residual morbidity. This resulted in a benefit-to-harm ratio of 3:1 in nonidiopathic NPH; the ratio was only 1.7:1 in idiopathic NPH.

Race

No racial predilection has been described in NPH.

Sex

NPH occurs with approximately equal frequency in males and females.

Age

NPH occurs more frequently with age and typically is diagnosed in the sixth or seventh decade of life.

Anatomy

NPH involves ventricular enlargement without increased CSF pressure. A disproportionate lack of sulcal enlargement exists because of the proposed transmantle pressure gradient.

Anatomically, this means an enlarged third ventricle exists along with dilation of the occipital, frontal, and temporal horns of the lateral ventricles. Presumably, the periventricular white matter is stretched and dysfunctional as a result of inadequate perfusion without actually being infarcted.^{9, 10, 11}

The proposed dysfunctional periventricular white matter tracts are related to the clinical presentation of NPH, since observed dementia is of a subcortical nature. Disruption of periventricular white matter tracts may explain gait disturbance and incontinence. Further, a perfusion deficit without infarction can explain the partial success of CSF shunting, which may reduce the stretching of the periventricular white matter tracts and restore some perfusion.

Some functional and neuroimaging data suggest corpus callosum functioning is impaired in NPH.^{12, 13}

Clinical Details

NPH classically presents with the clinical triad of gait disturbance, dementia, and urinary incontinence. Hydrocephalus, along with a normal CSF opening pressure, also is required to define NPH. The presence of hydrocephalus is ascertained via neuroimaging, while CSF pressures are determined by using lumbar puncture.

The gait disturbance in NPH has been described as appearing to be magnetic in nature, with the patient finding it difficult to initiate movement. The term gait apraxia frequently is used in NPH but is considered incorrect by some authors, since patients with NPH can exhibit near-normal walking movements when supported.^{14, 15} Patients with NPH demonstrate a short-stepped, shuffling gait with postural instability. Because this gait disorder is frequently the first clinical sign, the presentation may be confused with that of an extrapyramidal disorder, such as Parkinson disease.

The mental deterioration observed is frequently mild and is subcortical in nature. Memory problems, poor attention, and slowing of information processing are observed.

Urinary incontinence usually is present only in advanced cases and likely results from disruption of periventricular pathways to the sacral bladder center. This results in decreased inhibition of bladder contractions and, consequently, instability of bladder detrusors. Only in extremely advanced cases of NPH, with severe frontal lobe dysfunction, is incontinence a result of lack of concern for micturition.

Due to the high prevalence in the elderly of each independent feature of the NPH triad, paraclinical tests are paramount in attempting to predict who will benefit from neurosurgical CSF shunting. For example, clinical improvement resulting from large-volume CSF tapping may predict some success from shunting. Typically, the tapping procedure involves the removal of 40-50 mL of CSF, with monitoring of gait and memory. Unfortunately, this test is associated with a high rate of false negatives, and some authors have suggested that a more aggressive, continuous removal of CSF on the order of 150-200 mL be conducted daily for 3-5 days to better detect which patients will improve with shunting.¹⁶

Another invasive technique that has been utilized in an attempt to predict CSF-shunting success is lumbar infusion, wherein pressure dynamics are monitored following the infusion of saline. This test is rarely used in clinical practice, although it could be of reasonable value in certain circumstances.

A review of the above clinical tests and their value in predicting benefit from CSF shunting is provided by Marmarou and colleagues.¹⁷

Preferred Examination

Magnetic resonance imaging (MRI) of the brain is the preferred radiologic examination for the diagnosis of NPH, especially with T2-weighted images. Computed tomography (CT) scanning of the brain is useful if MRI is unavailable. Both radiologic techniques require clinical correlation.

Limitations of Techniques

The primary role of CT scanning and MRI is to assess for hydrocephalus with ventriculosulcal disproportion. This observation is a subjective assessment, and in patients with some sulcal widening or only minimal ventriculomegaly, the studies may not be sensitive or specific.

Patient Education: For excellent patient education resources, visit eMedicine's Dementia Center. Also, see eMedicine's patient education article Normal Pressure Hydrocephalus.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Obstructive hydrocephalus
Cerebral atrophy with ex vacuo ventricular dilatation

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Plain radiographs, in the form of pneumoencephalographs, have been replaced by CT scans and magnetic resonance images for the diagnosis of hydrocephalus and now remain only of historical interest. Pneumoencephalography was used to demonstrate nonobstructive hydrocephalus. Intrathecally introduced air (via lumbar puncture) was found, on radiographs, within the enlarged lateral ventricles and not in the subarachnoid convexities.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

In patients with NPH, CT scans demonstrate hydrocephalus, with ventriculomegaly that is out of proportion to sulcal atrophy. This so-called ventriculosulcal disproportion differentiates NPH from ex vacuo ventriculomegaly, in which sulcal atrophy should also be present.

In NPH, ventriculomegaly is prominent in all 3 horns of the lateral ventricles and in the third ventricle, with relative sparing of the fourth ventricle.

Frontal and occipital periventricular hypoattenuating areas, which may represent transependymal CSF flow, may be noted in NPH, but this sign is infrequent and often may represent periventricular leukoencephalopathy of microangiopathic disease.

Another finding possibly associated with NPH is corpus callosal thinning, although this finding is nonspecific and can be associated with many other conditions.

Degree of Confidence

CT scanning alone cannot be used to make a diagnosis of NPH, since the clinical picture and CSF pressures also are necessary in diagnosis. With an appropriate clinical picture and ventriculosulcal disproportion demonstrated on either CT or MRI scans, 50-70% of patients are likely to respond favorably to a CSF-shunting procedure (see MRI Degree of Confidence).

False Positives/Negatives

In the diagnosis of NPH, the exact percentage of false-positive and false-negative CT-scan findings is unknown. This is partially because NPH remains an incompletely understood entity, and no criterion standard test exists with which to make an unequivocal diagnosis. Assessing for the ability to predict response to surgery seems more appropriate. Unfortunately, individual patient response to CSF shunting in NPH is variable, and the exact percentage of false-positive and false-negative findings of suggestive CT scans is unclear. Disease entities that may mimic the CT-scan findings of NPH include obstructive hydrocephalus, ex vacuo dilatation secondary to cerebral atrophy, and idiopathic arrested hydrocephalus.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

As in CT scanning, the first abnormality that should be noted on MRI views is ventriculomegaly out of proportion with sulcal atrophy. More specifically, the temporal horns of the lateral ventricles may show dilatation out of proportion with hippocampal atrophy. 

Tsunoda and colleagues used 3-dimensional MRI volume-acquisition techniques to objectively assess ventriculosulcal disproportion.¹⁸ They measured ventricular volume (VV) and intracranial CSF space volume (ICV) and then calculated the VV/ICV ratio. They found that patients with NPH (n = 16) had significantly higher VV/ICV ratios than did the young control subjects (n = 14), the elderly control subjects (n = 13), and patients with cerebrovascular disease (n = 16). The authors found that 13 of the 16 patients with NPH had a VV/ICV ratio greater than 30%, while no patients in the other groups had ratios higher than 30%. Although the neuroimaging hallmark in NPH is ventriculomegaly out of proportion with sulcal atrophy, volumetric analysis via MRI does not seem to help predict patient response to CSF shunting.¹⁹

MRI imaging provides additional physiologic information on NPH compared with CT scanning because an estimate of CSF flow often can be made by using T2-weighted images.

• On T2-weighted images, regions of moving CSF demonstrate no signal instead of the increased signal observed in slow-moving CSF, similar to the flow effects seen with vascular flow voids.
• In patients with NPH, the cerebral aqueduct may demonstrate a pulsatile flow void.
• A jet of turbulent CSF flow may be observed distal to the aqueduct in the fourth ventricle. This finding appears as a hypointense or absent signal in the proximal fourth ventricle on proton density– and T2-weighted images, with surrounding CSF appearing isointense on proton density–weighted images or hyperintense on T2-weighted images.
• MRI may show transependymal CSF flow in the form of a periventricular high signal on T2-weighted images, primarily anterior to the frontal horns or posterior to the occipital horns of the lateral ventricles. However, as with CT imaging, these periventricular abnormalities may be confused with leukoencephalopathy resulting from microvascular ischemia.

Tullberg and colleagues differentiated between periventricular and deep white matter hyperintensity as seen on T2-weighted images and found that neither was predictive of the outcome of CSF shunting.²⁰ Thus, the authors caution that findings compatible with microvascular white matter disease do not predict a poor outcome of CSF shunting.

Jack and coworkers assessed the predictive value of 3 MRI findings with respect to positive response to CSF shunting.²¹ These included CSF flow void sign, periventricular increase signal on T2-weighted images, and corpus callosal thinning. The authors found that only the CSF flow void sign may be predictive of shunt responsiveness and that periventricular signal hyperintensity and corpus callosal morphology are not predictive of positive treatment results.

Bradley and colleagues assessed the predictive value of the presence of a CSF void for shunt responsiveness and found a significant correlation.²² However, in a later study, the researchers did not find a statistically significant relationship between responsiveness to CSF shunting and aqueductal flow void score, but they did find that MRI assessment of CSF flow stroke volume was predictive of shunt responsiveness.²³ Marmarou and colleagues concluded that "neither MRI CSF flow void sign nor quantitative CSF flow velocity seems to have significant diagnostic value," and they questioned whether stroke volume may have some benefit.¹⁷ However, Kahlon suggested that cine phase-contrast MRI measurements of stroke volume in the cerebral aqueduct are not useful in predicting patient response to CSF shunt surgery.²⁴

Tullberg and coworkers found that the presence of periventricular hyperintensity on T2-weighted images, which usually is considered to be evidence of transependymal CSF flow, is not predictive of a good outcome to shunt surgery.²⁰

Studies by Kizu and colleagues using proton chemical shift imaging have suggested that intraventricular lactate measurements may be useful in discriminating patients with NPH from those with other forms of dementia.²⁵ In the study, all 9 patients with clinically diagnosed NPH exhibited ventricular lactate peaks by way of proton chemical shift imaging. No lactate peaks were found in the 5 control subjects or in the 6 patients with other diagnosed dementias, including Alzheimer disease (4), Pick disease (1), and frontotemporal dementia (1).

Degree of Confidence

Degree of confidence in MRI in helping to diagnose NPH or, more importantly, in helping to predict a positive result with neurosurgical CSF shunting is unknown. Positive surgical results are demonstrated in 50-70% of patients with a strong clinical history of NPH and classic NPH findings on magnetic resonance images or CT scans.²⁶

False Positives/Negatives

Similar to CT scanning, MRI contributes to the diagnosis of NPH, but no criterion standard test exists with which to accurately assess the occurrence of false-positive and false-negative findings of MRI alone.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Ultrasonography is not used for the diagnosis of NPH, although some have suggested that reduced cerebral blood flow in NPH can be assessed by using transcranial Doppler ultrasonograms.^{27, 28}

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Traditionally, isotope cisternography and CT cisternography have been used in NPH to assess for disturbances in CSF dynamics, such as reversal of flow. This investigation is likely to be an unreliable predictor of NPH, despite its historical popularity.^{29, 30}

Using single-photon emission computed tomography (SPECT) and statistical brain mapping, Sasaki found regional cerebral blood flow reduction with frontal dominance and severe hypoperfusion around the corpus callosum.¹³ This was consistent with some of the regions of brain dysfunction that clinical assessment has indicated are involved.

Degree of Confidence

Isotope cisternography and CT cisternography appear to be unreliable in helping to predict whether patients with possible NPH will respond to CSF shunting.^{29, 30}

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Angiography is not used in the diagnosis of NPH.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

No radiologic interventions presently are used in the diagnosis or treatment of NPH. The condition has been treated with neurosurgical CSF shunting since NPH was first described in 1965.

Medical/Legal Pitfalls

• NPH treatment through neurosurgical CSF shunting has, in many studies, been found to demonstrate a poor benefit-to-harm ratio. However, with improvements in patient selection capabilities, this ratio also is likely to be improving. Consequently, many experts suggest that NPH is now underdiagnosed and undertreated.³¹
  
  • NPH is a relatively rare cause of gait disturbance and of cognitive decline in elderly persons, but diagnosis is important because many patients may respond to CSF shunting.
  • Unfortunately, no criterion standard test exists, response rates are only on the order of 50-70% at best, and CSF shunting has a significant complication rate (30-40%), with potential for substantial morbidity (5-15%).
  • This results in a poor benefit-to-harm ratio in all patients (3:1, according to Vanneste).²⁶
  • The ratio can be improved through selection of patients who have a high surgical risk and who may improve through assessment of the efficacy of continued CSF drainage for 1 or more weeks before consideration of a shunting procedure.
  • Kahlon assessed patients 5 years after the diagnosis of NPH and found that many patients were lost to follow-up due to other medical comorbidities.³² Of those available for follow-up at 5 years, 23/27 had surgery. The greatest improvement was seen in patients younger than 75 years (64%) as compared to those over 75 years (only 11%). Overall, a remaining improvement of gait was seen in 40%, whereas improvement in cognition was seen in fewer than 10%.
  • Using a mail-based questionnaire after shunting, Tisell found that 79% of responders felt subjective clinical improvements after an average of 4.2 years (range 2.3 to 6.2 years), and that 60% had persistent, observable improvements.³³  The standardized mortality ratio (observed/expected) was rather poor at approximately 3 years.
  • Meier found that 80% of patients who underwent shunting showed an immediate postoperative benefit and that 67% of patients demonstrated a sustained benefit an average of 34 months later.³⁴
  • Aygok and colleagues found a sustained benefit lasting from 3 months to 3 years as a result of shunting.³⁵ They recorded a slight decline in gait benefit over that time, from 91% to 75%, with retention-of-memory improvement at 80% and an improvement in incontinence problems from 70% to 82.5%.

• Overall, there still is unavoidable morbidity and mortality associated with the neurosurgical treatment of NPH. The improvement of patient selection criteria has helped to improve the benefit-to-harm ratio that has plagued the treatment of NPH. NPH remains one of the few treatable dementias, and every effort should be made to identify patients with this condition as effectively as possible. NPH is one of the reasons that all dementia patients should have neuroimaging with either CT scanning or MRI as part of their work-up.

Special Concerns

• MRI may have the potential to further determine which patients may respond to CSF shunting, and ongoing research involving cerebral perfusion, intraventricular lactate, and CSF flow may help to elucidate which potential patients with NPH will benefit from shunting, while excluding patients with comorbid neurodegenerative conditions.
• In a review article, Vanneste stressed that although a number of ancillary tests have been described that may help predict the outcome of CSF shunting, many are limited.³⁶
• Evaluation, when possible, of the clinical situation, MRI criteria, positive CSF tap testing, and B-wave monitoring is important when considering a CSF-shunting procedure in a patient with NPH.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Axial nonenhanced computed tomography (CT) scan of the head of a patient with normal pressure hydrocephalus at the level of the middle cranial fossa. Note the disproportionately enlarged temporal horns of the lateral ventricles compared with the relatively normal sulcal size.
	View Full Size Image
Media type:  CT

Media file 2:  Axial nonenhanced computed tomography (CT) scan at the level of the basal ganglia in a patient with normal pressure hydrocephalus. Note the prominent lateral ventricles, which are disproportionately dilated in comparison with the mild sulcal widening.
	View Full Size Image
Media type:  CT

Media file 3:  Axial T2-weighted magnetic resonance image of the brain in a patient with normal pressure hydrocephalus. Note the enlarged ventricular system, especially the atria of the lateral ventricles (V), which is out of proportion with sulcal atrophy.
	View Full Size Image
Media type:  MRI

Media file 4:  Axial T2-weighted magnetic resonance image through the level of the superior colliculi in a patient with normal pressure hydrocephalus. Note the enlarged temporal horns of the lateral ventricles (V). Also, note the cerebrospinal fluid (CSF) flow void in the cerebral aqueduct (arrow). This flow void lacks signal and appears black, while nonturbulent CSF, as imaged in the ventricles, is hyperintense on T2-weighted images.
	View Full Size Image
Media type:  MRI

Media file 5:  Midline sagittal T1-weighted magnetic resonance image in a patient with normal pressure hydrocephalus. Note the enlarged ventricular system (V), which is out of proportion with sulcal atrophy. Also note the thinned corpus callosum (arrow).
	View Full Size Image
Media type:  MRI

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT Scan
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

1. Hakim S, Adams RD. The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. Observations on cerebrospinal fluid hydrodynamics. J Neurol Sci. Jul-Aug 1965;2(4):307-27. [Medline].
2. Katzman R. Diagnosis and management of dementia. In: R Katzman, JW Rowe, eds. Principles of Geriatric Neurology. Philadelphia, Pa: FA Davis; 1992:167-206.
3. Larson EB, Reifler BV, Featherstone HJ, et al. Dementia in elderly outpatients: a prospective study. Ann Intern Med. Mar 1984;100(3):417-23. [Medline].
4. Clarfield AM. The reversible dementias: do they reverse?. Ann Intern Med. Sep 15 1988;109(6):476-86. [Medline].
5. Vanneste J, Augustijn P, Davies GA, et al. Normal-pressure hydrocephalus. Is cisternography still useful in selecting patients for a shunt?. Arch Neurol. Apr 1992;49(4):366-70. [Medline].
6. Laws ER, Mokri B. Occult hydrocephalus: results of shunting correlated with diagnostic tests. Clin Neurosurg. 1977;24:316-33. [Medline].
7. Black PM. Idiopathic normal-pressure hydrocephalus. Results of shunting in 62 patients. J Neurosurg. Mar 1980;52(3):371-7. [Medline].
8. Petersen RC, Mokri B, Laws ER Jr. Surgical treatment of idiopathic hydrocephalus in elderly patients. Neurology. Mar 1985;35(3):307-11. [Medline].
9. Graff-Radford NR, Rezai K, Godersky JC, et al. Regional cerebral blood flow in normal pressure hydrocephalus. J Neurol Neurosurg Psychiatry. Dec 1987;50(12):1589-96. [Medline].
10. Vorstrup S, Christensen J, Gjerris F, et al. Cerebral blood flow in patients with normal-pressure hydrocephalus before and after shunting. J Neurosurg. Mar 1987;66(3):379-87. [Medline].
11. Mamo HL, Meric PC, Ponsin JC, et al. Cerebral blood flow in normal pressure hydrocephalus. Stroke. Nov-Dec 1987;18(6):1074-80. [Medline].
12. Mataró M, Poca MA, Matarín M, et al. Corpus callosum functioning in patients with normal pressure hydrocephalus before and after surgery. J Neurol. May 2006;253(5):625-30. [Medline].
13. Sasaki H, Ishii K, Kono AK, et al. Cerebral perfusion pattern of idiopathic normal pressure hydrocephalus studied by SPECT and statistical brain mapping. Ann Nucl Med. Jan 2007;21(1):39-45. [Medline].
14. Nutt JG, Marsden CD, Thompson PD. Human walking and higher-level gait disorders, particularly in the elderly. Neurology. Feb 1993;43(2):268-79. [Medline].
15. Estanol BV. Gait apraxia in communicating hydrocephalus. J Neurol Neurosurg Psychiatry. Apr 1981;44(4):305-8. [Medline].
16. Haan J, Thomeer RT. Predictive value of temporary external lumbar drainage in normal pressure hydrocephalus. Neurosurgery. Feb 1988;22(2):388-91. [Medline].
17. Marmarou A, Bergsneider M, Klinge P, et al. The value of supplemental prognostic tests for the preoperative assessment of idiopathic normal-pressure hydrocephalus. Neurosurgery. Sep 2005;57(3 Suppl):S17-28; discussion ii-v. [Medline].
18. Tsunoda A, Mitsuoka H, Sato K, et al. A quantitative index of intracranial cerebrospinal fluid distribution in normal pressure hydrocephalus using an MRI-based processing technique. Neuroradiology. Jun 2000;42(6):424-9. [Medline].
19. Palm WM, Walchenbach R, Bruinsma B, et al. Intracranial compartment volumes in normal pressure hydrocephalus: volumetric assessment versus outcome. AJNR Am J Neuroradiol. Jan 2006;27(1):76-9. [Medline]. [Full Text].
20. Tullberg M, Jensen C, Ekholm S, et al. Normal pressure hydrocephalus: vascular white matter changes on MR images must not exclude patients from shunt surgery. AJNR Am J Neuroradiol. Oct 2001;22(9):1665-73. [Medline]. [Full Text].
21. Jack CR Jr, Mokri B, Laws ER Jr, et al. MR findings in normal-pressure hydrocephalus: significance and comparison with other forms of dementia. J Comput Assist Tomogr. Nov-Dec 1987;11(6):923-31. [Medline].
22. Bradley WG Jr, Whittemore AR, Kortman KE, et al. Marked cerebrospinal fluid void: indicator of successful shunt in patients with suspected normal-pressure hydrocephalus. Radiology. Feb 1991;178(2):459-66. [Medline].
23. Bradley WG Jr, Scalzo D, Queralt J, et al. Normal-pressure hydrocephalus: evaluation with cerebrospinal fluid flow measurements at MR imaging. Radiology. Feb 1996;198(2):523-9. [Medline].
24. Kahlon B, Annertz M, Stĺhlberg F, et al. Is aqueductal stroke volume, measured with cine phase-contrast magnetic resonance imaging scans useful in predicting outcome of shunt surgery in suspected normal pressure hydrocephalus?. Neurosurgery. Jan 2007;60(1):124-9; discussion 129-30. [Medline].
25. Kizu O, Yamada K, Nishimura T. Proton chemical shift imaging in normal pressure hydrocephalus. AJNR Am J Neuroradiol. Oct 2001;22(9):1659-64. [Medline]. [Full Text].
26. Vanneste JA. Three decades of normal pressure hydrocephalus: are we wiser now?. J Neurol Neurosurg Psychiatry. Sep 1994;57(9):1021-5. [Medline].
27. Fritz W, Kalbarczyk H, Schmidt K. Transcranial Doppler sonographic identification of a subgroup of patients with normal pressure hydrocephalus with coexistent vascular disease and treatment failure. Neurosurgery. Nov 1989;25(5):777-80. [Medline].
28. Droste DW, Krauss JK. Simultaneous recording of cerebrospinal fluid pressure and middle cerebral artery blood flow velocity in patients with suspected symptomatic normal pressure hydrocephalus. J Neurol Neurosurg Psychiatry. Jan 1993;56(1):75-9. [Medline].
29. Benzel EC, Pelletier AL, Levy PG. Communicating hydrocephalus in adults: prediction of outcome after ventricular shunting procedures. Neurosurgery. Apr 1990;26(4):655-60. [Medline].
30. Vanneste J, Augustijn P, Dirven C, et al. Shunting normal-pressure hydrocephalus: do the benefits outweigh the risks? A multicenter study and literature review. Neurology. Jan 1992;42(1):54-9. [Medline].
31. Stein SC, Burnett MG, Sonnad SS. Shunts in normal-pressure hydrocephalus: do we place too many or too few?. J Neurosurg. Dec 2006;105(6):815-22. [Medline].
32. Kahlon B, Sjunnesson J, Rehncrona S. Long-term outcome in patients with suspected normal pressure hydrocephalus. Neurosurgery. Feb 2007;60(20):327-32. [Medline].
33. Tisell M, Hellström P, Ahl-Börjesson G, et al. Long-term outcome in 109 adult patients operated on for hydrocephalus. Br J Neurosurg. Aug 2006;20(4):214-21. [Medline].
34. Meier U, Lemcke J. Clinical outcome of patients with idiopathic normal pressure hydrocephalus three years after shunt implantation. Acta Neurochir Suppl. 2006;96:377-80. [Medline].
35. Aygok G, Marmarou A, Young HF. Three-year outcome of shunted idiopathic NPH patients. Acta Neurochir Suppl. 2005;95:241-5. [Medline].
36. Vanneste JA. Diagnosis and management of normal-pressure hydrocephalus. J Neurol. Jan 2000;247(1):5-14. [Medline].
37. Adams RD, Fisher CM, Hakim S, et al. Symptomatic occult hydrocephalus with "normal" cerebrospinal-fluid pressure. A treatable syndrome. N Engl J Med. Jul 15 1965;273:117-26. [Medline].
38. del Mar Matarín M, Pueyo R, Poca MA, et al. Post-surgical changes in brain metabolism detected by magnetic resonance spectroscopy in normal pressure hydrocephalus: results of a pilot study. J Neurol Neurosurg Psychiatry. Jul 2007;78(7):760-3. [Medline].
39. Kiefer M, Eymann R, Steudel WI. Outcome predictors for normal-pressure hydrocephalus. Acta Neurochir Suppl. 2006;96:364-7. [Medline].

Article Last Updated: Sep 11, 2007