Secondary Logo

Journal Logo

Articles

Normal-Pressure Hydrocephalus: An Update

Stein, Sherman C.

Author Information
  • Free

Abstract

In the decade after normal-pressure hydrocephalus (NPH) was described, shunt insertion for this condition became one of the most frequently performed cranial neurosurgical procedures. Several negative reports in the mid-1970s raised the concern that we could not identify patients most likely to benefit from cerebrospinal fluid (CSF) diversion. This was followed by a sharp decline of interest and popularity in the topic, although research has continued in an attempt to understand its pathophysiology and refine diagnostic techniques. Several recent reports have reawakened interest in NPH and have inspired hope that the failures of the past can be avoided. This report is intended to review that research and to assess our progress.

BACKGROUND

In the 1950s it was recognized that hydrocephalus secondary to subarachnoid hemorrhage and other causes might be accompanied by normal pressures as measured by lumbar puncture. 1 Further, it was discovered that the neurologic deficits caused by such secondary hydrocephalus were often reversed after ventricular shunt insertion. Adams, Hakim, and their colleagues at the Massachusetts General Hospital described a group of such patients in whom the cause of the hydrocephalus was obscure and coined the term “normal-pressure hydrocephalus.”2,3 They described the characteristic clinical triad of gait disturbance, dementia, and urinary incontinence and stressed both that lumbar puncture pressures were normal and that symptoms were shunt-responsive.

Hakim and Adams 4 advanced a hydraulic explanation for the pathophysiology of the disease. If the subarachnoid flow of CSF is impeded (by an unrecognized process), intracranial pressure (ICP) rises and the ventricles start to expand. Ventricular expansion, however, causes a decrease in ICP, back to normal levels. Continued enlargement of the ventricles could, as explained by this “hydraulic press theory,” take place in the face of normal ICP. According to Pascal's law, fluid pressure is the same at all points on the walls of a closed container. Therefore, because the force exerted on the ventricular wall is the product of the pressure and the cross-sectional area of the wall, less ICP is necessary to expand already-enlarged ventricles. This is the same principle behind hydraulic presses such as automobile jacks. Additional hydraulic principles could be used to explain other pathophysiologic observations. For example, the relative ballooning of the largest sections of the ventricles, such as the frontal horns, could be explained by the Laplace law (the tension on the wall of a vessel is directly proportional to the vessel's radius). The disproportionate involvement of lower extremity function might result from greater stretching of lower extremity corticospinal fibers, which run near the ventricular walls, by the enlarged ventricles.

Early reports of shunt results in NPH were encouraging. 5 However, some shunt failures were noted, and overall results in idiopathic NPH were not as good as in hydrocephalus secondary to subarachnoid hemorrhage and other documented causes. It was recognized that Alzheimer's disease (hydrocephalus ex vacuo) could mimic NPH, and it was assumed that cerebral atrophy would not respond to shunting. Hence, authorities proposed laboratory tests that might be used to confirm the diagnosis of NPH, especially in patients with atypical clinical features. 5–7 These tests were based on the understood pathophysiology of NPH and related to structural changes in the CSF pathways or to dynamic flow properties. Benson et al. 6 first summarized the expected structural changes that might distinguish NPH from cerebral atrophy. Based on pneumoencephalography, they included the height and span of the frontal horns, the thickness of the cerebral mantle and the subarachnoid space, and the angle of the roof of the lateral ventricles in the anteroposterior projection (callosal angle). Other structural distinctions included the relative dilation of the temporal horns, the shape of the fourth ventricle, and others. 8,9 Hussey et al. 10 infused saline by lumbar puncture to reveal the underlying block to CSF flow in NPH, a block that would not be expected to be present in atrophy. Bannister et al. 11 reported on the pattern of CSF flow in NPH after the lumbar injection of a radioisotope tracer. The combination of ventricular penetration and stasis was considered characteristic for NPH and thought to distinguish it reliably from atrophy.

Unfortunately, most subsequent shunt series for NPH could not match the initial success rates. 12–25 Patient selection was often confounded by incomplete or atypical clinical presentations. 5–7 The results of laboratory studies were frequently contradictory, and there was no agreement as to which tests most accurately distinguished between NPH and Alzheimer's disease. 26–37 In one series, three patients whose clinical and laboratory features fit the strict definition of NPH were found on cortical biopsy to have atrophy/Alzheimer's disease 14 and did not improve after shunting. Clinical and laboratory results were not found to predict reliably relief of symptoms after shunt insertion in idiopathic 13,14,34,37 or secondary 38 hydrocephalus. There was even a report that patients with cerebral atrophy were as likely to respond to shunting as those with NPH. 39 By the mid-1970s it was recognized that the entity of NPH lacked a gold standard for diagnosis, that improvement after shunt insertion was often minor and unsustained, and that shunt response was unpredictable. It is therefore not surprising that the popularity of shunting for NPH plummeted at that time.

RECENT DIAGNOSTIC EFFORTS

Over the years, investigators have continued to seek factors that could reliably predict shunt success. It was accepted that these factors were unlikely to be absolute indicators; however, it was hoped they would provide reliable guidance to justify shunt insertion in individual patients. Most authorities agree that certain clinical findings increase the chances of shunt success. Fisher 40 and others 41 emphasized the importance of gait disturbance. The more prominent the “magnet gait” phenomenon compared with dementia, the greater the likelihood of the response to shunting. Other clinical findings posited as positive predictive factors include lack of dementia at onset of symptoms and brief symptom duration. 25

With the introduction of computed tomography and then magnetic resonance imaging (MRI), almost everyone expected that the detection of shunt-responsive NPH would be simplified. Structural changes amenable to neuroimaging studies and tested have included the size 16,42–51 and shape 16,44,45,47–50,52–55 of the ventricles and the convexity CSF spaces, 16,17,20,42–44,46–50,55–59 focal atrophy of the parenchyma, 60,61 and signal changes in the periventricular tissue. 20,44,48,49,51–55,58,61–70 However, no single pattern has gained wide acceptance. Table 1 highlights the lack of consensus regarding the use of structural changes to forecast shunt response.

TABLE 1
TABLE 1:
Predicting shunt response using neuroimaging studies

Intracranial pressure has been monitored for predictive value; factors such as intermittent increases, especially during sleep, 71–80 and the presence or relative frequency of B-waves 56,74,77–79,81–84 have been tested with equivocal results. ICP responses to the challenge of intrathecal infusion as a measure of the CSF absorption rate 10,59,75,84–95 or after Diamox administration 96 have not proven to be useful to all investigators (Table 2). Episodic elevated ICP and impaired absorption appear to predict high rates of shunt success; however, shunt results in the group with normal absorption rates were almost as high. 93 CSF pulse-pressure analysis has had limited success in predicting the outcome of shunt insertion. 97–99

TABLE 2
TABLE 2:
Predicting shunt response using ICP changes

Other measures of CSF dynamics once thought to be of value include isotope cisternography and dynamic MRI studies. Cisternography had adherents from the 1970s to the 1990s, 100,101 but most critical reviews have concluded it cannot predict shunt success. 22,102 The rate at which isotope clears from the CSF compartment has been promoted as an indicator of the CSF absorption rate and hence a predictor of shunt success. 83,103–105 Stein 106 mathematically proved that this measure is unreliable. The presence of CSF flow voids on MRI has been promoted as an indicator of shunt-responsive NPH, 107 as have measurements of flow velocity and flux on scans. 67,108–110 Again, however, the results of negative studies raise questions about their utility. 111–113

Investigators have attempted to correlate global 23,87,114–122 and regional 123–131 changes in cerebral blood flow and velocity or flow responses to lowering ICP 87,114,119–121,124,126,127,129–134 with clinical shunt response. As shown in Table 3, there is little agreement among the results. Indeed, there is confusion among proponents of cerebral blood flow determinations as to whether patients who respond to shunt insertion have higher or lower flow values than those who do not. Decreased autoregulation has been reported to be of predictive value, 118,122 but reports differ as to whether global or only focal changes are useful. Whereas one investigator reported that an impaired cerebrovascular response to Diamox predicts a good clinical response to shunt insertion, 132 another found that subnormal cerebrovascular responses to CO2 predicted shunt failure. 135 Studies of cerebral metabolism are likewise mixed. 21,114,136,137

TABLE 3
TABLE 3:
Predicting shunt response using CBF levels and responses

Isolated reports of biochemical markers in the CSF of patients with NPH 138–147 require confirmation, as does a report of genetic markers. 148 There is also a single study suggesting that motor evoked potentials may be helpful in predicting shunt response. 149 If there is a temporary response to a clinical trial of lumbar puncture or spinal or ventricular drainage, shunting is likely to be successful. 4,12,63,79,91,138–149 However, the same authorities agree that a negative trial is unreliable.

Some experts opine that only a combination of clinical and laboratory examinations can predict shunt outcome with any accuracy. 15,18,20,25,42,46,48,56,59,147,150–154 A glance at these combinations reveals that they are mutually exclusive and hence of limited acceptance. Not even biopsy results are universally relied on; there is significant disagreement as to whether either meningeal fibrosis or cortical atrophy can reliably predict shunt results. 14,24,35,137,155–168

Our failure in predicting shunt outcome can be traced in part to the bias in every study resulting from the selection of only certain patients for testing and shunt insertion. Each study demanded that prospective subjects fulfill certain clinical or laboratory criteria before inclusion, thus creating a number of self-fulfilling prophecies. Further, inclusion and outcome criteria vary from series to series, precluding accurate comparisons. Until we study the entire population of patients with dementia, we shall never know which of them are (and are not) likely to respond to shunting.

EFFECTIVE TREATMENT VERSUS PATIENT SELECTION

It could be argued that selecting the correct patients to treat is less critical than ensuring that treatment is administered properly. Various authors have recommended low, 148,169–171 medium, 172 or high 42,173 valve pressures for optimal shunt function in patients with NPH. Antisiphon devices have been reported to either improve 148,174–177 or worsen 178,179 outcome. Flow-regulated and programmable shunt valves 172,175 and lumboperitoneal shunts 171 have been used, with varying degrees of success.

Oi et al. 180,181 have emphasized that the optimal shunt parameters vary as the patient's hydrocephalus evolves over time. Williams et al. 182 found that nearly 80% of patients with NPH who did not initially respond to shunt insertion had inadequate shunt function; 70% of them responded to shunt revision. Others have also noted high failure rates in NPH shunts. 183 This of course suggests that many patients who do not exhibit clinical improvement after CSF diversion fail to do so because of shunt malfunction rather than inappropriate selection for surgery.

EVOLVING UNDERSTANDING OF PATHOPHYSIOLOGY

As happens so often in medicine, our original conception of NPH appears simplistic in retrospect. The hydrodynamic changes of the developing hydrocephalic process are more complicated than the original “hydraulic press” theory, as was later recognized by Hakim himself. 184 Abnormally elevated CSF pulse pressure 108,185,186 and pressure gradients across the cortical mantle 187–190) may contribute to hydrocephalus in the absence of absorption block or elevated intraventricular pressure. The hydrodynamic properties of the individual ventricular system change gradually in the course of the disease, affecting both the production of symptoms and the response to therapy. 180,181

However, ventricular enlargement both contributes to and results from parenchymal changes. As the ventricles expand, edema, plastic deformation, and shearing forces damage the periventricular white matter and vasculature. 23,87,148,191–193 This direct and ischemic damage increases tissue compliance, promoting even more ventricular enlargement. 194,195 Of course, the primary parenchymal effects of hypertensive and atherosclerotic disease have a similar effect on periventricular compliance. 153,159,164,196,197 This complex of interacting factors creates a vicious cycle of increasing ventricular growth and further periventricular damage (Fig. 1). All these mechanisms may produce symptoms. It is now clear that the characteristic gait disturbance is not the result of pyramidal fiber stretch. 149,198

Fig. 1.
Fig. 1.:
Hydrodynamic and parenchymal factors in normal-pressure hydrocephalus. Note that both primary white matter damage and cerebrospinal fluid absorption block may increase periventricular compliance. After sufficient damage has occurred, the vicious cycle of increasing ventricular growth and further periventricular damage (heavy arrows) continues in the absence of elevated pressure.

It no longer appears as critical to distinguish NPH from Alzheimer's disease and related causes of cortical atrophy as it once did. First, both neuroimaging studies 60,61 and neuropsychological testing 199 can readily distinguish between the two entities in their pure form. Second, as noted above, the results of biopsy and autopsy studies have shown that cortical atrophy frequently accompanies NPH 14,24,35,137,155–168 and, in some studies, does not preclude clinical response to shunting. 35,39,137,155–157,162,166

It is the relation between NPH and cerebrovascular disease that requires further examination. Strong associations between NPH and both hypertensive 159,192,200 and atherosclerotic cerebrovascular disease 148,164,196,201–204 have been noted. The clinical signs of arteriosclerotic subcortical encephalopathy (vascular dementia with lacunes, Binswanger's disease) resemble those of NPH. 202,205 Indeed, Vanneste, 23 in a review of NPH, claimed that arteriosclerotic subcortical encephalopathy is a much more common cause than NPH of the classic clinical triad of dementia, gait disturbance, and incontinence. As mentioned above, ischemic changes to the deep white matter can promote the process of NPH. 153,159,164,196,197 The frequency with which typical ischemic deep white matter lesions are found in NPH and the number of studies showing their association with improved shunt outcome 68–70 have led Noda et al. 206 to propose hypertensive vasculopathy as one of the causes of NPH. 206

COPING WITH UNPREDICTABILITY

The ideal test for predicting shunt response in NPH, sought by myself and others 14,207 for so long, will probably never be found. This is not surprising, considering the multitude of factors involved in the origin and pathogenesis of the condition. This multifactorial etiology has led some authorities to suggest we abandon the term “normal-pressure hydrocephalus” and replace it with “chronic hydrocephalus in the adult” or another generic term. 63,180

Hydrocephalus is a dynamic process, with the ICP and ventricular size gradually changing over time. 180 Their interrelationship, the details of which may vary among patients, is shown in Figure 2. Primary and secondary parenchymal changes are similarly time-dependent.

Fig. 2.
Fig. 2.:
Hydrodynamic changes in chronic hydrocephalus, evolving over time. As the cerebral ventricles grow, the intracranial pressure decreases, as does the valve pressure appropriate for drainage.

Shunt failure may have many causes. The hydrocephalus may be so severe or chronic that irreversible vascular or parenchymal changes have occurred. Associated degenerative disease may progress and obscure or reverse any shunt-related benefit. The shunt may be blocked or, if patent, be mismatched to intraventricular pressure.

DECISION TO TREAT

As of this writing, there is no effective treatment of dementia, save for shunting patients with NPH. This lack of alternative therapies must be taken into account when making therapeutic decisions. The evidence for predicting shunt outcomes in NPH is, as discussed in detail above, weak and contradictory. The few controlled studies that have been performed are not completely comparable, because neither entry criteria nor results are uniformly reported. Many authorities pass on previous recommendations without independent confirmation. Nevertheless, certain findings are most frequently reported to predict shunt success. These I list, in decreasing level of confidence: hydrocephalus of known etiology (e.g., subarachnoid hemorrhage), intermittent elevated ICP (by monitor), positive CSF drainage test (clinical response), infusion test showing CSF absorption block, a gait disturbance that is severe and that precedes dementia, and recent onset of symptoms. In contrast, severe and longstanding dementia, especially if there is neuroimaging evidence of advanced Alzheimer's disease, usually portends shunt failure. Cerebral blood blow studies and deep white matter changes on MRI are of questionable predictive utility.

Finally, the complication rate of the shunting procedure must be taken into account. Most large series report a complication rate of about 35% in NPH, 19,20,22,42,63,170–173,183 although Williams et al. 182 suggested that the incidence of unrecognized shunt malfunction is considerably higher.

REFERENCES

1. Foltz EL, Ward Jr. AA Communicating hydrocephalus from subarachnoid bleeding. J Neurosurg 1956; 13:546–66.
2. Hakim S. Some observations on cerebrospinal fluid pressure hydrocephalic syndrome in adults with “normal” cerebrospinal fluid pressure: Recognition of a new syndrome. Bogota, Columbia, Javeriana University School of Medicine, 1964 (English translation).
3. Adams RD, Fisher CM, Hakim S, et al. Symptomatic occult hydrocephalus with “normal” cerebrospinal fluid pressure: a treatable syndrome. N Engl J Med 1965; 273:117–26.
4. Hakim S, Adams RD. The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. Observations on cerebrospinal fluid hydrodynamics. J Neurol Sci 1965; 2:307–27.
5. Ojemann RG, Fisher CM, Adams RD, et al. Further experience with the syndrome of “normal”-pressure hydrocephalus. J Neurosurg 1969; 31:279–94.
6. Benson DF, LeMay M, Patten DH, Rubens AB. Diagnosis of normal-pressure hydrocephalus. N Engl J Med 1970; 283:609–15.
7. Ojemann RG. Normal-pressure hydrocephalus. Clin Neurosurg 1971; 18:337–70.
8. Sjaastad O, Skalpe IO, Engeset A. The width of the temporal horn in the differential diagnosis between pressure hydrocephalus and hydrocephalus ex vacuo. Neurology 1969; 19:1087–93.
9. LeMay M, New PF. Radiological diagnosis of occult normal-pressure hydrocephalus. Radiology 1970; 96:347–58.
10. Hussey F, Schanzer B, Katzman R. A simple constant-infusion manometric test for measurement of CSF absorption. II. Clinical studies. Neurology 1970; 20:665–80.
11. Bannister R, Gilford E, Kocen R. Isotope encephalography in the diagnosis of dementia due to communicating hydrocephalus. Lancet 1967; 2:1014–7.
12. Wood JH, Bartlet D, James AE. Normal-pressure hydrocephalus. Neurology 1973; 23:706–13.
13. Shenkin HA, Greenberg J, Bouzarth WF, et al. Ventricular shunting for relief of senile symptoms. JAMA 1973; 225:1486–9.
14. Stein SC, Langfitt TW. Normal-pressure hydrocephalus. Predicting the results of cerebrospinal fluid shunting. J Neurosurg 1974; 41:463–70.
15. Messert B, Wannamaker BB. Reappraisal of the adult occult hydrocephalus syndrome. Neurology 1974; 24:224–31.
16. Jacobs L, Conti D, Kinkel W, Manning E. “Normal-pressure” hydrocephalus. Relationship of clinical and radiographic findings to improvement following shunt surgery. JAMA 1976; 235:510–12.
17. Laws E, Mokri B. Occult hydrocephalus: results of shunting correlated with diagnostic tests. Clin Neurosurg 1977; 24:316–3.
18. Greenberg J, Shenkin H, Adam R. Idiopathic normal-pressure hydrocephalus: a report of 73 patients. J Neurol Neurosurg Psychiatry 1977; 40:336–41.
19. Hughes CP, Siegel BA, Coxe WS, et al. Adult idiopathic communicating hydrocephalus with and without shunting. J Neurol Neurosurg Psychiatry 1978; 41:961–71.
20. Black PM. Idiopathic normal-pressure hydrocephalus. Results of shunting in 62 patients. J Neurosurg 1980; 52:371–7.
21. Friedland RP. “Normal”-pressure hydrocephalus and the saga of the treatable dementias. JAMA 1989; 262:2577–81.
22. Vanneste J, Augustijn P, Dirven C, et al. Shunting normal-pressure hydrocephalus: do the benefits outweigh the risk? A multicenter study and literature review. Neurology 1992; 42:54–9.
23. Vanneste JA. Three decades of normal-pressure hydrocephalus: are we wiser now? J Neurol Neurosurg Psychiatry 1994; 57:1021–5.
24. Bech RA, Juhler M, Waldemar G, et al. Frontal brain and leptomeningeal biopsy specimens correlated with cerebrospinal fluid outflow resistance and B-wave activity in patients suspected of normal-pressure hydrocephalus. Neurosurgery 1997; 40:497–502.
25. Caruso R, Cervoni L, Vitale AM, Salvati M. Idiopathic normal-pressure hydrocephalus in adults: result of shunting correlated with clinical findings in 18 patients and review of the literature. Neurosurg Rev 1997; 20:104–7.
26. Heinz ER, Davis DO, Karp HR. Abnormal isotope cisternography in symptomatic occult hydrocephalus. A correlative isotopic-neuroradiological study in 130 subjects. Radiology 1970; 95:109–20.
27. James Jr, AE DeLand FH, Hodges 3d, FJ Wagner Jr. HN Normal-pressure hydrocephalus. Role of cisternography in diagnosis. JAMA 1970; 213:1615–22.
28. McCullough DC, Harbert JC, Di Chiro G, Ommaya AK. Prognostic criteria for cerebrospinal fluid shunting from isotope cisternography in communicating hydrocephalus. Neurology 1970; 20:594–8.
29. Greitz T, Grepe A. Encephalography in the diagnosis of convexity block hydrocephalus. Acta Radiol Diagn (Stockh) 1971; 11:232–42.
30. Tator CH, Murray S. A clinical, pneumoencephalographic and radioisotopic study of normal-pressure communicating hydrocephalus. Can Med Assoc J 1971; 105:573–9.
31. Bannister CM. A report of eight patients with low-pressure hydrocephalus treated by CSF diversion with disappointing results. Acta Neurochir (Wien) 1972; 27:11–5.
32. Guidetti B, Gagliardi FM. Normal-pressure hydrocephalus. Acta Neurochir (Wien) 1972; 27:1–9.
33. James Jr. AE Cisternography (cerebrospinal fluid imaging): a versatile diagnostic procedure. Am J Roentgenol Radium Ther Nucl Med 1972; 115:201–4.
34. Salmon JH. Adult hydrocephalus. Evaluation of shunt therapy in 80 patients. J Neurosurg 1972; 37:423–8.
35. Coblentz JM, Mattis S, Zingesser LH, et al. Presenile dementia. Clinical aspects and evaluation of cerebrospinal fluid dynamics. Arch Neurol 1973; 29:299–308.
36. Kieffer SA, Wolff JM, Westreich G. The borderline scinticisternogram. Radiology 1973; 106:133–40.
37. Wolinsky JS, Barnes BD, Margolis MT. Diagnostic tests in normal-pressure hydrocephalus. Neurology 1973; 23:706–13.
38. Yasargil MG, Yonekawa Y, Zumstein B, Stahl HJ. Hydrocephalus following spontaneous subarachnoid hemorrhage. Clinical features and treatment. J Neurosurg 1973; 39:474–9.
39. Salmon JH, Gonen JY, Brown L. Ventriculoatrial shunt for hydrocephalus ex-vacuo: psychological and clinical evaluation. Dis Nerv Syst 1971; 32:299–307.
40. Fisher CM. Hydrocephalus as a cause of disturbances of gait in the elderly. Neurology 1982; 32:1358–63.
41. Graff-Radford NR, Godersky JC. Normal-pressure hydrocephalus. Onset of gait abnormality before dementia predicts good surgical outcome. Arch Neurol 1986; 43:940–2.
42. Benzel EC, Pelletier AL, Levy PG. Communicating hydrocephalus in adults: prediction of outcome after ventricular shunting procedures. Neurosurgery 1990; 26:655–60.
43. Gleason PL, Black PM, Matsumae M. The neurobiology of normal-pressure hydrocephalus. Neurosurg Clin North Am 1993; 4:667–75.
44. Gunasekera L, Richardson AE. Computerized axial tomography in idiopathic hydrocephalus. Brain 1977; 100:749–54.
45. LeMay M, Hochberg FH. Ventricular differences between hydrostatic hydrocephalus and hydrocephalus ex vacuo by computed tomography. Neuroradiology 1979; 17:191–5.
46. Petersen R, Mokri B, Laws E. Surgical treatment of idiopathic hydrocephalus in elderly patients. Neurology 1985; 35:307–11.
47. Salibi NA, Lourie GL, Lourie H. A variant of normal-pressure hydrocephalus simulating Pick's disease on computerized tomography. Report of two cases. J Neurosurg 1983; 59:902–4.
48. Tans JT. Differentiation of normal-pressure hydrocephalus and cerebral atrophy by computed tomography and spinal infusion test. J Neurol 1979; 222:109–18.
49. Wikkelso C, Andersson H, Blomstrand C, et al. Computed tomography of the brain in the diagnosis of and prognosis in normal-pressure hydrocephalus. Neuroradiology 1989; 31:160–5.
50. Wilson RS, Fox JH, Huckman MS, et al. Computed tomography in dementia. Neurology 1982; 32:1054–7.
51. Yoshihara M, Tsunoda A, Sato K, et al. Differential diagnosis of NPH and brain atrophy assessed by measurement of intracranial and ventricular CSF volume with 3D FASE MRI. Acta Neurochir Suppl (Wien) 1998; 71:371–4.
52. George AE, Holodny A, Golomb J, de Leon MJ. The differential diagnosis of Alzheimer's disease. Cerebral atrophy versus normal-pressure hydrocephalus. Neuroimaging Clin North Am 1995; 5:19–31.
53. Jack CR, Mokri B, Laws ER, et al. MR findings in normal-pressure hydrocephalus: significance and comparison with other forms of dementia. J Comput Assist Tomogr 1987; 11:923–31.
54. Qureshi AI, Williams MA, Razumovsky AY, Hanley DF. Magnetic resonance imaging, unstable intracranial pressure and clinical outcome in patients with normal-pressure hydrocephalus. Acta Neurochir Suppl (Wien) 1998; 71:354–6.
55. Vassilouthis J. The syndrome of normal-pressure hydrocephalus. J Neurosurg 1984; 61:501–9.
56. Borgesen SE, Gjerris F. The predictive value of conductance to outflow of CSF in normal-pressure hydrocephalus. Brain 1982; 105(Pt 1):65–86.
57. Holodny AI, George AE, de Leon MJ, et al. Focal dilation and paradoxical collapse of cortical fissures and sulci in patients with normal-pressure hydrocephalus. J Neurosurg 1998; 89:742–7.
58. Kitagaki H, Mori E, Ishii K, et al. CSF spaces in idiopathic normal-pressure hydrocephalus: morphology and volumetry. AJNR Am J Neuroradiol 1998; 19:1277–84.
59. Thomsen AM, Børgesen SE, Bruhn P, Gjerris F. Prognosis of dementia in normal-pressure hydrocephalus after a shunt operation. Ann Neurol 1986; 20:304–10.
60. Holodny AI, Waxman R, George AE, et al. MR differential diagnosis of normal-pressure hydrocephalus and Alzheimer disease: significance of perihippocampal fissures. AJNR Am J Neuroradiol 1998; 19:813–9.
61. Savolainen S, Laakso MP, Paljarvi L, et al. MR imaging of the hippocampus in normal-pressure hydrocephalus: correlations with cortical Alzheimer's disease confirmed by pathologic analysis. AJNR Am J Neuroradiol 2000; 21:409–14.
62. Mori K, Murata T, Nakano Y, Handa H. Periventricular lucency in hydrocephalus on computerized tomography. Surg Neurol 1977; 8:337–40.
63. Bret P, Chazal J, Janny P, et al. [Chronic hydrocephalus in adults]. Neurochirurgie 1990; 36(suppl 1):1–159.
64. Sahuquillo J, Rubio E, Codina A, et al. Reappraisal of the intracranial pressure and cerebrospinal fluid dynamics in patients with the so-called “normal-pressure hydrocephalus” syndrome. Acta Neurochir (Wien) 1991; 112:50–61.
65. Tamaki N, Shirakuni T, Ehara K, Matsumoto S. Characterization of periventricular edema in normal-pressure hydrocephalus by measurement of water proton relaxation times. J Neurosurg 1990; 73:864–70.
66. Boon AJ, Tans JT, Delwel EJ, et al. Dutch Normal-Pressure Hydrocephalus Study: the role of cerebrovascular disease. J Neurosurg 1999; 90:221–6.
67. Bradley Jr. WG MR prediction of shunt response in NPH: CSF morphology versus physiology. AJNR Am J Neuroradiol 1998; 19:1285–6.
68. Hahnel S, Freund M, Munkel K, et al. Magnetisation transfer ratio is low in normal-appearing cerebral white matter in patients with normal-pressure hydrocephalus. Neuroradiology 2000; 42:174–9.
69. Krauss JK, Droste DW, Vach W, et al. Cerebrospinal fluid shunting in idiopathic normal-pressure hydrocephalus of the elderly: effect of periventricular and deep white matter lesions. Neurosurgery 1996; 39:292–9.
70. Krauss JK, Regel JP, Vach W, et al. White matter lesions in patients with idiopathic normal-pressure hydrocephalus and in an age-matched control group: a comparative study. Neurosurgery 1997; 40:491–5.
71. Symon L, Dorsch NW. Use of long-term intracranial pressure measurement to assess hydrocephalic patients prior to shunt surgery. J Neurosurg 1975; 42:258–73.
72. Hartmann A, Alberti E. Differentiation of communicating hydrocephalus and presenile dementia by continuous recording of cerebrospinal fluid pressure. J Neurol Neurosurg Psychiatry 1977; 40:630–40.
73. Crockard HA, Hanlon K, Duda EE, Mullan JF. Hydrocephalus as a cause of dementia: evaluation by computerised tomography and intracranial pressure monitoring. J Neurol Neurosurg Psychiatry 1977; 40:736–40.
74. Symon L, Hinzpeter T. The enigma of normal-pressure hydrocephalus: tests to select patients for surgery and to predict shunt function. Clin Neurosurg 1977; 24:285–315.
75. Lamas E, Lobato RD. Intraventricular pressure and CSF dynamics in chronic adult hydrocephalus. Surg Neurol 1979; 12:287–95.
76. Gucer G, Viernstein L, Walker AE. Continuous intracranial pressure recording in adult hydrocephalus. Surg Neurol 1980; 13:323–8.
77. Raftopoulos C, Deleval J, Chaskis C, et al. Cognitive recovery in idiopathic normal-pressure hydrocephalus: a prospective study. Neurosurgery 1994; 35:397–404.
78. Mazzone P, Fortuna L, Arena P, Pisani R. Multi-layer neural network analysis of cerebrospinal fluid pressure patterns in idiopathic normal-pressure hydrocephalus. Technol Health Care 1996; 4:393–401.
79. Williams MA, Razumovsky AY, Hanley DF. Comparison of Pcsf monitoring and controlled CSF drainage to diagnose normal-pressure hydrocephalus. Acta Neurochir Suppl (Wien) 1998; 71:328–30.
80. Takeuchi T, Kasahara E, Iwasaki M, et al. Indications for shunting in patients with idiopathic normal-pressure hydrocephalus presenting with dementia and brain atrophy (atypical idiopathic normal-pressure hydrocephalus). Neurol Med Chir (Tokyo) 2000; 40:38–46.
81. Chawla JC, Hulme A, Cooper R. Intracranial pressure in patients with dementia and communicating hydrocephalus. J Neurosurg 1974; 40:376–80.
82. Borgesen SE, Gjerris F, Sorensen SC. Intracranial pressure and conductance to outflow of cerebrospinal fluid in normal-pressure hydrocephalus. J Neurosurg 1979; 50:489–93.
83. Jensen F, Jensen FT. Acquired hydrocephalus. II. Diagnostic and prognostic value of quantitative isotope ventriculography (QIV), lumbar isotope cisternography (LIC), pneumoencephalography, and continuous intraventricular pressure recording (CIP). Acta Neurochir (Wien) 1979; 46:243–57.
84. Borgesen SE, Gjerris F, Sorensen SC. Cerebrospinal fluid conductance and compliance of the craniospinal space in normal-pressure hydrocephalus. A comparison between two methods for measuring conductance to outflow. J Neurosurg 1979; 51:521–5.
85. Nelson JR, Goodman SJ. An evaluation of the cerebrospinal fluid infusion test for hydrocephalus. Neurology 1971; 21:1037–53.
86. Sklar FH, Beyer Jr, CW Diehl JT, Clark WK. Significance of the so-called absorptive reserve in communicating hydrocephalus: a preliminary report. Neurosurgery 1981; 8:525–30.
87. Vorstrup S, Christensen J, Gjerris F, et al. Cerebral blood flow in patients with normal-pressure hydrocephalus before and after shunting. J Neurosurg 1987; 66:379–87.
88. Price DJ. Attempts to predict the probability of clinical improvement following shunting of patients with presumed normal-pressure hydrocephalus. In: Hoff JT, Betz AL, eds. Intracranial Pressure VII. Berlin: Springer Verlag; 1989:390–3.
89. Kosteljanetz M, Nehen AM, Kaalund J. Cerebrospinal fluid outflow resistance measurements in the selection of patients for shunt surgery in the normal-pressure hydrocephalus syndrome. A controlled trial. Acta Neurochir (Wien) 1990; 104:48–53.
90. Costabile G, Probst C. Hydrocephalus: analysis of 480 infusion tests. In: Avezaat CJJ, van Eijndhoven JHM, Maas AIR, Tans JTJ, eds. Intracranial Pressure VIII. Berlin: Springer Verlag; 1993:805–10.
91. Malm J, Kristensen B, Karlsson T, et al. The predictive value of cerebrospinal fluid dynamic tests in patients with the idiopathic adult hydrocephalus syndrome. Arch Neurol 1995; 52:783–9.
92. Hakim R, Black PM. Correlation between lumbo-ventricular perfusion and MRI-CSF flow studies in idiopathic normal-pressure hydrocephalus. Surg Neurol 1998; 49:14–9.
93. Boon AJ, Tans JT, Delwel EJ, et al. Does CSF outflow resistance predict the response to shunting in patients with normal-pressure hydrocephalus? Acta Neurochir Suppl (Wien) 1998; 71:331–3.
94. Meier U, Zeilinger FS, Kintzel D. Diagnosis in normal-pressure hydrocephalus: a mathematical model for determination of the ICP-dependent resistance and compliance. Acta Neurochir (Wien) 1999; 141:941–8.
95. Boon AJ, Tans JT, Delwel EJ, et al. The Dutch Normal-Pressure Hydrocephalus Study. How to select patients for shunting: an analysis of four diagnostic criteria. Surg Neurol 2000; 53:201–7.
96. Miyake H, Ohta T, Kajimoto Y, Deguchi J. Diamox challenge test to decide indications for CSF shunting in normal-pressure hydrocephalus. Acta Neurochir (Wien) 1999; 141:1187–93.
97. Foltz EL, Aine C. Diagnosis of hydrocephalus by CSF pulse analysis: a clinical study. Surg Neurol 1981; 15:283–93.
98. Barcena A, Mestre C, Canizal JM, et al. Idiopathic normal-pressure hydrocephalus: analysis of factors related to cerebrospinal fluid dynamics determining functional prognosis. Acta Neurochir (Wien) 1997; 139:933–41.
99. Droste DW, Krauss JK. Intracranial pressure B-waves precede corresponding arterial blood pressure oscillations in patients with suspected normal-pressure hydrocephalus. Neurol Res 1999; 21:627–30.
100. Alker Jr, GJ Glasauer FE, Leslie EV. Long-term experience with isotope cisternography. JAMA 1972; 219:1005–10.
101. Larsson A, Arlig A, Bergh AC, et al. Quantitative SPECT cisternography in normal-pressure hydrocephalus. Acta Neurol Scand 1994; 90:190–6.
102. Vanneste J, van Acker R. Normal-pressure hydrocephalus: did publications alter management? J Neurol Neurosurg Psychiatry 1990; 53:564–8.
103. Behrman S, Cast I, O'Gorman P. Two types of curves for transfer of RIHSA from cerebrospinal fluid to plasma in patients with normal-pressure hydrocephalus. J Neurosurg 1971; 35:677–80.
104. Mahaley Jr, MS Wilkinson Jr, RH Sivalingham S, et al. Radionuclide blood levels during cisternography of patients with normal-pressure hydrocephalus or Alzheimer's disease. J Neurosurg 1974; 41:471–80.
105. Jensen F, Jensen FT. Acquired hydrocephalus. I. A clinical analysis of 160 patients studied for hydrocephalus. Acta Neurochir (Wien) 1979; 46 (1–2):119–33.
106. Stein SC. Tracer clearance studies in hydrocephalus: a critique. Acta Neurochir (Wien) 1981; 55:247–51.
107. Bradley Jr, WG Whittemore AR, Kortman KE, et al. Marked cerebrospinal fluid void: indicator of successful shunt in patients with suspected normal-pressure hydrocephalus. Radiology 1991; 178:459–66.
108. Bradley Jr, WG Scalzo D, Queralt J, et al. Normal-pressure hydrocephalus: evaluation with cerebrospinal fluid flow measurements at MR imaging. Radiology 1996; 198:523–9.
109. Egeler-Peerdeman SM, Barkhof F, Walchenbach R, Valk J. Cine phase-contrast MR imaging in normal-pressure hydrocephalus patients: relation to surgical outcome. Acta Neurochir Suppl (Wien) 1998; 71:340–2.
110. Mase M, Yamada K, Banno T, et al. Quantitative analysis of CSF flow dynamics using MRI in normal-pressure hydrocephalus. Acta Neurochir Suppl (Wien) 1998; 71:350–3.
111. George AE. Chronic communicating hydrocephalus and periventricular white matter disease: a debate with regard to cause and effect. AJNR Am J Neuroradiol 1991; 12:42–4.
112. Mascalchi M, Arnetoli G, Inzitari D, et al. Cine-MR imaging of aqueductal CSF flow in normal-pressure hydrocephalus syndrome before and after CSF shunt. Acta Radiol 1993; 34:586–92.
113. Krauss JK, Regel JP, Vach W, et al. Flow void of cerebrospinal fluid in idiopathic normal-pressure hydrocephalus of the elderly: can it predict outcome after shunting? Neurosurgery 1997; 40:67–73.
114. Brooks DJ, Beaney RP, Powell M, et al. Studies on cerebral oxygen metabolism, blood flow, and blood volume, in patients with hydrocephalus before and after surgical decompression, using positron emission tomography. Brain 1986; 109:613–28.
115. Chang CC, Kuwana N, Ito S, Ikegami T. Prediction of effectiveness of shunting in patients with normal-pressure hydrocephalus by cerebral blood flow measurement and computed tomography cisternography. Neurol Med Chir (Tokyo) 1999; 39:841–5.
116. Chang CC, Kuwana N, Noji M, et al. Cerebral blood flow in patients with normal-pressure hydrocephalus. Nucl Med Commun 1999; 20:167–9.
117. Gideon P, Thomsen C, Gjerris F, et al. Measurement of blood flow in the superior sagittal sinus in healthy volunteers, and in patients with normal-pressure hydrocephalus and idiopathic intracranial hypertension with phase-contrast cine MR imaging. Acta Radiol 1996; 37:171–6.
118. Klinge PM, Berding G, Brinker T, et al. A positron emission tomography study of cerebrovascular reserve before and after shunt surgery in patients with idiopathic chronic hydrocephalus. Neurosurg Focus 2000;8(2).
119. Kushner M, Younkin D, Weinberger J, et al. Cerebral hemodynamics in the diagnosis of normal-pressure hydrocephalus. Neurology 1984; 34:96–9.
120. Meyer JS, Kitagawa Y, Tanahashi N, et al. Evaluation of treatment of normal-pressure hydrocephalus. J Neurosurg 1985; 62:513–21.
121. Tamaki N, Kusunoki T, Wakabayashi T, Matsumoto S. Cerebral hemodynamics in normal-pressure hydrocephalus. Evaluation by 133Xe inhalation method and dynamic CT study. J Neurosurg 1984; 61:510–4.
122. Tanaka A, Kimura M, Nakayama Y, et al. Cerebral blood flow and autoregulation in normal-pressure hydrocephalus. Neurosurgery 1997; 40:1161–5.
123. 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 1993; 56:75–9.
124. Graff-Radford NR, Rezai K, Godersky JC, et al. Regional cerebral blood flow in normal-pressure hydrocephalus. J Neurol Neurosurg Psychiatry 1987; 50:1589–96.
125. Ingvar DH, Gustafson L. Regional cerebral blood flow in organic dementia with early onset. Acta Neurol Scand 1970; 46(suppl 43):42–73.
126. Kimura M, Tanaka A, Yoshinaga S. Significance of periventricular hemodynamics in normal-pressure hydrocephalus. Neurosurgery 1992; 30:701–4.
127. Kristensen B, Malm J, Fagerland M, et al. Regional cerebral blood flow, white matter abnormalities, and cerebrospinal fluid hydrodynamics in patients with idiopathic adult hydrocephalus syndrome. J Neurol Neurosurg Psychiatry 1996; 60:282–8.
128. Larsson A, Bergh AC, Bilting M, et al. Regional cerebral blood flow in normal-pressure hydrocephalus: diagnostic and prognostic aspects. Eur J Nucl Med 1994; 21:118–23.
129. Lee EJ, Hung YC, Chang CH, et al. Cerebral blood flow velocity and vasomotor reactivity before and after shunting surgery in patients with normal-pressure hydrocephalus. Acta Neurochir (Wien) 1998; 140:599–604.
130. Moretti JL, Sergent A, Louarn F, et al. Cortical perfusion assessment with 123I-isopropyl amphetamine (123I-IAMP) in normal-pressure hydrocephalus (NPH). Eur J Nucl Med 1988; 14:73–9.
131. Waldemar G, Schmidt JF, Delecluse F, et al. High resolution with [99mTc]-d, 1-HMPAO in normal-pressure hydrocephalus before and shunt operation. J Neurol Neurosurg Psychiatry 1993; 56:655–64.
132. Chang CC, Kuwana N, Ito S, Ikegami T. Impairment of cerebrovascular reactivity to acetazolamide in patients with normal-pressure hydrocephalus. Nucl Med Commun 2000; 21:139–41.
133. Grubb Jr, RL Raichle ME, Gado MH, et al. Cerebral blood flow, oxygen utilization, and blood volume in dementia. Neurology 1977; 27:905–10.
134. Mathew NT, Meyer JS, Hartmann A, Ott EO. Abnormal cerebrospinal fluid-blood flow dynamics. Implications in diagnosis, treatment, and prognosis in normal-pressure hydrocephalus. Arch Neurol 1975; 32:657–64.
135. 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 1989; 25:777–80.
136. Jagust WJ, Friedland RP, Budinger TF. Positron emission tomography with [18F]fluorodeoxyglucose differentiates normal-pressure hydrocephalus from Alzheimer-type dementia. J Neurol Neurosurg Psychiatry 1985; 48:1091–6.
137. Tedeschi E, Hasselbalch SG, Waldemar G, et al. Heterogeneous cerebral glucose metabolism in normal-pressure hydrocephalus. J Neurol Neurosurg Psychiatry 1995; 59:608–15.
138. Hakim S, Adams RD. The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure: observations on cerebrospinal fluid hydrodynamics. J Neurol Sci 1965; 2:307–27.
139. Fisher CM. The clinical picture in occult hydrocephalus. Clin Neurosurg 1977; 24:270–84.
140. Wikkelso C, Andersson H, Blomstrand C, Lindqvist G. The clinical effect of lumbar puncture in normal-pressure hydrocephalus. J Neurol Neurosurg Psychiatry 1982; 45:64–9.
141. Wikkelso C, Andersson H, Blomstrand C, et al. Normal-pressure hydrocephalus. Predictive value of the cerebrospinal tap-test. Acta Neurol Scand 1986; 73:566–73.
142. Ahlberg J, Norlén L, Blomstrand C, Wikkelso C. Outcome of shunt operation on urinary incontinence in normal-pressure hydrocephalus predicted by lumbar puncture. J Neurol Neurosurg Psychiatry 1988; 51:105–8.
143. Haan J, Thomeer RT. Predictive value of temporary external lumbar drainage in normal-pressure hydrocephalus. Neurosurgery 1988; 22:388–91.
144. Di Lauro L, Bortoluzzi M. Temporary lumbar drainage in normal-pressure hydrocephalus. Neurosurgery 1989; 24:299.
145. Hanley DF, Borel CO, Herdman S. Normal-pressure hydrocephalus. In: Johnson RT, eds. Current Therapy in Neurological Disease. Philadelphia: BC Decker Inc; 1990:305–9.
146. Chen IH, Huang CI, Liu HC, Chen KK. Effectiveness of shunting in patients with normal-pressure hydrocephalus predicted by temporary, controlled-resistance, continuous lumbar drainage: a pilot study. J Neurol Neurosurg Psychiatry 1994; 57:1430–2.
147. Sand T, Bovim G, Grimse R, et al. Idiopathic normal-pressure hydrocephalus: the CSF tap-test may predict the clinical response to shunting. Acta Neurol Scand 1994; 89:311–6.
148. Mori K, Mima T. Can we predict the benefit of a shunting operation for suspected normal-pressure hydrocephalus? Crit Rev Neurosurg 1997; 7:263–75.
149. Krauss JK, Regel JP. The predictive value of ventricular CSF removal in normal-pressure hydrocephalus. Neurol Res 1997; 19:357–60.
150. Boon AJ, Tans JT, Delwel EJ, et al. Dutch Normal-Pressure Hydrocephalus Study: prediction of outcome after shunting by resistance to outflow of cerebrospinal fluid. J Neurosurg 1997; 87:687–93.
151. Corkill RG, Cadoux-Hudson TA. Normal-pressure hydrocephalus: developments in determining surgical prognosis. Curr Opin Neurol 1999; 12:671–7.
152. Meier U, Reichmuth B, Zeilinger FS, Lehmann R. The importance of xenon-computed tomography in the diagnosis of normal-pressure hydrocephalus. Int J Neuroradiol 1996; 2:153–60.
153. Moiri K, Mima T. To what extent has the pathophysiology of normal-pressure hydrocephalus been clarified? Crit Rev Neurosurg 1998; 8:232–43.
154. Vanneste JA. Diagnosis and management of normal-pressure hydrocephalus. J Neurol 2000; 247:5–14.
155. Appenzeller O, Salmon JH. Treatment of parenchymatous degeneration of the brain by ventriculo-atrial shunting of the cerebrospinal fluid. J Neurosurg 1967; 26:478–82.
156. Salmon JH, Armitage JL. Surgical treatment of hydrocephalus ex-vacuo. Ventriculoatrial shunt for degenerative brain disease. Neurology 1968; 18:1223–6.
157. DeLand FH, James Jr, AE Ladd DJ, Konigsmark BW. Normal-pressure hydrocephalus: a histologic study. Am J Clin Pathol 1972; 58:58–63.
158. Lorenzo AV, Bresnan MJ, Barlow CF. Cerebrospinal fluid absorption deficit in normal-pressure hydrocephalus. Arch Neurol 1974; 30:387–93.
159. Earnest MP, Fahn S, Karp JH, Rowland LP. Normal-pressure hydrocephalus and hypertensive cerebrovascular disease. Arch Neurol 1974; 31:262–6.
160. Vessal K, Sperber EE, James Jr. AE Chronic communicating hydrocephalus with normal CSE pressures: a cisternographic– pathologic correlation. Ann Radiol (Paris) 1974; 17:785–93.
161. Foncin JF, Redondo A, Le Beau J. [Cerebral cortex in normal-pressure hydrocephalus: an electron microscopy study]. Acta Neuropathol (Berlin) 1976 26;34:353–7.
162. Ball MJ. Neurofibrillary tangles in the dementia of “normal-pressure” hydrocephalus. Can J Neurol Sci 1976; 3:227–35.
163. Di Rocco C, Di Trapani G, Maira G, et al. Anatomo-clinical correlations in normotensive hydrocephalus. Reports on three cases. J Neurol Sci 1977; 33:437–52.
164. Koto A, Rosenberg G, Zingesser LH, et al. Syndrome of normal-pressure hydrocephalus: possible relation to hypertensive and arteriosclerotic vasculopathy. J Neurol Neurosurg Psychiatry 1977; 40:73–9.
165. Akai K, Uchigasaki S, Tanaka U, Komatsu A. Normal-pressure hydrocephalus. Neuropathological study. Acta Pathol Jpn 1987; 37:97–110.
166. Bech RA, Waldemar G, Gjerris F, et al. Shunting effects in patients with idiopathic normal-pressure hydrocephalus; correlation with cerebral and leptomeningeal biopsy findings. Acta Neurochir 1999; 141:633–9.
167. Savolainen S, Paljarvi L, Vapalahti M. Prevalence of Alzheimer's disease in patients investigated for presumed normal-pressure hydrocephalus: a clinical and neuropathological study. Acta Neurochir (Wien) 1999; 141:849–53.
168. Golomb J, Wisoff J, Miller DC, et al. Alzheimer's disease comorbidity in normal-pressure hydrocephalus: prevalence and shunt response. J Neurol Neurosurg Psychiatry 2000; 68:778–81.
169. McQuarrie IG, Saint-Louis L, Scherer PB. Treatment of normal-pressure hydrocephalus with low-versus medium-pressure cerebrospinal fluid shunts. Neurosurgery 1984; 15:484–8.
170. Boon AJ, Tans JT, Delwel EJ, et al. Dutch Normal-Pressure Hydrocephalus Study: randomized comparison of low-and medium-pressure shunts. J Neurosurg 1998; 88:490–5.
171. Chang CC, Kuwana N, Ito S. Management of patients with normal-pressure hydrocephalus by using lumboperitoneal shunt system with the Codman Hakim programmable valve. Neurosurg Focus 1999;7(4).
172. Schmitt J, Spring A. [Therapy of normal-pressure hydrocephalus with the transcutaneously magnetically adjustable shunt]. Neurochirurgia (Stuttg) 1990; 33(suppl 1):23–6.
173. Larsson A, Wikkelso C, Bilting M, Stephensen H. Clinical parameters in 74 consecutive patients shunt operated for normal-pressure hydrocephalus. Acta Neurol Scand 1991; 84:475–82.
174. Tokoro K, Chiba Y. Optimum position for an anti-siphon device in a cerebrospinal fluid shunt system. Neurosurgery 1991; 29:519–25.
175. Weiner HL, Constantini S, Cohen H, Wisoff JH. Current treatment of normal-pressure hydrocephalus: comparison of flow-regulated and differential-pressure shunt valves. Neurosurgery 1995; 37:877–84.
176. Pollay M, Harper DJ. Antisiphon devices and normal-pressure hydrocephalus. J Neurosurg 1996; 85:1192–3.
177. de Jong DA, Delwel EJ, Avezaat CJ. Hydrostatic and hydrodynamic considerations in shunted normal-pressure hydrocephalus. Acta Neurochir (Wien) 2000; 142:241–7.
178. Hassan M, Higashi S, Yamashita J. Risks in using siphon-reducing devices in adult patients with normal-pressure hydrocephalus: bench test investigations with Delta valves. J Neurosurg 1996; 84:634–41.
179. Bergsneider M, Peacock WJ, Mazziotta JC, Becker DP. Beneficial effect of siphoning in treatment of adult hydrocephalus. Arch Neurol 1999; 56:1224–9.
180. Oi S. Hydrocephalus chronology in adults: confused state of the terminology. Crit Rev Neurosurg 1998; 8:346–56.
181. Oi S, Shimoda M, Shibata M, et al. Pathophysiology of long-standing overt ventriculomegaly in adults. J Neurosurg 2000; 92:933–40.
182. Williams MA, Razumovsky AY, Hanley DF. Evaluation of shunt function in patients who are never better, or better than worse after shunt surgery for NPH. Acta Neurochir Suppl (Wien) 1998; 71:368–70.
183. Puca A, Anile C, Maira G, Rossi G. Cerebrospinal fluid shunting for hydrocephalus in the adult: factors related to shunt revision. Neurosurgery 1991; 29:822–6.
184. Hakim S, Venegas JG, Burton JD. The physics of the cranial cavity, hydrocephalus and normal-pressure hydrocephalus: mechanical interpretation and mathematical model. Surg Neurol 1976; 5:187–210.
185. Di Rocco C, Pettorossi VE, Caldarelli M, et al. Communicating hydrocephalus induced by mechanically increased amplitude of the intraventricular cerebrospinal fluid pressure: experimental studies. Exp Neurol 1978; 59:40–52.
186. Foltz EL. Hydrocephalus and CSF pulsatility: clinical and laboratory studies. In: Shapiro K, Marmarou A, Portnoy H, eds. Hydrocephalus. New York: Raven Press; 1984:337–62.
187. Fishman RA. Occult hydrocephalus [letter]. N Engl J Med 1966; 27:466–7.
188. Hoff J, Barber R. Transcerebral mantle pressure in normal-pressure hydrocephalus. Arch Neurol 1974; 31:101–5.
189. Conner ES, Foley L, Black PM. Experimental normal-pressure hydrocephalus is accompanied by increased transmantle pressure. J Neurosurg 1984; 61:322–7.
190. Pleasure SJ, Fishman RA. Ventricular volume and transmural pressure gradient in normal-pressure hydrocephalus. Arch Neurol 1999; 56:1199–200.
191. Sato O, Ohya M, Nojiri K, Tsugane R. Microcirculatory changes in experimental hydrocephalus: morphological and physiological studies. In: Shapiro K, Marmarou A, Portnoy H, eds. Hydrocephalus. New York: Raven Press; 1984.
192. Graff-Radford NR, Godersky JC. Idiopathic normal-pressure hydrocephalus and systemic hypertension. Neurology 1987; 37:868–71.
193. Mamo HL, Meric PC, Ponsin JC, et al. Cerebral blood flow in normal-pressure hydrocephalus. Stroke 1987; 18:1074–80.
194. Black PM, Ojemann RG, Tzouras A. CSF shunts for dementia, incontinence, and gait disturbance. Clin Neurosurg 1985; 32:632–51.
195. Black PM. Hydrocephalus in adults. In: Youmans JR, eds. Neurological Surgery, 4th ed. Philadelphia: WB Saunders; 1996:931.
196. Casmiro M, D'Alessandro R, Cacciatore FM, et al. Risk factors for the syndrome of ventricular enlargement with gait apraxia (idiopathic normal-pressure hydrocephalus): a case-control study. J Neurol Neurosurg Psychiatry 1989; 52:847–52.
197. Penar PL, Lakin WD, Yu J. Normal-ressure hydrocephalus: an analysis of aetiology and response to shunting based on mathematical modeling. Neurol Res 1995; 17:83–8.
198. Blomsterwall E, Bilting M, Stephensen H, Wikkelso C. Gait abnormality is not the only motor disturbance in normal-pressure hydrocephalus. Scand J Rehabil Med 1995; 27:205–9.
199. Iddon JL, Pickard JD, Cross JJ, et al. Specific patterns of cognitive impairment in patients with idiopathic normal-pressure hydrocephalus and Alzheimer's disease: a pilot study. J Neurol Neurosurg Psychiatry 1999; 67:723–32.
200. Haidri NH, Modi SM. Normal-pressure hydrocephalus and hypertensive cerebrovascular disease. Dis Nerv Syst 1977; 38:918–21.
201. Graff-Radford NR, Godersky JC. Idiopathic normal-pressure hydrocephalus and systemic hypertension. Neurology 1987; 37:868–71.
202. Shukla D, Singh BM, Strobos RJ. Hypertensive cerebrovascular disease and normal-pressure hydrocephalus. Neurology 1980; 30:998–1000.
203. Gallassi R, Morreale A, Montagna P, et al. Binswanger's disease and normal-pressure hydrocephalus. Clinical and neuropsychological comparison. Arch Neurol 1991; 48:1156–9.
204. Krauss JK, Regel JP, Vach W, et al. Vascular risk factors and arteriosclerotic disease in idiopathic normal-pressure hydrocephalus of the elderly. Stroke 1996; 27:24–9.
205. Bennett DA, Wilson RS, Gilley DW, Fox JH. Clinical diagnosis of Binswanger's disease. J Neurol Neurosurg Psychiatry 1990; 53:961–5.
206. Noda S, Fujita K, Kusunoki T, et al. [Hypertensive vasculopathy as a causative factor of normal-pressure hydrocephalus–a clinical analysis]. No Shinkei Geka 1981; 9:1033–9.
207. Sugar O. Meanwhile, back at the bedside [editorial]. JAMA 1976; 235:534.
Keywords:

Normal-pressure hydrocephalus; Hydrocephalus; Cerebrospinal fluid shunts; Patient selection

© 2001 Lippincott Williams & Wilkins, Inc.