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.
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.
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
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
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
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.
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.
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