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William G. Bradley Jr.

  
    	
American Journal of Neuroradiology June 1999,  20 (6) 1188-1189; 

  
  
  



  


  
  



			

		

	
	
 	
	  
  

		
		

			

			  

  
      
  
  

    
  


  
  



  
      
  
  

    

  

    

  
      
  
  

    
I have read Dr. Mori's letter concerning my commentary (1) on his article (2) and I wish to thank him for pointing out a mistake in a cited reference (3). Specifically, I had assumed that Dr. George's 1991 AJNR paper (3) contained information similar to his group's presentation (4) at the 1989 ASNR on large Sylvian cisterns in patients with NPH. Dr. Mori is correct in stating that large Sylvian cisterns are not mentioned as a feature of NPH in this article. On the other hand, the sign had been published by Dr. George 3 years earlier in a well-known textbook (5) in which he wrote, “Hydrocephalus, however, may coexist with large sulci and in particular with large Sylvian fissures… This occurs when the block is at the level of the high convexity or the pacchionian granulations. Consequently, the sulci and fissures dilate because of the damming of fluid proximal to the block. In effect, the sulci dilate in the same way as the ventricular system because of the distal obstruction.”
Having read this chapter and heard Dr. George's presentation, I naturally assumed that he was the first to describe the sign of large Sylvian cisterns in NPH; however, he never claimed priority. When I called him to confirm the references, he pointed out that Vassilouthis first described the sign in 1984 by using CT (6). Thus, I was correct in indicating that the sign of large Sylvian cisterns in NPH had been published previously; however, I was incorrect in my specific reference.
Concerning the issue of increased CSF flow void as an indicator of shunt-responsive NPH, I wish to point out that Dr. Mori's comments do not reflect the results as stated in either of his references, specifically in references 3 or 7. His reference 3 describes the finding of deep white matter ischemic changes with NPH (8). His reference 7 points out that the aqueductal CSF stroke volume (from quantitative phase contrast CSF velocity imaging) is increased with shunt-responsive NPH (9) not the flow void in itself.
Dr. Mori points out two articles (10, 11) that challenge the hyperdynamic CSF flow-void sign in NPH. The first of these investigators (10) used a fast spin-echo technique, and found the CSF flow void to be insensitive for predicting outcome in NPH. This is not surprising and, in fact, could have been predicted from our 1996 article in which we specifically stated that the current ubiquitous use of flow compensation minimizes the degree of signal loss attributable to CSF motion in the aqueduct (9). In that paper, 50% of the patients who were found to have hyperdynamic CSF flow by quantitative phase-contrast techniques did not have an increased flow void because the proton density–weighted images were flow-compensated. Similarly, with fast spin-echo images, the multiple 180° pulses achieve a marked degree of flow compensation, minimizing the degree of signal loss in the aqueduct and adjacent portions of the ventricular system (12). As noted (9), if flow-compensation (or fast spin-echo) techniques are used, the CSF flow void is intrinsically less marked, and if it is not seen in appropriately symptomatic patients, quantitative flow measurements should be made. The second citation (11) is an article written by two neurosurgeons. Unfortunately, they have not provided enough technical MR imaging information in their article to enable the reader to assess whether the CSF flow quantitation techniques were adequate or if the criteria for determining normal versus increased flow were appropriate.
In summary, we continue to believe firmly in the finding of hyperdynamic CSF flow as an indicator of shunt-responsive NPH—whether this is documented on proton density–weighted or conventional spin-echo images or through direct, quantitative phase-contrast CSF flow measurements. It has served us well for over 10 years of observation. Furthermore, we are grateful to Dr. Mori for making the finding of large Sylvian cisterns with NPH more accessible in the peer-reviewed radiologic literature.
References
  1. 18.↵
    Bradley WG.   MR prediction of shunt response in NPH: CSF morphology versus physiology.  AJNR Am J Neuroradiol  1998;19:1285-1286
    PubMed
  2. 19.↵
    Kitagaki H, Mori E, Ishii K,  et al.   CSF spaces in idiopathic normal pressure hydrocephalus: morphology and volumetry.  AJNR Am J Neuroradiol  1998;19:1277-1284
    Abstract
  3. 20.↵
    George AE.   Chronic communicating hydrocephalus and periventricular disease: a debate with regard to cause and effect.  AJNR Am J Neuroradiol  1991;12:42-44
    FREE Full Text
  4. 21.↵
    Shier CR, George AE, DeLeon MJ, Sheer-Williams M, Scyloponlos LA, Pinto R.   CT and MR features of hydrocephalus: paradoxical sylvian fissure enlargement and significance of the hippocampal luiency.   Presented at 27th Annual Meeting of American Society of Neuroradiology, March 18–24, 1989, Orlando, Florida 
  5. 22.↵
    George AE, DeLeon MJ.   Hydrocephalus, cerebral atrophy, and related disorders.   In: Haaga JR, Alfidie RJ, eds. Computed Tomography of the Whole Body, Chapter 10. St. Louis, Mo: CV Mosby & Co; 1988:326 
  6. 23.↵
    Vassilouthis J.   The syndrome of normal-pressure hydrocephalus.  J Neurosurg  1984;61(3):501-509
    PubMed
  7. 24.↵
    Bradley WG, Whittemore AR, Kortman KE, Homyak M, Teresi LM, David SJ.   Marked CSF flow void: an indicator of successful shunting in patients with suspected normal pressure hydrocephalus.  Radiology  1991;178:459-466
    PubMed
  8. 25.↵
    Bradley WG, Whittemore AR, Watanabe AS, Davis SJ, Teresi LM, Homyak M.   Association of deep white matter infarction with chronic communicating hydrocephalus: implications regarding the possible origin of normal-pressure hydrocephalus.  AJNR Am J Neuroradiol  1991;12:31-39
    Abstract/FREE Full Text
  9. 26.↵
    Bradley WG, Scalzo D, Queralt J, Nitz WN, Atkinson DJ, Wong P.   Normal-pressure hydrocephalus: evaluation with cerebrospinal fluid flow measurements at MR imaging.  Radiology  1996;198:523-529
    PubMed
  10. 27.↵
    Krause JK, Regel JP, Vach W, Jungling FD, Droats DW, Wakhloo AK.   Flow void of cerebrospinal fluid in idiopathic normal pressure hydrocephalus of the elderly: can it predict outcome after shunting.  Neurosurgery  1997;40:67-73
    PubMed
  11. 28.↵
    Hakim R, Black PM.   Correlation between lumbo-ventricular perfusion and MRI-CSF flow studies in idiopathic normal pressure hydrocephalus.  Surg Neurol  1998;49:14-19
    CrossRefPubMed
  12. 29.↵
    Bradley WG, Chen D-Y, Atkinson CJ.   Fast spin echo.   In: Bradley WG, Bydder GM, eds. Advanced MR Imaging Technology, Chapter 1. London: Martin Dunitz; 1997 
  


  
  



  
      
  
  

    
  


  
  



  




  


  
  



  
      
  
  

    
  


  
  



  
      
  
  

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