Acta Neurochir (Wien) (1989) 97:40-46
Ndurochirurgica 9 by Springer-Verlag1989
Age-dependent Changes of Cerebral Ventrieular Size Part I: Review of Intracranial Fluid Collections E. R. Cardoso, M. R. Del Bigio, and G. Schroeder Cerebral Hydrodynamics Laboratory, Department of Surgery, University of Manitoba, Winnipeg, Manitoba, Canada
Summary The age distributions of communicating hydrocephalus (CH), pseudotumour cerebri (PC) slit-ventricle syndrome (SVS), and chronic subdural haematomas (CSH) were reviewed in the medical literature. An age-related incidence was found: CH and CSH predominated in neonates less than 2 years and adults older than 55 years, while PC and SVS occurred mainly in older children and young adults. The latter two patient groups seem to show a greater resistance to ventricular dilatation in the presence of decreased CSF absorption. This may be related to larger volume and state of maturity of the cerebrum. On the other hand, neonates and the elderly more readily develop enlarged ventricles, in association with impairment of CSF absorption, or subdural fluid collections. Factors including status of cranial sutures, cerebral atrophy, cerebral water content, degree of cerebral myelination, and glial cell composition, may contribute to the age-related incidence of the four disorders investigated. Similarly, the development of ventriculomegaly may depend upon cerebral elastic properties besides the pri mary disturbance of CSF dynamics. The authors postulate that the size of cerebral ventricles in disorders of the ccrcbrospinal fluid (CSF) absorption is related to the elastic properties and volume of the brain. Furthermore, cerebral volume and elastic properties may also contribute to the age distribution of chronic subdural haematomas (CSH).
Keywords: Benign intracranial hypertension; chronic subdural haematoma; hydrocephalus; pseudotumour cerebri; slit-ventricle syndrome; cerebral ventricles.
Introduction T h e b i o m e c h a n i c a l principles t h a t d e t e r m i n e the size o f the c e r e b r a l ventricles are n o t well u n d e r s t o o d . Dist u r b a n c e o f c e r e b r o s p i n a l fluid ( C S F ) c i r c u l a t i o n is the best studied m e c h a n i s m which alters the ventricle size. U n d o u b t e d l y , the p h y s i c a l p r o p e r t i e s o f the c e r e b r u m are also i m p o r t a n t in d e t e r m i n i n g v e n t r i c u l a r size. T h e r e are a v a r i e t y o f d i s o r d e r s t h a t affect fluid-filled c o m p a r t m e n t s in the c r a n i u m a n d s u b s e q u e n t l y affect the v o l u m e o f the b r a i n p a r e n c h y m a .
R a i s e d i n t r a c r a n i a l pressure resulting f r o m cerebrospinal fluid s h u n t m a l f u n c t i o n m a y occur w i t h o u t acc o m p a n y i n g d i l a t a t i o n in h y d r o c e p h a l i c children, a c o n d i t i o n t e r m e d "slit-ventricle s y n d r o m e " (SVS) 11' 45, 65. T h e r e has been n o satisfactory e x p l a n a t i o n w h y ventricles t h a t h a d been p r e v i o u s l y d i l a t e d in these p a tients s u b s e q u e n t l y fail to r e - e x p a n d , as the defect o f CSF absorption probably remains unchanged. Similarly, after o b s t r u c t i o n o f c e r e b r a l v e n o u s d r a i n a g e raised i n t r a c r a n i a l pressure w i t h o u t ventricu l a r d i l a t a t i o n , o r p s e u d o t u m o u r cerebri (PC), m a y result in a d u l t s 3' 7, 23,134. H o w e v e r , similar venous b l o c k age in n e o n a t e s causes h y d r o c e p h a l u s 2I' 23, 25, 84,108. N o t o n l y i n t r a v e n t r i c u l a r a c c u m u l a t i o n o f C S F seems to be r e l a t e d to age, b u t also the c h r o n i c collection o f subd u r a l fluid which is m u c h m o r e c 6 m m o n a m o n g neonates a n d the elderly despite a m u c h higher incidence o f h e a d injuries d u r i n g the second a n d t h i r d decades 83' 88, 105, 119
T h e p u r p o s e o f the p r e s e n t s t u d y is to c o m p a r e the age d i s t r i b u t i o n s o f r e p o r t e d cases o f C H , PC, SVS, a n d c h r o n i c s u b d u r a l h a e m a t o m a s (CSH). W e speculate t h a t a g e - r e l a t e d changes in b o t h cerebral a n d ext r a c e r e b r a l tissues m a y c o n t r i b u t e to the susceptibility to f o r m a t i o n o f i n t r a c r a n i a l fluid collections o f all types.
Methods The medical literature was searched for reports of patients with CH, PC, SVS, or CSH and whose ages were specified or categorized by age divisions of five or fewer years. Patients were then grouped into three intervals for the first decade and 10-year intervals thereafter. Many reported series could not be included in the study because of incomplete information on patient age. No distinction were made between different aetiologies of a particular disorder.
E. R. Cardoso el aL: Age-dependent Changes of Cerebral Ventricular Size. I 40"
i "~',, .
5" t 6-2
012 3'-4 5[9 '//10'-19 20129 30!39 4o149 501s~ 60!69 -~'70
Fig. 1. Age distribution of communicating hydrocephalus (CH) (349 patients), pseudotumour cerebri (PC) (289 cases), slit-ventricle syndrome (SVS) (77 cases), and chronic subdural haematoma (CSH) (590 cases). The vertical axis represents the percentage of each age group in relation to the total number of cases for each disorder
A total of 68 studies involving 1,327 patients were reviewed. These included 349 cases of CH t' 9, 26, 34, 49, 5l, 54, 66, 67, 69, 71, 74, 90, 91, 92. 95, 102, 117, 118, 125. 128, 137 289 cases of PC 3" 5, 10, 12, 20, 43, 47, 6,-, 72, 106, 122,124,126,127, 133 77 cases of SVS 4' 8, 16, 17, 24, 36, 38, 41, 45, 46, 58, 61, 68, 113, 1151 116, 130, 14I, and 590 cases of CSH TM 14, 48, 59, 78, 82, 83, 88, 89, 98, 105. 119, 132
The age distributions for the four disorders are displayed in Fig. 1. Well defined peaks of incidence exist for each of them. CH and CSH present a bimodal age distribution with peaks in the first and seventh decades. There is striking overlap between the age incidence for the two diseases. Within the first decade 93% of hydrocephalic patients and 82 % of subdural patients were younger than 4 years of age. Although the graph indicates a peak for PC in the second decade, most of the large series, in which ages are often not specified, indicate a peak in the third or fourth decade 7' 44, 104, 111, 134 In notable contrast to CH and CSH, only 1.1% of the total number of PC patients were younger than 2 years. The age distribution of SVS predominates in the first decade, with only 2.1% of the patients below age 2 years. The age distribution curve for PC paralleled that for SVS, with no patients under 2 years and only 5.2% of patients older than 50 years. Diseussion
CSF absorption is a dynamic process involving various anatomic sites 87' 103. Impaired CSF absorption is
believed to be the main pathophysiologic disturbance in CH and SVS 9' iv, 77, 93. There is controversy whether cerebral vascular engorgement is involved in the development of PC 2' 32,42. However, information obtained from isotope cisternography and dynamic CSF infusion techniques suggest that impaired CSF reabsorption is the most important mechanism involved 63~si, 85,109. Yet the cerebral ventricles remain normal or small in size23' 32, 104, 135
While the disturbance of CSF dynamics in CH is similar to that observed in PC and SVS, ventriculomegaly develops only in CH. The ages of 2 and 50 years represent the lower and upper thresholds involved in the development of ventriculomegaly in diseases caused by diminished CSF absorption. CSF overdrainage in shunted patients may cause cerebral ventricles that are "slit-like ''15' 39. Collapse of the ventricle walls onto the shunt may cause intermittent elevations of intracranial pressure TM 45, 65. Although radiological evidence of "slit-like" ventricles is a common finding following CSF shunting in children, symptomatic SVS, is much less frequent. The reasons for the persistence of small ventricles are not fully understood. Foltz postulated the development of periventricular gliosis which leads to "stiffness" of the ventricular wall 4~ Pathological confirmation of the phenomenon is only suggestive 94. There has been no comparison of shunted hydrocephalics with and without SVS to assess the pathology, SVS follows CH on the same patient. The impaired CSF absorption that caused the initial hydrocephalus
E.R. Cardoso et al.: Age-dependent Changes of Cerebrai Ventricular Size. I
persists throughout the course of SVS17. The ventricles in these patients are initially enlarged. Following shunting the ventricles decrease in size and appear to become resistant to subsequent dilatation. This suggests that cerebral or extra-cerebral factors change with age and lead hydrocephalus to evolve into SVS. SVS in shunted patients is, therefore, analogous to PC. Indeed, there are documented cases of patients who developed alternatively CH and PC, suggesting a common mechanism between the two diseases s7. CH, PC, and SVS have common pathophysiological features of impaired CSF absorption 6' 17, 60, 85, 101,120, reduced cerebral compliance 121, and favourable response to CSF shunting2' 79. Ventriculomegaly, however, develops in CH, but not in PC or SVS, and thus seems to spare the middle years of life. Such an age distribution suggests that other variables, besides decreased CSF absorption, are responsible for the development of ventriculomegaly in neonates and elderly. Elevation of intracranial pressure is likely the factor that precipitates the initial development of ventriculomegaly in C H 33' 50, 99. Furthermore, for ventriculomegaly or chronic subdural collections to develop, gradients of pressure within the cerebral tissue must exist, in order to displace the parenchyma outward is' 100.The displacement of cerebral tissue is probably facilitated by two conditions: 1) diminished resistance of cerebral tissue to deformity and 2) decreased resistance to expansion by structures surrounding the brain. Both conditions are present during neonatal and senile life and they may therefore explain the predisposition to the development of ventriculomegaly or subdural collections in those age groups.
may explain why cerebral venous hypertension, which frequently leads to PC in older age groups, causes CH in children less than 20 months in age21' 23, 25, 27, 84, 86, 97, 107, 108, 112. Rosman and Shands also hypothesized that some alteration of brain consistency is responsible for that differenceI~ In the elderly, the brain parenchyma may be subject to less external resistance to distortion because of larger CSF-filled spaces over the convexities, secondary to senile atrophy of the cerebrum 142.
Composition of Cerebral Tissue Besides impaired CSF absorption and age-related extra-parenchymal resistance, the development of ventriculomegaly and subdural collections may depend upon the physical properties of the cerebral paren-
LEGEND ........ Skull Neuron
1~ o 0"
NO VENTRICULAR DILATATION
Extra-parenehymal Resistance to Cerebral Expansion Patency of cranial sutures, which begin to close at 1 year, partly accounts for diminished resistance to centrifugal cerebral displacement in neonates21. Internal centrifugal forces generated by elevated intracranial pressure can separate the skull bones, thus allowing hydrocephalus and subdural collections to develop. Hochwald et al. described a technique of removal of skull and dura over the convexity prior to induction of obstruction of CSF flow for consistent production of gross ventriculomegaly in cats 37' 55, 56. When only half of the calvavium was removed, the cats showed a greater degree of ventriculomegaly on the craniectomized side 11~ In the clinical setting subtemporal craniectomy also leads to ipsilateral ventricular expansion in patients with impaired CSF absorption 37' 141. This
Fig. 2. Diagramatic representation of cerebral and extra-cerebral factors that may contribute to the development of ventriculomegaly in disorders of CSF absorption or subdural collection of blood. Top: The infant brain with complete number of neurons, but with relatively few glial cells, incompletely myelinated axons, and high water content. The open skull sutures fascilitates the centrifugal displacement of cerebral tissue. Middle: In older children and young adults, ventriculomegaly is prevented by dense glial mass, complete myelination, low water content and closed s~:ull sutures. Bottom: In the elderly, neuronal loss contributes to cerebral atrophy and increase in size of the subarachnoid spaces. Those factors may predispose the development of extra-cerebral fluid collections
E. R. Cardoso etal.: Age-dependent Changes of Cerebral Ventricular Size. I c h y m a itself. Indeed ventriculomegaly precedes head enlargement at the onset o f neonatal hydrocephalus 35' 53, 64, 70. The cyto-architecture o f cerebral tissue varies with age, and m a y alter the ability of the cerebrum to undergo structural deformity such as ventriculomegaly (Fig. 2). A l t h o u g h m o s t neurons are present at birth, the cerebrum contains a relatively sparse population o f glial cells, incompletely myelinated axons, and high water content 3~ 31, 96, 114. The rapid increase in cerebral volume during the first 18 24 m o n t h s o f life is due mainly to proliferation o f glial cells 19' 28, 29, ao. While there is increase in cell and myelin mass, the water content gradually decreases and reaches adult values by 2 to 21/2 years 8~ 129, 138. A x o n a l myelination in the cerebral hemispheres begins after birth and proceeds at a very rapid rate till age 229,129,136, leo. The increasing population o f cellular elements, increase in myelin, and decrease in extracellular water content during the first 2 years o f life are likely to after the elasticity o f the cerebrum and to decrease its capacity to undergo deformity, thus explaining the reduced incidence o f ventriculomegaly after that age. Indeed, the reduction in size o f cerebral ventricles that occurs after infancy has been attributed to myelination 52' 76. After age 55, progressive reduction in weight and volume o f the brain is c o m m o n 22' 75, 123, 139. The resulting a t r o p h y causes enlargement o f sulci and cerebral ventricles. Senile enlargement o f ventricular surface m a y facilitate the development o f hydrocephalus 49. Additionally, senile enlargement o f subarachnoid spaces m a y decrease the resistance to centrifugal displacement o f cerebral tissue and thus facilitate the development o f hydrocephalus and subdural collections in elderly persons.
Conclusions The population distribution o f CH, PC, SVS, and C S H suggests that age-related properties o f the brain and extra-cerebral tissue m a y play a role in the develo p m e n t o f extra-parenchymal fluid collections. A m o n g the entities involving disturbances o f C S F absorption, PC and SVS seem to be closely related. Lack o f ventricular dilatation in both conditions is p r o b a b l y related to the greater volume and stiffness o f the brain. This m a y also explain the rare incidence o f C S H in this age group. The elderly and neonates are m o r e prone to develop both C H and CSH. Lack o f cerebral maturity and opening o f cranial sutures in neonates, and smaller
brains in the elderly m a y predispose the development of extra-cerebral fluid collections in these age groups. The data also suggest that the development o f ventriculomegaly in conditions associated with defective C S F absorption m a y depend u p o n cerebral elasticity and extra-cerebral resistance, in addition to the primary disturbance o f C S F hydrodynamics.
References 1. Adams RD, Fisher CM, Hakim S, Ojemann RG, Sweet WH (i965) Symptomatic occult hydrocephalus with "normal" cerebrospinal fluid pressure. A treatable syndrome. N Engl J Med 273:117-126 2. Ahlskog JE, O'Neill BP (1982) Pseudotumor cerebri. Ann Intern Med 97:249-256 3. Amacher AL, Spence JD (1985) Spectrum of benign intracranial hypertension in children and adolescents. Childs Nerv Syst 1:81-86 4. Ammiroti M, Eller T, Linton S (1986) Slit ventricles and shunt malfunction in an elderly patient. A case report. J Am Geriatric Soc 34:545-547 5. Bjerre P, Lindholm J, Gyldensted C (1982) Pseudotumor cerebri. A theory on aetiology and pathogenesis. Acta Neurol Scand 66:472M81 6. BlackP McL (1980) Idiopathic normal pressure hydrocephalus. Results of shunting 62 patients. J Neurosurg 52:371-377 7. Boddie HG, Banna M, Bradley WG (1974) "Benign" intracranial hypertension. Brain 97:313-326 8. Bode H, Habler W, Sauer M (1984) The slit-ventricule syndrome- causes, procedures of differential diagnosis and therapeutic problems. Klin Pediatr 196:40-43 9. Borgensen SE (1984) Conductance to outflow of CSF in normal pressure hydrocephalus. Acta Neurochir (Wien) 71:t-45 10. Brawanski A, Sorensen N (1985) Increased ICP without ventriculomegaly. Diagnostic and therapeutic problems in a 1-yearold boy. Childs Nerv Syst I: 66-68 11. Brenner A, Kalff R, Kocks W, Roosen C (1984) Slit-ventricle: clinical syndrome or radiological phenomenon? Neuropediatrics 15:241 (Abst) 12. Bullens C, DeVries WAEJ, van Crevel H (1979) Benign intracranial hypertension: a retrospective and follow-up study. J Neurol Sci 40:147-157 i3. Cameron M (1978) Chronic subdural hematoma. A review of 1I4 cases. J Neural Neurosurg Psychiatry 41:834 839 14. Carlton CK, Saunders RL (1983) Twist drill craniostomy and closed system drainage of chronic and subacute subdural haematomas. Neurosurgery 13:153-159 15. Carteri A, Longatti PL, Gerosa M, Mazza C, Pasqualin A (1980) Complications due to incongrous drainage of shunt operations. Adv Neurosurg 8:199-203 16. Chazal J, Janny P, Irthum B, Massini B (1983) Slit-ventricles. Report on 2 cases. Neurochirurgie 29:327-331 17. Collmann H, Mauersberger W, Mohr G (1980) Clinical observations and CSF absorption studies in the slit ventricle syndrome. Adv Neurosurg 8:183-186 18. Conner ES, Foley L, Black PM (1984) Experimental normalpressure hydrocephalus is accompanied by increased transmantle pressure. J Neurosurg 61:322-327
E.R. Cardoso etal.: Age-dependent Changes of Cerebral Ventricular Size. I
19. Coppoletta JM, Wolbach SB (1933) Body length and organ weights of infants and children. Am J Pathol 9:55-70 20. Couch R, Camfield PR, Tibbles JAR (1985) The changing picture of pseudotumour cerebri in children. Can J Neurol Sci 12:48-50 21. Coulson JD, Pitlick PT, Miller DC, French JW, Marshall WH, Fryer AD, Shumway NE (1984) Severe superior vena cava syndrome and hydrocephalus after the Mustard procedure: findings and a new surgical approach. Circulation 70 [Suppl] 1: 47-53 22. Creasey H, Rapaport SI (1985) The aging human brain. Ann Neurol 17:2-10 23. D'Avella D, Greenberg RP, Mingrino S, Scanarini M, Pardatscher K (1980) Alterations in ventricular size and intracranial pressure caused by sagittal sinus pathology in man. J Neurosurg 53:656-661 24. Dahlerup B, Gjerris F, Harmsen A, Sorensen PS (1985) Severe headaches as the only symptom of long-standing dysfunction in hydrocephalic children with normal or slit ventricles revealed by computed tomography. Child Nerv Syst 1:49-52 25. De Lange S, de Vlieger M (1970) Hydrocephalus associated with raised venous pressure. Dev Meal Child Neurol [Suppl] 22:28-32 26. De MolJ (1978) Troubles psychiques au eours d'hydrocephalie normotensive. Acta Neurol Belg 78:321-340 27. Dillon T, Berman W Jr, Yabek SM, Seigel R, Ahl B, Wernly J (1986) Communicating hydrocephalus: A reversible complication of the Mustard operation with serial hemodynamics and long-term follow-up. Ann Thorac Surg 41:146-149 28. Dobbing J, Undernutrition and the developing brain. Am J Dis Child 120:411~415 29. Dobbing J, Sands J (1973) Quantitative growth and development of human brain. Arch Dis Child 48:757-767 30. Dobbing J, Sands J (1970) Timing ofneuroblast muitiplication in developing human brain. Nature 226:639-640 31. Dobbing J, Smart JL (1973) Early undernutrition, brain development and behaviour. In: Barnett SA (ed) Ethology and development. Heinemann Medical Books, Ltd, London, pp 1636 32. Donaldson JO (I 981) Pathogenesis of pseudotumor cerebri syndromes. Neurology 31:877 880 33. Early CB, Fink LH (1976) Some fundamental applications of the law of Laplace in neurosurgery. Surg Neurol 6:185-189 34. Ekbom K, Greitz T, Kalmer M, Lopez J, Ottosson S (1969) Cerebrospinal fluid pulsations in occult hydrocephalus due to ectasia of the basilar artery. Acta Neurochir (Wien) 20:1-8 35. Ellison PH (1978) Re-evaluation of the approach to an enlarging head in infancy. Dev Med Child Neurol 20:738-745 36. Engel M, Carmel PW, Chutorian AM (1979) Increased intraventricular pressure without ventriculomegaly in children with shunts with "normal volume hydrocephalus". Neurosurgery 5:549-552 37. Epstein F, Rubin RC, Hochwald GM (1974) Restoration of the cortical mantle in severe feline hydrocephalus: A new Iaboratory model. Dev Med Child Neurol [Suppl] 32:49-53 38. Epstein FJ, Fleischer AS, Hochwald GM, Ransohoff J (1974) Subtemporal craniectomy for recurrent shunt obstruction secondary to small ventricles. J Neurosurg 41:2%31 39. Faulhauer K, Schmitz P (1978) Overdrainage phenomena in shunt treated hydrocephalus. Acta Neurochir (Wien) 45: 89101
40. Foltz EL (1984) Hydrocephalus and CSF pulsatility: clinical and laboratory studies. In: Shapiro K, Marmarou A, Portnoy H (eds) Hydrocephalus. Raven Press, New York, pp 337-362 41. Friedman P, Gass HH (1983) Lumboatrial shunt: case report. Neurosurgery 13:69-71 42. Gaab MR, Czech T, Korn A (1984) "Pseudotumor cerebri": Disturbance of "cerebrovenous outflow valve"? Neuropaediatrics 15:241 (Abst) 43. Gjerris F, Sorensen PS, Vorstrup S, Paulson OB (1985) Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow in patients with benign intracranial hypertension (pseudotumor cerebri). Ann Neurol 17:158-162 44. Grant DN (1971) Benign intracranial hypertension: a review of 79 cases in infancy and childhood. Arch Dis Child 46: 651655 45. Gruber R (1981) The relationship of ventricular shunt complications to the chronic overdrainage syndrome: A follow-up study. Z Kinderchir 34:346-352 46. Gruber R (1983) Should "normalization" of the ventricles be the goal of hydrocephalus therapy? Z Kinderchir 38 [Suppl] 2: 80-83 47. Gucer G, Viernstein L (1978) Long-term intracranial pressure recording in the management of pseudotumor cerebri. J Neurosurg 49:256-263 48. Gutierrez FA, Mclone DG, Raimondi AJ (1979) Physiopathology and a new treatment of chronic subdural hematoma in children. Child's Brain 5:216 232 49. Hakim S, Adams RD (1965) The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. Observations on cerebrospinal fluid dynamics. J Neurol Sci 2:307-327 50. Hakim S, Venegas JG, Burton JD (1976) The physics of the cranial cavity, hydrocephalus and normal pressure hydrocephalus: Medical interpretation and mathematical model. Surg Neurol 5:187-210 51. Hammock MK, Milhorat TH, Baron IS (1976) Normal pressure hydrocephalus in patients with myelomeningocele. Dev Med Child Neurol [Suppl] 37:55-68 52. Henningsen GJ, Jacobsen HH (1972) Abnormal pneumo-encephalogram in infancy subsequently normalized: three case histories from a child psychiatric department. Danish Med Bull 19:110 113 53. Hill A, Shactelford D, Volpe JJ (1984) A potential mechanism of pathogenesis for early posthemorrhagie hydrocephalus in the premature newborn. Pediatrics 73:19-21 54. Hill A, Volpe JJ (1981) Normal pressure hydrocephalus in the newborn. Pediatrics 68:623 629 55. Hochwald GM, Epstein F, Malhan C, Ransohoff J (1972) The role of skull and dura in experimental feline hydrocephalus. Dev Med Child Neurol [Suppl] 27:65-69 56. Hochwald GM, Ransohoff J (1973) The relationship of compensated to decompensated hydrocephalus in the cat. J Neurosurg 39:694-697 57. Hogan PA, Woolsey RM (1966) Hydrocephalus in the adult. JAMA 198:110-114 58. Holness RO, Hoffman HJ, Hendrick EB (1979) Subtemporal decompression for the slit-ventricle syndrome after shunting in hydrocephalic children. Child's Brain 5:137-144 59. Hubschamann OR (1980) Twist drill craniostomy in the treatment of chronic and subacute subdural haematomas in severely ill and elderly patients. Neurosurg 6:233-236
E. R. Cardoso etal.: Age-dependent Changes of Cerebral Ventricular Size. 1 60. Hughes CP, Siege1 BA, Coxe WS, Gado MH, Grubb RL, Coleman RE, Berg L (1978) Adult idiopathic communicating hydrocephalus with and without shunting. J Neurol Neurosurg Psychiatry 41:961-971 61. Hyde-Rowan MD, Rekate HL, Nulsen FE (1982) Re-expansion of previously collapsed ventricles. The slit ventricle syndrome. J Neurosurg 56:536 539 62. Johnston I0 Paterson A (1974) Benign intracranial hypertension. I. Diagnosis and prognosis. Brain 97:289 300 63. Johnston I (1975) The definition of a reduced CSF absorption syndrome: a reappraisal of benign intracranial hypertension and related syndromes. Med Hypoth 1:10-15 64. Kaiser AM, Whitelaw AGL (1985) CerebrospinaI fluid pressure during post hemorrhagic ventricular dilatation in newborn infants. Arch Dis Child 60:620-624 65. Kalff R, Bremer A, Kocks W, Roosen K, Lohr E (1985) SlitVentrikel - Klinisches Syndrom oder radiologisches Phfinomen? Radiologe 25:437~439 66. Katzman R (1977) Normal pressure hydrocephalus. Contemp Neurol Ser 15:69-92 67. Kendall B, Holland I (1981) Benign communicating hydrocephalus in children. Neuroradiology 21:93 96 68. Kiekens R, Mortier W, Pothman R, Bock WJ, Seibert H (1982) The slit-ventricle syndrome after shunting in hydrocephalic children. Neuropediatrics 13:190-i94 69. Knutsson E, Lying-Tunnell U (1985) Gait apraxia in normal pressure hydrocephalus: patterns of movement and muscle activation. Neurology 35:155 160 70. Korobkin R (1975) The relationship between head circumference and the development of communicating hydrocephalus in infants following intraventricular hemorrhage. Pediatrics 56: 74-77 71. Laws ER Jr, Mokri B (1977) Occult hydrocephalus: results of shunting correlated with diagnostic tests. Clin Neurosurg 24: 316-333 72. Lessell S, Rosman NP (1986) Permanent visual impairment in childhood pseudotumor cerebri. Arch Neurol 43:801-805 73. Linder M, Diehl J, Sklar FH (1983) Subtemporal decompression for shunt-dependent ventricles: Mechanism of action. Surg Neurol 19:520-523 74. Lobo Antunes J, Fahn S, Cote L (1983) Normal pressure hydrocephalus and Parkinson's disease. J Neural Trans [Suppl] 19:225 231 75. Leng DM (1985) Aging in the nervous system. Neurosurgery 17:348-354 76. Lerber J, Priestley BL (1981) Children with large heads: a practical approach to diagnosis in 557 children with special reference to 109 children with megalencephaly. Dev Med Child Neurol 23:494 504 77. Lorenzo AV, Page LK, Watters GV (1970) Relationship between cerebrospinal fluid formation, absorption and pressure in human hydrocephalus. Brain 93:679-692 78. Ludwig B, Nix W, Lanksch W (1983) Computed tomography of the "armored brain". Neuroradiology 25:39 43 79. Lundberg N (1960) Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiat Neurol Scand [Suppl] 149:1-193 80. MacArthur CG, Doisy EA (1918) Quantitative chemical changes in the human brain during growth. J Comp Neurol 30:445~486 81. Mann JD, Johnson RN, Butler AB, Bass NH (1983) Cerebro-
spinal fluid circulatory dynamics in pseudotumor cerebri and response to steroid therapy. In: Wood JH (ed) Neurobiology of cerebrospinal fluid 2. Plenum Press, New York, pp 739 751 82. Marcwalder TM, Seiler RW (1985) Chronic subdural hematomas. To drain or not to drain? Neurosurgery 16:185-188 83. Marcwalder TM, Steinsieppe KF, Rohner M, Reichenbach W (1981) The course of chronic subdural hematomas after burrhole craniostomy and closed system drainage. J Neurosurg 55: 390 396 84. Markowitz RI, Kleinman CS, Hellenbrand WE, KopfG, Ment LR (1984) Communicating hydrocephalus secondary to superior vena caval obstruction. Am J Dis Child 138:638-641 85. Martins AN (1973) Resistance to drainage of cerebrospinal fluid: Clinical measurement and significance. J Neurol Neurosurg Psychiatry 36:313-318 86. Mawk JR, McConnell J, Fulbright TD (1985) A suggested relationship between sagittal synostosis, intracranial hypertension and hydrocephalus. Minn Med 68:562-563 87. McComb JG (1983) Recent research into the nature of cerebrospinal fluid formation and absorption. J Neurosurg 59: 369383 88. McKissock W, Richardson A, Bloow W (1960) Subdural hematoma. A review of 389 cases. Lancet i: 1365-1369 89. McLauren R, Isaacs E, Lewis P (1971) Results of nonoperative treatment in 15 cases of infantile subdural hematoma. J Neurosurg 34:753-759 90. Messert B, Baker NH (1966) Syndrome of progressive spastic ataxia and apraxia associated with occult hydrocephalus. Neurology 16:440-452 91. Meyer JS, Kitagawa Y, Tanahashi N, Tachibana H, Kandula P, Cech DA, Clifton GL, Rose JE (1985) Evaluation of treatment of normal pressure hydrocephalus. J Neurosurg 62:513521 92. Meyer JS, Tachibana H, Hardenberg JP, Dowell RE Jr, Kitagawa Y, Mortel KF (1984) Normal pressure hydrocephalus. Influences on cerebral hemodynamic and cerebrospinal fluid pressure-chemical autoregulation. Surg Neurol 21:195-203 93. Milhorat TH (1972) Hydrocephalus and the cerebrospinal fluid. William and Wilkins Co, Baltimore, pp237 238 94. Oi S, Matsumoto S (1986) Morphological findings of postshunt slit ventricles in experimental canine hydrocephalus-aspects of causative factors of isolated ventricles and slit ventricle syndrome. Childs Nerv System 2:179-184 95. Ojemann RG, Fisher CM, Adams RD, Sweet WH, New PFJ (1969) Further experience with the syndrome of"normal" pressure hydrocephalus. J Neurosurg 31:279-294 96. Ordy JM, Kaack B (1975) Neurochemical changes in composition, metabolism and neurotransmitters in the human brain with age. Adv Behav Biol 16:253 285 97. Orr LS, Osher RH, Savino PJ (1978) The syndrome of facial nevi, anomalous cerebral venous return, and hydrocephalus. Ann Neurol 3:316-318 98. Orrison WW, Robertson WC, Sackett JF (1978) Computerized tomography in chronic subdural hematomas (effusions) of infancy. Neuroradiology 16:79-81 99. Paltesev EI, Sirovsky EB (1982) Intracranial physiology and biomechanics. Clinical data on pressure-volume relationships and their interpretation. J Neurosurg 57:500-510 100. Penn RD, Bacus JW (1984) The brain as a sponge. A computed tomographic look at Hakim's hypothesis. Neurosurgery 14: 670-675
E.R. Cardoso etal.: Age-dependent Changes of Cerebral Ventricular Size. I
101. Peterson RC, Mokri B, Laws ER Jr (1985) Surgical treatment of idiopathic hydrocephalus in elderly patients. Neurology 35: 307-311 102. Portenoy RK, Berger A, Gross E (1984) Familial occurrence of idiopathic normal-pressure hydrocephalus. Arch Neurol 4 h 335-337 103. Povlishock JT, Levine JE (1984) Cerebrospinal fluid absorption. In: Kapp JP, Schmidem HH (eds) Cerebral venous system and its disorders. Grune and Stratton Inc, pp251-274 104. Reid AC, Matheson MS, Teasdale G (1980) Volume of the ventricles in benign intracranial hypertension. Lancet 2:7-8 105. Robinson RG (1984) Chronic subduraI hematoma: Surgical management in 133 patients. J Neurosurg 61:263-268 106. Rose A, Matson DD (1967) Benign intraeranial hypertension in children. Pediatrics 39:227537 107. Rosman NP, Shands KN (1978) Hydrocephalus caused by increased intracranial venous pressure: a clinicopathological study. Ann Neurol 3:445-450 108. Ross RT (1983) Brain swelling and ventricle size. Can J Neurol Sci 10:110 113 109. Rottenberg DA, Foley KM, Posner JB (1980) Hypothesis: the pathogenesis of pseudotumour cerebri. Med Hypoth 6: 913918 110. Rubin RC, Hochward G, Tiell M, Liwnicz B, Epstein F (1975) Reconstitution of the cerebral cortical mantle in shunt-corrected hydrocephalus. Dev Med Child Neurol [Suppl] 35:151-156 111. Rush JA (1980) Pseudotumour cerebri. Clinical profile and visual outcome in 63 patients. Mayo Clin Proc 55:541-546 112. Saint-Rose C, LaCombe J, Pierre-Kehn A, Renier D, Hirsch JF (1984) Intra-cranial venous sinus hypertension: cause or consequence of hydrocephalus in infants? J Neurosurg 60: 727736 113. Salmon JH (1978) The collapsed ventricle: management and prevention. Surg Neurol 9:349-352 114. Samorajski T, Rolsten C (1973) Age and regional differences in the chemical composition of brains of mice, monkeys and humans. In: Fard DH (cd) Neurobiological aspects of maturation and aging. Elsevier Scientific Publ Co, Amsterdam. Prog Brain Res 40:253-265 115. Schutz H, Fleming JFR, Humphreys RP, Deck JHN, Keith WS (1980) Normal pressure hydrocephalus - high pressure normocephalus. Can J Neurol Sci 7:211-213 116. Serlo W, Heikkinen E, Saukkomen AL, Vomwendt L (1895) Classification and management of the slit ventricle syndrome. Child Nerv Syst h 194-199 117. Shapiro K, Fried A, Marmarou A (1985) Biomeehanical and hydrodynamic characterization of the hydrocephalic infant. J Neurosurg 63:69-75 118. Shapiro K, Takei F, Fried A, Kohn I (1985) Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats. J Neurosurg 63:82-87 119. Sepponen JT, Sepponen RE, Sivula A (1984) Chronic subdural haematoma: demonstration by magnetic resonance. Radiology 150:79-85 120. Singounas EG, Krasanakis C, Karvounis PC (1976) Observations on the pathogenesis of low pressure hydrocephalus. Analysis of 25 cases. Neurochirurgia 19:22-25 121. Sklar FH, Beyer CW, Clark WK (1980) Physiological features of the pressure-volume function of brain elasticity in man. J Neurosurg 53:166-172 122. Sklar FH, Diehl JT, Beyer CW, Clark WK (1980) Brain elasticity changes with ventriculomegaly. J Neurosurg 53:173-179
123. Skullerud K (1985) Variations in the size of the human brain. Influence of age, sex, body length, body mass index, alcoholism, Alzheimer changes, and cerebral atherosclerosis. Acta Neurol Scand [Suppl] 102:1-94 124. Smith TJ, Baker RS (1986) Perimetric findings in pseudotumor cerebri: using automated techniques. Ophthalmology 93:887 892 125. Sorensen PS, Gjerris F, Hammer M (1984) Cerebrospinal fluid vasopressin and increased intracranial pressure. Ann Neurol 15:435-440 126. Spector RH (1984) Pseudotumour cerebri caused by a synthetic vitamin A preparation. Neurology 34:150%1511 127. Spence JD, Amacher AL, Willis NR (1980) Benign intracranial hypertension without papilloedema: role of 24-hour cerebrospinal fluid pressure monitoring in diagnosis and management. Neurosurgery 7:326-336 128. Stein BM, Fraser RER, Tenner MS (1972) Normal pressure hydrocephalus: complication of posterior fossa surgery in children. Pediatrics 49:50-58 129. Tilney F, Rosett J (1931) The value of brain lipoids as an index of brain development. Bull Neurol Inst NY h 28-71 130. Walsh JW, James HE (1982) Subtemporal craniectomy and elevation of shunt valve opening pressure in the management of small ventricle-induced cerebrospinal fluid shunt dysfunction. Neurosurgery 10:698-703 131. Warwick R, Williams PL (eds) (1973) Gray's Anatomy 35th Ed. Longman, Edinburgh, 311 pp 132. Welsh JE, Tyson GW, Winn HR, Jane JA (1979) Chronic subdural haematoma presenting as transient neurologic deficits. Stroke 10:564-567 133. Weisberg LA, Chutorian AM (1977) Pseudotumor cerebri of childhood. Am J Dis Child 131:1243-1248 134. Weisberg LA (1975) Benign intracranial hypertension. Medicine 54:197-207 135. Weisberg LA (1985) Computed tomography in benign intracranial hypertension. Neurology 35:1075-1078 136. Wiggins RC (1986) Myelination- a critical stage in development. Neurotoxicology 7:103-120 137. Wikkelso C, Andersson H, Blomstrand C, Lindqvist G (1982) The clinical effect of lumbar puncture in normal pressure hydrocephalus. J Neurol Neurosurg Psychiatry 45:64-69 138. Winick M, Rosso P, Waterlow J (1970) Cellular growth of cerebrum, cerebellum, and brain stem in normal and marasmic children. Exp Neurol 26:393-400 139. Wree A, Braak H, Schleicher A, Zillcs K (1980) Biomathcmaticai analysis of the neuronal loss in the aging human brain of both sexes demonstrated in pigment preparations of the pars cerebellaris loci coerulei. Anat Embryol 160:105 119 140. Yakovlev PI, Lecours AR (1967) The myelogenetic cycles of regional maturation of the brain. In: Minhowski A (ed) Regional development of the brain in early life. Blackwell Scientific Publ, Oxford, pp 3-80 141. Yelin FS,. Ehni G (1969) Percallosal sump ventriculostomy for shunt-dependent hydrocephalic patient with small ventricles. J Neurosurg 31:570-573 142. Zeumer H, Hacke W, Hartwich P (1982) A quantitative approach to measuring the cerebrospinal fluid space with CT. Neuroradiology 22:193-197 Correspondence and Reprints: Dr. E. R. Cardoso, Cerebral Hydrodynamics Laboratory, Health Sciences Centre, MS-771,820 Sherbrook Street, Winnipeg, Manitoba, Canada R3A 1R9.