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�v J. Hydrocephalus, Vol. 1, No. 1, 2009

Journal of HydrocephalusVolume 1, Number 1　2009

EDITORIAL 1

ORIGINAL ARTICLES:Evolution Theory in Cerebrospinal Fluid Dynamics: A Hypothesis for Failure of Neuroendoscopic Ventriculostomy in Treatment of Hydrocephalus in Fetal, Neonatal and Early Infantile Periods.

Shizuo Oi, Wolf Luedemann, Amir Samii, Madjid Samii 2

Impact of a portable neuroendoscopic equipment system to provide an outreach service in Sub-Saharan Africa.

Mubashir Mahmood Qureshi, J Piquer Belloch 11

Complications of Neuroendoscopy Federico Di Rocco, M.D, Wolf Luedemann, Shizuo Oi 15

HYDROCEPHALUS RESEARCH WORLD RECORD RANKING [1950─2008]

The list of Top 10 researcher’s papers 21

INTERNATIONAL FEDERATION OF NEUROENDOSCOPY [IFNE] 37PRESIDENTIAL ADDRESS:

History of International Federation of Neuroendoscopy [IFNE] Shizuo Oi [IFNE President] 38

MEMORIAL ADDRESS: “Professor Axel Pernecsky” 1945-2009

Bernhard L. Bauer [IFNE Honorary President] 40

CONGRESS PRESIDENT WELCOME ADDRESS: 5th World Congress of the International Federation of Neuroendoscopy

Spyridon Sgouros [IFNE World Congress President] 42

COMMITTEE STRUCTURE OF INTERNATIONAL FEDERATION OF NEUROENDOSCOPY [IFNE] 43

PROGRAM of 5th World Congress of IFNE 44

CONSTITUTION AND BY-LAWS of INTERNATIONAL FEDERATION OF NEUROENDOSCOPY [IFNE] 62

ANNOUNCEMENTSpecial Issue: “NEUROENDOSCOPY”

　Journal of Hydrocephalus Volume 2, Number 1, 2010 66

Prof. Oi’s India Live-surgery Courses 2009 67

Journal of Hydrocephalus

�J. Hydrocephalus, Vol. 1, No. 1, 2009

“The basic facts permit an understanding of the dynamics of cerebrospinal fluid (CSF) circulation and of the various types of hydrocephalus” (Anthony J. Raimondi, 1972). Though not recognized as an independent specialty by international, regional, or national pediatric/adult neurosurgical organizations, Hydrocephalus Research is de facto recognized as a specific field of research by pediatricians, by all other medical and surgical specialties, and by society. Hydrocephalus is taught at the undergraduate level in medical schools, and at the graduate level in such specialties as neurosurgery, neuroradiology, neurology, pediatrics, obstetrics and basic neuroscience. Its principles are being established, its limits extended and defined, and its practitioners identified. However, even after one hundred years of Hydrocephalus Research, the various specific entities, pathophysiology, treatment modalities and indications, and fundamental basic science, remain controversial. A Journal specific to Hydrocephalus Research is needed. I chose to undertake this work together with an editorial board including major hydrocephalus researchers worldwide, attempting always to remember Anthony J. Raimondi’s words. The very different national origins and ultimate life goals of the board members form the basis for the truly humanistic group of Hydrocephalus Research: always foresquare in facing the reality that sick children are sick children everywhere in the world, that their parents suffer equally irrespective of the gravity of the illness, and that the child’s need for neurosurgical care must transcend the economic or academic needs of the physician. This same approach is essential when coping with adult patients suffering from “intractable hydrocephalus”. Still, when all is said and done, how does a journal that hopes to be a humanistic treatment of a scientific discipline, one composed of theoretical and technical elements, come into existence? We are beginning this work with an exhaustive review of the literature over the past half century, creating a Hydrocephalus Research World Record Ranking [HRWRR] as a means of critically analyzing various etiological, pathological, pathogenetic, diagnostic, and therapeutic aspects of hydrocephalus in the history of Hydrocephalus Research. In the critical review of neary 10,000 publications by the HRWRR committee, it was obvious that the Neuroendoscopy has been the source to advance the Hydrocephalus Research. The affiliation to the International Federation of Neuroendoscopy [IFNE] is essential. It is hoped that this “ ” may serve as an ongoing update on Hydrocephalus Research, while simultaneously stimulating present and future Hydrocephalus Researchers to advance the present knowledge and treatment modalities in hydrocephalus, more completely to head the sick patients suffering from this malady.

Shizuo Oi, M.D., Ph.D. Editor-in-Chief


EDITORIAL

� J. Hydrocephalus, Vol. 1, No. 1, 2009

Evolution Theory in Cerebrospinal Fluid Dynamics:A Hypothesis for Failure of Neuroendoscopic Ventriculostomy in Treatment of Hydrocephalus in Fetal, Neonatal and Early Infantile Periods

Shizuo Oi, M.D., Ph.D. 1, 2, Wolf Luedemann, M.D. 2, Amir Samii, M.D., Ph.D. 2, Madjid Samii, M.D., Ph.D. 2

Division of Pediatric Neurosurgery, The Jikei University Women’s & Children’s Medical Center, Tokyo Japan 1, and Department of Pediatric Neurosurgery, International Neuroscience Institute, Hannover, Germany 2

Corresponding author :Shizuo Oi, M.D., Ph.D.Division of Pediatric Neurosurgery,The Jikei University School of Medicine3-25-8 Nishi Shinbashi, Minato-ku 105-8461, Tokyo, JapanPhone: +81-3-3433-1111Fax: +81-3-3438-1161E-mail: [email protected]

[Object] The aim of this study was to discuss the underlying pathophysiology in failure of neuroendoscopic ventriculostomy during treatment of “non-communicating hydrocephalus” with reference to findings from analyses of specific cerebrospinal fluid (CSF) dynamics in the immature brain.

[Materials and Method] Prospective analysis was performed for 12 hydrocephalic neonates and infants suspected as non-communicating hydrocephalus as the initial impressions on magnetic resonance imaging (MRI) to undergo the preoperative CSF dynamic studies using cine-mode MRI and computed tomography (CT) ventriculo-cisternography.

[Results] Of the 12 cases, 9 (75%) in the prospective study of CSF dynamics revealed misdiagnosis compatible with “communicating hydrocephalus”. The pattern in the ventriculo-cisternography in all these cases revealed intra-parenchymal predominant CSF flow (minor pathway) in the CSF dynamics, rather than passage in the major pathway. Four patients were selected as displaying definitive indications for neuroendoscopic ventriculostomy. Postoperatively, all 4 patients were improved with stabilized intracranial pressure (ICP), as in the condition of “post-endoscopic ventriculostomy arrested hydrocephalus”. However, symptoms of increased ICP recurred in all 4 patients at a mean of 5.5 weeks (range, 4-9 weeks). Ventriculo-peritoneal (V-P) shunt was subsequently performed in all 12 patients except one who underwent craniotomy for cyst removal, with improvements noted in each case.

[Discussion and Conclusion] The high incidence of “failure of neuroendoscopic ventriculostomy” in treatment for hydrocephalus in the neonatal and infantile periods may depend on the specific CSF dynamics, in which the major CSF pathway has not developed and the minor pathway plays a significant role in the individual maturation process. This clinical evidence may be supported by the hypothesis that CSF dynamics develops according to evolutionary theory, from an immature brain as seen in animals with minor CSF pathway predominance,i.e., “Minor Pathway Hydrocephalus” towards a mature adult human brain together with completion of the major CSF pathway, i.e., “Evolution Theory in CSF Dynamics”.

Abstract

Key Words: evolution theory • CSF dynamics • neuroendoscopic ventriculostomy • hydrocephalus •major and minor pathway • age-difference • V-P shunt



I. Introduction

The t rea tment goa l fo r hydrocepha lus i s normalization of the disturbed cerebrospinal

fluid (CSF) dynamics, resulting in a state of “arrested hydrocephalus” 4), 24), 25). The most widely accepted treatment modalities at present involve either CSF diversion (shunt placement) or ventriculostomy (neuroendoscopic procedure). The final individual goal after treatment is defined as “shunt-dependent arrested hydrocephalus” in cases with shunt placement, or “post-ventriculostomy arrested hydrocephalus” after neuroendoscopic procedures.

Neuroendoscopic ventriculostomy is typically indicated for treatment of hydrocephalus in cases of “non-communicating hydrocephalus” (according to Dandy’s definition, 1919) 8), involving hydrocephalus due to a blockage located in the CSF

pathway between the (lateral) ventricles and the lumbar subarachnoid space 8), with marked tri-ventriculomegaly except of the fourth ventricle in cases of aqueductal stenosis. The success rate for “post-ventr iculostomy arrested hydrocephalus” under neuroendoscopic procedures is extremely high, approaching 100% in adulthood (long-standing overt ventriculomegaly in adult : LOVA, Oi S et al, 2000)26)

or late childhood 3) 17). However, success rates reported in treatment of hydrocephalus by neuroendoscopic procedure are much lower in the immature brain, at 0-64% in patients <1-year-old 6) 13) 17) 18) 20), and 53% under 2 years 3).

In our recent clinical experience, no successful cases of “post-ventriculostomy arrested hydrocephalus” have been encountered in patients <1-month-old, including hydrocephalus during fetal life, as in prematurely born neonates. Based on the literature and our own experience, we initiated prospective analyses of CSF dynamics in hydrocephalus of the immature brain using cine-mode magnetic resonance imaging (MRI) to observe CSF movements and computed tomography (CT) ventriculo-cisternography with water-soluble contrast to reveal CSF flow. In a preliminary study before designing the prospective study, early experience with CSF dynamics indicated specific patterns in this age group of immature patients, and we have already tentatively proposed a hypothesis concerning “Evolution Theory in CSF Dynamics” 28).

The purpose of this study was to analyze specific CSF dynamics in cases of hydrocephalus within 1 year after birth, including the fetal period for premature births, with special reference to possible mechanisms underlying the

failure of neuroendoscopic ventriculostomy in immature brain.

II. Material and Method

Analysis of CSF dynamics was scheduled prospectively for hydrocephalic neonates and infants under 1-year-old with hydrocephalus that was suspected as non-communicating hydrocephalus following plain CT and MRI. In order to select the most-indicated surgical modality, i.e., shunt placement vs. neuroendoscopic procedure, informed consent was obtained to analyze the pattern of disturbed CSF dynamics using CT ventriculo-cisternography. The patients selected to undergo this study were all macrocephalic with a head circumference enlarged by more than +2 standard deviations (SDs) and ventricles dilated more than 50% according to Evan’s Index (EI). All patients underwent preoperative studies of psychomotor development, with analysis of developmental quotient (DQ) using the new K-edition DQ test 29), CSF dynamics using cardiac-gated cine-mode MRI and CT ventriculo-cisternography using injection of 2 ml water-soluble contrast media (Omnipaque 240; iodine) via an Ommaya reservoir placed in the frontal horn of the lateral ventricle. CT scanning was repeated 1, 6 and 24 h (and 48 h, if requested) after contrast injection.

III. Results

1) Primary impression of hydrocephalus type on MRIBetween September 2001 and April 2004, a total of 12 hydrocephalic neonate/infants (9 girls, 3 boys) participated in this prospective study for selection of the most-indicated therapeutic modalities at Jikei University Hospital Women’s and Children’s Medical Center (JWCMC). Mean age at diagnosis was 17.2 weeks (range, 0-50 weeks). Underlying pathology was congenital/simple hydrocephalus (n = 6), intraventricular hemorrhage during fetal life (n = 3), arachnoid cyst (n = 1), encephalocele (n = 1), and myeloschisis (n = 1) (TABLE 1). Type of disturbed CSF circulation was considered “non-communicating hydrocephalus” as the initial impression, with MRI indicating occlusive changes in the major CSF path at the foramen of Monro (n = 1), aqueduct (n = 5), outlet of the fourth ventricle (n = 4) and basal cistern (n = 2) (TABLE 1). 2) Analyses of CSF DynamicsCSF dynamic studies with CT ventriculo-cisternography demonstrated definitive findings of communicating hydrocephalus in 9 of the 12 cases (75.0%), with free communication between the ventricular system and basal cistern at 6 h after injection of contrast into the lateral ventricle (TABLE 2 Note:75% of cases estimated as


“non-communicating hydrocephalus” were incorrect and CT ventriculo- cisternography confirmed “communicating hydrocephalus”; FIG. 1). Although cine-mode MRI was suggestive for detecting occlusive site, no definitive judgment could be obtained (FIG. 1-B) and final diagnosis was made using CT ventriculo-cisternography in all cases.

In CT ventriculo-cisternography at 24 h, contrast material filled the entire subarachnoid space over the cerebral convexity and Sylvian fissures in all except 2 of the 9 cases, in whom contrast material stayed in the basal cistern, suggesting a blockage or occlusion site around the tentorial notch. The finding allows communication between the ventricles and prepontine/posterior fossa cisterns but obstructing in the subarachnoid space: non-communicating by Dandy 8) but obstructive

hydrocephalus by Russell 32). Regardless of the pattern of disturbed CSF circulation in the major pathway, contrast distributed diffusely throughout the entire ventricular space and cerebral parenchyma (FIG. 1-C). Contrast tended to clear from the ventricle but remained much longer in the cerebral parenchyma (FIG. 2).

3) Operative Indications Based on CSF DynamicsBased on findings form the analysis of CSF dynamics, indications for neuroendoscopic ventriculostomy were discussed regarding 5 patients (non-communicating, n = 3; communicating-obstructive n = 2). The remaining 7 patients with communicating type hydrocephalus immediately underwent ventriculo-peritoneal (V-P) shunt, except in 1 case with posterior fossa cyst in which craniotomy was performed. Among the 5 patients discussed for treatment modalities, V-P shunt was performed in 1 patient with myeloschisis due to possible technical difficulties in such a small third ventricle with large massa intermedia. The other 4 patients underwent neuroendoscopic procedures, with third ventriculostomy alone (n = 2), and third ventriculostomy with either aqueductal plasty (n = 1) or septostomy (n = 1) (TABLE 1).

4) Post-ventriculostomy CSF DynamicsAt the end of each neuroendoscopic procedure, contrast media was injected into the ventricle and postoperative CT ventriculo-cisternography as well as by cine-mode MRI Post operative. cine-mode MRI suggested all ventriculostomied sites were patent. Postoperative

TABLE 1CSF dynamic study in neonatal/infantile hydrocephalus - 1: Indicated initial operative procedures based on CSF dynamics

Case No. Age (weeks)/ Sex

Underlying disease

Primary Impression for Occlusive Site

CSF Dynamics Initial Operative Modality

1 0/F Myeloschisis IV Ventricle Outlets Non-communicating Shunt

2 0/F Fetal IVH Aqueduct Communicating Shunt

3 0/M Fetal IVH IV Ventricle Outlets Non-communicating ETV/EAP

4 0/F Fetal IVH Foramen of Monro Non-communicating ESS

5 1/F Congenital Aqueduct Communicating Shunt

6 8/M Congenital Aqueduct Communicating Shunt

7 20/F Congenital IV Ventricle Outlets Communicating Shunt

8 24/M Congenital Aqueduct Communicating Shunt

9 28/F Congenital Basal Cistern Communicating- obstructive ETV

10 32/F Congenital Basal Cistern Communicating ETV

11 44/F Arachnoid Cyst IV Ventricle Outlets Communicating Craniotomy

12 50/F Encephalocele Aqueduct Communicating Shunt

IVH: intraventricular hemorrhage, ETV: endoscopic third ventriculostomy, EAP: endoscopic aqueductal plasty, ESS:endoscopic septostomy

TABLE 2Accuracy of indications for endoscopic ventriculostomy from initial

impression following MRI.

Primary Impression for Occlusive Site

CSF Dynamics with CT Ventriculo-

Communicating Non-

Aqueduct (5)5 (100%) 0

IV Ventricle Outlets (4)

2 (50.0%)2 (correct: 1,

incorrect site: 1)

Basal Cistern (2) 2 (100%)

Foramen of Monro (1) 0 1 (correct:1)

Total (12) 9 (75.0%)Occulusion Site

Correct : 2 (16.7%)Incorrect : 1 (8.3%)


A

B

C

D

A

B

C

DFIG. 1: Case #7. A 5-month-old girl with congenital hydrocephalus. A: T1-weighted midline-sagittal MRI revealing disproportionately large fourth ventricle with marked dilatation of all ventricles and aqueduct of Sylvius. The primary impression for the occlusive site was outlets of the fourth ventricle with a suggestive cystic lesion in the posterior fossa. B: Cardiac-gated cine-mode MRI midline-sagittal image. Findings were not definitive for communication or obstruction at the outlets of the fourth ventricle. C: CT Ventriculo-cisternography at 6 h after injection of water-soluble contrast via Ommaya reservoir. Note complete communication between ventricles and cisterns/subarachnoid space. This case was evaluated as “communicating hydrocephalus”. D: Pre- (left) and postoperative CT 1 month after ventriculo-peritoneal shunt (right). The brain mantle is in the process of reconstitution by shunt.

FIG. 2: Case #3. A 4-day-old girl with fetal IVH and Hydrocephalus. A: Primary impression for occlusive site was the outlets of the fourth ventricle. CSF dynamics confirmed non-communicating hydrocephalus with aqueductal occlusion.


ventriculo-cisternography revealed communicating CSF dynamics throughout the entire major CSF pathway between the ventricular system and convex subarachnoid space and Sylvian fissures. Contrast distribution, however, again revealed significant intraparenchymal stasis, even over 3 days after contrast injection, suggesting a condition of “post-ventriculostomy communicating hydrocephalus” (FIG. 2-B).

Postoperative courses were uneventful in all patients, with no developing morbidity or mortality. Patients who had undergone V-P shunt all displayed clinical improvements, with normalized head circumference within normal limits and significant brain mantle reconstruction on radiology (FIG. 1-D, 2-C). All 4 patients who had undergone neuroendoscopic procedures did well clinically without developing symptoms and signs of increased intracranial pressure, displaying soft and sunken or flat anterior fontanels and unchanged head circumferences. However, at a mean of 5.5 weeks (range, 4-9 weeks) after the operation, clinical symptoms and signs of increased intracranial pressure reappeared, with tense anterior fontanel and increased head circumference (TABLE 3). Postoperative CT and MRI revealed re-expanded ventriculomegaly, progressed beyond

preoperative findings from before neuroendoscopic ventriculostomy. All 4 patients consequently underwent V-P shunt. Before placing the ventricular tube, a 1.9-mm diameter fine rigid-rod neuroendoscopy lens (Oi-Samii Handy Pro; Karl Storz, Tuttlingen, Germany) 25) was inserted in the direction of the foramen of Monro and the patency of the third ventriculostomy fenestrated opening was confirmed. Post-shunt course was uneventful with satisfactory outcomes on clinical and radiological follow-up (FIG. 2) to a mean of 18 months (range, 8-36 months).

IV. Discussion

Patterns of Disturbed CSF Dynamics and Indications for Neuroendoscopic Ventriculostomy

The major CSF pathway starts from bilateral lateral ventricles with fluid from the choroid plexus, the major source of CSF, merging with fluid produced in the third and fourth ventricles. CSF then passes outside the ventricular system into the cisterns or subarachnoid space. An appreciable volume of CSF comes from sources other than choroid plexus in animals 4, 33). Absorption occurs primarily at the arachnoid granulation (Pacchionian

FIG. 2-B: Case #3. Post-endoscopic ventriculostomy CSF dynamic analysis. Contrast A. Post-ETV contrast injection: CT at 1 h later. B. Post-ETV contrast injection: CT at 24 h (1 day) later. C. Post-ETV contrast injection: CT at 72 h (3 days) later.

FIG. 2-B: Case #3. Post-endoscopic ventriculostomy CSF dynamic analysis. ContrastA. Post-ETV contrast injection: CT at 1 h later.B. Post-ETV contrast injection: CT at 24 h (1 day) later.C. Post-ETV contrast injection: CT at 72 h (3 days) later.

FIG. 2-C: Case #3 Post- shunt reconstitution of the cerebral mantle. A. CT: Pre-shunt. B. CT: Post-shunt, after 3 months.

FIG. 2-C: Case #3. Post- shunt reconstitution of the cerebral mantle.A. CT: Pre-shunt. B. CT: Post-shunt, after 3 months.

TABLE 3CSF dynamic study in neonatal/infantile hydrocephalus – 2: Post-

endoscopic ventriculostomy

Case No.

Age (weeks)/

Sex

Underlying disease

Occlusive Site

Post-Initial Op CSF Dynamics

Final Operative Modality*

3 0/M Fetal IVH AqueductPot-ETV/EAP communicating

Shunt

4 0/F Fetal IVForamen of Monro

Post-Ess communicating

Shunt

9 28/F CongenitalBasal

CisternPost-ETD Non-

obstructiveShunt

10 32/F CongenitalBasal

CisternPost-ETD Non-

obstructiveShunt


body) or villi that soak CSF into the sinus, mainly the superior sagittal sinus 35). With the bi-directional volume movement of CSF in the major pathway, CSF dynamics created bulk flow 9). Rate of CSF production is approximately 500 ml over 24 h in humans and the CSF major pathway contains some 130-140 ml, indicating a physiological turnover of CSF 3-4 times daily.

Based on these traditional concept of CSF dynamics, hydrocephalus has been defined as a state of “disturbed CSF circulation and classified classically into two types, communicating and non-communicating” 8). In the definition used by Dandy of communicating and non-communicating hydrocephalus, communications in the CSF pathway occur between the lateral ventricle and the lumbar subarachnoid space (confirmed by injection of dye into the lateral ventricle and subsequent detection by lumbar puncture). However, obstructive hydrocephalus 32) is defined as a condition of disturbed CSF circulation due to a blockage at any region in the major CSF pathway, including the ventricular system and cistern/subarachnoid apace, so the causes of non-obstructive hydrocephalus are limited to either CSF overproduction by choroid plexus papilloma or CSF malabsorption due to events such as sinus thrombosis. These two classifications are based on the classification of hydrocephalus from the perspective of disturbed CSF dynamics in the major CSF pathway alone, as “Major Pathway Hydrocephalus” 28).

The most crucial indication for neuroendoscopic ventriculostomy is the specific pattern of the disturbed CSF dynamics causing hydrocephalus in the individual case, if the shortest route is functioning as the alternative “major pathway”. On considering definitive indications for neuroendoscopic ventriculostomy, the classification “communicating vs. non-communicating” described by Dandy 8) may still be the most valid of the presently available classifications 24). Since the basic concept in this classification involves the site of occlusion in the major CSF pathway, particularly the outlet of the fourth ventricle or intraventricular passage, the interact draining route after each individual ventriculostomy procedure is key to normalization of the disturbed CSF dynamics. In a strict sense, there may be one exceptional condition, which cannot be included in this criterion. Even in “communicating-type hydrocephalus”, third ventriculostomy may still be indicated, if the blockage is localized and limited to the prepontine/quadrigeminal/ambient cisterns before the floor of the third ventricle. The classification of “non-obstructive vs. obstructive” hydrocephalus by Russell 32) is not suiTABLE when considering indications for any type of ventriculostomy. Actually, “obstructive hydrocephalus” can occur by occlusion not only within the ventricular system, but

also in any spot blocking CSF flow in the subarachnoid space before absorption via arachnoid granulations/villi (Pacchionian body). Third ventriculostomy, for example, may not be effective if covert blockage remains in the subarachnoid space before CSF absorption by the Pacchionian body.

Development of CSF Dynamics and Role of the “Minor Pathway”

CSF circulation starts to develop when the choroid plexus is created in the primitive lumen as the ventricle at embryonic day 41-44 embryonic days in the fourth ventricle, day 44 in the lateral ventricle and day 57 in the third ventricle 7). The roof of the fourth ventricle (area membranecca inferior; AMI) opens by gestational week 8, immediately after choroidal differentiation in the fourth ventricle is observed 36). The primitive meninx begins to develop at 8 weeks, with the arachnoid mater being first observed at 12 weeks and separating from the dura mater at gestational week 21) 29).

Regarding the development of CSF absorption sites, the absence of arachnoid granulations (Pacchionian body) in mice, rats, rabbits, cats and Japanese monkeys, even in adult animals, is well known 15). In large mammals and humans, arachnoid granulations (Pacchionian body) appear microscopically in postnatal life or just before birth as villi 12) 15), and begin to function as the route of CSF reabsorption in later life 23). Since the arachnoid villi are microscopic structures whereas granulations are prominent gross anatomical findings, the development of arachnoid granulations (Pacchionian body) 34) has been used as a marker of age in radiological identification with findings of parasagittal depression of the caldarium 1). Radiological evidence of the presence of arachnoid granulations is usually obtained first at around 7-years-old, developing progressively up to about 20-years-old 14). CSF reabsorption by the arachnoid graduations may begin from the late infantile period 23). Without the expected functional development of the arachnoid granulations, CSF dynamics may be maintained by the minor pathway with drainage via the perineural space to the lymphatic system 5) 10) 11) 23) 32), via transependymal-interstitial route to the perivascular /subpial space both in the brain and spinal cord 2) 16) 19), and via the epithelium of the choroid plexus to the fenestrated capillaries and finally to the Galenic venous system 15). These “minor CSF pathways” represent the main route for CSF dynamics in both rodents and other small mammals 30)

31) 33) 35) and the developing immature brain in humans 12,36) (See illustrative diagrams in reference 28) 28). We summarized the ontogenetic aspects of the development of CSF circulation and proposed the “Evolution Theory


in CSF Dynamics” 28). The developmental stage of CSF dynamics is also described in various processes, divided into Stages I-V (CSF Dynamics Maturation [CSFDM]: Stage I (gestational age, ≤22 weeks), primitive formation of the choroid plexus and sub-arachnoid space; Stage II ( gestational age, 23-32 weeks), organization of 3 layers of the meninges; Stage III (gestational age, 33-40 weeks), functional maturation of choroid plexus; Stage IV (neonatal period up to 4 weeks after birth), CSF formation approaching adult level.The meridian of “Minor CSF Pathway”; Stage V (infantile period, 5-50 weeks after birth) maturation of Pacchionian body and superior sagittal sinus [Maturation of Major CSF Pathway ]CSFDM stages are also compatible with our perspective classification of congenital hydrocephalus [PCCH] stages 27) (FIG. 3). Catala 7) reported that the epithelium of the choroid plexus in the human fetus contains large amounts of glycogen, as seen in the plexus in lower vertebrates (adult fish and amphibians). This high content of glycogen is likewise observed in hibernating mammals, in which choroid plexus cells are again filled with glycogen during hibernation. These data suggest that the glycogen content parallels the metabolic status of the subject and that human fetal life is very similar to a hibernating period.

“Minor CSF Pathway Hydrocephalus” and Failure of Neuroendoscopic Ventriculostomy

Since CSF dynamics during fetal and neonatal/early

infantile periods are mainly maintained by the “minor CSF pathways”, hydrocephalus occurring during these periods should be defined as disturbed CSF circulation in the “minor CSF pathway” (“Minor CSF Pathway Hydrocephalus”) 28). The mechanisms or pathogenesis of hydrocephalus may thus differ from “Major CSF Pathway Hydrocephalus”. The classical classification of “communicating vs. non-communicating” 8) or “obstructive vs. non-obstructive” 32) do not properly reflect the disturbance of CSF circulation at this stage in life. Causative underlying conditions may include various pathologies, as in our PCCH 27); i.e., primary dysgenesis or secondary causes such as intraventricular hemorrhage (IVH) in the fetal brain.

In the CSF circulation, as in the immature form, CSF absorption may possibly be disturbed at the various absorption sites including the subpial space -> perivascular space -> subarachnoid space -> neuroepithelium intracellular space, choroid plexus epithelium -> venous fenestrated capillary -> Galenic system, and/or perineural space -> lymphatic channel. Our data from CT ventriculo-cisternography demonstrated marked intraparenchymal CSF passage and delayed clearance of the contrast not only in the ventriculo-cisternal space (“major CSF pathway”) but moreover from the cerebral parenchyma as in the “minor CSF pathway” (Minor CSF Pathway Hydrocephalus). In several cases, the major CSF pathway was blocked by a certain lesion, such as clot from IVH blocking the foramen of Monro or aqueduct of

Embryo Fetus Neonate Infant Toddler

0 4 8 22 32 40 1 6 12(gestational weeks) (months)

-- ------ Stage I - Stage II - Stage III Stage IV Stage V

Choroid Plexus

Lepto-meninges

Arachnoid Villi(PachionianBody)

Minor CSF Pathwaywith CSF absorption via extra-arachnoid villus sites

Major CSF Pathwaywith CSF absorption via arachnoid villi

Minor CSF Pathwaywith CSF absorption via extra-arachnoid villus sitesMinor CSF Pathwaywith CSF absorption via extra-arachnoid villus sites

FIG. 3: CSF Dynamics Maturation [CSFDM] Stages I-V (Oi, S et al 2006, with permission) 28)


Sylvius, this did not represent the single cause underlying hydrocephalus. Neuroendoscopic ventriculostomy would represent the definitive therapeutic method if the above CSF absorption routes remained intact. However, after successful ventriculostomy CSF dynamics changed to “communicating hydrocephalus” with contrast stasis in all communicating ventricles, cisterns and the subarachnoid space. Furthermore, the prominent stasis of contrast material in the cerebral parenchyma was observed in some cases [Minor CSF Pathway Hydrocephalus] as a form of “post-ventriculostomy communicating hydrocephalus”.

T h e c o n d i t i o n o f “ m i n o r C S F p a t h w a y hydrocephalus”, however, can improve later with the development of the Pacchionian body in late infancy increasing CSF absorption. The high success rate of neuroendoscopic surgery, and even spontaneous arrested hydrocephalus and disappearance of external hydrocephalus are all expected after this period (CSFDM Stage V), when the “major CSF pathway” is completed.

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17. Hopf NJ, Grunert P, Fries G, Resch KD, Perneczky A: Endoscopic third ventriculostomy: outcome analysis of 100 consecutive procedures. Neurosurgery. 44 (4): 795-804; discussion 804─806, 1999

18. Javadpour M, Mallucci C, Brodbelt A, Golash A, May P: The impact of endoscopic third ventriculostomy on the management of newly diagnosed hydrocephalus in infants. Pediatr Neurosurg. 35 (3): 131─135, 2001

19. Katzman R, Schimmel. H, Wilson CE: Diffusion of insulin as a measure of extracellular fluid space in brain. Proc. Rudolf. Virchow Med. Sor. Suppl, 26: 254 ─ 280, 1968

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25. Oi S, Samii A, Samii M: Frameless free-hand maneuver of a handy small diameter rigid-rod neuroendoscope with working cannel under high-resolution imaging - technical note. J Neurosurg : Pediatrics 102: 113 ─ 118, 2005

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28. Oi S, Di Rocco C: Proposal of evolution theory in cerebrospinal fluid dynamics and minor pathway

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��J. Hydrocephalus, Vol. 1, No. 1, 2009

Impact of a portable neuroendoscopic equipment system to provide an outreach service in Sub-Saharan Africa Mubashir Mahmood Qureshi, FRCSEd (SN) 1 , J Piquer Belloch MD 2

1Section of Neurosurgery, Department of Surgery, Aga Khan University Hospital, Nairobi, Kenya , and Division of Neurosurgery, Kenyatta National Hospital, Nairobi, Kenya; 2Hospital de la Ribera, ALZIRA (Valencia), Spain Corresponding author:Mahmood M Qureshi, MBChB, M.Med (Surg), FCS-ECSA, FRCSEd (SN)Section of Neurosurgery, Dept of Surgery, Aga Khan University Hospital, P.O.Box 30272 GPO 00100Nairobi, KenyaPhone/Fax: +254-20-3742619Email: [email protected]

Hydrocephalus in the pediatric population is an enormous burden in developing countries worldwide. In Kenya, and its surrounding East, Central and Southern Africa region, with a population of 250,000 million, a conservative estimate suggests an annual incidence of nearly 14,000 infants developing hydrocephalus within the first year of life. Hydrocephalus, largely a disease of poverty in this region, becomes even more challenging to treat due to lack of neurosurgical manpower, inadequately equipped public health care facilities, meager resource allocation, high rates of neonatal infection including meningitis, difficulty of access to hospitals able to treat hydrocephalus, and high complication rates in patients who are able to access and receive shunting procedures.

Definitive treatment of Hydrocephalus, yet avoiding shunting procedures and long-term shunt dependence is a safer option. In environments such as Sub-Saharan Africa and, indeed, in other similar resource challenged regions, neuroendoscopic ventriculostomy (NEV), in appropriately selected patients, can overcome the problems associated with shunting, as well as long term shunt dependence.

Lack of neurosurgeons and those trained to perform neuroendoscopy, and non availability of neuroendoscopy equipment is a further challenge in such environments. Where such manpower and equipment is available, the challenge is for the multitude of patients in the rural population to access sites within their easy reach, which can offer NEV

The novel approach promoted by volunteer neurosurgical teams in Kenya is described, and the its potential role in successfully providing NEV at hospitals in regional sites away from main referral tertiary hospitals is outlined. Using a single portable neuroendscopy equipment system, and a versatile free-hand, single operator neuroendoscope, the outreach, and mobile portable model has been successfully utilized to perform 177 procedures including NEV, cyst fenestration, and cerebral abcess cavity washout, in 17 different hospital sites in 5 different countries within the East African region

The merits of performing this current best-practice procedure in a convenient, cost effective and safe way as an outreach, mobile service, for a condition that mainly affects children in rural populations, is highlighted.

Abstract

Key Words: Hydrocephalus • Neuroendoscopic ventriculostomy (NEV) • Portable outreach neuroendoscopy • East African neurosurgery

I. Introduction

The primary aim of treatment for hydrocephalus is normalization of impaired cerebrospinal

fluid (CSF) flow, aimed at achieving a state of “arrested

hydrocephalus” (1, 5). The final goal after treatment being defined as “shunt dependent arrested hydrocephalus” in cases of shunt placement, or “post-ventriculostomy arrested hydrocephalus” after neuroendoscopic ventriculostomy procedures. Of the large number of patients developing hydrocephalus within the first year


�� J. Hydrocephalus, Vol. 1, No. 1, 2009

of life, only about a fifth of the overall number are able to access shunting procedures in established centers in Kenya, and an even lower number can do so in other countries within this Sub-Saharan region, with the majority being treated by a handful of neurosurgeons, a few general surgeons and occasionally by pediatric surgeons. Shunts are expensive to purchase by the family, and often unavailable altogether. However even when affordable shunts are utilized, shunt failure through infection, shunt blockage, distal migration, scalp erosion, shunt extrusion through anal passage are a significant cause of morbidity and mortality in up to 25% of the treated patients (4). Thus, in developing regions, shunt placement procedures and shunt dependency pose an additional burden on the health care systems as well as on the care receivers and indeed upon the handful of specialist care providers, whose time is further expended in managing the disproportionately high rates of complications of shunting in these environments.

I t is therefore better to pursue a definit ive approach to treating Hydrocephalus, while, at the same time, avoiding shunt dependency. Neuroendoscopic ventriculostomy (NEV) has the advantage of achieving normalization of CSF flow dynamics and avoiding shunt related morbidities and dependency in the majority of children (2 , 3)

The equ ipmen t used fo r Neuroendoscop ic

Ventriculostomy (NEV) in centres able to provide this service include a Camera control Unit, a Cold Light Source unit, a High Frequency Electrosurgical cautery unit, a Flat screen Monitor Display unit, all placed on a mobile cart riding on casters, which incorporates shelves and drawers (FIG. 1)

The use of this set of equipment, albeit very robust and mobile within an operating suite of individual hospitals, is restricted to provision of NEV procedures to only those patients who are able to reach the hospital facility. It cannot be utilized as a convenie and readily accessible service to patients in low economic profile regions where the purchase cost of providing such equipment in distant and rural settings is neither feasible nor affordable, and nor is it safely and easily transportable. In essence this implies that the large majority of patients who reside in rural communities cannot be offered the preferred mode of treatment utilizing NEV procedures.

II. Material and Method

In October 2006, a neurosurgical team that had established an outreach mission program to provide specialized neurosurgical services in regional hospitals outside the capital Nairobi (FIG. 2), purchased a compact neuroendoscopic Karl Storz Telepack system (FIG. 3) This incorporates a processing unit, combined with a

FIG. 1 FIG. 3

FIG. 2


Camera Unit and Light source, all conveniently and safely transportable in a portable suitcase. An equally versatile and easy to use rigid rod neuroendoscope, the Oi Handy-Pro[Karl-storz, Tuttlingen, Germany] (6), with a 0 degree autoclavable Hopkins II Telescope (FIG. 4) was also purchased. The system offers a single surgeon the free hand ability to perform neuroendoscopy safely (FIG. 5). The image quality has been excellent. The system has revolutionized the management of children with hydrocephalus in this region.

III. Results

In tandem with providing an opportunity of treatment through NEV for patients (FIG. 6), the program has been a source of training of local teams, both neurosurgical and nursing, in performing the NEV procedure, sterilization and care of the equipment. The same single equipment system has been utilize to train 24 MDs (FIG.7), including 16 neurosurgeons and 8 neurosurgery residents to perform the procedure, and 14 operating room nurses in the care, assembly and sterilization of the equipment. The number of cases at sites served by one single unit include the following (Table. 1):

TABLE 1

KENYATTA NATIONAL HOSPITAL NAIROBI

KENYA ………..80

AGA KHAN UNIV HOSPITAL NAIROBI

KENYA………….6

ERTRUDE CHILDREN’s HOSPITA NAIROBI

KENYA …………6

L MOI TEACHING HOSPITAL ELDORE

KENYA …………5

COAST PROV GEN HOSP MOMBASA KENYA …………6

MEWA MISSION HOSP MOMBASA KENYA …………5

AGA KHAN HOSPITAL MOMBASA KENYA …………4

AGA KHAN HOSPITAL KISUMU KENYA …………2

KIJABE MISSION HOSPITAL RIFT VALLE

KENYA………….6

MULAGO MEDICAL COMPLEX KAMPALA

UGANDA ……....5

MUHIMBILI INSTITUTE DAR-ES-SALAAM

TANZANIA …...30

MNAZI MOJA HOSPITAL ZANZIBAR TANZANIA……..4

BLACK LION HOSPITAL ADDIS-ABABA

ETHIOPIA ……..3

BETHEL TEACHING HOSPITAL ADDIS-ABABA

ETHIOPIA ……..3

MYUNSUNG CHRISTIAN MISSIO ADDIS- ABABA

ETHIOPIA ……..4

KIGALI UNIVERSITY TEACHINGSP KIGALI

RWANDA………..8

TOTAL between October 2006 and Februa 2009

177 cases

FIG. 4

FIG. 5

FIG. 6

FIG. 7


Discussion

Post -ventriculitis aqueductal obstruction is amongst the commonest cause of hydrocephalus in East African studies, and the same is likely to be the case in other developing countries (8). Definitive treatment of hydrocephalus, while avoiding shunting , is a desirable mode of treatment, provided it can be achieved without increasing the management morbidity and mortality. NEV has been shown to have the potential for avoiding shunt dependency in the majority of children, with lower morbidity and mortality (3, 7). With the high burden of disease in developing regions, such as Sub-Saharan Africa, as well as the recognized dangers posed by shunt dependency, the cost of purchasing the shunt (as well as subsequent shunts, external drains, reservoirs, sterile collection bags, repeated CSF microbiology studies, etc, in the event of shunt infection and failure), the life long potential for shunt dysfunction, the wider use of NEV, as the primary option for treatment, has significant merit. On the other hand, the inadequate numbers of neurosurgical practitioners and their total absence in rural areas of developing countries, poses a challenge that require a novel approach. It is not feasible to offer expensive Neuroendoscopy equipment at rural sites, as this does not justify such large investment vis-à-vis the overall clinical workload at such rural hospitals. However, the population of hydrocephalus patients presenting at these rural sites cannot, equally, be denied appropriate care that is currently possible through NEV procedures.

IV. Conclusion

The outreach, portable, neuroendoscopy model developed in Kenya and now being promoted across the broader East African region, is one that can achieve the objectives of NEV treatment with ease, safety, convenience and in a cost effective manner. Its main requisites are a recognition that NEV is a preferred option of management, equipment that is readily portable in a safe and reliable way, and a dedicated team willing to volunteer its time and skills to, not only provide care, but also to organize a consistent and structured approach to training as many of the neurosurgical specialists available across the region.

References

1. Boulton M, Flessner M, Armstrong D, Hay J, Johnston M: Determination of Volumetric cerebrospinal fluid absorption into extracranial lymphatics in sheep. Am J Physiol. 274 (1 Pt2): R88─96, 1998

2. Cinalli G: Endoscopic Third Ventriculostomy in Pediatric Hydrocephalus, Springer-Verlag Italia, Milano, 2004, pp376─377

3. Hopf NJ, Grunert P, Fries G, Resch KD, Perneczky A:

Endoscpic third ventriculostomy: outcome analysis of 100 consecutive procedures, Neurosurgery, 44 (4): 795─804; discussion 804─806,1999

4. Noorani S : Complications of VP shunting seen at the Kenyatta National Hospital, Kenya: M. Med (Surgery), dissertation University of Nairobi 2004

5. Oi S: Classification and Definition of Hydrocephalus – Origin, Controversy and Assignment of the Terminology –G. Cinalli, C. Sainte-Rose, W. Maixner Ed. Pediatric Hydrocephalus. Chapter 6. pp95─112, 2005

6. Oi S, Samii A, Samii M: Frameless free-hand maneuver of a handy small diameter rigid-rod neuroendoscope with working channel under high resolution imaging – Technical note. J Neurosurg : Pediatrics 102: 113 ─ 118, 2005

7. Wa r f B C : N e u r o e n d o s c o p i c m a n a g e m e n t o f Hydrocephalus in African children. Results from 1000 ventriculoscopic procedures. Childs Nervous System 21: 507, ISGN abstract no 57, 2005

8. Warf BC: Hydrocephalus in Uganda: Predominance of infect ious or igin and pr imary management with endoscopic third ventriculostomy. Journal of Neurosurgery (Pediatric 1) 102: 1─15, 2005.


Complications of Neuroendoscopy

Federico Di Rocco, M.D, Wolf Luedemann, M.D, ², Shizuo Oi , M.D., Ph.D.3. 1Department of Pediatric Neurosurgery, Necker Enfants Malades Hospital, René Descartes University, Paris, France and ²Department of Neurosurgery, International Neuroscience Institute, Hannover, Germany and3Division of Pediatric Neurosurgery, Jikei University School of Medicine, Tokyo, Japan. Corresponding author:Federico Di Rocco, MD, Department of Paediatric NeurosurgeryNecker Enfants Malades Hospital, 156 rue de Vaugirard, 75015 Paris, FranceTel: 01-44-49-42-67Facsimile: +33 1 44 49 42 50Mail: [email protected]

The technical advances in endoscopic tools have extended the indications of neuroendoscopy in the neurosurgical practice. Endoscopy is currently used in most pediatric neurosurgical centers on a daily base. Hydrocephalus, intracranial cysts and intraventricular tumors are commonly treated nowadays with this minimally invasive technique.

While the advantages of this method have been the subject of many reports, its complications have not been described sufficiently and are difficult to evaluate on the grounds of the published reports. The knowledge of these complications is of paramount importance to try to reduce the steep learning curve of neurondoscopic procedures.

In the attempt to provide a pratical assessment of neuroendoscopic complications we have reviewed the recent literature classifying the complications according to their time of occurrence and/or clinical recognition: peroperative, immediate post-operative, and late.

Abstract

Key Words: endoscopic surgery • ventricles • hydrocephalus, • intraventricular tumors • intracranial cysts • morbidity • mortality

Since the first endoscopic procedures reported more than a century ago (6, 56) the improvement of

neuroendoscopic tools in the recent years has enlarged the spectrum of its indications (42). The anatomy of ventricular cavity lends in fact itself to a direct approach for hydrocephalus, intraventricular lesions (cysts or tumors) but the endoscope has been successfully used also to gain access to lesions adjacent to subarachnoid spaces such as sylvian cysts. Endoscopy is currently used to treat children with hydrocephalus, intracranial cysts and intraventricular tumors in most pediatric neurosurgical centers on daily base. While the advantages of the technique have been the subject of many reports, its complications have not been described sufficiently and are difficult to evaluate on the grounds of the published reports. In fact, the rate of complications of neurodoscopic procedures is extremely variable in the literature, going from 0 to 20% (59), and most of the papers dealing with

these subject are anecdotic case reports or coming from the same institutions and authors (10, 54, 55, 58, 59).

Though life threatening complications may occur during endoscopy (33), the endoscopic mortality and permanent morbidity are usually low in large series (0.6% and 4.4%, respectively in Schroeder et al series on 344 endoscopic procedures (59). The transient morbidity rate is higher. For instance in Schroeder et al series transient complications were found in 9.3% of the patients (59). The time distribution of the complications in most centers underlines the steep learning curve associated with these procedures, most of fatal and permanent complications occurring within the initial period of the series (11, 12,

23, 58). The knowledge of such events is of paramount importance to try to avoid the repetition of potential errors and mistakes and thus reduce the risk of complications. It might therefore be possible to reduce the steepness of the learning curve.

The evaluat ion of complicat ions re la ted to neuroendoscopy is also complicated by the fact that



they depend on the type of neuroendoscopic procedure: endoscopic third ventriculostomy (ETV) or septa fenestrations intracranial cyst fenestration, endoscopic biopsy for intraventricular lesions or endoscopic tumor removal (8, 22). All these procedures in fact carry a specific risk of morbidity (3, 8, 10, 15, 22, 50, 52 - 54,61- 64).

Complications can be further subdivided according to the impact they have on the outcome (transient vs permanent or symptomatic vs asymptomatic) or on the grounds of their occurrence (during the operation, in the immediate postoperative period or in the late postoperative phases).

In the attempt to provide a pratical evaluation of neuroendoscopic complications we have reviewed the recent literature classifying the complications according to their time of occurrence and/or clinical recognition: peroperative, immediate post-operative, and late.

Peroperative complications

1. Haemorrhagic complications and vascular injuries.Injuries to cerebral blood vessels or surgically induced haemorrhages from cerebral or tumoral tissue are a relatively common complication, mostly in the course of the operation. The haemorrhage is usually caused by mechanical and/or thermal (coagulation) direct injury. The bleeding might occur as early as at the introduction of the endoscope itself in the ventricle due to its impaction on subependymal vessels (FIG. 1). Usually it is only mild and can be controlled by irrigation. Sometimes the bleeding might be more important, coming from thalamic or septal veins. The visibility might be affected and the procedure abandoned (11, 36).

Endoscopic view at the insertion of the scope. The vision is blurred by an ependymal haemorrhage. The foramen of Monro in the center, the septal vein and choroid plexus on the left can be hardly recognized.

Arterial injuries are rare, occurring in about 1-2%

of ETV (1, 13; 58). The basilar artery or its branches within the interpeduncular cistern are involved (14).

Injury of such vessels is a dramatic event even if cases of successful management are reported (1, 60). The risk factors for vascular complications are represented by a poor intraoperative visibility and/or unfavourable anatomical conditions (14). Formation of traumatic basilar tip aneurysm after ETV has also been described (45). Involvement of anterior cerebral arteries and/or its branches has been exceptionally reported (7).

The control of intraoperative bleeding during endoscopic procedures is challenging. In fact, not only it is difficult to control it with the minimally invasive tools currently available, but blood can also rapidly and dramatically reduce the vision, consequently complicating or making impossible to continue the procedure. When irrigating during surgery, attention should be paid to several factors: infusion rate, temperature of the irrigation, inward and outward flow (48). Aggressive irrigation can in fact increase the ICP or in other cases distort the ventricular anatomy (37, 66). Cold saline has been reported to produce an altered mental status after surgery (48).

In some cases, the haemorrhage might be found on post-operative imaging within the parenchyma due to a damage of pial vessel during the introduction of the endoscope. However the occurrence of intracerebral haematoma is rather uncommon (58).

Epidural hematomas can also bee found (3/134 procedures in Oertel et al series (54)). The rate of haemorrhage seems similar in ETV and in intracranial cyst endoscopy. However, haemorrhage seems to be more frequent during endoscopic tumor biopsy or removal procedures. Intraoperative bleeding of any degree is, in fact, frequent. It was noted in 17 out of 31 cases in Depreitere et al series 14 of which from the tumor itself (18). But only rarely it results in an interrupted procedure or clinically significant sequelae (1/31 in Depreitere et al series, 3.5%.in Luther et al series (18, 43)).

2. Aborted procedures and technical failures

Although peroperative failures are mainly due to the interruption of the procedure for a bleeding that affect the visibility, the abort of the operation may be also due to an abnormal anatomy (12, 23, 48). In most cases the potential anatomical limitations can be predicted by a careful examination of preoperative MR especially taking into consideration axial and sagittal T2 weighted MR images which better delineate the shape of the ventricles, the position and thickness of the floor of the third ventricle and the size of the Monro foramen (47). However in some instances, an unexpected small foramen of Monro or an excessively malformed anatomy of the third ventricle as in myelomeningocele, may still be found during the procedure with the consequent impairment to introduce FIG. 1


the endoscope within the ventricle. In other cases the presence of thick membranes may hinder the recognition of the landmarks usually utilised to perforate the floor of the ventricle or cyst wall.

The reported rates of aborted procedures are higher in case of intraventricular tumors and intracranial cysts (1-9.5%) than in ETV (0.4-5.8%). In cases of intraventricular tumors, the procedure may also fail because of an excessive tumor consistency (59). Conversion to an open transcortical craniotomy with standard microsurgical technique might then be necessary (26, 64).

Technical failure can also be secondary to defective material during the procedure as in the case reported by Grotenhuis et al with a dislocation of the distal lens of the endoscope (30). A careful check of the tools, before any endoscopic procedure of all the elements from the scope and instruments, through the optic fibers and camera to the monitor should always be performed. In other cases, complications due to defective tools can be seen only in the postoperative period. Schroeder et al described multiple metal artefacts on the ventricular wall in one patient from an abraded trocar (58).

More in general, even though the success rate of intraventricular tumor biopsy remains high (52) some drawback may result from the histological analysis because of the limited sample size (16). Also this last limit might be considered as a complication of the neuroendoscopic procedure.

3. Hemodynamic modifications during neuroendoscopy

During endoscopic procedures, especially ETV, cardiac rhythm changes may be seen (bradycardia more commonly, tachycardia or arrest very rarely (14, 15, 21). Several hypothesis have been suggested: direct compression on the brain stem or on the basilar artery or its braches; increased ICP by irrigation, direct disturbance of hypothalamic nuclei in the floor of the third ventricle (2, 23).

Immediate post-operative

1. InfectionsInfection may occur in all types of procedures. CSF infections might occur in 1 to 7% of the cases (3, 15, 23, 58,

59, 61). Fatal septic multiorgan failure due to a meningitis following ETV has also be described (58, 60).In ETV procedures, however, postoperative meningitis might result in a closure of the stoma (25). Skin infection is a non specific complication of endoscopic procedures.2. Neurological complications

The incidence of neurological complications is low (3). In most of the cases they are transient. The rate of long term neurological complications reported in

the literature is lower than 1% (3, 58). More commonly clinically silent contusions of neurological structures such as fornix, thalamus or mamillary bodies can be found on postoperative imaging studies without any apparent clinical manifestations (58). The planning of the burr hole placement and endoscope trajectory are important to try to reduce any damage during the procedure.

Neurological complications might be secondary to vascular injuries or result by direct lesion.

The anatomical structures more often damaged during ETV are those delimiting the Monro foramen and the walls of the third ventricle. In some cases however postoperative focal deficits may be due to a lesion of the internal capsule (Hemiparesis, hemiplegy) or of the cranial nerves (palsies). Cases of Parinaud or Horner’s syndrome, peduncular hallucinosis due to mesencephalic/diencephalon injuries have also been described after ETV (14, 15).

The most frequent non-focal neurological deficits after ETV are the impairment of consciousness and confusion, late arousal or memory loss. They are due mainly to diencephalic or forniceal lesions. Personality disorders have been described after ETV (4).

Transient but also permanent hypothalamic and neurovegetative disorders have also been reported (increase in thirst and appetite, diabetes insipidus, hormonal changes , puber tas p raecox , thermic dysregulation …), the most common being transient diabetes insipidus and transient hyperthermia They result from injury or distortion of hypothalamic nuclei and infundibulum. (58, 63).

Similar complications are also found after the endoscopic management of intracranial cysts or intraventricular tumors depending on their location.

Seizures related to bleeding, hyponatremia, subdural effusions have also been reported after endoscopic procedures (3, 65). Seizure incidence following ETV is estimated around 1% (15, 19).

3. CSF related complications

Subgaleal CSF collections and CSF leak have been described after ETV with an overall incidence of 2% to 18% (14, 15, 58). CSF may tend to flow along the lower resistance pathway offered by the ETV tract. This phenomenon might occur during the first postoperative days secondarily to the transitory increase in ICP found after ETV (49). Lumbar punctures after the ETV might control the ICP protect the wound, and promote flow through the stoma while a normal CSF absorption is recovered.

Subdural collections are also found after endoscopic procedures with a ventricular access. Acute and


chronic collections have been reported (5, 23, 38, 46). Both symptomatic and asymptomatic collections have been described (58). In some cases surgery for the subdural collection is needed (35). Conversely, asymptomatic co l lec t ions a re se ldom repor ted and probably underestimated in the literature (5, 39, 45). Postoperative collections have been found in 20% of the cases in Hopf et al series (35). A packing of the endoscopic tract by fibrin glue and hemostatic mesh has been proposed to reduce the risk of such complication (41). Subdural spinal hematoma has also been reported (9) .

Pneumocephalus can occur due to the perioperative CSF leak (15). Only rarely it can become hypertensive (32).

These complications are also shared with the other types of endoscopic intraventricular procedures. 4. Failures

Symptom resolution is the best indicator of a functioning procedure and effective treatment (28). The success rate of ETV in the literature is estimated to 60-90% (11, 15, 19,

28). That means that in around 10-40% of the cases the ETV fails to treat the hydrocephalus. Some preoperative and intraoperative criteria have been proposed to predict the efficacy of the ETV. The stronger predictors of failure seem to be the intraventricular scarring or a distorted intraventricular anatomy (29).

A diminished ventricular volume, a flow void signal trough the stoma, as well as a modification of the ventricular shape are radiological criteria to assess on postoperative MR (25, 28, 40, 57). However the ventricular volume might remain enlarged in the early postoperative imaging so that persisting ventriculomegaly should not be considered necessarily a failure of the procedure (28, 40).

The failure of a technically successful ETV might occur early that is within the first days/weeks, marked by an initial resolution of the symptoms due to the ventricular tapping. In such a cases, symptoms recur in the early post-operative period despite the patency of the stoma confirmed at MR imaging. The cause of such failure is to be searched in an impaired CSF dynamics beyond the obstructed aqueduct (51). Post-infectious and post-haemorrhagic hydrocephalus for instance are less prone to respond to ETV (13, 24, 34). Age appears in some studies to play a role, with a progressive increase in success rate with increasing age (19).

In other cases, the patency of the stoma cannot be assessed, due to a cicatrisation of the stoma (FIG. 2) or an incomplete opening of the stoma. These cases will respond to a repeated procedure.

Endoscopic view of the floor of the third ventricle during a repeated ETV. The stoma is obliterated by a scarring tissue (arrow).

Late and delayed complications

Late complications of endoscopic procedures are mainly represented by the delayed reocclusion of the stoma with the risk of symptom recurrency.

Delayed failure after an initially successful ETV is uncommon (3.4% in Ershain et al series with a mean delay of 105 weeks (23)). However, late failure occurring after 6 years has been reported (11, 12). In some cases, the late closure may be recognized by a progressive clinical deterioration and symptom recurrence. In others, a rapid clinical deterioration can occur that needs to be promptly diagnosed. A repeated ETV is generally effective. However, cases of delayed sudden death after a functional ETV have also been reported (20, 31). All patients in whom an autopsy or repeated ETV were performed were found to have an occluded ETV (12, 20, 67) usually by a new membrane or scar and rarely by a clot or tumoral extension (25, 44). Education of patients and their families about the risk of a late deterioration is of paramount importance to allow for a rapid management and timely intervention. Similarly, cystostomies may close, with consequent cyst enlargement and symptoms recurrence (2/23 in Tamburrini et al series (62)). Large fenestrations in the cyst wall are often necessary to avoid cyst’s recurrence (27). The opening of the cyst in the ventricles and in the cisterns (ventriculo-cysto-cisternostomy) may reduce such risk of secondary closure (17).

References

1. Abtin K, Thompson BG, Walker ML. Basilar artery perforation as a complication of endoscopic third ventriculostomy. Pediatr Neurosurg. 28 (1): 35 ─ 41, 1998.

2. Anandh B, Madhusudan Reddy KR, Mohanty A, Umamaheswara Rao GS, Chandramouli BA. In t raopera t ive bradycard ia and pos topera t ive hyperkalemia in patients undergoing endoscopic third ventriculostomy. Minim Invasive Neurosurg. 45 (3): 154─7, 2002.

3. Beems T, Grotenhuis JA. Long-term complications and definition of failure of neuroendoscopic procedures. Childs Nerv Syst. 20 (11─12): 868─77, 2004

FIG. 2


4. Benabarre A, Ibáñez J, Boget T, Obiols J, Martínez-Aran A, Vieta E. Neuropsychological and psychiatric complications in endoscopic third ventriculostomy: a clinical case report. J Neurol Neurosurg Psychiatry. 71(2): 268-71, 2001.

5. Beni-Adani L, Siomin V, Segev Y, Beni S, Constantini S. Increasing chronic subdural hematoma after endoscopic III ventriculostomy. Childs Nerv Syst. 16 (7): 402-5, 2001.

6. Buxton N. Neuroendoscopic third ventriculostomy. Neurosurg Focus. 15; 6 (4): e2, 1999.

7. B u x t o n N , P u n t J . C e r e b r a l i n fa r c t i o n a f t e r neuroendoscopic third ventriculostomy: case report. Neurosurgery. 46 (4): 999-1001, 2000

8. Cappabianca P, Cinalli G, Gangemi M, Brunori A, Cavallo LM, de Divitiis E, Decq P, Delitala A, Di Rocco F, Frazee J, Godano U, Grotenhuis A, Longatti P, Mascari C, Nishihara T, Oi S, Rekate H, Schroeder HW, Souweidane MM, Spennato P, Tamburrini G, Teo C, Warf B, Zymberg ST. Application of neuroendoscopy to intraventricular lesions. Neurosurgery. 62 Suppl 2: 575-97, 2008;

9. Cartmill M, Vloeberghs M.Childs The fate of the cerebrospinal fluid after neuroendoscopic third ventriculostomy. Nerv Syst. 16 (12): 879-81, 2000.

10. Cinalli G, Spennato P, Ruggiero C, Aliberti F, Trischitta V, Buonocore MC, Cianciulli E, Maggi G. Complications following endoscopic intracranial procedures in children. Childs Nerv Syst. 23 (6): 633-44, 2007

11. Cinalli G, Sainte-Rose C, Chumas P, Zerah M, Brunelle F, Lot G, Pierre-Kahn A, Renier D. Failure of third ventriculostomy in the treatment of aqueductal stenosis in children. J Neurosurg. 90 (3): 448-54, 1999.

12. Cinalli G, Sainte-Rose C, Chumas P, Zerah M, Brunelle F, Lot G, Pierre-Kahn A, Renier D. Failure of third ventriculostomy in the treatment of aqueductal stenosis in children. Neurosurg Focus. 15; 6 (4): e3, 1999.

13. Cinalli G, Salazar C, Mallucci C, Yada JZ, Zerah M, Sainte-Rose C. The role of endoscopic third ven t r icu los tomy in the management o f shunt malfunction. Neurosurgery. 43 (6): 1323-7, 1998;

14. Di Rocco C, Cinalli G, Massimi L, Spennato P, Cianciulli E, Tamburrini G. Endoscopic third ventriculostomy in the treatment of hydrocephalus in pediatric patients. Adv Tech Stand Neurosurg. 31: 119-219, 2006.

15. Di Rocco C, Massimi L, Tamburrini G. Shunts vs endoscopic third ventriculostomy in infants: are there different types and/or rates of complications? A review. Childs Nerv Syst. 22 (12): 1573-89, 2006.

16. Di Rocco F, Nonaka Y, Hamada H, Yoshino M, Nakazaki H, Oi S. Endoscopic biopsy interpretation difficulties in a congenital diffuse intracranial teratoma. Childs Nerv Syst. 22 (1): 84-9, 2006.

17. Di Rocco F, Yoshino M, Oi S. Neuroendoscopic transventricular ventriculocystostomy in treatment for intracranial cysts. J Neurosurg. 103 (1 Suppl): 54-60, 2005.

18. Depreitere B, Dasi N, Rutka J, Dirks P, Drake J. Endoscopic biopsy for intraventricular tumors in children. J Neurosurg. 106 (5 Suppl): 340-6, 2007.

19. Drake JM; Canadian Pediatric Neurosurgery Study Group. Endoscopic third ventriculostomy in pediatric

patients: the Canadian experience. Neurosurgery. 60 (5): 881-6, 2007

20. Drake J, Chumas P, Kestle J, Pierre-Kahn A, Vinchon M, Brown J, Pollack IF, Arai H. Late rapid deterioration after endoscopic third ventriculostomy: additional cases and review of the literature. J Neurosurg. 105 (2 Suppl): 118-26, 2006

21. El-Dawlatly AA, Murshid WR, Elshimy A, Magboul MA, Samarkandi A, Takrouri MS. The incidence of bradycardia during endoscopic third ventriculostomy. Anesth Analg. 91 (5): 1142-4, 2000.

22. Enchev Y, Oi S. Historical trends of neuroendoscopic surgical techniques in the treatment of hydrocephalus. Neurosurg Rev. 31 (3): 249-62, 2008.

23. Erşahin Y, Arslan D. Complications of endoscopic third ventriculostomy. Childs Nerv Syst. 24 (8): 943-8, 2008.

24. Feng H, Huang G, Liao X, Fu K, Tan H, Pu H, Cheng Y, Liu W, Zhao D. Endoscopic third ventriculostomy in the management of obstructive hydrocephalus: an outcome analysis. J Neurosurg. 100 (4): 626-33, 2004.

25. Fukuhara T, Luciano MG, Kowalski RJ. Clinical features of third ventriculostomy failures classified by fenestration patency. Surg Neurol. 58 (2): 102-10, 2002.

26. Gaab MR, Schroeder HW. Neuroendoscopic approach to intraventricular lesions. Neurosurg Focus. 15; 6 (4): e5 1999.

27. Gangemi M, Maiuri F, Colella G, Sardo L. Endoscopic surgery for intracranial cerebrospinal fluid cyst malformations. Neurosurg Focus. 15; 6 (4): e6, 1999.

28. Goumnerova LC, Frim DM. Treatment of hydrocephalus with third ventriculocisternostomy: outcome and CSF flow patterns. Pediatr Neurosurg. 27 (3): 149-52, 1997.

29. Greenfield JP, Hoffman C, Kuo E, Christos PJ, Souweidane MM. Intraoperative assessment of endoscopic third ventriculostomy success. J Neurosurg Pediatrics. 2 (5): 298-303, 2008.

30. Grotenhuis JA, Bartels RH, Tacl S. Intraoperative dislocation of the distal lens of a neuroendoscope: a very rare complication: technical case report. Neurosurgery. 41 (3): 698-91997

31. Hader WJ, Drake J , Cochrane D, Sparrow O, Johnson ES, Kestle J. Death after late failure of third ventriculostomy in children. Report of three cases. J Neurosurg. 97 (1): 211-5, 2002.

32. Hamada H, Hayashi N, Kurimoto M, Umemura K, Hirash ima Y, Nogami K, Endo S . Tens ion pneumocephalus after a neuroendoscopic procedure--case report. Neurol Med Chir (Tokyo). 44 (4): 205-8, 2004.

33. Handler MH, Abbott R, Lee M. A near-fatal complication of endoscopic third ventriculostomy: case report. Neurosurgery. 35 (3): 525-7; discussion 527-8, 1994.

34. Hayashi N, Hamada H, Hirashima Y, Kurimoto M, Takaku A, Endo S. Clinical features in patients requiring reoperation after failed endoscopic procedures for hydrocephalus. Minim Invasive Neurosurg. 43 (4): 181-6, 2000.

35. Hopf NJ, Perneczky A. Endoscopic neurosurgery and endoscope-assisted microneurosurgery for the treatment of intracranial cysts. Neurosurgery. 43 (6): 1330-6, 1998

36. Hopf NJ, Grunert P, Fries G, Resch KD, Perneczky A. Endoscopic third ventriculostomy: outcome analysis


of 100 consecutive procedures. Neurosurgery. 44 (4): 795-804, 1999

37. Kalmar AF, Van Aken J, Caemaert J, Mortier EP, Struys MM. Value of Cushing reflex as warning sign for brain ischaemia during neuroendoscopy. Br J Anaesth. 94 (6): 791-9, 2005.

38. Kamel MH, Murphy M, Aquil ina K, Marks C. Subdural haemorrhage following endoscopic third ventriculostomy. A rare complication. Acta Neurochir (Wien). 148 (5): 591-3, 2006.

39. Kim BS, Jallo GI, Kothbauer K, Abbott IR. Chronic subdural hematoma as a complication of endoscopic third ventriculostomy. Surg Neurol. 62 (1): 64-8, 2004

40. Kulkarni AV, Drake JM, Armstrong DC, Dirks PB. Imaging correlates of successful endoscopic third ventriculostomy. J Neurosurg. 92 (6): 915-9, 2000.

41. Kurschel S, Ono S, Oi S. Risk reduction of subdural collections following endoscopic third ventriculostomy. Childs Nerv Syst. 23 (5): 521-6, 2007.

42. Li KW, Nelson C, Suk I, Jallo GI. Neuroendoscopy: past, present, and future. Neurosurg Focus. 15; 19 (6): E1, 2005.

43. Luther N, Cohen A, Souweidane MM. Hemorrhagic sequelae from intracranial neuroendoscopic procedures for intraventricular tumors. Neurosurg Focus. 15; 19 (1): E9, 2005.

44. Massimi L, Tamburrini G, Caldarelli M, Di Rocco F, Federica N, Di Rocco C. Late closure of the stoma by spreading of a periaqueductal glioma: an unusual failure of endoscopic third ventriculostomy. Case report. J Neurosurg. 104 (3 Suppl): 197-201, 2006.

45. McLaughlin MR, Wahlig JB, Kaufmann AM, Albright AL. Traumatic basilar aneurysm after endoscopic third ventriculostomy: case report. Neurosurgery. 41 (6): 1400-3, 1997.

46. Mohanty A, Anandh B, Reddy MS, Sastry KV. Contralateral massive acute subdural collection after endoscopic third ventriculostomy - a case report. Minim Invasive Neurosurg. 40 (2): 59-61, 1997.

47. Morota N, Watabe T, Inukai T, Hongo K, Nakagawa H. Anatomical variants in the floor of the third ventricle; implications for endoscopic third ventriculostomy. J Neurol Neurosurg Psychiatry. 69 (4): 531-4, 2000.

48. Navarro R, Gil-Parra R, Reitman AJ, Olavarria G, Grant JA, Tomita T. Endoscopic third ventriculostomy in children: early and late complications and their avoidance. Childs Nerv Syst. 22 (5): 506-13, 2006.

49. Nishiyama K, Mori H, Tanaka R. Changes in cerebrospina l f lu id hydrodynamics fo l lowing endoscopic third ventriculostomy for shunt-dependent noncommunicating hydrocephalus. J Neurosurg. 98 (5): 1027-31, 2003.

50. Oi S, Abbott R. Loculated ventricles and isolated compartments in hydrocephalus: their pathophysiology and the efficacy of neuroendoscopic surgery. Neurosurg Clin N Am. 15 (1): 77-87, 2004.

51. Oi S, Di Rocco C. Proposal of “evolution theory in cerebrospinal fluid dynamics” and minor pathway hydrocephalus in developing immature brain. Childs Nerv Syst. 22 (7): 662-9, 2006.

52. Oi S, Shibata M, Tominaga J, Honda Y, Shinoda M, Takei F, Tsugane R, Matsuzawa K, Sato O. Efficacy

of neuroendoscopic procedures in minimally invasive preferential management of pineal region tumors: a prospective study. J Neurosurg. 93 (2): 245-53, 2000.

53. Oi S, Hidaka M, Honda Y, Togo K, Shinoda M, Shimoda M, Tsugane R, Sato O. Neuroendoscopic surgery for specific forms of hydrocephalus. Childs Nerv Syst. 15 (1): 56-68, 1999.

54. Oertel J, Baldauf J, Schroeder HW , Gaab MR Endoscopic options in children: experience with 134 procedures. J Neurosurg Ped 3: 81-89, 2009.

55. Peretta P, Ragazzi P, Galarza M, Genitori L, Giordano F, Mussa F, Cinalli G. Complications and pitfalls of neuroendoscopic surgery in children. J Neurosurg. 105 (3 Suppl): 187-93, 2006.

56. Pettorini BL, Tamburrini G. Two hundred years of endoscopic surgery: from Philipp Bozzini’s cystoscope to paediatric endoscopic neurosurgery. Childs Nerv Syst. 23 (7): 723-4, 2007.

57. Preul C, Hübsch T, Lindner D, Tittgemeyer M. Assessment of ventricular reconfiguration after third ventriculostomy: what does shape analysis provide in addition to volumetry? AJNR Am J Neuroradiol. 27 (3): 689-93, 2006.

58. Schroeder HW, Niendorf WR, Gaab MR. Complications of endoscopic third ventriculostomy. J Neurosurg. 96 (6): 1032-40, 2002.

59. Schroeder HW, Oertel J, Gaab MR. Incidence of complications in neuroendoscopic surgery.Childs Nerv Syst. 20 (11-12): 878-83, 2004.

60. Schroeder HW, Warzok RW, Assaf JA, Gaab MR. Fatal subarachnoid hemorrhage after endoscopic third ventriculostomy. Case report. Neurosurg Focus. 15; 6 (4): e4, 1999.

61. Siomin V, Cinalli G, Grotenhuis A, Golash A, Oi S, Kothbauer K, Weiner H, Roth J, Beni-Adani L, Pierre-Kahn A, Takahashi Y, Mallucci C, Abbott R, Wisoff J, Constantini S. Endoscopic third ventriculostomy in patients with cerebrospinal fluid infection and/or hemorrhage. J Neurosurg. 97 (3): 519-24, 2002.

62. Tamburrini G, D'Angelo L, Paternoster G, Massimi L, Caldarelli M, Di Rocco C. Endoscopic management of intra and paraventricular CSF cysts. Childs Nerv Syst. 23 (6): 645-51, 2007.

63. Teo C, Jones R. Management of hydrocephalus by endoscopic third ventriculostomy in patients with myelomeningocele. Pediatr Neurosurg. 25 (2): 57-63, 1996.

64. Teo C Complete endoscopic removal of colloid cysts: issues of safety and efficacy. Neurosurg Focus. 15; 6 (4): e9, 1999.

65. Vaicys C, Fried A. Transient hyponatriemia complicated by seizures after endoscopic third ventriculostomy. Minim Invasive Neurosurg. 43 (4): 190-1, 2000.

66. van Aalst J, Beuls EA, van Nie FA, Vles JS, Cornips EM. Acute distortion of the anatomy of the third ventricle during third ventriculostomy. Report of four cases. J Neurosurg. 96 (3): 597-9, 2002.

67. Wellons JC 3rd, Tubbs RS, Banks JT, Grabb B, Blount JP, Oakes WJ, Grabb PA. Long-term control of hydrocephalus via endoscopic third ventriculostomy in children with tectal plate gliomas. Neurosurgery. 51 (1): 63-7, 2002.


Hydrocephalus ResearchWorld Record Ranking

1950-2008

“Hydrocephalus” Original English papers publication as the “first author” Data Base : Pub MedPeriod : 1950-2008Date of Retrieval : November 27, 2008On- line searching formula : hydrocephalus [majr] Limits: Publication Date from 1950, Journal Article, EnglishTotal Number : 7,494 papers “Cerebrospinal Fluid” original English papers publication as the “first author” Data Base : Pub MedPeriod : 1950-2008Date of Retrieval : December 2, 2008On-line searching formula : “cerebrospinal fluid” [majr] Limits: Publication Date from 1950, Journal Article, EnglishTotal Number : 4,901 papers * Confirmed by “Hydrocephalus Research World Record Ranking” [HRWRR] committee of “Journal of Hydrocephalus”.** Submission by the first author of any other original English paper (s), which is (are) not cited by the above on-line search formula, shall be accepted with approval of the HRWRR Committee. (See the submission guideline)


“Hydrocephalus”1950-2008

17 11 47 8 76 6 107 5

d

d

Hydrocephalus Research World Record Ranking

Rank First Author Papers Rank First Author Papers Rank First Author Papers Rank First Author Papers

1 J. Lorber 30 31 M. A. Poca 9 76 A. N. Guthkelch 6 107 C. Raftopoulos 52 H. C. Jones 25 31 M. Bergsneider 9 76 B. K. Owler 6 107 C. Sainte-Rose 52 S. Oi 25 31 N. Buxton 9 76 B. Tew 6 107 D. F. Kohn 54 M. R. Del Bigio 24 31 P. M. Black 9 76 C. Wikkelso 6 107 D. Goh 55 C. Di Rocco 22 31 R. S. Tubbs 9 76 D. Yashon 6 107 D. M. Frim 55 U. Meier 22 31 S. E. Borgesen 9 76 F. A. Chervenak 6 107 E. Alexander, Jr. 57 T. H. Milhorat 21 31 W. G. Bradley, Jr. 9 76 H. Miyake 6 107 E. R. Cardoso 58 K. M. Laurence 19 47 A. Mohanty 8 76 J. Malm 6 107 F. Takei 59 A. E. James, Jr. 18 47 A. Sahar 8 76 J. R. Kestle 6 107 G. S. Liptak 5

10 K. Mori 15 47 C. M. Bannister 8 76 L. Granholm 6 107 H. Hamada 511 E. L. Foltz 14 47 D. D. Matson 8 76 M. Castro-Gago 6 107 H. J. Hoffman 511 H. L. Rekate 14 47 F. Epstein 8 76 M. Gangemi 6 107 H. Kalter 513 E. Fernell 13 47 H. L. Brydon 8 76 M. Mataro 6 107 J. Jansen 513 H. E. James 13 47 P. Klinge 8 76 M. Michejda 6 107 J. Ransohoff 515 A. J. Raimondi 12 47 R. H. Pudenz 8 76 M. Tullberg 6 107 J. Sotelo 515 R. Bayston 12 47 R. O. Weller 8 76 N. Aoki 6 107 J. Vanneste 517 A V K lk iA. V. Kulkarni 11 47 S H kiS. Hakim 8 76 N T kiN. Tamaki 6 107 K OkK. Oka 517 A. Whitelaw 11 47 U. Kehler 8 76 P. Upadhyaya 6 107 K. P. Braun 517 J. E. Scarff 11 47 W. Serlo 8 76 P. W. Hanlo 6 107 K. Shulman 517 J. H. Piatt, Jr. 11 59 G. Kaiser 7 76 R. J. Edwards 6 107 K. Welch 517 J. H. Salmon 11 59 I. K. Pople 7 76 R. Kumar 6 107 M. A. Barnes 517 M. Czosnyka 11 59 J. F. Martinez-Lage 7 76 T. Fukuhara 6 107 M. J. Fritsch 523 D. B. Shurtleff 10 59 J. M. Fletcher 7 76 T. Lundar 6 107 M. Matsumae 523 G. A. Bateman 10 59 J. P. McAllister, 2n 7 76 T. P. Naidich 6 107 M. Vinchon 523 G. Cinalli 10 59 J. T. Tans 7 76 T. Takano 6 107 P. L. Longatti 523 G. M. Hochwald 10 59 M. Dennis 7 76 V. Etus 6 107 P. S. Sorensen 523 H. Yamada 10 59 M. Jouet 7 76 W. J. Gardner 6 107 P. W. Hayden 523 J. K. Krauss 10 59 M. Kiefer 7 76 Y. Ersahin 6 107 R. J. Hudgins 523 J. M. Drake 10 59 M. Tisell 7 107 A. B. Jamjoom 5 107 R. T. Johnson 523 P. K. Eide 10 59 N. G. Harris 7 107 A. Hill 5 107 S. Nakamura 531 A. Adeloye 9 59 N. R. Graff-Radfor 7 107 A. J. Boon 5 107 S. S. Nadvi 531 D. C. McCullough 9 59 P. Steinbok 7 107 A. R. Hansen 5 107 S. Tuli 531 D. G. McLone 9 59 R. F. Jones 7 107 B. Hagberg 5 107 T. Barreca 531 E. P. Strecker 9 59 S. C. Stein 7 107 B. Magnaes 5 107 T. Greitz 531 F. Jensen 9 59 S. Duckett 7 107 B. Simms 5 107 T. Lopponen 531 H. Andersson 9 59 S. Sood 7 107 B. Vachha 5 107 V. Rohde 531 H. D. Portnoy 9 76 A. L. Amacher 6 107 B. Williams 5 107 W. H. Clewell 531 J. L. Emery 9 76 A. Larsson 6 107 C. B. Wilson 531 K. Shapiro 9 76 A. Marmarou 6 107 C. Cedzich 5



“Cerebrospinal Fluid”1950-2008

“Cerebrospinal Fluid”

1950-2008Rank First Author Papers Rank First Author Papers Rank First Author Papers

1 H. Davson 18 37 C. Nilsson 5 65 G. Du Boulay 42 A. A. Artru 17 37 D. Oreskovic 5 65 H. Al-Sarraf 43 M. Spiegel-Adolf 14 37 D. R. Enzmann 5 65 H. F. Cserr 43 O. Gilland 14 37 E. M. Wright 5 65 H. L. Rekate 45 E. A. Bering, Jr. 10 37 G. Di Chiro 5 65 H. M. Canelas 45 W. W. Tourtellotte 10 37 H. D. Portnoy 5 65 H. Takizawa 47 B. Vigh 9 37 H. Link 5 65 J. B. Green7 E. Kovacs 9 37 I. Johnston 5 65 J. B. Rubin 47 M. W. Bradbury 9 37 I. R. Cameron 5 65 J. Booij 4

10 A. Sahar 8 37 J. Bekaert 5 65 J. D. Miller 410 B. P. Vogh 8 37 J. Clausen 5 65 J. De Reuck 410 G. M. Hochwald 8 37 J. D. Fenstermacher 5 65 J. P. Lakke 410 O. Sato 8 37 J. G. McComb 5 65 K. G. Go 414 A. Chodobski 7 37 K. Welch 5 65 K. Jensen 414 B. Mokri 7 37 L. Odessky 5 65 K. Ono 414 D. G. Potts 7 37 M. Czosnyka 5 65 M. Boulton 414 H. W. Ryder 7 37 M. Javid 5 65 M. C. Chamberlain 414 M. Lindvall 7 37 M. Oehmichen 5 65 M. Johnston 414 P. P. Harnish 7 37 P. H. Hashimoto 5 65 M. Kosteljanetz 414 R. A. Fishman 7 37 R. Grant 5 65 M. Lindvall-Axelss

4

o 414 S. Javaheri 7 37 R. J. Schain 5 65 M. Sandberg-Wollheim 414 T. H. Maren 7 37 R. M. Schmidt 5 65 N. H. Bass 423 A. E. James, Jr. 6 37 R. Sornas 5 65 P. Cinque 423 A. Lithander 6 37 R. W. Cutler 5 65 P. Winkler 423 A. N. Martins 6 37 W. W. Oppelt 5 65 R. A. Bhadelia 423 D. Greitz 6 65 A. Saifer 4 65 R. A. Mitchell 423 D. J. Reed 6 65 B. K. Siesjo 4 65 R. K. Jakoby 423 H. C. Jones 6 65 B. L. Wise 4 65 R. Spector 423 H. G. Sullivan 6 65 B. Williams 4 65 S. Bogoch 423 I. Vigh-Teichmann 6 65 C. B. Wilson 4 65 S. H. Bigner 423 J. R. Pappenheimer 6 65 C. M. Plum 4 65 S. Nakamura 423 J. W. Severinghaus 6 65 D. Bowsher 4 65 S. R. Heisey 423 M. Farstad 6 65 D. G. Davies 4 65 T. O. Kleine 423 M. Pollay 6 65 E. F. Rabe 4 65 V. Kronholm 423 R. E. Albright, Jr. 6 65 E. Roboz 4 65 W. G. Bradley, Jr. 423 T. H. Milhorat 6 65 F. Garcia-Bengochea 4 65 W. H. Sweet37 A. Guseo 5 65 F. H. Sklar 4 65 W. I. Schievink 437 A. Marmarou 5 65 F. Plum 4 116 A. Ames, 3rd 337 A. V. Lorenzo 5 65 F. R. Domer 4 116 A. B. Butler 3

4

22J. Hydrocephalus Volume 1 / Number 1 / May 2009



Rank First Author Papers Rank First Author Papers Rank First Author Papers116 A. D. Dayan 3 116 J. E. O'Connell 3 116 S. E. Borgesen 3116 A. K. Datta 3 116 J. L. Melnick 3 116 S. Majcherczyk 3116 A. Lowenthal 3 116 J. L. Sherman 3 116 S. Pelc 3116 A. Migliore 3 116 J. Lofgren 3 116 S. Seyfert 3116 A. N. Salt 3 116 J. M. Pearce 3 116 T. Ishibashi 3116 A. Naess 3 116 J. N. Cumings 3 116 T. J. Seabrook 3116 A. Peter 3 116 J. R. Atkinson 3 116 T. Lundar 3116 A. Petzold 3 116 J. Sedlacek 3 116 U. Ponten 3116 A. Pfefferbaum 3 116 K. Higashi 3 116 V. Fencl 3116 A. Walsted 3 116 K. Shulman 3 116 V. Kurtcuoglu 3116 A. Zakharov 3 116 L. Berg 3 116 W. A. Bonadio 3116 B. M. Greenwood 3 116 M. A. Maktabi 3 116 W. E. Stern 3116 C. P. Maurizi 3 116 M. A. Stoodley 3 116 W. F. House 3116 D. A. Nixon 3 116 M. B. Bowers, Jr. 3 116 W. H. Oldendorf 3116 D. G. Gomez 3 116 M. B. Segal 3116 D. G. McDowall 3 116 M. Buckell 3116 D. H. Harter 3 116 M. C. Calhoun 3116 D. K. Anderson 3 116 M. C. Henry-Feugea 3116 D. W. Palmer 3 116 M. D. Deck 3116 E. Appel 3 116 M. G. Marrosu 3116 E. E. Nattie 3 116 M. H. Wykoff 3116 E. G. Pavlin 3 116 M. J. Madonick 3116 E. P. Strecker 3 116 M. Pashenkov 3116 G. A. Rosenberg 3 116 M. R. Patel 3116 G. Bergstrand 3 116 M. W. Brightman 3116 G. Brocklehurst 3 116 O. Baledent 3116 G. D. Silverberg 3 116 P. C. Doherty 3116 G. Magram 3 116 P. E. Manconi 3116 G. Nagra 3 116 P. G. Osborne 3116 G. Schroth 3 116 P. Gideon 3116 H. H. Loeschcke 3 116 P. Kivisakk 3116 H. J. Safi 3 116 P. M. Black 3116 H. L. Rosomoff 3 116 R. G. Petersdorf 3116 H. S. Chang 3 116 R. H. Wilkins 3116 I. Leusen 3 116 R. K. Parkkola 3116 J. B. Posner 3 116 R. Katzman 3116 J. D. Mann 3 116 R. S. Bourke 3116 J. De Bersaques 3 116 S. Angelow 3116 J. E. Guinane 3 116 S. C. Wayte 3



“Hydrocephalus” Original English papers published as the “first author” (Nov.27, 2008) Ranking No.1-No.10

cran bifid l

#2 1985 and resistance l 90 0014-4886

"Hydrocephalus" Original English papers published as the "first author"(Nov.27,2008) Ranking No.1-No.47 (676 papers)

Rank Author No Year Title Journal Vol Pages ISBN/ISSN

1 J. Lorber #1 1961 The diagnosis and management of hydrocephalus in infancy N Z Med J 60 416-8 0028-8446(Print)

J. Lorber #2 1961 Systematic ventriculographic studies in infants born with meningomyelocele andencephalocele. The incidence and development of hydrocephalus

Arch DisChild

36 381-9 0003-9888(Print)

J. Lorber #3 1964 Two cases of achondroplasia Proc R SocMed

57 836-7 0035-9157(Print)

J. Lorber #4 1964 Spina bifida cystica. Heredit ary features Nurs Times 60 411-2 0954-7762(Print)

J. Lorber;J. L. Emery #5 1964 Intracerebral cysts complicating ventricular needling in hydrocephalic infants: Aclinico-pathological study

Dev MedChild Neurol

6 125-39 0012-1622(Print)

J. Lorber #6 1965 The family history of spina befida cystica Pediatrics 35 589-95 0031-4005(Print)

J. Lorber;U. Bassi #7 1965 The aetiology of neonatal hydrocephalus(Excluding cases with spina bifida) Dev MedChild Neurol

7 289-94 0012-1622(Print)

J. Lorber;D. Pickering #8 1966 Incidence and treatment of post-meningitic hydrocephalus in the newborn Arch DisChild

41 44-501468-2044(Electronic

J. Lorber #9 1967 Recovery of vision following prolonged blindness in children with hydrocephalusor following pyogenic meningitis

Clin Pediatr(Phila)

6 699-703

0009-9228(Print)

J. Lorber #10 1968 Puncture porencephaly Dev MedChild Neurol

10 233-4 0012-1622(Print)

J. Lorber #11 1968 The results of early treatment of extreme hydrocephalus Dev MedChild Neurol

Suppl16:21-9

0012-1622(Print)

J. Lorber;R. B. Zachary #12 1968 Primary congenital hydrocephalus. Long-term results of controlled therapeutictrial

Arch DisChild

43 516-271468-2044(Electronic

J. Lorber #13 1969Ventriculo-cardiac shunts in the first week of life. Results of a controlled trial inthe treatment of hydrocephalus in infants born with spina bifida cystica orcranium bifidumium um

Dev MedChild NeurolSupplSupp

20 13-22 0419-0238(Print)

J. Lorber;A. K. Tunstill #14 1969 The Sheffield Congenital Anomalies Research Unit Med BiolIllus

19 100-4 0025-6978(Print)

J. Lorber #15 1971 Medical and surgical aspects in the treatment of congenital hydrocephalus Neuropadiatrie

2 239-46 0028-3797(Print)

J. Lorber #16 1972 The use of isosorbide in the treatment of hydrocephalus Dev MedChild Neurol

27 87-93 0419-0238(Print)

J. Lorber #17 1973 Isosorbide in the medical treatment of infantile hydrocephalus J Neurosurg 39 702-11 0022-3085(Print)

J. Lorber #18 1973 Neonatal E. coli meningitis, hydrocephalus, respiratory distress syndrome, fullrecovery after temporary blindness

Proc R SocMed

66 221-2 0035-9157(Print)

J. Lorber;U. S. Bhat #19 1974 Posthaemorrhagic hydrocephalus. Diagnosis, differential diagnosis, treatment, andlong-term results

Arch DisChild

49 751-621468-2044(Electronic

J. Lorber #20 1975 Ethical problems in the management of myelomeningocele and hydrocephalus.The Milroy Lecture 1975

J R CollPhysicians

10 47-60 0035-8819(Print)

J. Lorber #21 1975 Isosorbide in the treatment of infantile hydrocephalus. Observations with a newdrug

Clin Pediatr(Phila)

14 916-9 0009-9228(Print)

J. Lorber #22 1975 Isosorbide in treatment of infantile hydrocephalus Arch DisChild

50 431-61468-2044(Electronic

J. Lorber #23 1976 The medical treatment of hydrocephalus using isosorbide Mod ProblPaediatr

18 178-80 0303-884X(Print)

J. Lorber #24 1976 Ethical problems in the management of myelomingocele and hydrocephalus. 2 Nurs Times 72 suppl:9-11

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#7 1991 The cerebral cortex in congenital hydrocephalus in the H-Tx rat: a quantitativelight microscopy study

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#8 1993 Inherited hydrocephalus in H-Tx rat pups: treatment monitored with magneticresonance imaging

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#11 1995 Shunt treatment at two postnatal ages in hydrocephalic H-Tx rats quantified usingMR imaging

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#12 1995 Learning deficits in congenitally hydrocephalic rats and prevention by early shunttreatment

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#13 1996 Spatial learning and visual discrimination tests in hydrocephalic rat pupsperformed using the Morris water maze

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#18 2000 Progressive tissue injury in infantile hydrocephalus and prevention/reversal withshunt treatment

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#15 1998 Monoamine neurotransmitters and their metabolites in the mature rabbit brainfollowing induction of hydrocephalusfollowing induction of hydrocephalus

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#16 1993 Postprandial and postural dyspnea: a clinical sign of intraperitoneal pseudocyst inpatients with hydrocephalus and ventriculo-peritoneal shunt

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#18 1994A survey of the first complication of newly implanted CSF shunt devices for thetreatment of nontumoral hydrocephalus. Cooperative survey of the 1991-1992Education Committee of the ISPN

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U. Meier;J. Lemcke #19 2006Is it possible to optimize treatment of patients with idiopathic normal pressurehydrocephalus by implanting an adjustable Medos Hakim valve in combinationwith a Miethke shunt assistant?


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U. Meier;J. Lemcke #21 2006First clinical experiences in patients with idiopathic normal-pressurehydrocephalus with the adjustable gravity valve manufactured by Aesculap(proGAV(Aesculap))

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0001-6306(Print)

T. H. Milhorat;M. K.Hammock

#11 1971 Isotope ventriculography. Interpretation of ventricular size and configuration inhydrocephalus

Arch Neurol 25 1-8 0003-9942(Print)

T. H. Milhorat;M. K.Hammock;R. S. Chandra. S.

#12 1971 The subarachnoid space in congenital obstructive hydrocephalus. 2. Microscopicfindings

J Neurosurg 35 7-15 0022-3085(Print)(Print)

T. H. Milhorat;M. K.Hammock;G. Di Chiro

#13 1971 The subarachnoid space in congenital obstructive hydrocephalus. 1.Cisternographic findings



Bull

in 33

T. H. Milhorat #14 1974 Failure of choroid plexectomy as treatment for hydrocephalus SurgGynecol

139 505-8 0039-6087(Print)

T. H. Milhorat;M. K.Hammock;D. L. Breckbill

#15 1975 Acute unilateral hydrocephalus resulting from oedematous occlusion of foramenof Monro: complication of intraventricular surgery

J NeurolNeurosurg

38 745-8 0022-3050(Print)

T. H. Milhorat;J. E.McClenathan

#16 1975 Direct cardiac shunt for hydrocephalus of infancy and childhood. Technical note J Neurosurg 42 605-8 0022-3085(Print)

T. H. Milhorat;T. Chien;M.Majd;D. L. Breckbill

#17 1976 Unreliability of combined pneumoencephalography and scinticisternography J Nucl Med 17 54-6 0161-5505(Print)

T. H. Milhorat;M. K.Hammock;T. Chien;D. A.Davis

#18 1976 Normal rate of cerebrospinal fluid formation five years after bilateral choroidplexectomy. Case report J Neurosurg 44 735-9

0022-3085(Print)

T. H. Milhorat;M. K.Hammock;D. A. Davis;J.D. Fenstermacher

#19 1976 Choroid plexus papilloma. I. Proof of cerebrospinal fluid overproduction Childs Brain 2 273-890302-2803(Print)

T. H. Milhorat #20 1987 Acute hydrocephalus after aneurysmal subarachnoid hemorrhage Neurosurgery

20 15-20 0148-396X(Print)

T. H. Milhorat #21 1992 Classification of the cerebral edemas with reference to hydrocephalus andpseudotumor cerebri

Childs NervSyst

8 301-6 0256-7040(Print)

8 K. M. Laurence #1 1957 The urinary phenolsulphonphthalein (phenol red) excretion test in hydrocephalus Arch DisChild

32 413-6 0003-9888(Print)

K. M. Laurence #2 1958 The natural history of hydrocephalus Lancet 2 1152-4 0140-6736(Print)

K. M. Laurence #3 1959 Some applications of the urinary phenolsulphonphthalein excretion test inhydrocephalus and related conditions

Brain 82 551-65 0006-8950(Print)

K. M. Laurence #4 1959 The pathology of hydrocephalus Ann R CollSurg Engl

24 388-401

0035-8843(Print)

K. M. Laurence #5 1960 The natural history of hydrocephalus PostgradMed J

36 662-7 0032-5473(Print)

K. M. Laurence #6 1960 Infantile hydrocephalus: its diagnosis and natural history Q RevPediatr

15 5-12

K. M. Laurence #7 1960 Hydrocephalus and disability Cereb PalsyBull

2 170-9

K. M. Laurence #8 1960 Hydrocephalus and disability Cereb PalsyBull

2 170-9

K. M. Laurence;S. Coates #9 1962 Further thoughts on the natural history of hydrocephalus Dev MedChild Neurol

4 263-7 0012-1622(Print)

K. M. Laurence #10 1964 A case of unilateral megalencephalyC Dev MedChild Neurol

6 585-90 0012-1622(Print)

K. M. Laurence #11 1964 The natural history of spina bifida cystica: Detailed analysis of 407 cases Arch DisChild

39 41-57 0003-9888(Print)

K. M. Laurence #12 1966 The survival of untreated spina bifida cystica Dev MedChild Neurol

Suppl11:10-9

0012-1622(Print)

K. M. Laurence #13 1967 Brain damage in hydrocephalic patients Proc R SocMed

60 1265-6 0035-9157(Print)

K. M. Laurence;S. Coates #14 1967 Spontaneously arrested hydrocephalus. Results of the re-examination of 82survivors from a series of 182 unoperated cases

Dev MedChild Neurol

Suppl13:4-13

0012-1622(Print)

K. M. Laurence;C. O.Carter;P. A. David

#15 1968 Major central nervous system malformations in South Wales. II. Pregnancyfactors, seasonal variation, and social class effects

Br J PrevSoc Med

22 212-22 0007-1242(Print)

K. M. Laurence;C. O.Carter;P. A. David

#16 1968 Major central nervous system malformations in South Wales. I. Incidence, localvariations and geographical factors

Br J PrevSoc Med

22 146-60 0007-1242(Print)

K. M. Laurence #17 1969 Neurological and intellectual sequelae of hydrocephalus Arch Neurol 20 73-81 0003-9942(Print)

K. M. Laurence #18 1979 The biology of choroid plexus papilloma in infancy and childhood ActaNeurochir

50 79-90 0001-6268(Print)

K. M. Laurence #19 1984 Genetic aspects of "uncomplicated" hydrocephalus and its relationship to neuraltube defect

Z Kinderchir 39Suppl 2

96-9 0174-3082(Print)

9A. E. James, Jr.;F. H.DeLand;F. J. Hodges,3rd;H. N. Wagner, Jr.

#1 1970 Normal-pressure hydrocephalus. Role of cisternography in diagnosis JAMA 2131615-

220098-7484(Print)

A. E. James, Jr.;J. P.Dorst;E. S. Mathews;V. A. #2 1972 Hydrocephalus in achondroplasia studied by cisternography Pediatrics 49 46-9 0031-4005

(Print)

A. E. James, Jr.;P. F.New;E. R. Heinz;F. J.Hodges;F. H. DeLand

#3 1972 A cisternographic classification of hydrocephalus

Am JRoentgenolRadium TherNucl Med

115 39-490002-9580(Print)

A. E. James, Jr.;E. P.Strecker

#4 1973 Use of silastic to produce communicating hydrocephalus InvestRadiol

8 105-10 0020-9996(Print)

A. E. James, Jr.;E. P.Strecker;M. Bush

#5 1973 A catheter technique for the production of communicating hydrocephalus Radiology 106 437-9 0033-8419(Print)

A. E. James, Jr.;E. P.Strecker;G. Novak;B.Strecker;G. Novak;B.

#6 1973 Correlation of serial cisternograms and cerebrospinal fluid pressure measurementsin experimental communicating hydrocephalusexperimental communicating hydrocephalus

Neurology 23 1226-33

0028-3878(Print)(Print)

A. E. James, Jr.;W. J.Flor;M. Bush;T. Merz;B.

#7 1974 An experimental model for chronic communicating hydrocephalus J Neurosurg 41 32-7 0022-3085(Print)


Neurochirur 0028

(Print)

A. E. James, Jr.;W. J.Flor;T. Merz;E. P.Strecker;B. Burns

#8 1974A pathophysiologic mechanism for ventricular entry of radiopharmaceutical andpossible relation to chronic communicating hydrocephalus


122 38-430002-9580(Print)

A. E. James, Jr.;E.Sperber;E. P. Strecker;C.Digel;G. Novak;M. Bush

#9 1974 Use of serial cisternograms to document dynamic changes in the development ofcommunicating hydrocephalus: a clinical and experimental study

Acta NeurolScand

50 153-700001-6314(Print)

A. E. James, Jr.;E. P.Strecker;E. Sperber;W. J.Flor;T. Merz;B. Burns

#10 1974 An alternative pathway of cerebrospinal fluid absorption in communicatinghydrocephalus. Transependymal movement Radiology 111 143-6

0033-8419(Print)

A. E. James, Jr.;B.Burns;W. F. Flor;E. P.Strecker;T. Merz;M.

#11 1975Pathophysiology of chronic communicating hydrocephalus in dogs (Canisfamiliaris). Experimental studies J Neurol Sci 24 151-78

0022-510X(Print)

A. E. James, Jr.;M. H.Epstein;T. C. Smith

#12 1975 In vitro measurement of respiration of choroid plexus cells in communicatinghydrocephalus

InvestRadiol

10 366-70 0020-9996(Print)

A. E. James, Jr.;M.Epstein;G. Novak;B. Burns

#13 1977 Evaluation of cerebrospinal fluid production in the development ofcommunicating hydrocephalus

Radiology 122 143-7 0033-8419(Print)

A. E. James, Jr.;W. J.Flor;G. R. Novak;E. P.Strecker;B. Burns;M.

#14 1977 Experimental hydrocephalus Exp Eye Res 25Suppl 435-59

0014-4835(Print)

A. E. James, Jr.;G.Novak;A. L. Bahr;B. Burns

#15 1977 The production of cerebrospinal fluid in experimental communicatinghydrocephalus

Exp BrainRes

27 553-7 0014-4819(Print)

A. E. James, Jr.;G. R.Novak;E. P. Strecker;W. J.Flor

#16 1977 The central canal of the spinal cord in experimental hydrocephalus: preliminaryresults Radiology 125 417-20

0033-8419(Print)

A. E. James, Jr.;W. J.Flor;G. R. Novak;E. P.Strecker;B. Burns

#17 1978 Evaluation of the central canal of the spinal cord in experimentally inducedhydrocephalus J Neurosurg 48 970-4

0022-3085(Print)

A. E. James, Jr.;W. J.Flor;G. R. Novak;J. L.Ribas;J. L. Parker;W. L.

#18 1980 The ultrastructural basis of periventricular edema: preliminary studies Radiology 135 747-50 0033-8419(Print)

10 K. Mori;A. J. Raimondi #1 1975 Submicroscopic changes in the periventricular white matter of hydrocephalic chmouse

NipponGeka Hokan

44 159-68 0003-9152(Print)

K. Mori;H. Handa #2 1977 Subdural haematoma (effusion) and internal hydrocephalus Neurochirurgia (Stuttg)

20 154-61 0028-3819-3819(Print)

K. Mori;T. Murata;Y.Nakano;H. Handa

#3 1977 Periventricular lucency in hydrocephalus on computerized tomography Surg Neurol 8 337-40 0090-3019(Print)

K. Mori;H. Handa;T.Murata;Y. Nakano

#4 1980 Periventricular lucency in computed tomography of hydrocephalus and cerebralatrophy

J ComputAssist

4 204-9 0363-8715(Print)

K. Mori;K. Fujito;Y.Kamimura

#5 1984 Binding assay for muscarinic cholinergic receptors in kaolin inducedhydrocephalus

NipponGeka Hokan

53695-702

0003-9152(Print)

K. Mori;M. Morimoto;Y.Kamimura

#6 1985 Post-traumatic epidural hematoma in two patients with long-standing "arrested"hydrocephalus

Childs NervSyst

1 288-90 0256-7040(Print)

K. Mori #7 1990 Hydrocephalus--revision of its definition and classification with special referenceto "intractable infantile hydrocephalus"

Childs NervSyst

6 198-204

0256-7040(Print)

K. Mori;K. Tsutsumi;M.Kurihara;T. Kawaguchi;M.Niwa

#8 1990 Alteration of atrial natriuretic peptide receptors in the choroid plexus of rats withinduced or congenital hydrocephalus

Childs NervSyst

6 190-3 0256-7040(Print)

K. Mori;H. Miyake;M.Kurisaka;T. Sakamoto

#9 1993 Immunohistochemical localization of superoxide dismutase in congenitalhydrocephalic rat brain

Eur J PediatrSurg

3 Suppl1

35 0939-7248(Print)

K. Mori;H. Miyake;M.Kurisaka;T. Sakamoto

#10 1993 Immunohistochemical localization of superoxide dismutase in congenitalhydrocephalic rat brain

Childs NervSyst

9 136-41 0256-7040(Print)

K. Mori #11 1995 Current concept of hydrocephalus: evolution of new classifications Childs NervSyst

11523-31;discussi

0256-7040(Print)

K. Mori;J. Shimada;M.Kurisaka;K. Sato;K.Watanabe

#12 1995 Classification of hydrocephalus and outcome of treatment Brain Dev 17 338-480387-7604(Print)

K. Mori #13 2000 Actualities in hydrocephalus classification and management possibilities Neurol Res 22 127-30 0161-6412(Print)

K. Mori #14 2001 Management of idiopathic normal-pressure hydrocephalus: a multiinstitutionalstudy conducted in Japan


K. Mori;M. Maeda;S.Asegawa;J. Iwata

#15 2002Quantitative local cerebral blood flow change after cerebrospinal fluid removal inpatients with normal pressure hydrocephalus measured by a double injectionmethod with N-isopropyl-p-[(123)I] iodoamphetamine

ActaNeurochir(Wien)

144

255-62;discussion 262-

3

0001-6268(Print)

11 E. L. Foltz;D. B. Shurtleff #1 1963 Five-Year comparative study of hydrocephalus in children with and withoutoperation(113 cases)

J Neurosurg 20 1064-79

0022-3085(Print)

E. L. Foltz;D. B. Shurtleff #2 1966 Conversion of communicating hydrocephalus to stenosis or occlusion of theaqueduct during ventricular shunt


E. L. Foltz #3 1968 Hydrocephalus--the value of treatment South Med J 61 443-54 0038-4348(Print)

E. L. Foltz;R. Kronmal;D.B. Shurtleff

#4 1973 Chapter 10. To treat or not to treat: a neurosurgeon's perspective ofmyelomeningocele

ClinNeurosurg

20 147-63 0069-4827(Print)


“Cerebrospinal Fluid” Original English papers published as the “first author” (Dec.2, 2008) Ranking No.1-No.10

(

"Cerebrospinal Fluid" Original English papers published as the "first author" (Dec.2,2008) Ranking No.1-No.10 Rank Author No Year Title Journal Volume Pages ISBN/ISSN

1 H. Davson;C. Purvis #1 1954 Cryoscopic apparatus suitable for studies on aqueous humour and cerebro-spinalfluid J Physiol 124 12-3P

0022-3751(Print)

H. Davson;C. P. Luck #2 1955 The distribution of bicarbonate between aqueous humour, cerebrospinal fluid andplasma in several mammalian species J Physiol 130 48-9P 0022-3751

(Print)

H. Davson;C. P. Luck #3 1956 A comparative study of the total carbon dioxide in the ocular fluids, cerebrospinalfluid, and plasma of some mammalian species J Physiol 132 454-64

0022-3751(Print)

H. Davson;C. P. Luck #4 1957The effect of acetazoleamide on the chemical composition of the aqueous humourand cerebrospinal fluid of some mammalian species and on the rate of turnover of24Na in these fluids

J Physiol 137 279-93 0022-3751(Print)

H. Davson;H. V. Smith #5 1957 Physiological aspects of the penetration of drugs into the cerebrospinal fluid Proc R SocMed

50 963-6 0035-9157(Print)

H. Davson;C. R.Kleeman;E. Levin

#6 1962 Quantitative studies of the passage of different substances out of the cerebrospinalfluid

J Physiol 161 126-42 0022-3751(Print)

H. Davson;E. Spaziani #7 1962 Effect of hypothermia on certain aspects of the cerebrospinal fluid Exp Neurol 6 118-28 0014-4886(Print)

H. Davson #8 1963 The cerebrospinal fluid ErgebPhysiol

52 20-72 0080-2042(Print)

H. Davson;M. Pollay #9 1963 The turnover of 24Na in the cerebrospinal fluid and its bearing on the blood-brainbarrier

J Physiol 167 247-55 0022-3751(Print)

H. Davson;M. Bradbury #10 1965 The fluid exchange of the central nervous system Symp SocExp Biol

19 349-64 0081-1386(Print)

H. Davson #11 1966 Formation and drainage of the cerebrospinal fluidSci BasisMed AnnuRev

238-590080-7729(Print)

H. Davson;C. A. Purvis;M.B. Segal

#12 1969 Measurement of resistance to flow of cerebrospinal fluid J Physiol 202 62P-64P 0022-3751(Print)

H. Davson;M. B. Segal #13 1969 Effect of cerebrospinal fluid on volume of distribution of extracellular markers Brain 92 131-6 0006-8950(Print)

H. Davson;G.Hollingsworth;M. B. Segal

#14 1970 The mechanism of drainage of the cerebrospinal fluid Brain 93 665-78 0006-8950(Print)

H. Davson;M. B. Segal #15 1971 Secretion and drainage of the cerebrospinal fluid Acta NeurolLatinoam

1 ppl 1:99-0001-6306(Print)

H. Davson;K. Welch #16 1971 The permeation of several materials into the fluids of the rabbit's brain J Physiol 218 337-510022-3751(Print)

H. Davson #17 1972 Dynamic aspects of cerebrospinal fluidDev MedChild NeurolSuppl

27 1-160419-0238(Print)

H. Davson;F. R. Domer;J.R. Hollingsworth

#18 1973 The mechanism of drainage of the cerebrospinal fluid Brain 96 329-36 0006-8950(Print)

2 A. A. Artru;M. Nugent;J.D. Michenfelder

#1 1982 Enflurane causes a prolonged and reversible increase in the rate of CSFproduction in the dog

Anesthesiology

57 255-60 0003-3022(Print)

A. A. Artru;M. Nugent;J.D. Michenfelder

#2 1982 Closed recirculatory spinal subarachnoid perfusion for determining CSF dynamics J Neurosurg 56 368-720022-3085(Print)

A. A. Artru #3 1983 Effects of halothane and fentanyl on the rate of CSF production in dogs AnesthAnalg

62 581-5 0003-2999(Print)

A. A. Artru #4 1984 Effects of enflurane and isoflurane on resistance to reabsorption of cerebrospinalfluid in dogs

Anesthesiology

61 529-33 0003-3022(Print)

A. A. Artru #5 1984 Isoflurane does not increase the rate of CSF production in the dog Anesthesiology

60 193-7 0003-3022(Print)

A. A. Artru #6 1984 Effects of halothane and fentanyl anesthesia on resistance to reabsorption of CSF J Neurosurg 60 252-6 0022-3085(Print)

A. A. Artru;T. F. Hornbein #7 1986 Closed ventriculocisternal perfusion to determine CSF production rate andpressure

Am J Physiol 251 R996-9 0002-9513(Print)

A. A. Artru #8 1987 Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebralblood volume, cerebrospinal fluid volume, and brain tissue water and electrolytes

J CerebBlood FlowMetab

7 471-90271-678X(Print)

A. A. Artru;T. F. Hornbein #9 1987 Prolonged hypocapnia does not alter the rate of CSF production in dogs duringhalothane anesthesia or sedation with nitrous oxide

Anesthesiology

67 66-71 0003-3022(Print)

A. A. Artru #10 1988Dose-related changes in the rate of cerebrospinal fluid formation and resistance toreabsorption of cerebrospinal fluid following administration of thiopental,midazolam, and etomidate in dogs

Anesthesiology

69 541-6 0003-3022(Print)

A. A. Artru #11 1988 Muscle relaxation with succinylcholine or vecuronium does not alter the rate ofCSF production or resistance to reabsorption of CSF in dogs

Anesthesiology

68 392-60003-3022(Print)

A. A. Artru;R. A. Katz #12 1988 Comparison of spinal needles, epidural catheters, and cordis lumbar catheters forintraoperative removal of cerebrospinal fluid

Neurosurgery

22 101-4 0148-396X(Print)

A. A. Artru #13 1990 The rate of CSF formation, resistance to reabsorption of CSF, and aperiodicanalysis of the EEG following administration of flumazenil to dogs

Anesthesiology

72 111-70003-3022(Print)

A. A. Artru #14 1993 Propofol combined with halothane or with fentanyl/halothane does not alter therate of CSF formation or resistance to reabsorption of CSF in rabbits

J NeurosurgAnesthesiol

5 250-70898-4921(Print)





A. A. Artru #15 1993Rate of cerebrospinal fluid formation, resistance to reabsorption of cerebrospinalfluid, brain tissue water content, and electroencephalogram during desfluraneanesthesia in dogs


5 178-86 0898-4921(Print)

A. A. Artru;C. M.Bernards;D. S. Mautz;K.M. Powers

#16 1997Intravenous lidocaine decreases but cocaine does not alter the rate of cerebrospinalfluid formation in anesthetized rabbits


9 31-430898-4921(Print)

A. A. Artru;T. Momota #17 2000 Rate of CSF formation and resistance to reabsorption of CSF during sevofluraneor remifentanil in rabbits


12 37-430898-4921(Print)

3 M. Spiegel-Adolf;H. T.Wycis

#1 1951 Ultraspectrophotometry of cerebrospinal fluids in tumors of the central nervoussystem

ConfinNeurol

11 87-97 0010-5678(Print)

M. Spiegel-Adolf;H. T.Wycis;E. A. Spiegel

#2 1951 Chemical analysis of spectrophotometric findings in the cerebrospinal fluid J Nerv MentDis

113 529-37 0022-3018(Print)

M. Spiegel-Adolf #3 1952 Cerebrospinal fluid Prog NeurolPsychiatry

7 275-91 0079-6506(Print)


8 283-99 0079-6506(Print)

M. Spiegel-Adolf;C. W.Umlauf;E. G. Szekely

#5 1953 Effects of convulsions induced by various types of electric stimulation upon thecerebrospinal fluid

JNeuropatholExp Neurol

12 363-67 0022-3069(Print)


9 283-3040079-6506(Print)

M. Spiegel-Adolf;H. W.Baird, 3rd;E. G. Szekely;H.T. Wycis

#7 1954 Cerebrospinal fluid studies in infant children with cerebral palsy and otherneurologic disorders Pediatrics 14 215-21

0031-4005(Print)


10 293-3150079-6506(Print)


11 145-680079-6506(Print)


12 277-3010079-6506(Print)

M. Spiegel-Adolf;H. Baird,3rd;D. Kollias

#11 1957 Lipases in the cerebrospinal fluid in various neurological conditions, especiallyinfantile amaurotic idiocy (Tay-Sachs disease)

ConfinNeurol

17 310-5 0010-5678(Print)


16 283-309 0079-6506(Print)


18 392-4100079-6506(Print)


20 455-81 0079-6506(Print)

3 O. Gilland #1 1965 CSF dynamic diagnosis of spinal block. II. The spinal CSF pressure-volume curve Acta NeurolScand

41 487-96 0001-6314(Print)

O. Gilland #2 1965CSF dynamic diagnosis of spinal block IV: demands on electromanometricequipment

Acta NeurolScand Suppl

13 Pt 1 75-1050065-1427(Print)

O. Gilland #3 1965 CSF dynamic diagnosis of spinal block 3: an equation for block influence oncisterno-lumbar electromanometrics

Acta NeurolScand Suppl

13 Pt 1 47-74 0065-1427(Print)

O. Gilland #4 1966 Cerebrospinal fluid dynamic diagnosis of spinal block V. Uniform lumbarelectromanometrics

Neurology 16 1110-7 0028-3878(Print)

O. Gilland #5 1966 CSF dynamic diagnosis of spinal block. VII. Reliability of lumbarelectromanometrics

Acta NeurolScand

42 ppl 21:450001-6314(Print)

O. Gilland #6 1966 CSF dynamic diagnosis of spinal block. VI. Reliability of combined cisterno-lumbar electromanometrics

Acta NeurolScand

42 uppl 21:1-0001-6314(Print)

O. Gilland #7 1968 Cerebrospinal fluid Prog NeurolPsychiatry

23 338-51 0079-6506(Print)

O. Gilland #8 1969 Normal cerebrospinal-fluid pressure N Engl JMed

280 904-5 0028-4793(Print)

O. Gilland #9 1969 How to take the headache out of spinal taps Headache 8 154-8 0017-8748(Print)

O. Gilland #10 1969 Cerebrospinal fluid Prog NeurolPsychiatry

24 272-91 0079-6506(Print)

O. Gilland;F. Chin;W. B.Anderson;J. R. Nelson

#11 1969 A cinemyelographic study of cerebrospinal fluid dynamics


106 369-750002-9580(Print)

O. Gilland #12 1970 Lumbar electromanometrics. New equipment and long-term accuracy evaluationin 100 patients

Acta NeurolScand

46 uppl 43:2 0001-6314(Print)

O. Gilland #13 1970 Cerebrospinal fluidProg NeurolPsychiatry

25 214-370079-6506(Print)

O. Gilland #14 1971 Cerebrospinal fluidProg NeurolPsychiatry

26 329-610079-6506(Print)

5 E. A. Bering, Jr. #1 1951 A simplified apparatus for constant ventricular drainage J Neurosurg 8 450-2 0022-3085(Print)

E. A. Bering, Jr. #2 1954 Water exchange in the brain and cerebrospinal fluid; studies on theintraventricular instillation of deuterium (heavy water) J Neurosurg 11 234-42

0022-3085(Print)


E. A. Bering, Jr. #3 1955Choroid plexus and arterial pulsation of cerebrospinal fluid; demonstration of thechoroid plexuses as a cerebrospinal fluid pump

AMA ArchNeurolPsychiatry

73 165-720096-6886(Print)

E. A. Bering, Jr. #4 1957 Problems of the dynamics of the cerebrospinal fluid with particular reference tothe formation of cerebrospinal fluid and its relationship to cerebral metabolism

ClinNeurosurg

5 discussio0069-4827(Print)

E. A. Bering, Jr. #5 1958 Composition of cerebrospinal fluid under varying conditions Neurology 8 129-30 0028-3878(Print)

E. A. Bering, Jr. #6 1959 Cerebrospinal fluid production and its relationship to cerebral metabolism andcerebral blood flow Am J Physiol 197 825-8

0002-9513(Print)

E. A. Bering, Jr. #7 1959Cerebrospinal fluid production and its relationship to cerebral metabolism andcerebral blood flow Am J Physiol 197 825-8

0002-9513(Print)

E. A. Bering, Jr.;O. Sato #8 1963 Hydrocephalus: Changes in formation and absorption of cerebrospinal fruidwithin the cerbral ventricles J Neurosurg 20 1050-63 0022-3085

(Print)

E. A. Bering, Jr. #9 1966 Cerebrospinal fluid Prog NeurolPsychiatry

21 358-73 0079-6506(Print)

E. A. Bering, Jr. #10 1974 The cerebrospinal fluid and the extracellular fluid of the brain. Introductoryremarks Fed Proc 33 2061-6

0014-9446(Print)

5W. W. Tourtellotte;R. N.Dejong;S. Janich;K.Gustafson

#1 1962A study of lipids in the cerebrospinal fluid (and serum). VIII. Further commentson the normal lipid profile

Med Bull(Ann Arbor)

28 114-260196-5336(Print)

W. W. Tourtellotte #2 1963 Multiple sclerosis and cerebrospinal fluid Med ClinNorth Am

47 1619-28 0025-7125(Print)

W. W. Tourtellotte;R. J.Allen;A. F. Haerer;S. A.Kelly;K. A. Gustafson;E. R.Bryan;R. N. Dejong

#3 1963 A study of lupids in the cerebrospinal fluid. IX. Two new laboratory observationson the cerebrospinal fluid in tay-saches disease

Trans AmNeurolAssoc

88 104-7 0065-9479(Print)

W. W. Tourtellotte;K. C.Quan;A. F. Haerer;E. R.Bryan

#4 1963 Neoplastic cells in the cerebrospinal fluid. Report of a case of metasticmelanoblastoma.

Neurology 13 866-8 0028-3878(Print)

W. W. Tourtellotte;A. F.Haerer

#5 1964A study of lipids in the cerebrospinal fluid (and serum). Present state ofknowledge in health and disease

RevNeuropsiquiatr

27 339-560034-8597(Print)

W. W. Tourtellotte;A. F.Haerer;J. A. Parker

#6 1964 A study of the blood-cerebrospinal fluid-central nervous system barrier in multiplesclerosis. II. A possible model study for other diseases

RevNeuropsiquiatr

27 260-76 0034-8597(Print)

W. W. Tourtellotte;L. N.Metz;E. R. Bryan;R. N.Dejong

#7 1964Spontaneous subarachnoid hemorrhage. Factors affecting the rate of clearing ofthe cerebrospinal fluid Neurology 14 301-6

0028-3878(Print)

W. W. Tourtellotte;R. J.Allen;A. F. Haerer;E. R.Bryan

#8 1965 Study of lipids in cerebrospinal fluid and serum Arch Neurol 12 300-100003-9942(Print)

W. W. Tourtellotte #9 1967 Cerebrospinal fluid examination in meningoencephalitis Mod Treat 4 879-97 0026-8526(Print)

W. W. Tourtellotte;H.Itabashi;R. P. Tucker;E. R.Bryan

#10 1968 Cerebrospinal fluid cytologyTrans AmNeurolAssoc

93 288-90065-9479(Print)

7 B. Vigh;I. Vigh-Teichmann;B. Aros

#1 1970 Ultrastructure of the CSF contacting neurons of the spinal cord in the newt,triturus cristatus

ActaMorpholAcad SciHung

18 369-82 0001-6217(Print)

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IFNE

INTERNATIONAL FEDERATION

OF NEUROENDOSCOPY


Presidential Address

History of International Federation of Neuroendoscopy [IFNE]

Shizuo Oi, M.D., Ph.D.First President of IFNE

In the year of bright lights shinning on the earth starting the 21st century, 2001, the International Study Group of Neuroendoscopy [ISGNE] was established. The 15 pioneering neurosurgeons from the world in this research field of the rapidly and widely expanding new neurosurgical treatment modalities, “Neuroendoscopic Surgery”, gathered in Awaji International Park, Kobe, Japan on September 25th, 2001 against the violence power of the terrorism on September 11th.

The objective of the Study Group was to contribute to the advancement of neuroendoscopy by serving:・ as the International Study Group to promote worldwide collaborative research in the field of neuroendoscopy. ・ as a forum for effective communication among neurosurgeons actively practicing neuroendoscopic operations and

with basic scientists, engineers and other specialists in related fields. ・ as a medium for development and promotion of scientific knowledge, surgical technique, instrumentation and

minimally-invasive neurosurgery within the area of neuroendoscopy

The scientific activities of ISGNE have promoted the cooperative studies on the controversial unsolved clinical problems and created new aspects on instrumentation, surgical techniques and treatment strategies of neuroendoscopic surgery, as shown in the series of publications on its academic achievements. The ISGNE has been managed as a purely scientific study group ever since.

“The World Congress of Neuroendoscopy” by ISGNE has convened every two years with great success:・ 2001: The 1st World Congress of Neuroendoscopy of ISGNE, Kobe, Japan, Congress President : Shizuo Oi ・ 2003: The 2nd World Congress of Neuroendoscopy of ISGNE, Naples, Italy, Congress President : Giuseppe

Cinalli ・ 2005: The 3rd World Congress of Neuroendoscopy of ISGNE, Marburg, Germany, Congress President : Dieter

Hellwig ・ 2007: The 4th World Congress of Neuroendoscopy of ISGNE, Versailles, France, Congress Presidents : Phillipe

Decq & Paulo Cappabianca ・ 2009: The 5th World Congress of Neuroendoscopy of IFNE, Athens, Greece, Congress President: Spyridon

Sgouros

Along with those scientific activities by ISGNE, there have been several Study Groups on Neuroendoscopy created in the different regions/countries in the world. Based on this historical background, it was strongly supported to create a


The founding members of ISGNE in Awaji, 25th September 2001

world-wide association in the spirit of ISGNE by those who have contributed to the academic achievements of ISGNE and rapidly growing various regional Study Groups or Societies of Neuroendoscopy.

The IFNE, “THE INTERNATIONAL FEDERATION OF NEUROENDOSCOPY” was established as it transformed from ISGNE based on this historical trend and current status of the world-wide support. The objective of the Federation shall be to contribute to the advancement of neuroendoscopy by serving:・ as an association of societies and/or individuals interested in the field of neuroendoscopy, locally, nationally, and

internationally. ・ as a forum for effective communication among neurosurgeons actively practicing neuroendoscopic operations and

with basic scientists, engineers and other specialists in related fields. ・ as a medium for development and promotion of scientific knowledge, surgical technique, instrumentation and

minimally-invasive neurosurgery within the area of neuroendoscopy. ・ as a parent organization to the International Study Group of Neuroendoscopy [ISGNE], which will continue to

exist and function as a Committee of IFNE, with main aim to promote worldwide collaborative research in the field of neuroendoscopy.

・ as a workshop to promote active co-operation among its members, education, teaching and training to neuroendoscopic surgeons world-wide.

・ as a body to promote high standards of training in the specialty at an international level for present or prospective neuroendoscopic surgeons and develop guidelines and indications for neuroendoscopic procedures.

Such purpose shall be served by meetings, publications, committee activities, and any other action which may be deemed appropriate.

I, as the President of IFNE, would like to invite all of you to our academic activities in the field of “Neuroendoscopy” to promote the advanced minimally-invasive neurosurgery in the world.

The spirit of ISGNE shall contribute to the academic and scientific collaboration of world-wide activities of “neuroendoscopy” among the individual and society/study group members of IFNE in 21st century. Shizuo Oi, M.D., Ph.D.President of IFNEProfessor of Neurosurgery, The Jikei University School of Medicine, Tokyo, Japan& International Neuroscience Institute, Hannover, Germany


Memorial Address: “Professor Axel Pernecsky” 1945-2009

A man is known by his work. Curriculum vitae and contributions to NeurosurgeryBernhard L. Bauer, M.D., Ph.D.

It is a great honor for me to give the laudation on my friend Professor Axel Perneczky, laureate on occasion of the V. World Congress of IFNE. I hope to succeed in conveying his human and professional dimension. I am well aware that such attempt must fall short of a true reflection.

Professor Axel Perneczky was born November 01. 1945 in Krasnogorsk near Moscow .From 1946 to 1965 he lived in Budapest and started studying medicine at the University Medical School of Budapest in 1964. He went in 1965 to the University of Vienna and continued the medical studies. During the last three years of his studies he worked at the department of Anatomy with Professor Hajed and Platzer, simultaneously he started his studies in surgical anatomy. After graduation from medical science at the University of Vienna in 1971 he spent at first 2 years at the departments of general surgery and traumatology. In 1973 he started training in neurosurgery at the Neurosurgical University Department in Vienna with Professor Kraus. Because of his very earliest interest in microsurgery and surgical anatomy he spent one year with Professor G. Yasargil as assistant surgeon in Zürich. In 1980 he became to be an associate professor for neurosurgery in Vienna under Professor Koos. In October 1988 he was elected and appointed Professor of neurosurgery and chairman of the Neurosurgical Department of the Medical School, University of Mainz, Germany and joined the staff of the world famous Neurosurgeon Professor K. Schürmann.His main fields of activity are microsurgical anatomy and the implicating surgical strategies in neurosurgery, aneurysm and angioma surgery, and skull base surgery with special consideration of the cavernous sinus. The development of microsurgical strategies resulted in a further refinement of surgical technique and so since 1989 he is working on the application of endoscopy in neurosurgery, wide field use of minimally invasive techniques, such as stereotactic


guided microsurgery, endoscopic assisted microsurgery and neuronavigation. A special technique has been developed for the extended use of the keyhole strategy. He organised the “First International Congress on Minimally Invasive Techniques in Neurosurgery” (Wiesbaden, June 1993) and he is the editor in chief of the International Journal of “Minimally Invasive Neurosurgery” (MIN). Hands-on-courses on microsurgical planning and neuroendoscopy are held six times per year in Mainz and Tuttlingen. He has been the president of a Symposium on Neuronavigation in November 1997 in Mainz and of the 1st International Congress on Endoscope Assisted Microsurgery in June 1998 in Frankfurt. During the last year his interest was focused on the intraoperative imaging modalities using for surgical planning and navigation.

His published scientific contributions count more than 250 papers. He is co-author of the “Colour Atlas of Microneurosurgery” (Thieme, 1984 and 1993), “Endoscopic Anatomy for Neurosurgery” (Thieme 1993), he is also author of the book “Keyhole Concept in Neurosurgery” including “Endoscope Assisted Microsurgery” (Thieme 1999). The book “Keyhole approaches in Neurosurgery” is in press.

As founder and president of the German Society for Endoscope assisted Neurosurgery and Neuronavigation e.V. he remains unforgotten. A new center for “Minimally Invasive Neurosurgery” at the University of Mainz is now under construction, including a special concept for development and application of new concepts and technologies in the neurosurgical operating unit with special innovation in intraoperative visualization and imaging.

We bemoan together with his family and his children: Alexa (1973), Ines (1976), Paul (1977), Julia (1986), Max (1997) and Tom (1998). We remember his passion and brilliance as member of the “Skull-Base-All-Stars” band playing jazz guitar. Gifted with talent beyond neurosurgery we remember him as a painter and last not least as a sportsman on the tennis court, in the swimming pool and skiing snowy mountains.

Professor Axel Perneczky had a brilliant career in academic neurosurgery, devoting himself to solving many of the problems that existed with microsurgery and neuroendoscopy. He took a truly intellectual approach to these problems, starting with basic laboratory work, devising ingenious surgical methods, carefully applying new concepts and a new technique to previously unmanageable neurosurgical problems in patients, and doing all of this with the kindness, compassion and consummate skill of a great physician and surgeon. No one who has met him and has read his writings could fail to feel a growing respect for his wide knowledge, his directness, and his broad cultural background.

He devoted himself to the education of young neurosurgeons, in large numbers they are his scholars and reside worldwide. On the clinical side, he is best remembered for his major contributions to neuroendoscopy and his continuous endeavor to reconcile microsurgery with neuroendoscopy. His proposal to collect and to combine microsurgery and neuroendoscopy as the minimal invasive and tissue saving procedure called “key hole surgery “shall be connected for ever with his name. He has molded modern days neurosurgical practice. The minor and major setbacks and sad moments in his life did not achieve to hinder this man’s work and did not influence his character negatively. He was able to control the situation and continue onward both externally as well as with his spirit. He has given neuroendoscopy worldwide a solid reputation and he has implanted his methods and spirit in many of us. We, his collegues and the great family of former scholars are thankful and indebted. His name and his work occupy a worthy and honourable place in the annals of IFNE and a special place in our heart. World Neurosurgery has lost a friend, an invaluable teacher and a great master of Neurosurgery.

Bernhard L. Bauer M.D. Ph.D. Honorary President IFNEProfessor emerit. of Neurosurgery Senior Professor INI Hannover/Germany


Congress President Welcome Address

5th World Congress of the International Federation of Neuroendoscopy30th May-3rd June 2009

Athens, Greece

Spyridon Sgouros, M.D., FRCS (SN)

Dear Colleagues and Friends,

Neuroendoscopy has seen tremendous progress in the last decade. Although it was first employed in the surgical treat-ment of neurosurgical diseases early in the 20th century by pioneers such as Walter Dandy, it did not become an estab-lished practice for a long time, mainly because of poor technology and clinical results. We could call the first 2 decades of the 20th century the invention phase. After decades of neglect, a kind of “dark ages”, neuroendoscopy is enjoying a sustained resurgence. After a slow timid re-appearance in the 1980s, the 1990s saw an explosion of techniques and instrumentation. We could call the 1980s the re-invention phase, when modern pioneers endured the criticism of their colleagues and tried successfully techniques that everybody thought were not working. We could call the 1990s the expansion phase. As it is common with many other “inventions”, there was an early phase of enthusiasm, which lasted several years, when endoscopy was used almost for everything, if one was allowed to exaggerate. This expansion was couple by development of the technological armamentarium, which goes hand-in-hand with improvement of surgical techniques and results. During that phase the International Study Group for Neuroendoscopy (ISGNE) was born. I feel that now we are entering a phase of consolidation, marked by the transformation of ISGNE to the International Federa-tion of Neuroendoscopy. We have crystallised indications and mapped out success. This does not mean that endoscopy will not expand any longer, in the contrary. But expansion will follow a mature course, as it will not meander aimless in futureless avenues. In these important crossroads comes the 5th Word Congress of Neuroendoscopy, which I have the privilege and honour to organise.

In the timeless setting of Athens, a city with rich past and vibrant present, in the birth country of modern Medicine and the Western Civilisation, and the luxurious surroundings of a historic hotel in the centre of town, we will have the op-portunity to exchange ideas, but also meet old friends and make new ones. A balanced blend of science and social in-teraction will give us the opportunity to map the future of Neuroendoscopy in the new millennium. There is something for everybody: pre-Congress cadaveric workshop for colleagues who want to improve their skills, scientific sessions for those who have something to say and those who want to hear them, and a social programme in timeless venues. And af-ter the Congress, everyone can enjoy the summer weather in the coastal region of Athens or one of the many wonderful islands nearby.

I hope you will all enjoy the Congress

Yours Sincerely,

Spyridon Sgouros, M.D., FRCS (SN)Congress PresidentDepartment of Neurosurgery at the University of Athens and Department at “Attikon” University Hospital


IFNE Executive Board 2007-2009

Honorary President: Bernhard BauerPresident: Shizuo OiVice-President and ISGNE Chairman: Shlomi ConstantiniSecretary: Spyridon SgourosTreasurer: Dieter HellwigEducation: Tai-Tong WongScientific: Giuseppe CinalliLiaison: Benjamin Warf

Guidelines & Ethics: Chandrashaker DeopujariAudit: Henry SchroederChairmen of 4th World Congress of ISGNE2007: Philippe Decq and Paolo Cappabianca5th World Congress of IFNE 2009 Congress President: Spyridon SgourosRegional & Continental Registration Committee [RCRC]: Mahmood Qureshi, Andre Grotenhuis

Representative of ISPN: Ezzio Di RoccoRepresentative of GLEN: Carlos de AlencastroRepresentative of Italian SN: Giuseppe CinalliRepresentative of Japan JSHCSF: Takayuki Inagaki AFRICA:Algeria　Country Representative. KA Bouyucef 　Members Iguertsira, SI Saber, Sidi Maamar MokhbatMorocco　Country Representaive. Abdslam Ouahabi Egypt　Country Representative Mohamed El Fiki　Member Omar HammadGhana　Country Representative Nii Andrews Nigeria　Country Representative Tayo ShokunbiEthiopia　Country Representative Gadlie T Zenebe　Members Gabriel Lende Tadios MunieKenya　Country Representative D Oluoch-Olunya　Members. Mahmood Qureshi PK Wanyoike, PG Mwangi, J Kiboi J Boore, K Koech Uganda　Country Representative J Mugamba　Members J Kiryabirwe, M Muhumuza H Ssenyongo, JB Mukasa D Kitya Tanzania　Country Representative J Kahamba 　Members A Kinasha, M Shabaan Rwanda　Country Representative Severien Muneza 　Member E Nkusi

Zambia　Country Representative Latson Chikoya

EUROPE:Bulgaria　Country Representative Yavor Enchev Spain　Country Representative Jose Piquer Belloch 　Member Pedro RiesgoEngland　Country Representative Silvia Gatscher

ASIA:India　Country Representative S Venkatesh　Member Chandrashekar Deopujari Saudip ChatterjeeSaudi Arabia　Country Representative Ahmed Ammar

LATIN AMERICA:Dr. Luiz Carlos de Alencastro　Presidente　Latin American Group of Neuroendoscopy 　Sociedade Brasileira de Neurocirurgia Dr. Samuel Zymberg　Secretary 　Latin American Group of Neuroendoscopy 　Sociedade Brasileira de Neurocirurgia Dr. Guillermo Molina Fernandez　President　III Latin American Congress of Neuroendoscopy　　　Rua Ramiro Barcelos, 910 conj 703　　　Porto Alegre - 90035 001 - Brazil　　　Fone: +55 51 99841529 / 81826130　　　E-mail: [email protected]

IFNE certified Societies / Study Groups and the Representatives [proved by RCRC]


5th World Congress of the International Federation of NeuroendoscopyIFNE 　　　　　　　　　　　　　Athens, Greece, 30 May-3 June 2009

Congress Organizing Bureau

Erasmus Conferences Tours & Travel S.A.

1 Kolofontos & Evridikis str., 161 21 Athens, Greece

Tel.: +30.210.7257693 - Fax: +30.210.7257532

Email: [email protected] - Website: www.erasmus.gr

IFNE President: Shizuo Oi

Congress President: Spyros Sgouros

IFNE Scienti�c Programme: Giuseppe Cinalli

www.ifneuroendoscopy.org

International Federation for Neuroendoscopy

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