Progressive posthämorrhagische Ventrikelerweiterung des Frühgeborenen Inzidenz, Prognose und Therapie

Background. 35% of preterm infants with intraventricular hemorrhage develop ventricular dilatation. The posthemorrhagic ventricular dilatation can persist, be transient or be progressive. Finally 1–2% of all very low birthweight (VLBW <1500 g) infants require shunt placement for the treatment of the posthemorrhagic hydrocephalus. Outcome. The neurodevelopmental outcome is extremely poor in children surviving progressive posthemorrhagic ventricular dilatation. Therapy. There are no uniform guidelines for the treatment of preterm infants with progressive posthemorrhagic ventricular dilatation. Randomised multicenter trials demonstrated, that inhibition of cerebrospinal fluid production with acetazolamide and furosemide or early cerebrospinal fluid tapping did not reduce the need for shunt placement and may worsen the outcome or can be associated with adverse side-effects. Preterm infants with posthemorrhagic ventricular dilatation should be treated by standard therapy with uniform guidelines for cerebrospinal fluid tapping and shunt placement.     

Phase I study of intraventricular recombinant tissue plasminogen activator for treatment of posthaemorrhagic hydrocephalus.

AIM: Phase I study to evaluate intraventricular fibrinolytic treatment with recombinant tissue plasminogen activator (tPA) as a method of clearing blood from the cerebrospinal fluid, and thus preventing permanent hydrocephalus. METHODS: Twenty two preterm infants, aged 7 to 26 days, with progressive posthaemorrhagic ventricular dilatation (ventricular width > 4 mm over 97th centile) received one to five intraventricular bolus injections of 1.0 mg or 0.5 mg tPA at intervals of one to seven days. RESULTS: The mean cerebrospinal fluid concentration of tPA 24 hours after 1 mg was 1860 micrograms/ml. The half life of tPA in cerebrospinal fluid was about 24 hours. Twenty one (95%) infants survived, 12 (55%) without shunt surgery. One infant had secondary intraventricular haemorrhage. CONCLUSION: Intraventricular tPA resulted in survival without a shunt for most of the infants, but with some risk. Failure may have been due to plasminogen deficiency, an inhibitor, or late intervention.     

Management of posthaemorrhagic ventricular dilatation

Intraventricular haemorrhage and posthaemorrhagic ventricular dilatation remain an important challenge in the management of prematurity and are associated with significant permanent morbidity. Progressive ventricular dilatation causes white matter injury by pressure, distortion, free radical injury and inflammation. Therapeutic interventions include serial lumbar punctures, only useful when the ventricles remain in communication with the lumbar subarachnoid space, and repeated aspiration through a ventricular access device. Reduction of cerebrospinal fluid production by acetazolamide and frusemide in a large multicentre randomised trial showed a worse outcome in the treated arm. A trial of drainage, irrigation and fibrinolytic therapy did not demonstrate a reduced need for permanent cerebrospinal fluid diversion, but did show a significant reduction in severe cognitive disability at two years. Ventriculoperitoneal shunting is indicated when the ventricles continue to enlarge at a body weight of around 2.5 kg and cerebrospinal fluid protein levels are below 1.5 g /L. This review summarises current concepts on the pathophysiology and management of posthaemorrhagic ventricular dilatation, underlining clinical challenges and ongoing research. Although the percentage of small preterm infants developing intraventricular haemorrhage (IVH) has been greatly reduced in the last three decades, increased survival of very immature infants has meant that large IVH with subsequent posthaemorrhagic ventricular dilatation is still a serious unsolved problem.     

Soluble Fas (CD95/Apo-1), soluble Fas ligand,and activated caspase 3 in the cerebrospinal fluid of infants with posthemorrhagic and nonhemorrhagic hydrocephalus

Hydrocephalus may result in loss of tissue associated with neuronal degeneration, axonal damage, and reactive gliosis. The soluble form of the anti-apoptotic regulator Fas (sFas) and the pro-apoptotic factors soluble FasL (sFasL) and activated caspase 3 were studied in the cerebrospinal fluid of infants with hydrocephalus. Fifteen preterm infants with posthemorrhagic hydrocephalus undergoing serial reservoir puncture and seven term or near-term infants with nonhemorrhagic hydrocephalus and shunt surgery were included in the study. Twenty-four age-matched patients with lumbar puncture for the exclusion of meningitis served as controls. Elevated levels of sFas were observed in infants with posthemorrhagic hydrocephalus [median (range), 131 ng/mL (51-279 ng/mL)] and in nonhemorrhagic hydrocephalus [127 ng/mL (35-165 ng/mL)]. sFas concentrations were highest in a subgroup of eight patients with posthemorrhagic hydrocephalus developing periventricular leukomalacia [164 ng/mL (76-227 ng/mL)]. In contrast, in 24 control infants, sFas was low, in 15 cases below detection limit (0.5 ng/mL) and in nine cases, 24 ng/mL (20-43 ng/mL). sFasL and activated caspase 3 did not differ from control infants in all groups of patients. Increased intrathecal release of sFas in the cerebrospinal fluid of infants with hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilatation.     

Treatment of progressive posthemorrhagic hydrocephalus with temporary external ventricular drainage. Preliminary results

Peri-intraventricular hemorrhage (PIVH) is a major problem of preterm neonates: over 40% of infants with birth weight less than 1500 g have been found to experience this disorder. The posthemorrhagic hydrocephalus (PHH) is generally believed to occur secondary to obliterative posterior fossa arachnoiditis. Its management in critically ill premature infants with multiple medical problems has thus become quite significant. This paper reports the results of the placement of a temporary external ventricular drainage in three patients in whom progressive ventricular dilatation began within two weeks after severe neonatal PIVH. In all patients the hydrocephalus and increased intracranial pressure were controlled within three weeks of treatment. One infant died from other problems associated with his prematurity. Early demonstration of progressive ventricular dilatation by ultrasound and prompt external drainage has been found to be a safe initial method to treat PHH in preterm infants.     

Posthaemorrhagic ventricular dilatation: new mechanisms and new treatment

Post haemorrhagic ventricular dilatation is associated with a high rate of disability, multiple impairments and adverse effects of shunt surgery for hydrocephalus. Post haemorrhagic ventricular dilatation results initially from multiple small blood clots throughout the cerebrospinal fluid channels impeding circulation and re-absorption. Transforming growth factor β is released into the cerebrospinal fluid and there is evidence that this cytokine stimulates the laying down of extracellular matrix proteins which produce permanent obstruction to the cerebrospinal fluid pathways. Prolonged raised pressure, pro-inflammatory cytokines and free radical damage from iron may contribute to periventricular white matter damage and subsequent disability. Interventions such as early lumbar punctures, diuretic drugs to reduce cerebrospinal fluid production and intraventricular fibrinolytic therapy have been tested and, not only fail to prevent shunt dependence, death or disability, but have significant adverse effects. Surgical interventions such as subcutaneous reservoir, external drain, choroid plexus coagulation and third ventriculostomy have not been subject to controlled trial. Ventriculoperitoneal shunt is not feasible in the early phase after intraventricular haemorrhage but, despite the problems with blockages and infections, remains the only option for infants with excessive head expansion over periods of weeks. We have piloted drainage, irrigation and fibrinolytic therapy as a way of removing blood early enough to stop the progressive deposition of matrix proteins, permanent hydrocephalus and shunt dependence.     

Posthaemorrhagic ventricular dilatation: new mechanisms and new treatment

Post haemorrhagic ventricular dilatation is associated with a high rate of disability, multiple impairments and adverse effects of shunt surgery for hydrocephalus. Post haemorrhagic ventricular dilatation results initially from multiple small blood clots throughout the cerebrospinal fluid channels impeding circulation and re-absorption. Transforming growth factor beta is released into the cerebrospinal fluid and there is evidence that this cytokine stimulates the laying down of extracellular matrix proteins which produce permanent obstruction to the cerebrospinal fluid pathways. Prolonged raised pressure, pro-inflammatory cytokines and free radical damage from iron may contribute to periventricular white matter damage and subsequent disability. Interventions such as early lumbar punctures, diuretic drugs to reduce cerebrospinal fluid production and intraventricular fibrinolytic therapy have been tested and, not only fail to prevent shunt dependence, death or disability, but have significant adverse effects. Surgical interventions such as subcutaneous reservoir, external drain, choroid plexus coagulation and third ventriculostomy have not been subject to controlled trial. Ventriculoperitoneal shunt is not feasible in the early phase after intraventricular haemorrhage but, despite the problems with blockages and infections, remains the only option for infants with excessive head expansion over periods of weeks. We have piloted drainage, irrigation and fibrinolytic therapy as a way of removing blood early enough to stop the progressive deposition of matrix proteins, permanent hydrocephalus and shunt dependence.     

Ventricular volume in infantile hydrocephalus and its relationship to intracranial pressure and cerebrospinal fluid clearance before and after treatment. A preliminary study

The present study examines ventricular volume before and after shunting in 16 infants with hydrocephalus and mixed aetiology and relates this parameter to rates of cerebrospinal fluid clearance, intracranial pressure and outcome. Following treatment all patients showed reduction in intracranial pressure and amelioration of the clinical manifestations of hydrocephalus. Nevertheless, 4 patients showed persistence of marked ventriculomegaly, 4 had moderate ventricular enlargement, while 8 showed small or normal ventricles. Although the series was small there appeared to be a clear correlation between persistent ventriculomegaly, poor cerebrospinal fluid clearance and poor outcome despite reduction in intracranial pressure. The question is raised as to whether pressure-determined cerebrospinal fluid drainage provides optimum treatment of hydrocephalus in infants given the particular physical characteristics pertaining to the non-rigid cranium.     

新生儿脑室内出血致脑积水的储液囊埋植引流治疗15例报告

目的 脑室内出血后脑积水是新生儿严重的并发症,存活后往往伴有严重的神经系统后遗症,目前对脑室内出血后脑积水处理仍然相当棘手,没有统一的方案.用储液囊埋植引流治疗新侣生儿脑室出血后脑积水,就其疗效和安全性作一初步评价.方法 对2003年1月至2005年12月期间,相继入住我院的15例新生儿脑窜内出血Ⅲ度以上合并脑积水,且1周内脑室进行性扩大,头围每天增大>2 mm伴有颅内压增高症状患儿,进行储液囊埋植引流治疗.储液囊埋植后根据临床和头颅超声或头颅CT检查结果,决定脑脊液引流次数,间歇引流时间和引流量,并观察脑脊液中细胞数、蛋白质和葡萄糖浓度的变化及术中和术后的并发症.若储液囊引流无效,改行脑室-腹腔分流术.出院后临床随访1.5～3年.结果 15例患儿中早产儿11例,孕龄(31.5±0.5)周;足月儿4例,其中3例为维生素K缺乏性颅内出血.脑室出血Ⅲ级13例,Ⅳ级2例.脑室出血平均诊断日龄:早产儿(9±1)d,足月儿(22±7)d.埋植Ommaya囊时日龄:早产儿(18±1)d,足月儿(31±7)d.平均每例患儿脑脊液引流次数(21.5±4.6)次,每次引流量为(10.2±1.3)ml/kg.15例经储液囊脑脊液引流后30 d脑脊液中细胞计数和葡萄糖分别为(14±6)×106个/L、(2.2±0.2)mmol/L;引流后39 d蛋白质为(0.48±0.10)g/L.13例经储液囊脑脊液引流后在1～4周内头围增长速度每周<1 cm,病情改善,其中12例至12～18个月时脑室恢复正常大小,1例在36个月时仍有轻度扩大.2例储液囊脑脊液引流无效,其中1例转行脑室.腹腔分流术后好转,1例放弃治疗出院后3个月死亡.术中和术后病情稳定,1例术后16 d储液囊出现渗漏,并发颅内感染(感染发生率为1/15),加用抗菌素治疗痊愈.14例术后1.5～3年时间随访:11例生长发育正常;2例早产儿发生两下肢痉挛性脑瘫,其中1例合并弱视;1例足月儿有癫癎发作.结论 采用储液囊脑室埋植引流治疗新生儿重型脑室出血合并脑积水,初步显示疗效满意和比较安全,为进一步明确其疗效需前瞻性临床多中心随机对照试验.     

Transforming growth factor-beta1: a possible signal molecule for posthemorrhagic hydrocephalus?

Posthemorrhagic hydrocephalus remains a complication of preterm birth for which we lack a clear understanding and a curative therapy. Transforming growth factor beta (TGF-beta) is a cytokine that upregulates the production by fibroblasts of extracellular matrix proteins. We hypothesized that TGF-beta might be released into cerebrospinal fluid (CSF) after intraventricular hemorrhage and play a role in posthemorrhagic hydrocephalus. Total TGF-beta1 and TGF-beta2 were measured by immunoassay in CSF samples from 12 normal preterm infants, nine preterm infants with transient posthemorrhagic ventricular dilation, and 10 infants who subsequently developed permanent hydrocephalus. Five infants received intraventricular tissue plasminogen activator, and two infants were treated by drainage irrigation and fibrinolytic therapy. Median TGF-beta1 in normal CSF was 0.495 ng/mL. In infants with transient posthemorrhagic ventricular dilation, median initial CSF TGF-beta1 was 2.1 ng/mL. Infants who subsequently had permanent hydrocephalus had median initial CSF TGF-beta1, 9.7 ng/mL (differences between groups p < 0.01). Intraventricular recombinant tissue plasminogen activator was followed by a rise in CSF TGF-beta1 (p = 0.0007). Drainage irrigation and fibrinolytic therapy was followed by a fall in CSF TGF-beta1. TGF-beta2 was detected in CSF and showed similar trends, but the CSF concentration of TGF-beta1 was more than 20 times higher. These findings support the hypothesis that TGF-beta1 is released into CSF after intraventricular hemorrhage and may play an important part in hydrocephalus. The results help to explain the failure of intraventricular fibrinolytic therapy.     

Early prognosis of low birthweight infants treated for progressive posthaemorrhagic hydrocephalus.

Twelve low birthweight preterm infants were treated for progressive posthaemorrhagic hydrocephalus by ventriculoperitoneal diversion of cerebrospinal fluid. At a median postnatal age of 20 months, 6 were moderately or severely retarded. Convulsions in the first week of life were associated with a poorer prognosis and frequent taps to remove cerebrospinal fluid with a better outcome.     

Incidence of infections of ventricular reservoirs in the treatment of post-haemorrhagic ventricular dilatation: a retrospective study (1992-2003)

BACKGROUND: Since 1992, infants with progressive posthaemorrhagic ventricular dilatation (PHVD) have been treated in the Neonatal Intensive Care Unit, Wilhelmina Children's Hospital, Utrecht, The Netherlands, with a ventricular reservoir. OBJECTIVE: To retrospectively study the incidence of infection using this invasive procedure. METHODS: Between January 1992 and December 2003, 76 preterm infants were treated with a ventricular reservoir. Infants admitted during two subsequent periods were analysed: group 1 included infants admitted during 1992-7 (n = 26) and group 2 those admitted during 1998-2003 (n = 50). Clinical characteristics and number of reservoir punctures were evaluated. The incidence of complications over time was assessed, with a focus on the occurrence of infection of the reservoir. RESULTS: The number of punctures did not change during both periods. Infection was significantly less common during the second period (4% (2/50) v 19.2% (5/26), p = 0.029). CONCLUSION: The use of a ventricular reservoir is a safe treatment to ensure adequate removal of cerebrospinal fluid in preterm infants with PHVD. In experienced hands, the incidence of infection of the ventricular reservoir or major complications remains within acceptable limits.     

Intracranial pressure and cerebral blood flow velocity in preterm infants with posthaemorrhagic ventricular dilatation

AIM: To determine the volume of cerebrospinal fluid (CSF) that should be tapped in preterm infants with posthaemorrhagic ventricular dilatation as guided by intracranial pressure (ICP) and cerebral blood flow velocity (CBFV). METHODS: The total number of measurements was 106 in 22 infants. Birth weights ranged from 630 to 2050 g, gestational age from 24.5 to 30.3 weeks, and age at insertion from 12 to 67 days. A subcutaneous ventricular catheter reservoir for repetitive CSF drainage was placed when the diameter of a ventricle was > 4 mm above the 97th centile. A volume of 5 ml/kg body weight was removed twice daily. ICP and CBFV were determined before and after CSF tapping. RESULTS: If the ICP after tapping exceeded 7 cm H(2)O, tapping did not result in a significant improvement in CBFV. If the ICP before tapping was less than 6 cm H(2)O, tapping also had no effect on CBFV. Longitudinal studies in individual infants showed a slight correlation between ICP and CBFV. CONCLUSION: Volume of repetitive CSF drainage in preterm infants with posthaemorrhagic ventricular dilatation guided by ICP and CBFV may be a useful technique. An ICP of about 6 cm H(2)O is the cut off point for CSF drainage.     

Erhöhte Konzentrationen des excitotoxischen Neurotransmiters Glutamat im Liquor von Frühgeborenen mit progressiver posthämorrhagischer Ventrikelerweiterung

Objective. Glutamate mediated excitotoxicity is responsible for neuronal injury in a variety of pathologic conditions. As cerebrospinal fluid (CSF) reflects the composition of the extracellular fluid of the brain, CSF-glutamate concentrations were determined in preterm infants with posthemorrhagic ventricular dilatation. Patients and Methods. 16 premature infants at the gestational age of 23–32 weeks who developed progressive posthemorrhagic ventricular dilatation were investigated during the first six months of life. CSF was obtained on 39 occasions by lumbar (n=4) or ventricular (n=23) puncture and during treatment with external drainage (n=12). Results. In 13 CSF samples from 7 patients (44% of the examined preterms) glutamate was increased (>7,2 μM). Extremely high CSF glutamate concentrations of 126 and 77 μM were observed in one patient during ventriculitis and during an episode with excessive increased intracranial pressure (67 cm H₂O). No correlation could be demonstrated between glutamate in the CSF and increased intracranial pressure or parenchym lesions. Elevated concentrations of glutamate in the CSF were associated with increased CSF lactate. Conclusion. These data demonstrate the occurrence of increased CSF glutamate up to the excitotoxic range in preterm infants with progressive posthemorrhagic ventricular dilatation. Glutamate may be part of the final pathway leading to neuronal injury in these patients.     

Computer Assisted Tomography in Children

Sixty-two infants and children were examined during the first 12 months in which computer assisted tomography was available at the Sir Charles Gairdner Hospital, and our early local experience is presented.
All ten tumours were correctly diagnosed. Diagnostic features are discussed. Seventeen cases showed ventricular dilatation. The difficulties in assessment of marginal hydrocephalus and in differentiation of communicating from non-communicating hydrocephalus are outlined. Less commonly encountered lesions and their diagnostic features are enumerated.     

Post-haemorrhagic hydrocephalus in the preterm infant

This prospective study documents the incidence, clinical features and risk factors for post-haemorrhagic hydrocephalus (PHH) as well as the short-term outcome after serial CSF taps. Serial real-time ultrasound scans were performed on 220 infants: on all admissions less than or equal to 1250 g and on an additional 130 infants with birthweights greater than 1250 g with risk factors for intraventricular haemorrhage (IVH). Based on percentile charts of postnatal increase in ventricular size and head circumference growth rate, PHH was defined as ventricular dilatation greater than 95th centile associated with either a head circumference growth greater than 95th centile or with clinical features of raised intracranial pressure (ICP). Forty-eight (22%) infants were found to have IVH of whom 14 had intracerebral extension of IVH. Sixteen (40%) of 40 infants who survived the acute episode of IVH developed PHH. PHH occurred more commonly in those who survived severe birth asphyxia and/or intracerebral extension of IVH. Fifteen infants who developed clinical features of raised ICP were treated with serial CSF taps. This procedure was effective in a staged treatment for PHH in relieving clinical symptoms and deferring ventriculo-peritoneal (VP) shunting. Morbidity associated with serial CSF taps and VP shunting is minimal. A high red cell count and protein concentration in the CSF at diagnosis of PHH identified all five infants who subsequently required VP shunting.     

Post-haemorrhagic hydrocephalus in the preterm infant

Abstract This prospective study documents the incidence, clinical features and risk factors for post-haemorrhagic hydrocephalus (PHH) as well as the short-term outcome after serial CSF taps. Serial real-time ultrasound scans were performed on 220 infants: on all admissions ≤1250 g and on an additional 130 infants with birthweights >1250 g with risk factors for intraventricular haemorrhage (IVH). Based on percentile charts of postnatal increase in ventricular size and head circumference growth rate, PHH was defined as ventricular dilatation >95th centile associated with either a head circumference growth >95th centile or with clinical features of raised intracranial pressure (ICP). Forty-eight (22%) infants were found to have IVH of whom 14 had intracerebral extension of IVH. Sixteen (40%) of 40 infants who survived the acute episode of IVH developed PHH. PHH occurred more commonly in those who survived severe birth asphyxia and/or intracerebral extension of IVH. Fifteen infants who developed clinical features of raised ICP were treated with serial CSF taps. This procedure was effective in a staged treatment for PHH in relieving clinical symptoms and deferring ventriculo-peritoneal (VP) shunting. Morbidity associated with serial CSF taps and VP shunting is minimal. A high red cell count and protein concentration in the CSF at diagnosis of PHH identified all five infants who subsequently required VP shunting.     

Cerebrospinal fluid concentrations of atrial natriuretic peptide in children

Concentrations of atrial natriuretic peptide (ANP) in plasma and in cerebrospinal fluid (CSF) were measured in preterm neonates, in infants and in children with hydrocephalus. Plasma ANP in preterm neonates were elevated compared to infants and children with hydrocephalus. CSF-ANP in all groups were lower than plasma levels. ANP concentrations in the liquor exhibited higher values in children with hydrocephalus. No correlation was found between plasma and CSF-ANP levels while CSF-pressure and ANP concentration in the liquor correlated positively. Our data provide evidence for the existence of a cerebral ANP system in humans. The CSF-ANP system seems to be independent from the systemic, atrial ANP. CSF-ANP may be of great importance in the regulation of water and ion content of central nervous system and probably liquor formation.     

Accumulation of transforming growth factor-beta2 and nitrated chondroitin sulfate proteoglycans in cerebrospinal fluid correlates with poor neurologic outcome in preterm hydrocephalus

BACKGROUND: Progressive post-hemorrhagic hydrocephalus in preterm infants strongly predicts abnormal neurologic development, and often accompanies cystic periventricular leukomalacia (cPVL). Transforming growth factor-beta1 (TGF-beta1), associated with hydrocephalus, can upregulate the chondroitin sulfate proteoglycan (CSPG) synthesis. To date, CSPG and their nitrated metabolites (NT-CSPG) have not been evaluated in hydrocephalus. OBJECTIVES: We hypothesized that TGF-beta1, TGF-beta2, CSPG, and NT-CSPG would accumulate in cerebrospinal fluid (CSF) in preterm hydrocephalus, and their concentrations would correlate with poor long-term outcomes. METHODS: TGF-beta1, TGF-beta2, CSPG, and NT-CSPG concentrations in CSF were measured prospectively by ELISA in 29 preterm newborns with (n=22) or without (n=34) progressive post-hemorrhagic hydrocephalus, and correlated with progressive neonatal hydrocephalus and neurologic outcome. Only concentrations from each patient's initial CSF sample were used for statistical analysis. RESULTS: Compared to neonates without hydrocephalus, CSF [TGF-beta1], [TGF-beta2], [CSPG] and [NT-CSPG] were significantly greater by >3-, >35-, >8-, and >3-fold, respectively. Unlike CSF [TGF-beta2] and [CSPG], [TGF-beta1] correlated with CSF [total protein]. Only CSF [NT-CSPG] correlated with cPVL. Unlike [TGF-beta2] or [CSPG], [NT-CSPG] correlation with preterm progressive post-hemorrhagic hydrocephalus (PPHH) was explained entirely by the presence of cPVL among these patients. [TGF-beta2] was >20-fold greater in preterm survivors who required a ventriculoperitoneal shunt for PPHH (n=9), as compared to survivors who did not require a shunt (n=2), or those without hydrocephalus (n=12). [TGF-beta2] and [NT-CSPG] correlated inversely with Bayley Index Scores (15.0 months median adjusted age). CONCLUSIONS: This is the first report that [TGF-beta2], [CSPG], and [NT-CSPG], measured well before term, accumulate abnormally in preterm progressive post-hemorrhagic hydrocephalus CSF, and correlate with adverse neurologic outcome.     

Intraventricular neurocysticercus cyst(s) in Indian children

Eleven cases of intraventricular neurocysticercosis were managed over a 10-year period. All patients presented with features of hydrocephalus. In 9 cases the cysts were blocking the cerebrospinal fluid (CSF) pathway resulting in hydrocephalus. The 4 cases of lateral ventricular cyst had communicating hydrocephalus, while 2 of these had asymmetrical ventriculomegaly. Two of 4 cases had more than one cyst. One of 4 children with lateral ventricular cyst had narrowing of the foramen of Monro causing asymmetrical hydrocephalus. Following cyst removal, CSF diversion was not required in 6 cases, while 5 required CSF diversion despite removal of their cysts in 4 of 5. One patient had a cyst at the aqueductal inlet and he was managed by shunt and albendazole therapy. Thus, we managed 6 of our cases with excision of the cysts obstructing the CSF pathway, and in 4 cases excision of cysts with ventriculoperitoneal shunt was adequate.