Recurrent Headaches in a Child with Tuberculous Meningitis: Unmasking Slit Ventricle Syndrome

Recurrent Headaches in a Child with Tuberculous Meningitis: Unmasking Slit Ventricle Syndrome | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Recurrent Headaches in a Child with Tuberculous Meningitis: Unmasking Slit Ventricle Syndrome Yiyuan Li, YU Zhu, Qin Guo This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5395813/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Slit ventricle syndrome (SVS) is a severe and potentially life-threatening complication associated with chronic overdrainage of cerebrospinal fluid. However, its clinical manifestations and imaging characteristics are often overlooked due to insufficient awareness among clinicians.. Case Presentation We report the case of a pediatric patient diagnosed with tuberculous meningitis, who received standard anti-tuberculosis treatment and underwent ventriculoperitoneal shunting for hydrocephalus. Four years after completing treatment, the patient presented with recurrent headaches, which were eventually diagnosed as SVS. The patient's condition improved following an upward adjustment of the shunt valve pressure. Conclusion This case highlights the critical need for heightened awareness of SVS among pediatric specialists. Early recognition and timely intervention are crucial for optimizing clinical outcomes in patients with a history of shunt surgery and hydrocephalus. Slit ventricle syndrome Children Tuberculous Meningitis Figures Figure 1 Background Tuberculous meningitis (TBM) is associated with high mortality and morbidity rates, particularly in young children [ 1 ]. The clinical presentation of TBM typically includes symptoms such as headache, fever, vomiting, irritability, signs of meningeal irritation, and elevated intracranial pressure (ICP) [ 2 ]. In pediatric patients with TBM who undergo ventriculoperitoneal shunting (VPS) for hydrocephalus, recurrent headaches may indicate the presence of a less commonly recognized complication knows as slit ventricle syndrome (SVS). SVS is a severe and potentially life-threatening complication associated with chronic overdrainage of cerebrospinal fluid (CSF),which can lead to ventricular collapse, and a characteristic slit-like appearance on imaging [ 3 ]. SVS is clinically characterized by a triad of intermittent headaches, delayed filling of the shunt reservoir, and radiological evidence of slit-like ventricles [ 3 ]. A significant barrier to the timely diagnosis and effective management of SVS is the lack of awareness among clinicians regarding its clinical manifestations and imaging features. In this report, we present a pediatric patient with TBM who received standard anti-tuberculosis treatment and VPS for hydrocephalus. Four years after completing treatments, the patient developed recurrent headaches, which were ultimately diagnosed as SVS. This case underscores the critical need to enhance awareness of SVS among pediatric specialists, enabling earlier diagnosis and timely intervention, thereby improving clinical outcomes. Case Presentation An 11-year-old male patient was admitted with a five-day history of fever, cough, and vomiting, accompanied by a three-day history of somnolence. The fever occurred three times daily, with peak temperatures reaching 39°C, and accompanied by chills, rigors, lethargy, and decreased appetite. The patient also experienced intermittent cough, bilateral eye pain, headache, and ,postprandial non-projectile vomiting. Three days prior to admission, he progressively developed somnolence, gait instability, worsening cough, and urinary and fecal incontinence. At a local hospital, a cranial computed tomography (CT) scan revealed heterogeneous density in the soft tissues of the right frontal and parietal regions, along with several small nodular hyperdense lesions within the intracranial space. The patient received one day of intravenous therapy, but the conditions did not ameliorate. The patient had not received the Bacillus Calmette-Guérin vaccine. Five years prior, he was diagnosed with TBM and pulmonary tuberculosis, presenting with lethargy, fever, cough, and altered consciousness. He underwent one year of anti-tuberculosis treatment and subsequently had a VPS for hydrocephalus management. The initial two-month intensive phase of treatment consisted of isoniazid, rifampin, ethambutol (which was replaced by levofloxacin on day seventeen due to abnormal visual evoked potentials), and pyrazinamide. This was followed by a ten-month continuation phase with isoniazid and rifampin. Over the past two years, the patient experienced intermittent headaches and vomiting. His two maternal uncles had a history of tuberculosis. The remaining personal, family, and medical history were unremarkable. Physical examinations were performed and documented. The patient presented with a body temperature of 36.5°C, a heart rate of 55 beats per minute, a respiratory rate of 12 breaths per minute, and a blood pressure of 122 over 77 millimeter of mercury. The patient's weight was recorded at 30.3 kilograms. He appeared somnolent and displayed signs of emaciation. The Glasgow Coma Scale score was 12, with an eye-opening response of 2, a verbal response of 4, and a motor response of 6. The patient responded appropriately to stimuli. A palpable drainage tube was noted beneath the skin at the right parietal region of the scalp, and a five-centimeter surgical scar was observed in the right lower abdominal quadrant. Although the patient was unable to stand independently, he could maintain stability with support. Neurological examination revealed positive neck stiffness and bilateral Babinski signs while the remainder of the neurological examination was unremarkable. Auxiliary investigations revealed that routine blood cell counts and C-reactive protein levels were within normal limits. The nucleic acid test for Influenza A virus returned positive. Cerebrospinal fluid (CSF) analysis demonstrated elevated ICP exceeding 250 mmH₂O, a negative protein qualitative test, a nucleated cell count of 0, a chloride level of 117.3 mmol/L, and a glucose level of 3.71 mmol/L, and negative results for pathogen culture. Routine electroencephalogram findings were characterized by slowed background rhythm. A chest CT revealed a calcified nodule in the posterior-basal segment of the left lower lobe, accompanied by calcified lymph nodes in the mediastinum. An abdominal CT demonstrated a catheter positioned within the abdominal and pelvic cavities, as well as a small volume of pelvic fluid. Compared to an abdominal CT conducted three years prior, no significant changes were observed. Cranial magnetic resonance imaging (MRI) showed abnormal strip-like signals in the left basal ganglia, left insular cortex, and left temporal horn, with evidence of encephalomalacia and gliosis. The left lateral ventricle appeared pulled and dilated (Fig. 1 ). The patient was diagnosed with a disturbance of consciousness, with intracranial hypertension syndrome and intracranial infection considered as possible underlying causes. Additionally, the diagnoses inlcuded severe influenza A, acute bronchitis, ventriculoperitoneal shunt, and growth retardation. The patient received antiviral treatment with peramivir, along with intracranial pressure reduction therapy using mannitol and glycerol fructose. These interventions temporarily alleviated the patient's headache and somnolence. After ruling out cerebrospinal fluid drainage obstruction and influenza-associated encephalopathy, the shunt valve was adjusted to reduce pressure and facilitate drainage in an effort to lower intracranial pressure. However, somnolence and headache persisted, and the patient’s condition worsened, leading to severe headache, increased somnolence, and vomiting. Pupillary asymmetry developed, with the right pupil measuring approximately 4 millimeters and the left pupil 3 millimeters, both exhibiting sluggish light reflexes. Aggressive intracranial pressure-lowering interventions provided only temporary relief. Interdisciplinary consultations between pediatric infectious disease and neurosurgical teams considered SVS. The shunt valve pressure was subsequently adjusted upward, resulting in successful alleviation of the patients’s headache, somnolence, and vomiting. The patient gradually regained independent ambulation and was discharged in satisfactory condition. Discussion and Conclusions The patient presented with fever, vomiting, and altered consciousness, accompanied by ocular pain, headache, and somnolence. Bradycardia was noted, along with positive signs of neck stiffness and bilateral Babinski reflexes, as well as elevated CSF pressure, all indicative of intracranial hypertension. Initially, an intracranial infection or infection-related encephalopathy was suspected. However, CSF analysis was unremarkable, failing to support a bacterial etiology. Additionally, cranial MRI, along with chest and abdominal CT scans, revealed no progression of tuberculosis lesions, making a relapse of tuberculous meningitis unlikely. The possibility of influenza-associated encephalopathy was also considered. However, the cranial MRI findings typically associated with this condition are characterized by multiple symmetric lesions primarily affecting the thalamus, midbrain, pons, and brainstem, which were absent in this patient[ 4 ]. The patient was neither immunocompromised nor undergoing immunosuppressive therapy, reducing the likelihood of a fungal intracranial infection. The patient had a history of VPS placement for TBM and hydrocephalus, but shunt obstruction as a cause of intracranial hypertension was ruled out based on cranial MRI and chest/abdominal CT findings. Despite adjustments to the shunt valve pressure to enhance drainage, the patient's clinical symptoms persisted. After extensive multidisciplinary discussions involving infectious disease and neurosurgery teams, SVS was considered. Increasing the shunt valve pressure subsequently led to a gradual improvement in the patient’s clinical symptoms and signs. SVS is a complication that can occur in pediatric patients following shunt surgery. It is characterized by chronic over-drainage of CSF, leading to ventricular narrowing with slit-like ventricles visible on imaging. SVS typically manifests months to years after the initial shunt procedure, with an average onset of approximately 6.5 years postoperatively [ 5 ]. The primary symptom, a posture-dependent headache, often termed "spinal headache," which may be accompanied by neck or upper back pain, nausea, vomiting, dizziness, fatigue, irritability, gait disturbances, diplopia, seizures, and lethargy[ 3 , 6 , 7 ]. Radiological findings on CT scans typically reveal slit-like alterations in the lateral ventricles, as well as abnormal thickening of the cranial bones [ 8 ], The pathophysiological mechanisms underlying SVS remain incompletely understood and ar e thought to be multifactorial. A primary pathological basis involves siphoning effects that lead to excessive CSF drainage and hemodynamic alterations within the CSF venous system[ 9 ]. Excessive CSF drainage from the cranial cavity disrupts the cranial-to-brain ratio, resulting in morphological changes in the ventricles, where ventricular walls may collapse and occlude the internal shunt catheter. Additionally, the siphoning effected of the shunt promotes chronic over-drainage of CSF, reducing ventricular size. This reduction ca n lead to functional obstruction of the ventricular end of the shunt catheter, presenting symptoms of intracranial hypertension [ 3 ]. In the early stages, slight ventricular expansion may temporarily restore shunt function and alleviate obstruction, providing transient relief from intracranial hypertension. However, ongoing over-drainage and abnormal fluctuations in intracranial pressure contribute to the formation of scar tissue in the periventricular white matter, diminishing ventricular compliance and heightens the patient’s sensitivity to changes in intracranial pressure. This can result in chronic, intermittent headaches and vomiting, potentially accompanied by other neurological signs, such as seizures, papilledema, vision loss, and cognitive decline[ 3 , 10 ]. SVS is a complex complication that may arise following shunt surgery. Treatment options include pharmacological therapy, shunt valve pressure adjustment, and surgical intervention. Postural therapy, such as bed rest, may help reduce drainage volume and siphoning pressure, and in some cases, increasing the shunt valve pressure may be beneficial [ 11 ]. Diuretics such as furosemide, mannitol, dexamethasone, and anti-migraine medications may provide symptomatic relief. However, they do not address the underlying issue of cerebrospinal fluid drainage obstruction. Surgical intervention is indicated when conservative treatments prove ineffective or when complications such as subdural effusion, microcephaly, Chiari malformation, or isolated ventricles arised, particularly if symptoms significantly impacted the patient’s quality of life [ 11 ]. Various surgical approaches were available, including the replacement with an adjustable anti-siphon shunt, re-establishment of a ventriculoperitoneal shunt, or placement of a lumbar cistern-peritoneal shunt. The specific technique is chosen based on the patient’s clinical status and individual needs. In patients experiencing intracranial hypertension following shunt surgery, the presence of slit-like ventricles on CT imaging, rather than ventricular enlargement, suggests a possible diagnosis of SVS. In cases where intracranial pressure is significantly elevated and unresponsive to pharmacological treatment, timely surgical intervention is essential to restore an effective cerebrospinal fluid circulation pathway. Abbreviations TBM Tuberculous meningitis ICP intracranial pressure VPS ventriculoperitoneal shunting SVS slit ventricle syndrome CSF cerebrospinal fluid CT tomography MRI magnetic resonance imaging Declarations Ethics approval and consent to participate Publication of this case report followed the regulations of the Ethical Board of the West China Second Hospital and was conducted according to the latest version of the Helsinki Declaration. Written informed consent for publication was obtained from the patient's guardian. All identifiable patient information was omitted during the manuscript's initial development. Thank the patient and her family for allowing us to develop this manuscript. Clinical trial number Not applicable Consent for publication Written informed consent was obtained from the patient's legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal Availability of data All data generated or analyzed during this study are included in this published article. The datasets used and/or analyzed during the current study available from the corresponding author on reasonable request Competing interests The authors declare that they have no competing interests. Funding This study was financially supported by no funding. Author contribution YL collect the data and write the manuscript; YL and QG revise the manuscript; YL and YZ performed literature review. All authors have reviewed the final manuscript. Acknowledgments Not applicable. References Thwaites GE, van Toorn R, Schoeman J: Tuberculous meningitis: more questions, still too few answers . Lancet Neurol 2013, 12 (10):999-1010. Chatterjee S: Brain tuberculomas, tubercular meningitis, and post-tubercular hydrocephalus in children . J Pediatr Neurosci 2011, 6 (Suppl 1):S96-S100. Ros B, Iglesias S, Martin A, Carrasco A, Ibanez G, Arraez MA: Shunt overdrainage syndrome: review of the literature . Neurosurg Rev 2018, 41 (4):969-981. Dadak M, Pul R, Lanfermann H, Hartmann H, Hehr U, Donnerstag F, Michels D, Tryc AB: Varying Patterns of CNS Imaging in Influenza A Encephalopathy in Childhood . Clin Neuroradiol 2020, 30 (2):243-249. Hanak BW, Bonow RH, Harris CA, Browd SR: Cerebrospinal Fluid Shunting Complications in Children . Pediatr Neurosurg 2017, 52 (6):381-400. Hart MG, Czosnyka M, Czosnyka ZH, Fernandes HM: Combined intracranial pressure monitoring and cerebrospinal fluid infusion study to guide management of slit ventricle syndrome . Pediatr Neurosurg 2013, 49 (2):113-118. Schuhmann MU, Sood S, McAllister JP, Jaeger M, Ham SD, Czosnyka Z, Czosnyka M: Value of overnight monitoring of intracranial pressure in hydrocephalic children . Pediatr Neurosurg 2008, 44 (4):269-279. Chernov MF, Kamikawa S, Yamane F, Ishihara S, Hori T: Neurofiberscope-guided management of slit-ventricle syndrome due to shunt placement . J Neurosurg 2005, 102 (3 Suppl):260-267. Sainz LV, Hockel K, Schuhmann MU: Chronic overdrainage syndrome: pathophysiological insights based on ICP analysis: a case-based review . Childs Nerv Syst 2018, 34 (3):401-408. Kraemer MR, Sandoval-Garcia C, Bragg T, Iskandar BJ: Shunt-dependent hydrocephalus: management style among members of the American Society of Pediatric Neurosurgeons . J Neurosurg Pediatr 2017, 20 (3):216-224. Agarwal N, Shukla RM, Agarwal D, Gupta K, Luthra R, Gupta J, Jain S: Pediatric Ventriculoperitoneal Shunts and their Complications: An Analysis . J Indian Assoc Pediatr Surg 2017, 22 (3):155-157. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-5395813","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":381336747,"identity":"c2f108af-d2c8-434e-be83-0dd9c6af73a9","order_by":0,"name":"Yiyuan Li","email":"","orcid":"","institution":"West China Second University Hospital of Sichuan University","correspondingAuthor":false,"prefix":"","firstName":"Yiyuan","middleName":"","lastName":"Li","suffix":""},{"id":381336749,"identity":"096b159d-c6db-47ac-bd2d-a7d8f25939e0","order_by":1,"name":"YU Zhu","email":"","orcid":"","institution":"West China Second University Hospital of Sichuan University","correspondingAuthor":false,"prefix":"","firstName":"YU","middleName":"","lastName":"Zhu","suffix":""},{"id":381336755,"identity":"82fa52b0-f9c0-41fb-884a-f3045557f27b","order_by":2,"name":"Qin Guo","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAzklEQVRIiWNgGAWjYDACZhBhICHHz97Y+OAD8VoKLIwlew43G84g3qoPFYkbbqS3SXMQo5jvOO8Bxi8GEowNNx82SDMw2MnpNhDQInmYL4FZxkCCmXF2YoNxAUOysdkBAloMDvMYMEsYSLAxSyc2JM9gOJC4jVgtPGySBxsO8xCrhfGDgYQEjwRjYzNRWiRBtgDjBWhPYjPjDAMi/MJ3/owB448/dfX7jx9//uNDhZ0cQS0MBxjYf/Mg3ElIOUQLA+MPYhSOglEwCkbByAUAhGQ+lOR9K1MAAAAASUVORK5CYII=","orcid":"","institution":"West China Second University Hospital of Sichuan University","correspondingAuthor":true,"prefix":"","firstName":"Qin","middleName":"","lastName":"Guo","suffix":""}],"badges":[],"createdAt":"2024-11-05 13:38:28","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-5395813/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-5395813/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":71633457,"identity":"29de5c51-d711-45a3-8481-f4a30d3af18d","added_by":"auto","created_at":"2024-12-17 09:52:29","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":169628,"visible":true,"origin":"","legend":"\u003cp\u003eCranial MRI showed strip-like abnormal signals in the left basal ganglia and left insular cortex, accompanied by encephalomalacia with gliosis, as well as traction and dilation of the left lateral ventricle.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-5395813/v1/13f25209650898715f58eaa3.png"},{"id":77660415,"identity":"d1416853-43c1-46de-bd9c-3ff43fd0d2d5","added_by":"auto","created_at":"2025-03-04 04:31:50","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":908909,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-5395813/v1/b059488f-a4a6-414a-8249-f5718049e4f4.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Recurrent Headaches in a Child with Tuberculous Meningitis: Unmasking Slit Ventricle Syndrome","fulltext":[{"header":"Background","content":"\u003cp\u003eTuberculous meningitis (TBM) is associated with high mortality and morbidity rates, particularly in young children [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. The clinical presentation of TBM typically includes symptoms such as headache, fever, vomiting, irritability, signs of meningeal irritation, and elevated intracranial pressure (ICP) [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. In pediatric patients with TBM who undergo ventriculoperitoneal shunting (VPS) for hydrocephalus, recurrent headaches may indicate the presence of a less commonly recognized complication knows as slit ventricle syndrome (SVS).\u003c/p\u003e \u003cp\u003eSVS is a severe and potentially life-threatening complication associated with chronic overdrainage of cerebrospinal fluid (CSF),which can lead to ventricular collapse, and a characteristic slit-like appearance on imaging [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. SVS is clinically characterized by a triad of intermittent headaches, delayed filling of the shunt reservoir, and radiological evidence of slit-like ventricles [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. A significant barrier to the timely diagnosis and effective management of SVS is the lack of awareness among clinicians regarding its clinical manifestations and imaging features.\u003c/p\u003e \u003cp\u003eIn this report, we present a pediatric patient with TBM who received standard anti-tuberculosis treatment and VPS for hydrocephalus. Four years after completing treatments, the patient developed recurrent headaches, which were ultimately diagnosed as SVS. This case underscores the critical need to enhance awareness of SVS among pediatric specialists, enabling earlier diagnosis and timely intervention, thereby improving clinical outcomes.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eAn 11-year-old male patient was admitted with a five-day history of fever, cough, and vomiting, accompanied by a three-day history of somnolence. The fever occurred three times daily, with peak temperatures reaching 39\u0026deg;C, and accompanied by chills, rigors, lethargy, and decreased appetite. The patient also experienced intermittent cough, bilateral eye pain, headache, and ,postprandial non-projectile vomiting. Three days prior to admission, he progressively developed somnolence, gait instability, worsening cough, and urinary and fecal incontinence. At a local hospital, a cranial computed tomography (CT) scan revealed heterogeneous density in the soft tissues of the right frontal and parietal regions, along with several small nodular hyperdense lesions within the intracranial space. The patient received one day of intravenous therapy, but the conditions did not ameliorate.\u003c/p\u003e \u003cp\u003eThe patient had not received the Bacillus Calmette-Gu\u0026eacute;rin vaccine. Five years prior, he was diagnosed with TBM and pulmonary tuberculosis, presenting with lethargy, fever, cough, and altered consciousness. He underwent one year of anti-tuberculosis treatment and subsequently had a VPS for hydrocephalus management. The initial two-month intensive phase of treatment consisted of isoniazid, rifampin, ethambutol (which was replaced by levofloxacin on day seventeen due to abnormal visual evoked potentials), and pyrazinamide. This was followed by a ten-month continuation phase with isoniazid and rifampin. Over the past two years, the patient experienced intermittent headaches and vomiting. His two maternal uncles had a history of tuberculosis. The remaining personal, family, and medical history were unremarkable.\u003c/p\u003e \u003cp\u003ePhysical examinations were performed and documented. The patient presented with a body temperature of 36.5\u0026deg;C, a heart rate of 55 beats per minute, a respiratory rate of 12 breaths per minute, and a blood pressure of 122 over 77 millimeter of mercury. The patient's weight was recorded at 30.3 kilograms. He appeared somnolent and displayed signs of emaciation. The Glasgow Coma Scale score was 12, with an eye-opening response of 2, a verbal response of 4, and a motor response of 6. The patient responded appropriately to stimuli. A palpable drainage tube was noted beneath the skin at the right parietal region of the scalp, and a five-centimeter surgical scar was observed in the right lower abdominal quadrant. Although the patient was unable to stand independently, he could maintain stability with support. Neurological examination revealed positive neck stiffness and bilateral Babinski signs while the remainder of the neurological examination was unremarkable.\u003c/p\u003e \u003cp\u003eAuxiliary investigations revealed that routine blood cell counts and C-reactive protein levels were within normal limits. The nucleic acid test for Influenza A virus returned positive. Cerebrospinal fluid (CSF) analysis demonstrated elevated ICP exceeding 250 mmH₂O, a negative protein qualitative test, a nucleated cell count of 0, a chloride level of 117.3 mmol/L, and a glucose level of 3.71 mmol/L, and negative results for pathogen culture. Routine electroencephalogram findings were characterized by slowed background rhythm. A chest CT revealed a calcified nodule in the posterior-basal segment of the left lower lobe, accompanied by calcified lymph nodes in the mediastinum. An abdominal CT demonstrated a catheter positioned within the abdominal and pelvic cavities, as well as a small volume of pelvic fluid. Compared to an abdominal CT conducted three years prior, no significant changes were observed. Cranial magnetic resonance imaging (MRI) showed abnormal strip-like signals in the left basal ganglia, left insular cortex, and left temporal horn, with evidence of encephalomalacia and gliosis. The left lateral ventricle appeared pulled and dilated (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThe patient was diagnosed with a disturbance of consciousness, with intracranial hypertension syndrome and intracranial infection considered as possible underlying causes. Additionally, the diagnoses inlcuded severe influenza A, acute bronchitis, ventriculoperitoneal shunt, and growth retardation.\u003c/p\u003e \u003cp\u003eThe patient received antiviral treatment with peramivir, along with intracranial pressure reduction therapy using mannitol and glycerol fructose. These interventions temporarily alleviated the patient's headache and somnolence. After ruling out cerebrospinal fluid drainage obstruction and influenza-associated encephalopathy, the shunt valve was adjusted to reduce pressure and facilitate drainage in an effort to lower intracranial pressure. However, somnolence and headache persisted, and the patient\u0026rsquo;s condition worsened, leading to severe headache, increased somnolence, and vomiting. Pupillary asymmetry developed, with the right pupil measuring approximately 4 millimeters and the left pupil 3 millimeters, both exhibiting sluggish light reflexes. Aggressive intracranial pressure-lowering interventions provided only temporary relief. Interdisciplinary consultations between pediatric infectious disease and neurosurgical teams considered SVS. The shunt valve pressure was subsequently adjusted upward, resulting in successful alleviation of the patients\u0026rsquo;s headache, somnolence, and vomiting. The patient gradually regained independent ambulation and was discharged in satisfactory condition.\u003c/p\u003e"},{"header":"Discussion and Conclusions","content":"\u003cp\u003eThe patient presented with fever, vomiting, and altered consciousness, accompanied by ocular pain, headache, and somnolence. Bradycardia was noted, along with positive signs of neck stiffness and bilateral Babinski reflexes, as well as elevated CSF pressure, all indicative of intracranial hypertension. Initially, an intracranial infection or infection-related encephalopathy was suspected. However, CSF analysis was unremarkable, failing to support a bacterial etiology. Additionally, cranial MRI, along with chest and abdominal CT scans, revealed no progression of tuberculosis lesions, making a relapse of tuberculous meningitis unlikely. The possibility of influenza-associated encephalopathy was also considered. However, the cranial MRI findings typically associated with this condition are characterized by multiple symmetric lesions primarily affecting the thalamus, midbrain, pons, and brainstem, which were absent in this patient[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. The patient was neither immunocompromised nor undergoing immunosuppressive therapy, reducing the likelihood of a fungal intracranial infection. The patient had a history of VPS placement for TBM and hydrocephalus, but shunt obstruction as a cause of intracranial hypertension was ruled out based on cranial MRI and chest/abdominal CT findings. Despite adjustments to the shunt valve pressure to enhance drainage, the patient's clinical symptoms persisted. After extensive multidisciplinary discussions involving infectious disease and neurosurgery teams, SVS was considered. Increasing the shunt valve pressure subsequently led to a gradual improvement in the patient\u0026rsquo;s clinical symptoms and signs.\u003c/p\u003e \u003cp\u003eSVS is a complication that can occur in pediatric patients following shunt surgery. It is characterized by chronic over-drainage of CSF, leading to ventricular narrowing with slit-like ventricles visible on imaging. SVS typically manifests months to years after the initial shunt procedure, with an average onset of approximately 6.5 years postoperatively [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. The primary symptom, a posture-dependent headache, often termed \"spinal headache,\" which may be accompanied by neck or upper back pain, nausea, vomiting, dizziness, fatigue, irritability, gait disturbances, diplopia, seizures, and lethargy[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Radiological findings on CT scans typically reveal slit-like alterations in the lateral ventricles, as well as abnormal thickening of the cranial bones [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e],\u003c/p\u003e \u003cp\u003eThe pathophysiological mechanisms underlying SVS remain incompletely understood and ar\u003cspan type=\"Underline\" class=\"Underline\" name=\"Emphasis\"\u003ee\u003c/span\u003e thought to be multifactorial. A primary pathological basis involves siphoning effects that lead to excessive CSF drainage and hemodynamic alterations within the CSF venous system[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Excessive CSF drainage from the cranial cavity disrupts the cranial-to-brain ratio, resulting in morphological changes in the ventricles, where ventricular walls may collapse and occlude the internal shunt catheter. Additionally, the siphoning effected of the shunt promotes chronic over-drainage of CSF, reducing ventricular size. This reduction ca\u003cspan type=\"Underline\" class=\"Underline\" name=\"Emphasis\"\u003en\u003c/span\u003e lead to functional obstruction of the ventricular end of the shunt catheter, presenting symptoms of intracranial hypertension [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. In the early stages, slight ventricular expansion may temporarily restore shunt function and alleviate obstruction, providing transient relief from intracranial hypertension. However, ongoing over-drainage and abnormal fluctuations in intracranial pressure contribute to the formation of scar tissue in the periventricular white matter, diminishing ventricular compliance and heightens the patient\u0026rsquo;s sensitivity to changes in intracranial pressure. This can result in chronic, intermittent headaches and vomiting, potentially accompanied by other neurological signs, such as seizures, papilledema, vision loss, and cognitive decline[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eSVS is a complex complication that may arise following shunt surgery. Treatment options include pharmacological therapy, shunt valve pressure adjustment, and surgical intervention. Postural therapy, such as bed rest, may help reduce drainage volume and siphoning pressure, and in some cases, increasing the shunt valve pressure may be beneficial [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Diuretics such as furosemide, mannitol, dexamethasone, and anti-migraine medications may provide symptomatic relief. However, they do not address the underlying issue of cerebrospinal fluid drainage obstruction. Surgical intervention is indicated when conservative treatments prove ineffective or when complications such as subdural effusion, microcephaly, Chiari malformation, or isolated ventricles arised, particularly if symptoms significantly impacted the patient\u0026rsquo;s quality of life [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Various surgical approaches were available, including the replacement with an adjustable anti-siphon shunt, re-establishment of a ventriculoperitoneal shunt, or placement of a lumbar cistern-peritoneal shunt. The specific technique is chosen based on the patient\u0026rsquo;s clinical status and individual needs.\u003c/p\u003e \u003cp\u003eIn patients experiencing intracranial hypertension following shunt surgery, the presence of slit-like ventricles on CT imaging, rather than ventricular enlargement, suggests a possible diagnosis of SVS. In cases where intracranial pressure is significantly elevated and unresponsive to pharmacological treatment, timely surgical intervention is essential to restore an effective cerebrospinal fluid circulation pathway.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eTBM Tuberculous meningitis\u003c/p\u003e\n\u003cp\u003eICP intracranial pressure\u003c/p\u003e\n\u003cp\u003eVPS ventriculoperitoneal shunting\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eSVS slit ventricle syndrome\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCSF cerebrospinal fluid\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCT tomography\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eMRI magnetic resonance imaging\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePublication of this case report followed the regulations of the Ethical Board of the West China Second Hospital and was conducted according to the latest version of the Helsinki Declaration. Written informed consent for publication was obtained from the patient\u0026apos;s guardian. All identifiable patient information was omitted during the manuscript\u0026apos;s initial development. Thank the patient and her family for allowing us to develop this manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient\u0026apos;s legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data generated or analyzed during this study are included in this published article. The datasets used and/or analyzed during the current study available from the corresponding author on reasonable request\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was financially supported by no funding.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contribution\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eYL collect the data and write the manuscript; YL and QG revise the manuscript; YL and YZ performed literature review. All authors have reviewed the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgments\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eThwaites GE, van Toorn R, Schoeman J: \u003cstrong\u003eTuberculous meningitis: more questions, still too few answers\u003c/strong\u003e. \u003cem\u003eLancet Neurol \u003c/em\u003e2013, \u003cstrong\u003e12\u003c/strong\u003e(10):999-1010.\u003c/li\u003e\n\u003cli\u003eChatterjee S: \u003cstrong\u003eBrain tuberculomas, tubercular meningitis, and post-tubercular hydrocephalus in children\u003c/strong\u003e. \u003cem\u003eJ Pediatr Neurosci \u003c/em\u003e2011, \u003cstrong\u003e6\u003c/strong\u003e(Suppl 1):S96-S100.\u003c/li\u003e\n\u003cli\u003eRos B, Iglesias S, Martin A, Carrasco A, Ibanez G, Arraez MA: \u003cstrong\u003eShunt overdrainage syndrome: review of the literature\u003c/strong\u003e. \u003cem\u003eNeurosurg Rev \u003c/em\u003e2018, \u003cstrong\u003e41\u003c/strong\u003e(4):969-981.\u003c/li\u003e\n\u003cli\u003eDadak M, Pul R, Lanfermann H, Hartmann H, Hehr U, Donnerstag F, Michels D, Tryc AB: \u003cstrong\u003eVarying Patterns of CNS Imaging in Influenza A Encephalopathy in Childhood\u003c/strong\u003e. \u003cem\u003eClin Neuroradiol \u003c/em\u003e2020, \u003cstrong\u003e30\u003c/strong\u003e(2):243-249.\u003c/li\u003e\n\u003cli\u003eHanak BW, Bonow RH, Harris CA, Browd SR: \u003cstrong\u003eCerebrospinal Fluid Shunting Complications in Children\u003c/strong\u003e. \u003cem\u003ePediatr Neurosurg \u003c/em\u003e2017, \u003cstrong\u003e52\u003c/strong\u003e(6):381-400.\u003c/li\u003e\n\u003cli\u003eHart MG, Czosnyka M, Czosnyka ZH, Fernandes HM: \u003cstrong\u003eCombined intracranial pressure monitoring and cerebrospinal fluid infusion study to guide management of slit ventricle syndrome\u003c/strong\u003e. \u003cem\u003ePediatr Neurosurg \u003c/em\u003e2013, \u003cstrong\u003e49\u003c/strong\u003e(2):113-118.\u003c/li\u003e\n\u003cli\u003eSchuhmann MU, Sood S, McAllister JP, Jaeger M, Ham SD, Czosnyka Z, Czosnyka M: \u003cstrong\u003eValue of overnight monitoring of intracranial pressure in hydrocephalic children\u003c/strong\u003e. \u003cem\u003ePediatr Neurosurg \u003c/em\u003e2008, \u003cstrong\u003e44\u003c/strong\u003e(4):269-279.\u003c/li\u003e\n\u003cli\u003eChernov MF, Kamikawa S, Yamane F, Ishihara S, Hori T: \u003cstrong\u003eNeurofiberscope-guided management of slit-ventricle syndrome due to shunt placement\u003c/strong\u003e. \u003cem\u003eJ Neurosurg \u003c/em\u003e2005, \u003cstrong\u003e102\u003c/strong\u003e(3 Suppl):260-267.\u003c/li\u003e\n\u003cli\u003eSainz LV, Hockel K, Schuhmann MU: \u003cstrong\u003eChronic overdrainage syndrome: pathophysiological insights based on ICP analysis: a case-based review\u003c/strong\u003e. \u003cem\u003eChilds Nerv Syst \u003c/em\u003e2018, \u003cstrong\u003e34\u003c/strong\u003e(3):401-408.\u003c/li\u003e\n\u003cli\u003eKraemer MR, Sandoval-Garcia C, Bragg T, Iskandar BJ: \u003cstrong\u003eShunt-dependent hydrocephalus: management style among members of the American Society of Pediatric Neurosurgeons\u003c/strong\u003e. \u003cem\u003eJ Neurosurg Pediatr \u003c/em\u003e2017, \u003cstrong\u003e20\u003c/strong\u003e(3):216-224.\u003c/li\u003e\n\u003cli\u003eAgarwal N, Shukla RM, Agarwal D, Gupta K, Luthra R, Gupta J, Jain S: \u003cstrong\u003ePediatric Ventriculoperitoneal Shunts and their Complications: An Analysis\u003c/strong\u003e. \u003cem\u003eJ Indian Assoc Pediatr Surg \u003c/em\u003e2017, \u003cstrong\u003e22\u003c/strong\u003e(3):155-157.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Slit ventricle syndrome, Children, Tuberculous Meningitis","lastPublishedDoi":"10.21203/rs.3.rs-5395813/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5395813/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eSlit ventricle syndrome (SVS) is a severe and potentially life-threatening complication associated with chronic overdrainage of cerebrospinal fluid. However, its clinical manifestations and imaging characteristics are often overlooked due to insufficient awareness among clinicians..\u003c/p\u003e\u003ch2\u003eCase Presentation\u003c/h2\u003e \u003cp\u003eWe report the case of a pediatric patient diagnosed with tuberculous meningitis, who received standard anti-tuberculosis treatment and underwent ventriculoperitoneal shunting for hydrocephalus. Four years after completing treatment, the patient presented with recurrent headaches, which were eventually diagnosed as SVS. The patient's condition improved following an upward adjustment of the shunt valve pressure.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis case highlights the critical need for heightened awareness of SVS among pediatric specialists. Early recognition and timely intervention are crucial for optimizing clinical outcomes in patients with a history of shunt surgery and hydrocephalus.\u003c/p\u003e","manuscriptTitle":"Recurrent Headaches in a Child with Tuberculous Meningitis: Unmasking Slit Ventricle Syndrome","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-12-17 09:52:24","doi":"10.21203/rs.3.rs-5395813/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"a35d4738-53bd-4c06-bfeb-835f5ca9d3fa","owner":[],"postedDate":"December 17th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-03-04T04:23:36+00:00","versionOfRecord":[],"versionCreatedAt":"2024-12-17 09:52:24","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-5395813","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5395813","identity":"rs-5395813","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}