Pediatric Syringomyelia

Disease/Disorder

Definition

Syringomyelia is a condition caused by a fluid-filled cavity, or syrinx, which forms within the spinal cord. A syrinx can refer to an abnormal glial cell-lined, fluid-filled cavity located within the spinal cord parenchyma (syringomyelia) or a focal dilation of the central canal (hydromyelia).¹ These two terms are occasionally combined into syringohydromyelia; however, separating these entities based on clinical and radiographical findings is under discussion.
The syrinx can span one or more spinal levels or even the entire length of the spinal cord, causing a variety of motor, sensory, and autonomic symptoms based on location.
In the pediatric population, syringomyelia is most often found in the setting of congenital abnormalities such as Chiari I or tethered cord, though it can be seen with trauma, tumors, and years after infections like meningitis as well. Caring for these patients requires complex, multidisciplinary medical and rehabilitation care.

Etiology

Causes of syringomyelia are varied and typically categorized as congenital, acquired, or idiopathic. Common causes are outlined below.

Congenital

• Neural tube defects
  • Myelomeningocele
  • Tethered cord syndrome
• Chiari malformations

Acquired

• Post-infectious
  • Meningitis, arachnoiditis
• Post-inflammatory
  • Transverse myelitis, sarcoidosis, multiple sclerosis
• Post-traumatic
  • Spinal cord injury, postsurgical, arachnoid scarring
• Neoplastic
  • Spinal cord tumors (ependymomas and hemangioblastomas)
  • Extramedullary tumors
• Familial

Idiopathic

• underlying cause is unknown

The most common etiology of syringomyelia in both adult and pediatric patients is Chiari I malformation, representing 48-50% of adult cases^2,3 and 43.2% of pediatric cases.⁴ In pediatric populations with syrinx, the next most associated conditions are idiopathic (30.6%), spinal dysraphism (7.4%), tumor (5.5%), and tethered cord (4.8%).⁴

Epidemiology including risk factors and primary prevention

General prevalence
Syringomyelia most commonly presents in young adults ages 20 to 40, although all ages may be affected.⁵ Estimates of prevalence vary between 1.94-8.4 per 100,000.^2,3 Men and women are equally affected.^2,5

Risk factors
There are multiple risk factors for developing a syringomyelia.

Chiari I malformation (CM-I): In approximately 12-22.9% of pediatric patients with CM-I, a syrinx is also present.^6,9 Estimates are higher in patients undergoing surgery for CM-I, in which syrinx is seen in as high as 60-85% of patients.⁷ The syrinx is commonly located in the cervical spinal cord There is an increased likelihood of spinal syrinx with lower tonsil position.⁷

Myelomeningocele: Reported incidence of syrinx varies from 25 to 45%.⁸ There is an association between untreated or inadequately treated hydrocephalus and symptomatic syringomyelia in patients with myelomeningocele.⁹

Trauma-associated:  The incidence of post-traumatic syringomyelia ranges from <1 to 7% in patients with clinical symptoms and is as high as >50% on imaging studies.¹⁰ Increased risk of development of syringomyelia within 5 years after spinal cord injury may be associated with complete SCI and age greater than 30 years.¹⁰ Dislocated spine fractures and spinal stenosis may also increase risk of development of posttraumatic syrinx.¹¹

Tumor-associated: Syrinx occurs in 25 to 58% of patients with intramedullary spinal cord tumors and are typically seen in the lower cervical and upper thoracic regions. Ependymomas are most frequent, followed by hemangioblastomas and cavernomas.¹²

Familial: Familial syringomyelia is rare. Familial cases of both autosomal dominant and recessive inheritance patterns have been reported and are felt to be due to gene abnormalities in spinal cord development.¹³ Some cases have been associated with Chiari I malformation while others have revealed isolated thoracic syringomyelia with only mild symptoms.^13,14

Pathophysiology

The pathophysiology of syringomyelia is not completely understood. Theories regarding pathogenesis of syringomyelia can be divided into three categories as outlined by Blegvad, et al³

• Altered cerebrospinal fluid flow dynamics.
  • Direct communication between the fourth ventricle and syrinx.
  • Transmedullary infiltration of CSF through the perivascular space.
  • Parenchymal formation due to blood plasma ultrafiltration.
• Intramedullary tissue damage due to hemorrhage or infarction.
• Intramedullary tumor with secretory capabilities. In syringomyelia due to spinal cord tumors, tumor syringes have been found to have an elevated protein concentration compared to normal CSF and syrinx fluid associated with other etiologies, suggesting a possible unique mechanism related to the secretory ability of the tumor itself.¹²

Disease progression: Clinical features and presentation over time

The natural history of syringomyelia is variable and dependent on etiology. While some patients may remain asymptomatic, others will develop worsening progression of symptoms overtime.

CM-I: Syringomyelia has been shown to improve in 78% of patients with CM-I who undergo surgery. Clinically, 75% of patients experience improvement, 17% have no change, and 9% experience worsening of neurological outcomes post-operatively.¹⁵

Idiopathic:  In one study, 36% of pediatric patients with idiopathic syringomyelia had a neurologic deficit at presentation. At 13 month follow up, deficits were stable or improved in 64% of cases.¹⁶

Myelomeningocele: Syringomyelia usually develops around age four to seven in patients who have had surgical repair of the defect during the neonatal period.⁸ There is a lack of data regarding the natural history of syringomyelia in patients with myelomeningocele. Although there is a high estimate for the prevalence of syringomyelia based on imaging studies (25-45%), only an estimated 2.3% of patients with myelomeningocele will develop clinically active syringomyelia.⁹

Trauma-associated: Most patients with post-traumatic syringomyelia who are asymptomatic or with mild symptoms will remain stable over time.¹¹ Deterioration of motor and sensory function, pain and increased spasticity are the most commonly observed symptoms in patients with post-traumatic syringomyelia.¹⁰ In patients who underwent surgical intervention, 52% had improvement in their symptoms, 37% remained stable, and 11% had progression.¹⁷ Many patients (51%) required more than one surgical intervention.¹⁷

When a patient presents with symptomatic syringomyelia, progressive neurologic deterioration may appear; however, diagnosis may be delayed due to the slow progression of symptoms, particularly when the cervical spinal cord is involved.

With extension of the syrinx, progression of clinical symptoms may include the following

• Sensory loss due to injury to the spinothalamic fibers with resultant alteration of pain and temperature sensation. There can be preservation of light touch, vibration, and proprioception. This can occur in one or both arms or across the upper torso
• Posterior column enlargement causes lower extremity loss of position and vibration sense.
• Dysesthesias, often described as severe deep aching pain, sometimes following a radicular distribution in the upper extremities and trunk.
• Motor loss with extension to anterior horns with diffuse muscle atrophy beginning in the hands progressing proximally to the forearm and shoulder girdle.
• Impaired bowel, bladder, and sexual dysfunction are typically signs of end-stage spinal cord dysfunction.
• Horner’s syndrome, reflecting damage to sympathetic fibers in the intermediary cell columns.
• With extension into the medulla (syringobulbia), symptoms may include dysphagia, nystagmus, pharyngeal and palatal weakness, tongue atrophy, and sensory loss in the trigeminal nerve distribution.
• Lumbar syringomyelia may present with lower motor neuron signs, including leg muscle atrophy with sensory loss in lumbosacral dermatomes and decreased or absent reflexes.

Specific secondary or associated conditions and complications

• Scoliosis may be seen in 25% to 85% of pediatric cases of syringomyelia associated with CM-I.¹⁸ The presence of syrinx has been found to be independently associated with scoliosis in this subset of patients, suggesting that low tonsillar position is not itself a risk factor for development of scoliosis.⁶ Left thoracic curve, young age, severity, and rapid progression may raise suspicion for intraspinal anomaly in a patient presenting with scoliosis.⁸ Patient’s with Chiari malformation and scoliosis should be followed closely for higher risk of curve progression.²⁴
• Painless ulcers of the hands (aphthous ulcers) caused by decreased peripheral sensation.
• Neurogenic arthropathies of shoulder, elbow, and wrist (Charcot joints); painful enlargement of the shoulder because of humeral destruction. The most common cause of upper extremity Charcot joint is syringomyelia.
• Pain complaints are more common in adults than children.

Essentials of Assessment

History

Symptoms range from asymptomatic to severe impairment and are variable depending on location of the syrinx within the spinal cord. Onset of symptoms and progression over time are important to determine as symptoms often progress slowly.

Common symptoms seen in syringomyelia

• Pain
  • Pain and stiffness in the back, shoulders and extremities.
  • Symptoms aggravated by postural changes or Valsalva maneuver.
• Motor
  • Weakness, gait changes or clumsiness.
• Sensory symptoms
  • “Cape-like” loss of pain and temperature sensation in the back and arms, although this is rare in clinical practice.¹
  • Sensory deficits may be asymmetric and may not follow a dermatomal distribution^.8
• Autonomic symptoms
  • Dry skin or hyperhidrosis.⁸
  • Bowel and bladder dysfunction.
• Brainstem symptoms (syringobulbia)
  • Facial numbness, dysarthria, dysphagia, vision and hearing changes, and respiratory dysfunction.⁸
• Associated symptoms
  • New onset scoliosis.
  • Joint pain or swelling.
  • Weight loss, anorexia, fatigue, history of cancer and back pain exacerbated by the supine position may be indicative of tumor.
  • Previous or family history of brain or spinal cord malformations may increase suspicion of syringomyelia.

Factors related to specific patient populations

• History of spinal cord injury or myelomeningocele:
  • It is critical to establish a baseline level of neurological function.
  • New neurologic deficits in the lower extremities, pain, bowel or bladder changes, and scoliosis may suggest development of syringomyelia. If the syrinx extends upward to the cervical spinal cord, patients can present with new hand weakness and sensory symptoms.¹

Physical examination

Detailed neurologic examination is required with special attention to motor and sensory deficits or asymmetries. A gait assessment can be beneficial to assess for ataxia, disturbance in balance, or lack of coordination. It is also imperative to test reflexes, including pathologic reflexes such as Hoffman or Babinski.

Other aspects of the physical exam to be mindful of when syringomyelia is suspected includes a musculoskeletal exam looking for atrophy, scoliosis, or Charcot joints and a skin exam to assess for aphthous ulcers.

Findings are dependent on spinal cord level

Syringobulbia

• Cranial nerve dysfunction and cerebellar signs

Cervical syringomyelia

• Upper extremity hyporeflexia
• Lower extremity hyperreflexia, spasticity with paraparesis, and Babinski reflex
• Horner’s syndrome or other evidence of dysautonomia

Lumbar syringomyelia

• Lower extremity hyporeflexia and paresis

Functional assessment

A functional assessment allows for better understanding of a patient’s ability to perform daily tasks independently or with assistance. This can also help with assessing how severe or progressed the symptom burden has become, which can aid in determining best next steps in management.

Patients must be evaluated for development of the following

• Gross motor skills
  • Bed mobility
  • Transfers
  • Ambulation with/without assistive devices
  • Static/dynamic balance
  • Active/passive range of motion
• Fine motor skills
• Eye-hand coordination
• Activities of daily living status
• Speech/language and other oral skills
  • Indicators of dysphagia (cough, hypoxia, or dysphonia may require additional studies)
  • Nutritional status
• Cognitive skills
  • Executive functioning, at school and home
  • Short- and long-term memory
  • Concentration/focus
  • Safety awareness, judgment

It is important to note changes in the physical exam, especially new onset or worsening spasticity, alterations in deep tendon reflexes, or changes in the sensory levels as this may indicate progression of the syrinx.

Laboratory studies

There are no known lab studies to diagnose syringomyelia.

Imaging

Contrast-enhanced spinal MRI is the gold standard for detection of syringomyelia as contrast can help to differentiate syringomyelia from tumor or inflammatory disease. Three-dimensional constructive interference in steady state (CISS) sequences may be helpful for determining anatomical details of syringes with multiple septa and for detecting extramedullary arachnoid adhesions or membranes.^1,8 Four-dimensional phase contrast MRI is a new technique that can be used to study CSF flow dynamics.¹

Additional imaging studies

• Computed tomography (CT) myelogram can be considered if MRI is unavailable or unsafe.
• Spine radiographs can evaluate for coexisting scoliosis.
• MRI of the head and craniocervical junction can be considered to evaluate for hydrocephalus and Chiari malformation.¹
• MRI of the lumbosacral spine should be included if there is concern for tethered cord¹
• CSF flow MRI can be utilized to assess the cerebrospinal fluid.

Supplemental assessment tools

• Videofluoroscopy Swallow Study (VFSS), fiberoptic endoscopic evaluation of swallowing, or other studies for dysphagia; laryngoscopy for dysphonia and vocal cord dysfunction.
• Electrodiagnosis for decreased hypothenar muscle action potentials or abnormal tibial nerve somatosensory evoked potentials related to impaired proprioception in the lower extremities.¹⁹
• Urodynamic studies can be considered pre and post spinal cord untethering to evaluate for retethering or progression of syringomyelia.⁸

Early predictions of outcomes

Morbidity/mortality and assessment of treatment results are difficult because of rarity, variable presentation, and limited follow-up with small numbers in most studies. This may be lower in modern studies, given neurosurgical intervention, better imaging techniques, and treatment of complications.

CM-I: Studies show that a shorter duration of symptoms before surgical decompression favorably influences clinical outcome.²⁰ Syrinx shape also influences pain and symptoms. Recovery is slower in patients with deviated or dorsal horn involvement compared to enlarged or central syrinx.²¹

Idiopathic syringomyelia: Children with idiopathic syrinx remain asymptomatic, stable, or improved in 64% of cases.¹⁶ Orthopedic and neurologic studies reviewing pain, neurologic symptoms, and rate of scoliosis progression found no correlation between location or size of syrinx and magnitude of major curve or severity of neurologic deficit.¹⁸

Myelomeningocele: Patients with myelomeningocele who are asymptomatic with syringomyelia identified on imaging are likely to remain asymptomatic.⁹ In patients with hydrocephalus, shunt obstruction can lead to deterioration in syringomyelia.⁸

Trauma-associated: During the acute phase of spinal cord injury, operative restoration of spinal alignment may decrease the risk of  development of post-traumatic syringomyelia.^11,17 The extent of intradural scarring and arachnoiditis leads to more difficult surgical intervention and may result in recurrence or worsening of syringomyelia and need for surgical revision.¹⁷ This may be especially problematic in patients with motor incomplete injuries (ASIA C or D) who have been shown to have higher rates of neurological deterioration after 5 years postoperatively (39%) compared to 14% in ASIA A or B and 6% in ASIA E.¹¹ This may be due to the intraoperative difficulty in performing complete arachnolysis and untethering while trying to preserve as much residual cord function as possible in patients with partially preserved motor function at baseline.¹¹

Tumor-associated: Tumors with associated syringomyelia tend to be non-infiltrative. After tumor removal, the syrinx will typically resolve.¹²

Environmental

It is imperative to ensure a safe home environment, as well as optimizing mobility in the home and community for patients with syringomyelia. Physicians can help facilitate maximum functionality for their patients, whether with a caregiver, assistive device, or independently. Inquire about the home environment particularly regarding stairs, width of corridors or doors, and accessibility for durable medical equipment if there is paralysis or gait dysfunction. Barrier-free school environment should also be assessed, particularly for pediatric patients. Assistance with establishing an education plan or adaptive learning environment is available for patients.

Race is associated with age and timing of diagnosis for both CM1 and syringomyelia, non-whites and male patients were more likely present at an older age.²⁵ Lower socio-economic status can also play a role in patients’ ability to seek care, obtain transportation to appointments, and afford durable medical equipment not provided through insurance.

Social role and social support system

Providers need comprehensive understanding of the living situation, including the number of primary caretakers and their roles in daily management of the patient’s functional and medical needs. Direct questions must be asked of the caretaker to ensure they can meet the patient’s needs (e.g., who will provide bladder, bowel, and skin care management).

Rehabilitation Management and Treatments

Available or current treatment guidelines

N/A.

At different disease stages

Asymptomatic patients require expectant management with monitoring of MRI and clinical symptoms. If a patient presents with decline in function or worsened symptom burden, it is imperative to refer for neurosurgical evaluation. When surgery is indicated, the goal is restoration of normal CSF flow dynamics with different techniques dependent on etiology.¹

Rehabilitation assessment and intervention include the following

• Multimodal pain management including medications, modalities, behavioral pain coping strategies, and alternative/complementary medicine
• Physical therapy
• Occupational therapy
• Speech and language therapy (if deficits in brainstem function)
• Nutrition

Short- and long-term goals include the following

• Injury prevention
• Continence
• Contracture prevention
• Strengthening and conditioning
• Balance: static/dynamic
• Transfers
• Ambulation
• Fine motor skills
• Activities of daily living with/without assistive devices
• Swallowing, phonation, and respiration
• Verbal and written communication
• Family education/training

Coordination of care

Care of this complex condition requires coordination with the following

• Primary physician
• Physiatrist
• Neurosurgeon
• Orthopedic surgeon
• Therapists
• Psychiatrist/psychologist
• Social worker/case manager
• Third-party payers

Parents require a supportive team approach and development of a support network including the following

• Family
• Social workers
• Clergy
• Peers
• Respite care

Parents must learn how to advocate effectively for their child while promoting independence and must understand all issues involved in their child’s diagnosis and be involved in all treatment decisions. When able, the child should be involved in their own personal care.

Early developmental and neuropsychologic assessment and periodic re-evaluation are needed to ascertain ability to make decisions regarding care. A legal guardian should be appointed if capacity as a legal adult is lacking.

Patient & family education

For the benefit of patients and their families, it is important to have open communication between the families and the multidisciplinary team. Families must be aware of symptoms to monitor and bring to medical attention. Education and training in skin protection and bowel/bladder care are essential. If primary caretakers are unable to provide adequate support, referral to social services is required.

External resources include the following

• Chiari and Syringomyelia Foundation
• American Syringomyelia & Chiari Alliance Project

Teenage female patients should receive counseling from their Obstetrician regarding pregnancy, vaginal delivery is not contraindicated but epidurals should be pursued with caution due to risk for Dural puncture. ²⁶

Emerging/unique interventions

There are no specific syringomyelia outcome measures. Functional scales (e.g., WeeFIM) that address mobility, self-care, and cognition can be used for children ages 3 to 8 years. There is presently no valid, specific, reliable outcome scale for syringomyelia.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Syringomyelia requires complex management over the life span. Vigilant monitoring of patients with a history of Chiari malformation, spinal cord injury, or myelomeningocele is necessary. Changes in neurologic function should be evaluated with imaging to assess the presence/expansion of syrinx or spine instability. ²⁶

Cutting Edge/ Emerging and Unique Concepts and Practice

Dynamic 4D phase contrast-enhanced MRI to analyze CSF flow dynamics within the syrinx.

Gaps in the Evidence-Based Knowledge

A survey of the pediatric section of the American Association of Neurological Surgeons favors surgical intervention for cranial nerve dysfunction, motor/sensory loss, and scoliosis associated with syringomyelia.²² Treatment of asymptomatic patients with CM-I and syringomyelia with conservative management versus early surgical intervention is unclear.²³ Although posterior fossa decompression is the most common treatment modality for children with CM-I and syringomyelia, optimal surgical technique has not been determined.²³ Consideration may also be given to the timing of neurosurgical intervention before scoliosis surgery.

Current research in syringomyelia (www.clinicaltrials.gov):

• The therapeutic effect of betaine in syringomyelia
• Development of a patient-reported outcome measure for Chiari malformation and syringomyelia
• Impact of peripheral afferent input on central neuropathic pain
• Subarachnoid-subarachnoid bypass versus adhesion lysis in spinal arachnoiditis and syringomyelia

References

1. Vandertop WP. Syringomyelia. Neuropediatrics. 2014;45(1):3-9.
2. Sakushima K, Tsuboi S, Yabe I, et al. Nationwide survey on the epidemiology of syringomyelia in japan. J Neurol Sci. 2012;313(1-2):147-152.
3. Brickell KL, Anderson NE, Charleston AJ, Hope JK, Bok AP, Barber PA. Ethnic differences in syringomyelia in new zealand. J Neurol Neurosurg Psychiatry. 2006;77(8):989-991.
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5. Syringomyelia. https://rarediseases.org/rare-diseases/syringomyelia/. Updated 2017. Accessed May 31, 2018.
6. Strahle J, Smith BW, Martinez M, et al. The association between chiari malformation type I, spinal syrinx, and scoliosis. J Neurosurg Pediatr. 2015;15(6):607-611.
7. Kahn EN, Muraszko KM, Maher CO. Prevalence of chiari I malformation and syringomyelia. Neurosurg Clin N Am. 2015;26(4):501-507.
8. Tsitouras V, Sgouros S. Syringomyelia and tethered cord in children. Childs Nerv Syst. 2013;29(9):1625-1634.
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10. Krebs J, Koch HG, Hartmann K, Frotzler A. The characteristics of posttraumatic syringomyelia. Spinal Cord. 2016;54(6):463-466.
11. Klekamp J. Treatment of posttraumatic syringomyelia. J Neurosurg Spine. 2012;17(3):199-211.
12. Samartzis D, Gillis CC, Shih P, O’Toole JE, Fessler RG. Intramedullary spinal cord tumors: Part I-epidemiology, pathophysiology, and diagnosis. Global Spine J. 2015;5(5):425-435.
13. Demirci S, Ünlü MD. Familial syringomyelia: Incidental or hereditary? Turk J Neurol 2025;31(1):80-86 Doi: 10.55697/tnd.2025.228
14. Dhawan A, Dhawan J, Sharma A, Azzam D, Cherry A, Fehlings M. Familial Chiari malformation: a systematic review and illustrative cases. Journal of Neurosurgery. 41(1), 105–114. https://doi.org/10.3171/2024.1.SPINE231277
15. Arnautovic A, Splavski B, Boop FA, Arnautovic KI. Pediatric and adult chiari malformation type I surgical series 1965-2013: A review of demographics, operative treatment, and outcomes. J Neurosurg Pediatr. 2015;15(2):161-177.
16. Rodriguez A, Kuhn EN, Somasundaram A, Couture DE. Management of idiopathic pediatric syringohydromyelia. J Neurosurg Pediatr. 2015 Oct;16(4):452-7. doi: 10.3171/2015.3.PEDS14433. Epub 2015 Jul 24. PMID: 26207665.
17. Karam Y, Hitchon PW, Mhanna NE, He W, Noeller J. Post-traumatic syringomyelia: Outcome predictors. Clin Neurol Neurosurg. 2014;124:44-50.
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19. Akan O, Baslo MB. (2018). Electrophysiologic Abnormalities in a Patient with Syringomyelia Referred for Asymmetrical Lower Limb Atrophy. Turk J Neurol 2018;24:186-187 https://doi.org/10.4274/tnd.04372
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21. Nakamura M, Chiba K, Nishizawa T, Maruiwa H, Matsumoto M, Toyama Y. Retrospective study of surgery-related outcomes in patients with syringomyelia associated with chiari I malformation: Clinical significance of changes in the size and localization of syrinx on pain relief. J Neurosurg. 2004;100(3 Suppl Spine):241-244.
22. Haroun RI, Guarnieri M, Meadow JJ, Kraut M, Carson BS. Current opinions for the treatment of syringomyelia and chiari malformations: Survey of the pediatric section of the american association of neurological surgeons. Pediatr Neurosurg. 2000;33(6):311-317.
23. Rocque BG, George TM, Kestle J, Iskandar BJ. Treatment practices for chiari malformation type I with syringomyelia: Results of a survey of the american society of pediatric neurosurgeons. J Neurosurg Pediatr. 2011;8(5):430-437.
24. Zhang T, Bao H, Zhang X, et al. Brace treatment for scoliosis secondary to chiari malformation type 1 or syringomyelia without neurosurgical intervention: A matched comparison with idiopathic scoliosis. European Spine Journal. 2021;30(12):3482-3489. doi:10.1007/s00586-021-06958-2
25. Akbari, Syed Hassan A., et al. “Socioeconomic and Demographic Factors in the Diagnosis and Treatment of Chiari Malformation Type I and Syringomyelia.” Journal of Neurosurgery: Pediatrics, vol. 29, no. 3, 1 Mar. 2022, pp. 288–297, 10.3171/2021.9.peds2185. Accessed 22 Mar. 2022.
26. Flint, Graham. “Syringomyelia: Diagnosis and Management.” Practical Neurology, vol. 21, no. 5, 25 Aug. 2021, pp. 403–411, 10.1136/practneurol-2021-002994. Accessed 8 Dec. 2021.

Original Version of the Topic

Meg A. Krilov, MD, Jennifer Gomez, MD. Pediatric Syringomyelia. 9/20/2014

Previous Revision(s) of the Topic

Amanda Kole Morrow, MD Frank Pidcock, MD. Pediatric Syringomyelia. 9/7/2018

Rajashree Srinivasan, MD, MBBS, Sarah Matthews, MD, Cristina Sanders, DO. Pediatric Syringomyelia. 6/16/2022

Author Disclosure

Cristina Marie Sanders, DO, MS
Nothing to Disclose

Olivia Tincher, DO
Nothing to Disclose

Grace Meehan, DO
Nothing to Disclose

Rajashree Srinivasan, MD, MBBS
Nothing to Disclose