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Syringomyelia

MedGen UID:
21449
Concept ID:
C0039144
Disease or Syndrome
Synonyms: Myelosyringoses; Myelosyringosis; Syringomyelias; Syringomyelus
SNOMED CT: Syringomyelia (111496009); Syringomyelia-anesthesia syndrome (111496009); Myelosyringosis (111496009)
Modes of inheritance:
Autosomal recessive inheritance
MedGen UID:
141025
Concept ID:
C0441748
Intellectual Product
Source: Orphanet
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in individuals with two pathogenic alleles, either homozygotes (two copies of the same mutant allele) or compound heterozygotes (whereby each copy of a gene has a distinct mutant allele).
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Source: Orphanet
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
Not genetically inherited
MedGen UID:
988794
Concept ID:
CN307044
Finding
Source: Orphanet
clinical entity without genetic inheritance.
 
HPO: HP:0003396
Monarch Initiative: MONDO:0017987
Orphanet: ORPHA3280

Definition

Dilated, glial-lined cavity in spinal cord. This cavity does not communicate with the central canal, and usually is between the dorsal columns unilaterally or bilaterally along the side of the cord. [from HPO]

Conditions with this feature

Cleidocranial dysostosis
MedGen UID:
3486
Concept ID:
C0008928
Disease or Syndrome
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia that represents a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities) to mild CCD to isolated dental anomalies without the skeletal features. Most individuals come to diagnosis because they have classic features. At birth, affected individuals typically have abnormally large, wide-open fontanelles that may remain open throughout life. Clavicular hypoplasia can result in narrow, sloping shoulders that can be opposed at the midline. Moderate short stature may be observed, with most affected individuals being shorter than their unaffected sibs. Dental anomalies may include supernumerary teeth, eruption failure of the permanent teeth, and presence of the second permanent molar with the primary dentition. Individuals with CCD spectrum disorder are at increased risk of developing recurrent sinus infections, recurrent ear infections leading to conductive hearing loss, and upper-airway obstruction. Intelligence is typically normal.
Radial aplasia-thrombocytopenia syndrome
MedGen UID:
61235
Concept ID:
C0175703
Disease or Syndrome
Thrombocytopenia absent radius (TAR) syndrome is characterized by bilateral absence of the radii with the presence of both thumbs, and thrombocytopenia that is generally transient. Thrombocytopenia may be congenital or may develop within the first few weeks to months of life; in general, thrombocytopenic episodes decrease with age. Cow's milk allergy is common and can be associated with exacerbation of thrombocytopenia. Other anomalies of the skeleton (upper and lower limbs, ribs, and vertebrae), heart, and genitourinary system (renal anomalies and agenesis of uterus, cervix, and upper part of the vagina) can occur.
Neurocutaneous melanocytosis
MedGen UID:
154259
Concept ID:
C0544862
Congenital Abnormality
Neurocutaneous melanosis, or neuromelanosis, is characterized by the presence of melanin-producing cells within the brain parenchyma or leptomeninges, which may lead to clinically apparent neurologic signs and symptoms, such as seizures. Other neurologic abnormalities, including hydrocephalus, arachnoid cysts, tumors, and syringomyelia, may also occur. The disorder is a rare but severe manifestation of congenital melanocytic nevus syndrome (CMNS; 137550). Some patients with neurocutaneous melanosis or CMNS may develop malignant melanoma. The incidence of neurologic involvement, development of malignant melanoma, and death is significantly associated with the projected adult size of the largest congenital melanocytic nevus, particularly those greater than 40 cm (summary by Kinsler et al., 2008; Kinsler et al., 2013).
Chiari type II malformation
MedGen UID:
108222
Concept ID:
C0555206
Congenital Abnormality
Chiari malformation type II (CM2), also known as the Arnold-Chiari malformation, consists of elongation and descent of the inferior cerebellar vermis, cerebellar hemispheres, pons, medulla, and fourth ventricle through the foramen magnum into the spinal canal. CM2 is uniquely associated with myelomeningocele (open spina bifida; see 182940) and is found only in this population (Stevenson, 2004). It is believed to be a disorder of neuroectodermal origin (Schijman, 2004). For a general phenotypic description of the different forms of Chiari malformations, see Chiari malformation type I (CM1; 118420).
Chiari type I malformation
MedGen UID:
196689
Concept ID:
C0750929
Congenital Abnormality
Arnold-Chiari type I malformation refers to a relatively mild degree of herniation of the posteroinferior region of the cerebellum (the cerebellar tonsils) into the cervical canal with little or no displacement of the fourth ventricle. It is characterized by one or both pointed (not rounded) cerebellar tonsils that project 5 mm below the foramen magnum, measured by a line drawn from the basion to the opisthion (McRae Line)
Microcephalic osteodysplastic dysplasia, Saul-Wilson type
MedGen UID:
722057
Concept ID:
C1300285
Disease or Syndrome
Saul-Wilson syndrome (SWS) is a skeletal dysplasia characterized by profound short stature, distinctive craniofacial features, short distal phalanges of fingers and toes, and often clubfoot. Early development (primarily speech and motor) is delayed; cognition is normal. Other findings can include hearing loss (conductive, sensorineural, and mixed), lamellar cataracts, and/or rod-cone retinal dystrophy. To date, 16 affected individuals have been reported.
Spondyloepimetaphyseal dysplasia-short limb-abnormal calcification syndrome
MedGen UID:
338595
Concept ID:
C1849011
Disease or Syndrome
Spondyloepimetaphyseal dysplasia-short limb-abnormal calcification syndrome is a rare, genetic primary bone dysplasia disorder characterized by disproportionate short stature with shortening of upper and lower limbs, short and broad fingers with short hands, narrowed chest with rib abnormalities and pectus excavatum, abnormal chondral calcifications (incl. larynx, trachea and costal cartilages) and facial dysmorphism (frontal bossing, hypertelorism, prominent eyes, short flat nose, wide nostrils, high-arched palate, long philtrum). Platyspondyly (esp. of cervical spine) and abnormal epiphyses and metaphyses are observed on radiography. Atlantoaxial instability causing spinal compression and recurrent respiratory disease are potential complications that may result lethal.
Lateral meningocele syndrome
MedGen UID:
342070
Concept ID:
C1851710
Disease or Syndrome
NOTCH3-related lateral meningocele syndrome (LMS) is characterized by multiple lateral spinal meningoceles (protrusions of the arachnoid and dura through spinal foramina), distinctive facial features, joint hyperextensibility, hypotonia, and skeletal, cardiac, and urogenital anomalies. Neurologic sequelæ of the meningoceles depend on size and location and can include neurogenic bladder, paresthesia, back pain, and/or paraparesis. Other neurologic findings can include Chiari I malformation, syringomyelia, and rarely, hydrocephalus. Additional findings of LMS include developmental delay, mixed or conductive hearing loss, and cleft palate. Skeletal abnormalities may include scoliosis, vertebral fusion, scalloping of vertebrae, and wormian bones. Infants may demonstrate feeding difficulties with poor weight gain.
Primary basilar invagination
MedGen UID:
400018
Concept ID:
C1862299
Disease or Syndrome
Primary basilar impression of the skull is a developmental defect of the cranium in which there is invagination of the foramen magnum upward into the posterior cranial fossa. Basilar impression is often associated with other malformations of the notochord and craniovertebral junction, such as occipitalization of the atlas, Klippel-Feil anomaly (see 118100), Chiari type I malformation (118420), and syringomyelia (186700) (Paradis and Sax, 1972; Bhangoo and Crockard, 1999). Secondary basilar impression occurs as a result of generalized skeletal diseases, including hyperparathyroidism (see 145000), Paget disease (see 167250), and osteogenesis imperfecta (see, e.g., 166200). Platybasia refers to a skull base with an abnormally obtuse angle between the planes of the clivus and the anterior fossa. Platybasia may occur in basilar impression, but it is not of medical significance on its own (Bhangoo and Crockard, 1999). Historically, basilar impression was defined radiologically by numerous parameters, including the lines defined by Chamberlain (1939), McGregor (1948), and Fischgold and Metzger (1952), and the angle defined by Bull et al. (1955).
Alveolar capillary dysplasia with pulmonary venous misalignment
MedGen UID:
755478
Concept ID:
C2960310
Congenital Abnormality
Congenital alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is characterized histologically by failure of formation and ingrowth of alveolar capillaries that then do not make contact with alveolar epithelium, medial muscular thickening of small pulmonary arterioles with muscularization of the intraacinar arterioles, thickened alveolar walls, and anomalously situated pulmonary veins running alongside pulmonary arterioles and sharing the same adventitial sheath. Less common features include a reduced number of alveoli and a patchy distribution of the histopathologic changes. The disorder is associated with persistent pulmonary hypertension of the neonate and shows varying degrees of lability and severity (Boggs et al., 1994). Affected infants present with respiratory distress resulting from pulmonary hypertension in the early postnatal period, and the disease is uniformly fatal within the newborn period (Vassal et al., 1998). Additional features of ACDMPV include multiple congenital anomalies affecting the cardiovascular, gastrointestinal, genitourinary, and musculoskeletal systems, as well as disruption of the normal right-left asymmetry of intrathoracic or intraabdominal organs (Sen et al., 2004).
CHROMOSOME 1p32-p31 DELETION SYNDROME
MedGen UID:
462386
Concept ID:
C3151036
Disease or Syndrome
Craniosynostosis and dental anomalies
MedGen UID:
481703
Concept ID:
C3280073
Disease or Syndrome
CRSDA is an autosomal recessive disorder characterized by craniosynostosis, maxillary hypoplasia, and dental anomalies, including malocclusion, delayed and ectopic tooth eruption, and/or supernumerary teeth. Some patients also display minor digit anomalies, such as syndactyly and/or clinodactyly (summary by Nieminen et al., 2011).
Hereditary spastic paraplegia 54
MedGen UID:
761341
Concept ID:
C3539495
Disease or Syndrome
Spastic paraplegia-54 (SPG54) is a complicated form of spastic paraplegia, a neurodegenerative disorder affecting fibers of the corticospinal tract. Affected individuals have delayed psychomotor development, intellectual disability, and early-onset spasticity of the lower limbs. Brain MRI shows a thin corpus callosum and periventricular white matter lesions. Brain magnetic resonance spectroscopy shows an abnormal lipid peak (summary by Schuurs-Hoeijmakers et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive spastic paraplegia, see 270800.
Distal tetrasomy 15q
MedGen UID:
766772
Concept ID:
C3553858
Disease or Syndrome
Spondylocostal dysostosis 5
MedGen UID:
901825
Concept ID:
C4083048
Disease or Syndrome
Spondylocostal dysostosis (SCDO), defined radiographically as multiple segmentation defects of the vertebrae (M-SDV) in combination with abnormalities of the ribs, is characterized clinically by: a short trunk in proportion to height; short neck; non-progressive mild scoliosis in most affected individuals, and occasionally, more significant scoliosis. Respiratory function in neonates may be compromised by reduced size of the thorax. By age two years lung growth may improve sufficiently to support relatively normal growth and development; however, even then life-threatening complications can occur, especially pulmonary hypertension in children with severely restricted lung capacity from birth. Males with SCDO appear to be at increased risk for inguinal hernia.
Luscan-Lumish syndrome
MedGen UID:
898669
Concept ID:
C4085873
Disease or Syndrome
Luscan-Lumish syndrome (LLS) is characterized by macrocephaly, intellectual disability, speech delay, low sociability, and behavioral problems. More variable features include postnatal overgrowth, obesity, advanced carpal ossification, developmental delay, and seizures (Luscan et al., 2014; Lumish et al., 2015)
Palatal anomalies-widely spaced teeth-facial dysmorphism-developmental delay syndrome
MedGen UID:
895943
Concept ID:
C4225229
Disease or Syndrome
Palatal anomalies-widely spaced teeth-facial dysmorphism-developmental delay syndrome is a rare, genetic multiple congenital anomalies/dysmorphic syndrome characterized by global developmental delay, axial hypotonia, palate abnormalities (including cleft palate and/or high and narrow palate), dysmorphic facial features (including prominent forehead, hypertelorism, downslanting palpebral fissures, wide nasal bridge, thin lips and widely spaced teeth), and short stature. Additional manifestations may include digital anomalies (such as brachydactyly, clinodactyly, and hypoplastic toenails), a single palmar crease, lower limb hypertonia, joint hypermobility, as well as ocular and urogenital anomalies.
PMP22-RAI1 contiguous gene duplication syndrome
MedGen UID:
894862
Concept ID:
C4225255
Disease or Syndrome
Yuan-Harel-Lupski syndrome is a complex neurodevelopmental disorder characterized by global developmental delay and early-onset peripheral neuropathy. The disorder comprises features of both demyelinating Charcot-Marie-Tooth disease type 1A (CMT1A; 118220), which results from duplication of the PMP22 gene on 17p12, and Potocki-Lupski syndrome (PTLS; 610883), which results from duplication of a slightly proximal region on 17p11.2 that includes the RAI1 gene. These 2 loci are about 2.5 Mb apart. The resultant YUHAL phenotype may be more severe in comparison to the individual contributions of each gene, with particularly early onset of peripheral neuropathy and features of both central and peripheral nervous system involvement (summary by Yuan et al., 2015).
Au-Kline syndrome
MedGen UID:
900671
Concept ID:
C4225274
Disease or Syndrome
Au-Kline syndrome is characterized by developmental delay and hypotonia with moderate-to-severe intellectual disability, and typical facial features that include long palpebral fissures, ptosis, shallow orbits, large and deeply grooved tongue, broad nose with a wide nasal bridge, and downturned mouth. There is frequently variable autonomic dysfunction (gastrointestinal dysmotility, high pain threshold, heat intolerance, recurrent fevers, abnormal sweating). Congenital heart disease, hydronephrosis, palate abnormalities, and oligodontia are also reported in the majority of affected individuals. Additional complications can include craniosynostosis, feeding difficulty, vision issues, osteopenia, and other skeletal anomalies.
Osteogenesis imperfecta type 17
MedGen UID:
903845
Concept ID:
C4225301
Disease or Syndrome
Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. The term "osteogenesis imperfecta" means imperfect bone formation. People with this condition have bones that break (fracture) easily, often from mild trauma or with no apparent cause. Multiple fractures are common, and in severe cases, can occur even before birth. Milder cases may involve only a few fractures over a person's lifetime.\n\nThere are at least 19 recognized forms of osteogenesis imperfecta, designated type I through type XIX. Several types are distinguished by their signs and symptoms, although their characteristic features overlap. Increasingly, genetic causes are used to define rarer forms of osteogenesis imperfecta. Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis imperfecta. Type II (also known as perinatally lethal osteogenesis imperfecta) is the most severe. Other types of this condition, including types III (progressively deforming osteogenesis imperfecta) and IV (common variable osteogenesis imperfecta with normal sclerae), have signs and symptoms that fall somewhere between these two extremes.\n\nOther types of osteogenesis imperfecta are more severe, causing frequent bone fractures that are present at birth and result from little or no trauma. Additional features of these types can include blue sclerae of the eyes, short stature, curvature of the spine (scoliosis), joint deformities (contractures), hearing loss, respiratory problems, and a disorder of tooth development called dentinogenesis imperfecta. Mobility can be reduced in affected individuals, and some may use a walker or wheelchair. The most severe forms of osteogenesis imperfecta, particularly type II, can include an abnormally small, fragile rib cage and underdeveloped lungs. Infants with these abnormalities may have life-threatening problems with breathing and can die shortly after birth.\n\nThe milder forms of osteogenesis imperfecta, including type I, are characterized by bone fractures during childhood and adolescence that often result from minor trauma, such as falling while learning to walk. Fractures occur less frequently in adulthood. People with mild forms of the condition typically have a blue or grey tint to the part of the eye that is usually white (the sclera), and about half develop hearing loss in adulthood. Unlike more severely affected individuals, people with type I are usually of normal or near normal height.
Syringomyelia, isolated
MedGen UID:
1622554
Concept ID:
C4538540
Disease or Syndrome
Syringomyelia (Greek: 'syrinx,' pipe, and 'myelos,' marrow) is a tubular cavity in the spinal cord. It can occur sporadically in association with spinal cord tumors, inflammatory arachnoiditis, or posttraumatically. It is rarely idiopathic (less than 1% of cases). The vast majority of cases of syringomyelia are cervical, noncommunicating, and associated with an abnormality at the foramen magnum, particularly the Chiari malformation type I (CM1; 118420), as well as basilar impression (109500) and Dandy-Walker malformation (220200) (Speer et al., 2003; Levine, 2004); these cases have shown familial segregation. The form of syringomyelia discussed here is 'noncommunicating' with the fourth ventricle, but may communicate with the subarachnoid space. In contrast, 'communicating' syringomyelia, or 'hydromelia,' opens rostrally into the fourth ventricle and almost always occurs in children with hydrocephalus, Chiari malformation type II (CM2; 207950), and spina bifida (see 182940) (Levine, 2004).
Pontocerebellar hypoplasia type 10
MedGen UID:
1676575
Concept ID:
C5190575
Disease or Syndrome
Pontocerebellar hypoplasia type 10 is an autosomal recessive neurodevelopmental and neurodegenerative disorder characterized by severely delayed psychomotor development, progressive microcephaly, spasticity, seizures, and brain abnormalities, including brain atrophy and delayed myelination. Some patients have dysmorphic features and an axonal sensorimotor neuropathy (summary by Karaca et al., 2014 and Schaffer et al., 2014). For a general phenotypic description and a discussion of genetic heterogeneity of PCH, see PCH1 (607596).

Professional guidelines

PubMed

Rosenblum JS, Pomeraniec IJ, Heiss JD
Neurol Clin 2022 May;40(2):297-307. Epub 2022 Mar 31 doi: 10.1016/j.ncl.2021.11.007. PMID: 35465876Free PMC Article
Flint G
Pract Neurol 2021 Oct;21(5):403-411. Epub 2021 Aug 25 doi: 10.1136/practneurol-2021-002994. PMID: 34433683
Giner J, Pérez López C, Hernández B, Gómez de la Riva Á, Isla A, Roda JM
Neurologia (Engl Ed) 2019 Jun;34(5):318-325. Epub 2016 Dec 9 doi: 10.1016/j.nrl.2016.09.010. PMID: 27939111

Recent clinical studies

Etiology

Zheng YC, Liu YT, Wei KC, Huang YC, Chen PY, Hsu YH, Lin CL
Asian J Surg 2023 Feb;46(2):705-711. Epub 2022 Jul 20 doi: 10.1016/j.asjsur.2022.06.150. PMID: 35868963
Ciaramitaro P, Massimi L, Bertuccio A, Solari A, Farinotti M, Peretta P, Saletti V, Chiapparini L, Barbanera A, Garbossa D, Bolognese P, Brodbelt A, Celada C, Cocito D, Curone M, Devigili G, Erbetta A, Ferraris M, Furlanetto M, Gilanton M, Jallo G, Karadjova M, Klekamp J, Massaro F, Morar S, Parker F, Perrini P, Poca MA, Sahuquillo J, Stoodley M, Talamonti G, Triulzi F, Valentini MC, Visocchi M, Valentini L; International Experts Jury of the Chiari Syringomyelia Consensus Conference, Milan, November 11-13, 2019
Neurol Sci 2022 Feb;43(2):1327-1342. Epub 2021 Jun 15 doi: 10.1007/s10072-021-05347-3. PMID: 34129128
Saletti V, Farinotti M, Peretta P, Massimi L, Ciaramitaro P, Motta S, Solari A, Valentini LG
Neurol Sci 2021 Dec;42(12):4965-4995. Epub 2021 Sep 30 doi: 10.1007/s10072-021-05565-9. PMID: 34591209
Knafo S, Picard B, Morar S, Aghakhani N, Samadi M, Parker F, Benhamou D
J Gynecol Obstet Hum Reprod 2021 Mar;50(3):101970. Epub 2020 Nov 4 doi: 10.1016/j.jogoh.2020.101970. PMID: 33157323
Chatrath A, Marino A, Taylor D, Elsarrag M, Soldozy S, Jane JA Jr
Childs Nerv Syst 2019 Oct;35(10):1793-1799. Epub 2019 Jul 30 doi: 10.1007/s00381-019-04310-0. PMID: 31363830

Diagnosis

Flint G
Pract Neurol 2021 Oct;21(5):403-411. Epub 2021 Aug 25 doi: 10.1136/practneurol-2021-002994. PMID: 34433683
Leclerc A, Matveeff L, Emery E
Rev Neurol (Paris) 2021 May;177(5):498-507. Epub 2020 Aug 18 doi: 10.1016/j.neurol.2020.07.004. PMID: 32826067
Giner J, Pérez López C, Hernández B, Gómez de la Riva Á, Isla A, Roda JM
Neurologia (Engl Ed) 2019 Jun;34(5):318-325. Epub 2016 Dec 9 doi: 10.1016/j.nrl.2016.09.010. PMID: 27939111
Vandertop WP
Neuropediatrics 2014 Feb;45(1):3-9. Epub 2013 Nov 22 doi: 10.1055/s-0033-1361921. PMID: 24272770
Williams B
Neurol Res 1986 Sep;8(3):130-45. doi: 10.1080/01616412.1986.11739745. PMID: 2877406

Therapy

Gallo P, Kaliaperumal C
Adv Tech Stand Neurosurg 2022;45:317-338. doi: 10.1007/978-3-030-99166-1_10. PMID: 35976455
Yokota H, Tamaki R, Sugimoto T, Horiuchi K, Mori K, Miyamae S, Yaegaki T, Tanaka H, Iida JI
World Neurosurg 2020 Aug;140:96-100. Epub 2020 May 17 doi: 10.1016/j.wneu.2020.05.073. PMID: 32434025
Hachem LD, Ahuja CS, Fehlings MG
J Spinal Cord Med 2017 Nov;40(6):665-675. Epub 2017 Jun 1 doi: 10.1080/10790268.2017.1329076. PMID: 28571527Free PMC Article
Ahuja CS, Wilson JR, Nori S, Kotter MRN, Druschel C, Curt A, Fehlings MG
Nat Rev Dis Primers 2017 Apr 27;3:17018. doi: 10.1038/nrdp.2017.18. PMID: 28447605
Newsom-Davis J
Rev Neurol (Paris) 2004 May;160(5 Pt 2):S85-9. doi: 10.1016/s0035-3787(04)71010-3. PMID: 15269665

Prognosis

Zheng YC, Liu YT, Wei KC, Huang YC, Chen PY, Hsu YH, Lin CL
Asian J Surg 2023 Feb;46(2):705-711. Epub 2022 Jul 20 doi: 10.1016/j.asjsur.2022.06.150. PMID: 35868963
McClugage SG, Oakes WJ
J Neurosurg Pediatr 2019 Sep 1;24(3):217-226. doi: 10.3171/2019.5.PEDS18382. PMID: 31473667
Chatrath A, Marino A, Taylor D, Elsarrag M, Soldozy S, Jane JA Jr
Childs Nerv Syst 2019 Oct;35(10):1793-1799. Epub 2019 Jul 30 doi: 10.1007/s00381-019-04310-0. PMID: 31363830
Langridge B, Phillips E, Choi D
World Neurosurg 2017 Aug;104:213-219. Epub 2017 Apr 21 doi: 10.1016/j.wneu.2017.04.082. PMID: 28435116
Vandertop WP
Neuropediatrics 2014 Feb;45(1):3-9. Epub 2013 Nov 22 doi: 10.1055/s-0033-1361921. PMID: 24272770

Clinical prediction guides

Zheng YC, Liu YT, Wei KC, Huang YC, Chen PY, Hsu YH, Lin CL
Asian J Surg 2023 Feb;46(2):705-711. Epub 2022 Jul 20 doi: 10.1016/j.asjsur.2022.06.150. PMID: 35868963
Chatrath A, Marino A, Taylor D, Elsarrag M, Soldozy S, Jane JA Jr
Childs Nerv Syst 2019 Oct;35(10):1793-1799. Epub 2019 Jul 30 doi: 10.1007/s00381-019-04310-0. PMID: 31363830
Langridge B, Phillips E, Choi D
World Neurosurg 2017 Aug;104:213-219. Epub 2017 Apr 21 doi: 10.1016/j.wneu.2017.04.082. PMID: 28435116
Gower DJ, Pollay M, Leech R
J Child Neurol 1994 Jan;9(1):14-21. doi: 10.1177/088307389400900103. PMID: 8151075
Sequeira W
Clin Exp Rheumatol 1994 May-Jun;12(3):325-37. PMID: 8070170

Recent systematic reviews

Jankovic D, Hanissian A, Rotim K, Splavski B, Arnautovic KI
World Neurosurg 2022 Feb;158:1-10. Epub 2021 Oct 21 doi: 10.1016/j.wneu.2021.10.105. PMID: 34687932
Saletti V, Farinotti M, Peretta P, Massimi L, Ciaramitaro P, Motta S, Solari A, Valentini LG
Neurol Sci 2021 Dec;42(12):4965-4995. Epub 2021 Sep 30 doi: 10.1007/s10072-021-05565-9. PMID: 34591209
Garvey GP, Wasade VS, Murphy KE, Balki M
Anesth Analg 2017 Sep;125(3):913-924. doi: 10.1213/ANE.0000000000001987. PMID: 28598915
Langridge B, Phillips E, Choi D
World Neurosurg 2017 Aug;104:213-219. Epub 2017 Apr 21 doi: 10.1016/j.wneu.2017.04.082. PMID: 28435116
Wang J, Alotaibi NM, Samuel N, Ibrahim GM, Fallah A, Cusimano MD
World Neurosurg 2017 Feb;98:800-808.e2. Epub 2016 Nov 25 doi: 10.1016/j.wneu.2016.11.080. PMID: 27894943

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