Sports Concussion Assessment Tool 5 (SCAT5) is a standardized concussion assessment, available as a pdf or online , used by healthcare providers when a concussion is suspected in athletes ages 12 and older.

The Fifth International Conference on Concussion in Sport was held in Berlin in October 2016. A series of 12 questions and subquestions was developed and the expert panel members were required to perform a systematic review to answer each question. Following presentation at the Berlin meeting of the systematic review, poster abstracts and audience discussion, the summary Consensus Statement was produced. Further, a series of tools for the management of sport-related concussion was developed, including the Sport Concussion Assessment Tool Fifth edition (SCAT5), the Child SCAT5, and the Concussion Recognition Tool Fifth edition 1).



The SCAT5 cannot be performed correctly in less than 10 minutes.

The revision of the SCAT3 (first published in 2013) culminated in the SCAT5. The revision was based on a systematic review and synthesis of current research, public input and expert panel review as part of the 5th International Consensus Conference on Concussion in Sport held in Berlin in 2016. The SCAT5 is intended for use in those who are 13 years of age or older. The Child SCAT5 is a tool for those aged 5-12 years, which is discussed elsewhere 2).

The Sports Concussion Assessment Tool-5th Edition (SCAT5) and the child version (Child SCAT5) are the current editions of the SCAT and have updated the memory testing component from previous editions.

To achieve consensus, via an international panel of SRC experts, on which athlete/player and parent/caregiver demographic variables should be considered for inclusion in future editions of the SCAT/Child SCAT respectively.

Methods: A two-round modified Delphi technique, overseen by a steering committee, invited 41 panellists to achieve expert consensus (≥80% agreement). The first round utilised open questions to generate demographic variables; the second round used a five-point ordinal item to rank the importance of including each variable in future editions of the SCAT/Child SCAT.

Results: 15 experts participated in at least one Delphi round. 29 athlete/player and eight parent/caregiver variables reached consensus for inclusion in the SCAT, whereas two parent/caregiver variables reached consensus for exclusion. 28 athlete/player and four parent/caregiver variables reached consensus for the Child SCAT, whereas two parent/caregiver variables reached consensus for exclusion. Key categories of variables included the following: concussion/sport details, personal medical conditions and family medical history.

Conclusion: This study provides a list of athlete/player and parent/caregiver demographic variables that should be considered in future revisions of the SCAT/Child SCAT. By considering (and ultimately likely including) a wider and standard set of additional demographic variables, the Concussion in Sport experts will be able to provide clinicians and researchers with data that may enhance interpretation of the individual’s data and the building of larger datasets 3).

In a prospective observational study, the ability of the SCAT5 and ChildSCAT5 to differentiate between children with and without a concussion was examined. Concussed children (n=91) and controls (n=106) were recruited from an emergency department in three equal-sized age bands (5-8/9-12/13-16 years). Analysis of covariance models (adjusting for participant age) were used to analyze group differences on components of the SCAT5. On the SCAT5 and ChildSCAT5, respectively, youth with concussion reported a greater number (d=1.47; d=0.52) and severity (d=1.27; d=0.72) of symptoms than controls (all p<0.001). ChildSCAT5 parent-rated number (d=0.98) and severity (d=1.04) of symptoms were greater for the concussion group (all p<0.001). Acceptable levels of between-group discrimination were identified for SCAT5 symptom number (AUC=0.86) and severity (AUC=0.84) and ChildSCAT5 parent-rated symptom number (AUC=0.76) and severity (AUC=0.78). The findings support the utility of the SCAT5 and ChildSCAT5 to accurately distinguish between children with and without a concussion 4).

A study aimed to validate this new memory component against the Rey Auditory Verbal Learning Test (RAVLT) as the validated standard. This prospective, observational study, carried out within The Royal Children’s Hospital Emergency Department, Melbourne, Australia, recruited 198 participants: 91 with concussion and 107 upper limb injury or healthy sibling controls. Partial Pearson correlations showed that memory acquisition and recall on delay aspects of the SCAT5 were significantly correlated with the RAVLT equivalents when controlling for age (p < 0.001, r = 0.565 and p < 0.001, r = 0.341, respectively). Factor analysis showed that all RAVLT and SCAT5 memory components load on to the same factor, accounting for 59.13% of variance. Logistic regression models for both the RAVLT and SCAT5, however, did not predict group membership (p > 0.05). Receiver operating curve analysis found that the area under the curve for all variables and models was below the recommended 0.7 threshold. This study demonstrated that the SCAT5 and Child SCAT5 memory paradigm is a valid measure of memory in concussed children 5).

The two-week test-retest reliability of the SCAT5 baseline scores varied from moderate to high. However, there was considerable individual variability on the SAC and mBESS scores and most players have notable short-term fluctuation on performance even if uninjured. Recommendations for interpreting change on the SCAT5 are provided 6).


Davis GA, Ellenbogen RG, Bailes J, Cantu RC, Johnston KM, Manley GT, Nagahiro S, Sills A, Tator CH, McCrory P. The Berlin International Consensus Meeting on Concussion in Sport. Neurosurgery. 2018 Feb 1;82(2):232-236. doi: 10.1093/neuros/nyx344. PMID: 29106653.

Echemendia RJ, Meeuwisse W, McCrory P, Davis GA, Putukian M, Leddy J, Makdissi M, Sullivan SJ, Broglio SP, Raftery M, Schneider K, Kissick J, McCrea M, Dvořák J, Sills AK, Aubry M, Engebretsen L, Loosemore M, Fuller G, Kutcher J, Ellenbogen R, Guskiewicz K, Patricios J, Herring S. The Sport Concussion Assessment Tool 5th Edition (SCAT5): Background and rationale. Br J Sports Med. 2017 Jun;51(11):848-850. doi: 10.1136/bjsports-2017-097506. Epub 2017 Apr 26. PMID: 28446453.

Shanks MJ, McCrory P, Davis GA, Echemendia RJ, Gray AR, Sullivan SJ. Developing common demographic data elements to include in future editions of the SCAT and Child SCAT: a modified international Delphi study. Br J Sports Med. 2020 Aug;54(15):906-912. doi: 10.1136/bjsports-2018-100482. Epub 2019 Oct 11. PMID: 31604697.

Babl FE, Anderson V, Rausa VC, Anderson N, Pugh R, Chau T, Clarke C, Fabiano F, Fan F, Hearps S, Parkin G, Takagi M, Davis G. Accuracy of Components of the SCAT5 and ChildSCAT5 to Identify Children with Concussion. Int J Sports Med. 2021 Aug 16. doi: 10.1055/a-1533-1700. Epub ahead of print. PMID: 34399426.

Shapiro JS, Hearps S, Rausa VC, Anderson V, Anderson N, Pugh R, Chau T, Clarke C, Davis GA, Fabiano F, Fan F, Parkin GM, Takagi M, Babl FE. Validation of the SCAT5 and Child SCAT5 Word-List Memory Task. J Neurotrauma. 2021 May 10. doi: 10.1089/neu.2020.7414. Epub ahead of print. PMID: 33765839.

Hänninen T, Parkkari J, Howell DR, Palola V, Seppänen A, Tuominen M, Iverson GL, Luoto TM. Reliability of the Sport Concussion Assessment Tool 5 baseline testing: A 2-week test-retest study. J Sci Med Sport. 2021 Feb;24(2):129-134. doi: 10.1016/j.jsams.2020.07.014. Epub 2020 Aug 5. PMID: 32868203.

Pediatric cerebrovascular disease epidemiology

Pediatric cerebrovascular disease epidemiology

The incidence of pediatric stroke is 1 in 5000, and if hemiplegic cerebral palsy due to vaso-occlusive stroke is included, the number could be as high as 1 in 3000. Additionally, cerebrovascular disease is 1 of the top 10 causes of death in infants younger than 1 year. Finally, 20% to 30% of children with arterial ischemic stroke will have recurrent strokes, even with treatment. Stroke in children differs from stroke in adults. Not only is it rare, but its presentation is subtle—particularly in infants—and even with a focal hemiplegia there is a wide differential diagnosis. Coagulation mechanisms, the arteries, and the neurological systems are all different in children, and each of these plays a large role in stroke. The causes of pediatric stroke do not include atherosclerosis, so a myriad of other risk factors and associations exist and are unique for each age group. The causes of pediatric stroke are poorly understood, and although this is a fertile area of research, clinical trials in the field are lacking. Currently, any treatment guidelines or tools being used to treat children with stroke either come from the field of adult stroke or are based on empirical information.

More than 95% of children with ischemic stroke have an underlying thrombus occluding an artery or a vein, and our understanding of clot pathogenesis in children is increasing. Whereas in adults, platelet clots predominantly form secondary to atherosclerosis, in children and infants there is likely a higher fibrin composition, which may require a different treatment strategy. Although anticoagulation is typically used, it is not known whether anticoagulation is more effective than aspirin. There are also major clinical challenges, the most significant of which is that the diagnosis is not made and the stroke is missed entirely or that the diagnosis is severely delayed and by the time the diagnosis is made, the infarct is much larger 1).

In 1978 A 10-year review of the Mayo Clinic experience with childhood cerebrovascular disease unrelated to birth, intracranial infection, or trauma identified 69 patients (38 with ischemic stroke, and 31 with subarachnoid or intracerebral hemorrhage). Although children with cerebral infarction had better survival, they experienced more residual disability than children with cerebral hemorrhage. The medical records-linkage system for Rochester, Minnesota residents made it possible for the first time to study cerebrovascular disease in a well-defined childhood population. Records from all medical facilities serving this population (average of 15,834 resident children) showed four strokes over 10 years (average annual incidence rate of 2.52 cases per 100,000 per year) 2).

In 2018 a study reported the period prevalence, incidence, and risk factors of pediatric stroke in Taiwan.

All Taiwan inhabitants aged 1 month to 18 years registered in the National Health Insurance Research Database between 2010 and 2011 were enrolled in this study. Factors including age, sex, location, and household income levels were collected. Incidence, period prevalence, mortality rate, and the possible risks were completely evaluated. Outcomes and results: Hemorrhagic stroke has a significantly higher mortality rate than ischemic stroke (27.6% vs. 10.2%, P<0.05). Risk factors or underlying diseases for stroke were identified in 77.8% of the patients and 16.2% had more than one risk factor. The most common risk factors were vascular diseases (26.3%), infection (14.0%), and cardiac disorders (9.1%).

Infants younger than 2 years, boys, and children in lower socioeconomic status have a significantly higher risk of stroke. Hemorrhagic stroke has a significantly higher mortality rate than ischemic stroke. More than half of the children with stroke had underlying diseases and the causes of hemorrhagic stroke are significantly different from ischemic stroke 3).

In 2019 Surmava et al. sought to evaluate in -Ontario, the incidence and characteristics of pediatric stroke and TIA including care gaps and the predictive value of International Classification of Diseases (ICD) codes.

A retrospective chart review was conducted at 147 Ontario pediatric and adult acute care hospitals. Pediatric stroke and TIA cases (age < 18 years) were identified using ICD-10 code searches in the 2010/11 Canadian Institute for Health Information’s Discharge Abstract Database (CIHI-DAD) and National Ambulatory Care Reporting System (NACRS) databases in the Ontario Stroke Audit.

Among 478 potential pediatric strokes and TIA cases identified in the CIHI-DAD and NACRS databases, 163 were confirmed as cases of stroke and TIA during the 1-year study period. The Ontario stroke and TIA incidence rate was 5.9 per 100,000 children (3.3 ischemic, 1.8 hemorrhagic, and 0.8 TIA). The mean age was 6.4 years (16% neonate). Nearly half were not imaged within 24 h of arrival in emergency and only 56% were given antithrombotic treatment. At discharge, 83 out of 121 (69%) required health care services post-discharge. Overall positive predictive value (PPV) of ICD-10 stroke and TIA codes was 31% (range 5-74%) and yield ranged from 2.4 to 29% for acute stroke or TIA event; code I63 achieved maximal PPV and yield.

This population-based study yielded a higher incidence rate than prior North-American studies. Important care gaps exist including delayed diagnosis, lack of expert care, and departure from published treatment guidelines. Variability in ICD PPV and yield underlines the need for prospective data collection and for improving the pediatric stroke and TIA coding processes 4).

It is believed that the incidence in the Hospital Universitario “Dr. Jose Eleuterio Gonzalez,” Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon, Mexico is higher than it appears.

A study by Garza-Alatorre et al. aimed to assess the incidence and characteristics of pediatric stroke in this university hospital. Likewise, this study seeks to evaluate if a longer symptoms-to-diagnosis time is associated with mortality in patients with ischemic stroke.

Methods: A retrospective study including children with stroke admitted to the UANL University Hospital from January 2013 to December 2016.

Results: A total of 41 patients and 46 stroke episodes were admitted. About 45.7% had an ischemic stroke and 54.3% had a hemorrhagic stroke. Mortality of 24.4% and morbidity of 60.9% were recorded. Regarding ischemic and hemorrhagic stroke, and increased symptoms-to-diagnosis time and a higher mortality were obtained with a relative risk of 2.667 (95% confidence interval [CI]: 1.09-6.524, p = 0.013) and 8.0 (95% CI: 2.18-29.24, p = < 0.0001), respectively. A continuous increase in the incidence rate, ranging from 4.57 to 13.21 per 1,000 admissions comparing the first period (2013) versus the last period (2016), p = 0.02, was found in our center.

Pediatric stroke is a rare disease; however, its incidence shows a continuous increase. More awareness toward pediatric stroke is needed 5).


Bowers KJ, Deveber GA, Ferriero DM, Roach ES, Vexler ZS, Maria BL. Cerebrovascular disease in children: recent advances in diagnosis and management. J Child Neurol. 2011 Sep;26(9):1074-100. doi: 10.1177/0883073811413585. Epub 2011 Jul 21. PMID: 21778188; PMCID: PMC5289387.

Schoenberg BS, Mellinger JF, Schoenberg DG. Cerebrovascular disease in infants and children: a study of incidence, clinical features, and survival. Neurology. 1978 Aug;28(8):763-8. doi: 10.1212/wnl.28.8.763. PMID: 567292.

Chiang KL, Cheng CY. Epidemiology, risk factors and characteristics of pediatric stroke: a nationwide population-based study. QJM. 2018 Jul 1;111(7):445-454. doi: 10.1093/qjmed/hcy066. PMID: 29648667.

Surmava AM, Maclagan LC, Khan F, Kapral MK, Hall RE, deVeber G. Incidence and Current Treatment Gaps in Pediatric Stroke and TIA: An Ontario-Wide Population-Based Study. Neuroepidemiology. 2019;52(3-4):119-127. doi: 10.1159/000493140. Epub 2019 Jan 17. PMID: 30654369.

Garza-Alatorre G, Carrion-Garcia AL, Falcon-Delgado A, Garza-Davila EC, Martinez-Ponce de Leon AR, Botello-Hernandez E. Characteristics of Pediatric Stroke and Association of Delayed Diagnosis with Mortality in a Mexican Tertiary Care Hospital. Neuropediatrics. 2021 Jul 14. doi: 10.1055/s-0041-1731802. Epub ahead of print. PMID: 34261144.

Cleidocranial dysostosis

Cleidocranial dysostosis

Cleidocranial dysplasia is a rare genetic condition that affects teeth and bones, such as the skullfacespine, collarbones, and legs. The bones in people with CCD might be formed differently or might be more fragile than normal, and certain bones such as collarbones may be absent.

Runx2, also known as Cbfa1, is a multifunctional transcription factor essential for osteoblast differentiation. It also plays a major role in chondrocyte maturation, mesenchymal stem cell differentiation, cleidocranial dysplasia, and the growth and metastasis of tumors.

A review encountered several cases of orthodontic implications but a few cases on cranial defect approach.

The articles present literature that is unanimous on the recommendation of expectant conduct in children since the cranial block can occur spontaneously, even if the delayed form 1).

Hypophosphatasia (HPT) and cleidocranial dysplasia (CCD) are characterized by both defective ossification and bone mineralization. Patients usually present with craniosynostosis and cranial defects which in many cases require surgical repair.

There re only 2 reported case of combined HPT and CCD in the literature.

The reported case of Blionas et al. involves a 3.5-year-old girl with concomitant homozygous CCD and heterozygous HPT. The child had an extended cranial defect since birth which improved with the administration of Strensiq and was followed until preschool age. Bone defects were relatively minor on revaluation. Due to the limited final defect, we decided not to intervene. In HPT-CCD patients, bone defects are overestimated due to osteomalacia, and thus, management strategy should be less aggressive. They should undergo surgical repair with cranioplasty with the use of cement and/or titanium meshes in case of extended final defects 2).

A case of posterior fossa subdural hematoma (PFSDH) after vaginal delivery in a neonate with CCD, which presented with several clinical symptoms such as apnea, vomiting, and bradycardia. Our patient, who had a family history of CCD, developed apnea and vomiting shortly after birth; PFSDH was detected by head computed tomography, and the patient recovered well following standard medical treatment.

The prognosis of intracranial hemorrhage in neonates with CCD is generally poor. In neonates, PFSDH occurs by the following mechanism: the distortion of the infant’s cranium during delivery, by the strong force, causes elongation of the falx and angulation of the tentorium that leads to tears in the posterior fossa venous structures, which then cause bleeding into the subdural space. In CCD, the forces occurring during vaginal delivery may cause excessive distortion of the fragile skull. An awareness of CCD is hence important to avoid vaginal delivery in prenatally diagnosed CCD cases with a family history of CCD 3).

A 40-yr-old woman presented with sensory disturbance on the left side of the body. Magnetic resonance imaging (MRI) revealed cerebellar tonsil herniation into the foramen magnum with cervical syringomyelia, and computed tomography additionally revealed skull anomalies: fontanel closure insufficiencies, cranial dysraphism, thin cranial bone, and dentition abnormalities. We diagnosed as symptomatic CM1 with syringomyelia associated with cleidocranial dysplasia, which is a dominantly inherited autosomal bone disease. Cerebral angiography revealed a developed right occipital sinus and hypoplasia of the bilateral transverse sinus. We performed FMD, paying special attention to the developed occipital sinus using ICG-VA to ensure a safe duraplasty. The angiography clearly highlighted a right-sided occipital sinus with a high contrast ratio, and no left-sided occipital sinus was visible. After a dural incision in a unilateral curvilinear fashion was safely completed, expansive duraplasty was performed. The sensory disorders experienced by the patient disappeared postoperatively. Postoperative MRI revealed elevation of the cerebellar tonsil and decreasing of the syringomyelia.

Conclusion: Additional assessment using intraoperative ICG-VA provides useful information for a safe FMD, particularly in patients with complicated cerebral venous circulation anomalies 4).

A rare case of successful cranioplasty using a modified split calvarial graft technique in a patient with cleidocranial dysplasia 5).


Azevedo Almeida LC, Faraj de Lima FB, Matushita H, Valença MM, Ferreira Castro TL, de Mendonça RN. Cleidocranial dysplasia, a rare skeletal disorder with failure of the cranial closure: case-based update. Childs Nerv Syst. 2020 Dec;36(12):2913-2918. doi: 10.1007/s00381-020-04831-z. Epub 2020 Jul 30. PMID: 32734401.

Blionas A, Friehs GM, Zerris VA. Hypophosphatasia and cleidocranial dysplasia-a case report and review of the literature: the role of the neurosurgeon. Childs Nerv Syst. 2021 Jun 15. doi: 10.1007/s00381-021-05261-1. Epub ahead of print. PMID: 34131769.

Nagasaka S, Suzuki K, Saito T, Tanaka K, Yamamoto J. Posterior fossa subdural hematoma in a neonate with cleidocranial dysostosis after a spontaneous vaginal delivery: a case report. Childs Nerv Syst. 2021 Feb;37(2):683-686. doi: 10.1007/s00381-020-04689-1. Epub 2020 Jun 5. PMID: 32504170.

Omoto K, Takeshima Y, Nishimura F, Nakagawa I, Motoyama Y, Park YS, Nakase H. Additional Assessment of Developed Occipital Sinus Using Intraoperative Indocyanine Green Videoangiography for a Safe Foramen Magnum Decompression-Technical Case Report. Oper Neurosurg (Hagerstown). 2020 Oct 15;19(5):E533-E537. doi: 10.1093/ons/opaa125. PMID: 32421802.

Jung YT, Cho JI, Lee SP. Cranioplasty Using a Modified Split Calvarial Graft Technique in Cleidocranial Dysplasia. J Korean Neurosurg Soc. 2015 Jul;58(1):79-82. doi: 10.3340/jkns.2015.58.1.79. Epub 2015 Jul 31. PMID: 26279819; PMCID: PMC4534745.
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