Table 1.

Summary of studies reporting direct cerebellar injury (n=12)

Studies	Design	Populations (complete data)	Lesions	Imaging	Cerebellar outcomes	Developmental outcomes	Conclusions
Bednarek [24]	Retrospective  case series	6 PT 24–28 w GA with CBI	CBI, cerebral  injury	HUS	Presence of CBI	Heterogeneous evaluation  and variable time	6/6 (100 %) PT children with CBI presented  with adverse outcome: 3 died and 3 had  impaired neurological development.
Dyet [28]	Prospective  cohort	119 PT <30 w GA	CBI, cerebral  injury	ptMRI and tMRI	Presence of CBI	18–36 months: Griffiths Mental  Developmental Scales,  CP	6/8 (75 %) PT children with CBI presented with  adverse outcome: 3 died and 3 had severe  developmental delay including 1 with CP.
Johnsen [32]	Retrospective  case series	67 PT <28 w GA, ≤1,000 g  with CP	CBI, cerebral  injury	Follow-up MRI	Presence of CBI	1.5–20 years Neurological status at  clinical follow-up	PT born subjects with CBI were more unlikely to  walk (59 %) or talk (77 %) than those with a  normal CBL (24 % and 19 %).
Limperopoulos  [22]	Retrospective  case–control	35 PT ≤32 w GA with  isolated CBI, 35 controls PT ≤32 w with  no CBI or cerebral injury,  16 PT with CBI + cerebral  injury	CBI, cerebral  injury	HUS, follow-up  MRI for PT  with an abnor-  mal HUS	Presence of  isolated CBI or  combined CBI  with cerebral  injury	2–5 years: Neuro exam MSEL PDMS VABS CBCL M-CHAT SCQ	Isolated CBI was significantly associated with  severe developmental delay in motor skills  (40–54 %), language (37–40 %), and  cognition (40–46 %); deficits in daily living  activities performance (40 %), internalizing  behavioral problems (34 %) and autistic  features (37 %). Cerebral injury and more extended cerebellar  lesions (bilateral vs unilateral) were associated  with greater deficits. Vermal injury was associated with socialization  difficulties (VABS) and positive autism  screening (M-CHAT+SCQ).
Limperopoulos  [26]	Prospective  cohort	40 PT ≤32 w GA with  isolated CBI	CBI	HUS, follow-up  MRI	Regional cerebral  volume  contralateral to  CBI	18–63 months: Neuro exam MSEL PDMS CBCL M-CHAT	Greater dorsolateral prefrontal volume was  associated with better M-CHAT and CBCL  internalizing scores. Greater sensorimotor volume was associated  with higher PDMS gross motor score. Greater premotor volume was associated with  higher Mullen cognitive scores. Greater midtemporal volume was associated with  higher Mullen Expressive language score.
Mercuri [11]	Retrospective  case series	10 PT ≤33 w GA with CBI	CBI, cerebral  injury	HUS, follow-up  MRI	Presence of CBI	7 month–8 years: Neuro exam, motor  development	All PT children with CBI had mild (40 %) to  severe (60 %) motor delay.
Messerchmidt  [23]	Retrospective  case–control	31 PT ≤31 w GA with severe  volume reduction in CBL  on HUS; 31 PT GA and gender  matched with cerebral  injury but normal CBL on  HUS	CBL volume  reduction,  cerebral injury	HUS	Presence of CBI	24–36 months: Neuro exam BSID-II: Motor +  cognitive composites	PT children with CBI had significantly worse  neurodevelopmental outcomes than children  without CBI. All children with CBI (100 %) had CP and had  neurodevelopmental delay (motor and  cognitive).
Steggerda [9]	Prospective  cohort	108 PT <32 w GA	CBI, cerebral  injury	HUS, tMRI	Presence of small  CBI	2 years: Neuro exam GMFCS BSID-III: Motor +  cognitive composites CBCL	In PT infants with small CBI, behavioral  problems were found in 15–23 %, motor  delay in 15 %and mild or severe  neurodevelopmental outcome in 61.5 %.  None of the children with small CBI had  cognitive delay. Small CBI was not significantly associated with  poorer neurodevelopmental outcomes or  problematic behavior when compared to  preterm without CBI.
Tam [29]	Prospective  cohort	94 PT ≤34 w GA	CBI, cerebral  injury	HUS, ptMRI &  tMRI	Presence of CBI	3–6 years: Neuro exam WPPSI-III (IQ)	Of the 8 PT infants with CBI detectable on MRI  only, 4 (50 %) presented with abnormal  neurological examination findings at  3–6 years of age. CBI was significantly associated with  neurological anomalies, but not with IQ  evaluated at follow-up.
Van Kooji [30]	Prospective  cohort	112 PT <31 w GA	CBI, cerebral  injury	tMRI,	Presence of CBI,  CBL volume  and H1-MRS	2 years: BSID-III: Motor +  cognitive composites	No significant differences in BSID-III scores  between PT children with and without CBI. Cognitive scores were associated with CBL  volume and CBL NAA/Cho ratio but not CBI. No significant association was found between  CBL variables and the motor composite.
Zafeiriou [31]	Retrospective  case series	12 PT <28 w GA with  pontocerebellar  hypoplasia	Pontocerebellar  hypoplasia,  cerebral injury	Follow-up MRI	Presence of  pontocerebellar  hypoplasia	21–90 months: Neuro exam, motor  development	All PT children with pontocerebellar hypoplasia  (100 %) had CP and presented with  movement disorders.
Zayek [25]	Retrospective  cohort	1120 PT <28 w GA	CBI, cerebral  injury	HUS	Presence of CBI	12–18 months: BSID-II or BSID-III: Motor + cognitive  composites	PT infants with CBI had significantly more  neurodevelopmental impairments. Of the 32 children with CBI, 15 (50 %) had  cognitive impairment, 18 (56 %) motor  impairment including CP in 10 (32 %). Lesions isolated to the cerebellar hemispheres  were associated with lower cognitive scores,  but not with motor skills. Lesions involving the vermis were associated  with motor and cognitive impairments.

BSID Bayley Scale for Infant Development, CBCL Child Behavior Checklist, CBI cerebellar injury, CBL cerebellum, CP cerebral palsy, GA gestational age, H¹ -MRS proton magnetic resonance spectroscopy, HUS head ultra sound, M-CHAT Modified Checklist for Autism in Toddlers, MSEL Mullen Scales for Early Learning, PDMS Peabody Developmental Motor Scales, PT preterm, ptMRI preterm MRI, SCQ Social Communication Questionnaire, tMRI term or term-equivalent MRI, VABS Vineland Adaptative Behavior Scale, w week, WPPSI Wechsler Preschool and Primary Scale of Intelligence