Temporal dynamics of cerebral blood flow during the first year after moderate-severe traumatic brain injury: A longitudinal perfusion MRI study

Gaggi, Naomi; Ware, Jeffrey B.; Dolui, Sudipto; Brennan, Daniel; Torrellas, Julia; Wang, Ze; Whyte, John; Kim, Junghoon

doi:10.1016/j.nicl.2023.103344

Cited by 11 publications

(11 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…102 Similar findings have been reported in individuals with mild 70 and in moderate severe TBI. 103 Our correlations measure the interdependent blood flow across brain regions highlighting bilateral effects specific to TBI animals. Specifically, global blood flow correlations were reduced at 3dpi with recovery by 30dpi followed by a dramatic decline at 60dpi.…”

Section: Discussionmentioning

confidence: 99%

Delayed cerebrovascular dysfunction and social deficits after traumatic brain injury

Singh,

Gong,

et al. 2024

Preprint

View full text Add to dashboard Cite

Traumatic brain injury (TBI) survivors face debilitating long-term psychosocial consequences, including social isolation and depression. Acute TBI modifies neurovascular physiology and behavior but a gap in our understanding are the chronic physiological implications of altered brain perfusion on behavioral activities, particularly social interactions.We investigated longitudinal functional vascular networks across the brain for 2-months post- TBI and its impact on social behavior. Adult C57/BL6 male mice received a moderate cortical TBI. Behavior (foot-fault, open-field, 3-chamber social preference) was assessed at baseline, 3-, 7-, 14-, 30-, and 60-days post injury (dpi) followed by magnetic resonance imaging (MRI, 9.4T). Anatomical MRI (T2-weighted), dynamic susceptibility contrast (DSC) perfusion weighted MRI (PWI) were acquired at each temporal epoch. After the final 60dpi MRI, animals underwent transcardial perfusion fixation to map angioarchitecture. MRI data were analyzed using standardized protocols followed by cross-correlations between social behavior, cerebral perfusion, and vascular metrics.Social behavior deficits at 60dpi emerged as reduced interaction with a familiar cage-mate (partner). We observed multiphasic decrements in cerebral blood flow (CBF) encompassing lesion and perilesional cortex where acute reductions at 3-14dpi partially recovered by 30dpi, followed by significant reductions in perfusion at 60dpi. The CBF perturbations extended antero-posteriorly from the ipsilateral TBI impact site but also adulterated contralateral brain regions. CBF reductions impacted regions known to regulate social behavior including hippocampus, hypothalamus, and rhinal cortex. Alongside perfusion deficits at 60dpi, social isolation in TBI-mice emerged with a significant decline in preference to spend time with a cage mate. Cortical vascular density was also reduced corroborating the decline in brain perfusion and social interaction.Thus, the novel temporal neurovascular loss, and subsequent recovery followed by chronic decrements are broadly reflected by social interaction perturbations. Our correlations strongly implicate a linkage between vascular density, cerebral perfusion, and social interactions, where early evaluation can potentially predict long-term outcomes. Thus, our study provides a clinically relevant timeline of alterations in functional vascular recovery that can guide research for future therapeutics.

show abstract

Section: Discussionmentioning

confidence: 99%

Delayed cerebrovascular dysfunction and social deficits after traumatic brain injury

Singh,

Gong,

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…More than half of patients with severe TBI showed decreased cerebral blood flow (CBF) between one and six weeks after injury [ 38 ]. Furthermore, the CBF of GM is lower in moderate to severe TBI patients than in controls at six months and one year post-injury [ 39 ]. Additionally, moderate to severe TBI patients with DAI in the chronic phase had lower CBF than controls [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Brain Temperature as an Indicator of Cognitive Function in Traumatic Brain Injury Patients

Kitagawa,

Abiko,

Sheriff

et al. 2023

Metabolites

View full text Add to dashboard Cite

Whether brain temperature noninvasively extracted by magnetic resonance imaging has a role in identifying brain changes in the later phases of mild to moderate traumatic brain injury (TBI) is not known. This prospective study aimed to evaluate if TBI patients in subacute and chronic phases had altered brain temperature measured by whole-brain magnetic resonance spectroscopic imaging (WB-MRSI) and if the measurable brain temperature had any relationship with cognitive function scores. WB-MRSI was performed on eight TBI patients and fifteen age- and sex-matched control subjects. Brain temperature (T) was extracted from the brain’s major metabolites and compared between the two groups. The T of the patients was tested for correlation with cognitive function test scores. The results showed significantly lower brain temperature in the TBI patients (p < 0.05). Brain temperature derived from N-acetylaspartate (TNAA) strongly correlated with the 2 s paced auditory serial addition test (PASAT-2s) score (p < 0.05). The observation of lower brain temperature in TBI patients may be due to decreased metabolic activity resulting from glucose and oxygen depletion. The correlation of brain temperature with PASAT-2s may imply that noninvasive brain temperature may become a noninvasive index reflecting cognitive performance.

show abstract

“…Altered CBF often accompanies TBI as early as hours after injury in the very acute post-injury phase with decreases observed in patients ( Bouma et al, 1992 ; Soustiel et al, 2005 ; Salehi et al, 2017 ), although an increase in CBF is reported in day 1–5 post-injury and is associated with better outcome ( Kelly et al, 1997 ). Intriguingly, CBF is also reported to be reduced at 6 and 12 months post-injury in TBI survivors compared to healthy controls ( Gaggi et al, 2023 ). There are physiologic, neurologic, and immunologic changes that mediate changes in neurovascular hemodynamics to affect CBF and link alterations in sleep.…”

Section: Tbi-induced Mechanisms That Dysregulate Sleepmentioning

confidence: 99%

Sleep, inflammation, and hemodynamics in rodent models of traumatic brain injury

Green,

Carey,

Mannino

et al. 2024

Front. Neurosci.

View full text Add to dashboard Cite

Traumatic brain injury (TBI) can induce dysregulation of sleep. Sleep disturbances include hypersomnia and hyposomnia, sleep fragmentation, difficulty falling asleep, and altered electroencephalograms. TBI results in inflammation and altered hemodynamics, such as changes in blood brain barrier permeability and cerebral blood flow. Both inflammation and altered hemodynamics, which are known sleep regulators, contribute to sleep impairments post-TBI. TBIs are heterogenous in cause and biomechanics, which leads to different molecular and symptomatic outcomes. Animal models of TBI have been developed to model the heterogeneity of TBIs observed in the clinic. This review discusses the intricate relationship between sleep, inflammation, and hemodynamics in pre-clinical rodent models of TBI.

show abstract

Temporal dynamics of cerebral blood flow during the first year after moderate-severe traumatic brain injury: A longitudinal perfusion MRI study

Cited by 11 publications

References 81 publications

Delayed cerebrovascular dysfunction and social deficits after traumatic brain injury

Delayed cerebrovascular dysfunction and social deficits after traumatic brain injury

Brain Temperature as an Indicator of Cognitive Function in Traumatic Brain Injury Patients

Sleep, inflammation, and hemodynamics in rodent models of traumatic brain injury

Contact Info

Product

Resources

About