Cerebral Hemodynamic Changes After Wartime Traumatic Brain Injury

Razumovsky, Alexander Y.; Tigno, Teodoro; Hochheimer, Sven M.; Stephens, Fred L.; Bell, Randy S.; Vo, Alexander H.; Severson, Meryl A.; Marshall, Scott; Oppenheimer, Stephen; Ecker, Robert D.; Armonda, Rocco A.

doi:10.1007/978-3-7091-1192-5_19

Cited by 16 publications

(14 citation statements)

References 20 publications

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“…The authors noted that radiographic vasospasm incidence correlated with extent of injury. In a study of combat victims with TBI, TCD signs of mild, moderate, and severe vasospasms were observed in 37%, 22%, and 12% of patients [14]. Zubkov et al prospectively assessed 90 head injury patients.…”

Section: Evaluation Of Vasospasm In Traumatic Subarachnoid Hemorrhagementioning

confidence: 99%

Cerebral Vasospasm in Traumatic Brain Injury

Kramer

Winer

Pease

et al. 2013

Neurology Research International

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Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%–68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%–16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinical course tends to be milder, although extreme cases may occur. Traumatic vasospasm can occur in the absence of subarachnoid hemorrhage. Surveillance transcranial Doppler ultrasonography (TCD) has been utilized to monitor for radiographic vasospasm following TBI. However, effective treatment modalities remain limited. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be used judiciously in TBI patients, and calcium-channel blockers have offered mixed clinical results. Currently, the paucity of large prospective cohort studies and level-one data limits the ability to form evidence-based recommendations regarding the diagnosis and management of vasospasm associated with TBI.

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Section: Evaluation Of Vasospasm In Traumatic Subarachnoid Hemorrhagementioning

confidence: 99%

Cerebral Vasospasm in Traumatic Brain Injury

Kramer

Winer

Pease

et al. 2013

Neurology Research International

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“…166 Recently, signs of mild, moderate, and severe VSP were observed in wartime TBI patients by TCD in 37%, 22%, and 12% of patients, respectively. 167 VSP detected by TCD may precede neurologic deficits and prompt earlier intervention. 168 Hemodynamic changes seen in intracerebral vasculature after tSAH can be diagnosed and monitored using TCD; therefore, the primary application of TCD in tSAH is in the daily surveillance of VSP.…”

Section: Tcd and Vasospasm Diagnosis After Subarachnoid Hemorrhagementioning

confidence: 99%

“…168 Hemodynamic changes seen in intracerebral vasculature after tSAH can be diagnosed and monitored using TCD; therefore, the primary application of TCD in tSAH is in the daily surveillance of VSP. 151,167 Angiographic VSP has been classically reported to occur between Days 4 and 14 after aSAH, 169 but variations to this timeline do occur, and VSP has been reported as early as within 48 h in up to 13% of patients and as late as Day 16 170 or 17. 171-174 VSP could be evident up to Day 20 by TCD.…”

Section: Tcd and Vasospasm Diagnosis After Subarachnoid Hemorrhagementioning

confidence: 99%

A Review of the Effectiveness of Neuroimaging Modalities for the Detection of Traumatic Brain Injury

Amyot

Arciniegas

et al. 2015

Journal of Neurotrauma

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183

147

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The incidence of traumatic brain injury (TBI) in the United States was 3.5 million cases in 2009, according to the Centers for Disease Control and Prevention. It is a contributing factor in 30.5% of injury-related deaths among civilians. Additionally, since 2000, more than 260,000 service members were diagnosed with TBI, with the vast majority classified as mild or concussive (76%). The objective assessment of TBI via imaging is a critical research gap, both in the military and civilian communities. In 2011, the Department of Defense (DoD) prepared a congressional report summarizing the effectiveness of seven neuroimaging modalities (computed tomography [CT], magnetic resonance imaging [MRI], transcranial Doppler [TCD], positron emission tomography, single photon emission computed tomography, electrophysiologic techniques [magnetoencephalography and electroencephalography], and functional near-infrared spectroscopy) to assess the spectrum of TBI from concussion to coma. For this report, neuroimaging experts identified the most relevant peer-reviewed publications and assessed the quality of the literature for each of these imaging technique in the clinical and research settings. Although CT, MRI, and TCD were determined to be the most useful modalities in the clinical setting, no single imaging modality proved sufficient for all patients due to the heterogeneity of TBI. All imaging modalities reviewed demonstrated the potential to emerge as part of future clinical care. This paper describes and updates the results of the DoD report and also expands on the use of angiography in patients with TBI.

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“…Vasospasms resulting from TBI can lead to ischemic episodes, energy depletion and cell necrosis; in other words, an inability for brain cells to compensate for increased metabolic functional overload (97). Vasospasms are frequently associated with recurrent intracranial hypertension and subarachnoid hemorrhage (142, 181). Blast TBI, in particular, can cause cerebral vasospasms that last for more than 30 days and are associated with altered mental status (103).…”

Section: Vasospasms Subarachnoid Hemorrhage Edema and Ischemic Hypoxiamentioning

confidence: 99%

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

Logsdon

Lucke‐Wold

Turner

et al. 2015

Comprehensive Physiology

127

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Traumatic brain injury (TBI) is acquired from an external force, which can inflict devastating effects to the brain vasculature and neighboring neuronal cells. Disruption of vasculature is a primary effect that can lead to a host of secondary injury cascades. The primary effects of TBI are rapidly occurring while secondary effects can be activated at later time points and may be more amenable to targeting. Primary effects of TBI include diffuse axonal shearing, changes in blood brain barrier (BBB) permeability, and brain contusions. These mechanical events, especially changes to the BBB, can induce calcium perturbations within brain cells producing secondary effects, which include cellular stress, inflammation, and apoptosis. These secondary effects can be potentially targeted to preserve the tissue surviving the initial impact of TBI. In the past, TBI research had focused on neurons without any regard for glial cells and the cerebrovasculature. Now a greater emphasis is being placed on the vasculature and the neurovascular unit following TBI. A paradigm shift in the importance of the vascular response to injury has opened new avenues of drug treatment strategies for TBI. However, a connection between the vascular response to TBI and the development of chronic disease has yet to be elucidated. Long-term cognitive deficits are common amongst those sustaining severe or multiple mild TBIs. Understanding the mechanisms of cellular responses following TBI is important to prevent the development of neuropsychiatric symptoms. With appropriate intervention following TBI, the vascular network can perhaps be maintained and the cellular repair process possibly improved to aid in the recovery of cellular homeostasis.

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Cerebral Hemodynamic Changes After Wartime Traumatic Brain Injury

Cited by 16 publications

References 20 publications

Cerebral Vasospasm in Traumatic Brain Injury

Cerebral Vasospasm in Traumatic Brain Injury

A Review of the Effectiveness of Neuroimaging Modalities for the Detection of Traumatic Brain Injury

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

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