Early Single‐Photon Emission Computed Tomography in Mild Head Trauma

Masdeu, Joseph C.; Heertum, Ronald L. Van; Kleiman, Anne; Anselmi, Gregory; Kissane, Kevin; Horng, J.; Yudd, Anthony P.; Luck, Dana; Grundman, Michael

doi:10.1111/jon199444177

Cited by 44 publications

(19 citation statements)

References 25 publications

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“…Specifically, investigators have found a greater number of abnormalities detected earlier on SPECT images compared to CT [20,25,26]. Abu-Judeh et al [27] concluded that brain perfusion SPECT is valuable and sensitive for the evaluation of cerebral perfusion changes following mild TBI; that these changes can occur without loss of consciousness; that SPECT is more sensitive than CT in detecting brain lesions; and the changes observed on SPECT imaging may explain a neurological component of the patient's symptoms in the absence of morphological abnormalities.…”

Section: Discussionmentioning

confidence: 98%

Voxel-based statistical analysis of cerebral blood flow using Tc-99m ECD brain SPECT in patients with traumatic brain injury: Group and individual analyses

Shin¹,

Kim²,

Kim³

et al. 2006

Brain Injury

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From this study, group and individual analyses of SPM2 could clearly identify the perfusion abnormalities of brain SPECT in patients with TBI. Group analysis of SPM2 showed hypoperfusion pattern in the areas including medial frontal gyrus of both hemispheres, cingulate gyrus, anterior cingulate gyrus, parahippocampal gyrus and hippocampus in the left hemisphere compared to age-matched normal controls. Also, left parahippocampal gyrus and left hippocampus were additional hypoperfusion areas. However, these findings deserve further investigation on a larger number of patients to be performed to allow a better validation of objective SPM analysis in patients with TBI.

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Section: Discussionmentioning

confidence: 98%

Voxel-based statistical analysis of cerebral blood flow using Tc-99m ECD brain SPECT in patients with traumatic brain injury: Group and individual analyses

Shin¹,

Kim²,

Kim³

et al. 2006

Brain Injury

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“…This applies to traumatic brain injury [1][2][3][4][5][6][7][8], whiplash injury [9,10], migraine [11], or Alzheimer's disease [12,13], and also neuropsychiatric systemic lupus erythematosus (SLE) [14][15][16]. Neuropsychiatric SLE has in most cases been studied in late stages of the disease; little is known of early neuropsychiatric SLE.…”

Section: Introductionmentioning

confidence: 99%

Brain glucose utilization in systemic lupus erythematosus with neuropsychiatric symptoms: A controlled positron emission tomography study

et al. 1997

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Abstract. In contrast to morphological imaging [such as magnetic resonance imaging (MRI) or computed tomography], functional imaging may be of advantage in the detection of brain abnormalities in cases of neuropsyehiatric systemic lupus erythematosus (SLE). Therefore, we studied 13 patients (aged 40_+14 years, 11 female, 2 male) with neuropsychiatric SLE who met four of the American Rheumatism Association criteria for the classification of SLE. Ten clinically and neurologically healthy volunteers served as controls (aged 40+12 years, 5 female, 5 male). Both groups were investigated using fluorine-18-1abelled fluorodeoxyglucose brain positron emission tomography (PET) and cranial MRI. The normal controls and 11 of the 13 patients showed normal MRI scans. However, PET scan was abnormal in all 13 SLE patients. Significant group-to-group differences in the glucose metabolic index (GMI=region of interest uptake/global uptake at the level of the basal ganglia and thalamus) were found in the parieto-occipital region on both sides: the GMI of the parieto-oceipital region on the right side was 0.922+0.045 in patients and 1.066+0.081 in controls (P<0.0001, Mann Whitney U test), while on the left side it was 0.892+0.060 in patients and 1.034+0.051 in controls (P=0.0002). Parietooccipital hypometabolism is a conspicuous finding in mainly MRl-negative neuropsychiatric SLE. As the parieto-occipital region is located at the boundary of blood supply of all three major arteries, it could be the most vulnerable zone of the cerebrum and may be affected at an early stage of the cerebrovascular disease.

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“…Mild human TBI is not typically associated with macroscopic structural central nervous system lesions, 28 but posttraumatic edema formation 94 or changes in cerebral blood flow and metabolic rates 55,70 have been reported. Additionally, authors of a number of studies have suggested that TAI results from TBI over a wide range of severity in humans.…”

Section: J Neurosurg / Volume 95 / November 2001mentioning

confidence: 99%

Mild head injury increasing the brain's vulnerability to a second concussive impact

Laurer¹,

Bareyre²,

Lee³

et al. 2001

Journal of Neurosurgery

291

234

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Object. Mild, traumatic repetitive head injury (RHI) leads to neurobehavioral impairment and is associated with the early onset of neurodegenerative disease. The authors developed an animal model to investigate the behavioral and pathological changes associated with RHI. Methods. Adult male C57BL/6 mice were subjected to a single injury (43 mice), repetitive injury (two injuries 24 hours apart; 49 mice), or no impact (36 mice). Cognitive function was assessed using the Morris water maze test, and neurological motor function was evaluated using a battery of neuroscore, rotarod, and rotating pole tests. The animals were also evaluated for cardiovascular changes, blood—brain barrier (BBB) breakdown, traumatic axonal injury, and neurodegenerative and histopathological changes between 1 day and 56 days after brain trauma. No cognitive dysfunction was detected in any group. The single-impact group showed mild impairment according to the neuroscore test at only 3 days postinjury, whereas RHI caused pronounced deficits at 3 days and 7 days following the second injury. Moreover, RHI led to functional impairment during the rotarod and rotating pole tests that was not observed in any animal after a single impact. Small areas of cortical BBB breakdown and axonal injury, observed after a single brain injury, were profoundly exacerbated after RHI. Immunohistochemical staining for microtubule-associated protein—2 revealed marked regional loss of immunoreactivity only in animals subjected to RHI. No deposits of β-amyloid or tau were observed in any brain-injured animal. Conclusions. On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma.

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Early Single‐Photon Emission Computed Tomography in Mild Head Trauma

Cited by 44 publications

References 25 publications

Voxel-based statistical analysis of cerebral blood flow using Tc-99m ECD brain SPECT in patients with traumatic brain injury: Group and individual analyses

Voxel-based statistical analysis of cerebral blood flow using Tc-99m ECD brain SPECT in patients with traumatic brain injury: Group and individual analyses

Brain glucose utilization in systemic lupus erythematosus with neuropsychiatric symptoms: A controlled positron emission tomography study

Mild head injury increasing the brain's vulnerability to a second concussive impact

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