A quantitative immunohistochemical study on the time-dependent course of acute inflammatory cellular response to human brain injury

Hausmann, Roland; Kaiser, A.; Lang, C.W.; Bohnert, Michael; Betz, P.

doi:10.1007/s004140050241

Cited by 75 publications

(55 citation statements)

References 17 publications

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“…The evaluation of injury patterns and types can be further impaired if vascular reactions are primarily involved and if such disturbances lead to tissue damage only secondarily [12,13].…”

Section: Introductionmentioning

confidence: 99%

No stress - no whiplash?

Castro¹,

Meyer²,

Becke³

et al. 2001

International Journal of Legal Medicine

123

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Volunteer studies of experimental, low-velocity rear-end collisions have shown a percentage of subjects to report short-lived symptoms, but the cause of these symptoms remains unknown. It is unclear whether the symptoms arise from biomechanical stress causing injury or from psychological stress causing symptom expectation and anxiety. Similarly, the cause of symptoms remains obscure in virtually all "whiplash" patients because it is impossible to identify acute pathology in many cases. In this study subjects were exposed to placebo collisions that almost completely lacked biomechanical stress. It was highly probable that if the symptoms reported following low-velocity collisions were not due to injury but to other factors (including misattribution of symptoms from other sources), then the proportion of subjects reporting symptoms would be similiar to that reported for volunteers in true (experimental) low-velocity, rear-end collisions. A total of 51 volunteers (33 males and 18 females, mean age 32.4 years) were recruited through local newspaper advertisements. An experimental set-up for a placebo collision was constructed using two standard European cars. At time T0, prior to the placebo collision, a history and physical examination was performed, including a psychological analysis (Freiburger Personality Inventory). A symptom history and physical examination were also performed at time T1, immediately after the placebo collision, and the subjects completed symptom questionnaires 3 days (time T2) and 4 weeks (time T3) after the placebo collision. Data analysis included a determination of the predictive value of psychological data for the presence of symptoms following exposure to a placebo collision. At time T1, 9 out 51 participants (17.6%) indicated symptoms. Within 3 days (time T2) after the placebo collision, 10 (19.6%) of the subjects had symptoms, and within 4 weeks (time T3) 5 subjects (9.8%) had symptoms. Of the last group, two of the five did not relate these symptoms to the "collision". Subjects who endorsed symptoms at time T1 had significantly higher scores on the psychological scale of psychosomatic disorders (measured at time T0). Subjects endorsing symptoms at time T2 had significantly higher scores on emotional instability. There was also a tendency to higher scores on this sub-scale for subjects with whiplash-associated disorders (WAD) at time T3. A discriminant analysis using all four psychological scales from time T0 had a power of 87%, 83% and 92% for correct classification of subjects as asymptomatic times T1, T2 and T3, respectively. Approximately 20% of subjects exposed to placebo, low-velocity rear-end collisions will thus indicate WAD, even though no biochemical potential for injury exists. Certain psychological profiles place an individual at higher risk for phenomenon.

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“…The evaluation of injury patterns and types can be further impaired if vascular reactions are primarily involved and if such disturbances lead to tissue damage only secondarily [12,13].…”

Section: Introductionmentioning

confidence: 99%

No stress - no whiplash?

Castro¹,

Meyer²,

Becke³

et al. 2001

International Journal of Legal Medicine

123

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“…Changes in these proteins and related acute reactants have been studied by the immunohistochemical and biochemical methods in fire fatalities [15,16,17], brain injury [18,19,20,21,22,23,24,25,26,27,28], asphyxia [9] and sudden infant death [29,30]. No studies have been undertaken of the central nervous system (CNS) in fire deaths.…”

Section: Introductionmentioning

confidence: 99%

Intranuclear ubiquitin immunoreactivity in the pigmented neurons of the substantia nigra in fire fatalities

Quan

Zhu

Oritani

et al. 2001

International Journal of Legal Medicine

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To evaluate the significance of immunohistochemical staining of ubiquitin (heat shock protein) in the midbrain for medico-legal investigation of death in fires, we examined forensic autopsy cases of fire fatalities (n = 35) in comparison with controls (n = 27; brain stem injury, acute myocardial infarction and carbon monoxide poisoning other than fire fatality). There were two intranuclear staining patterns in the nuclei of pigmented substantia nigra neurons: a type of inclusion (possible Marinesco bodies) and a diffuse staining. Percentage of nuclear ubiquitin positivity (Ub-positive %) in fire fatalities (2.7-44.7%; mean, 18.5%) was significantly higher than in brain stem injury (n = 9; 0-10.4%; mean, 4.5%) and myocardial infarction (n = 14; 1.5-14.6%; mean, 6.9%), independently of blood carboxyhemoglobin (COHb) levels. Age-dependent increase in Ub-positive % was observed in lower COHb (< 60%) cases. The intranuclear diffuse ubiquitin staining was not observed in cases of high blood cyanide level (> 1.0 microg/ml). These observations showed that intranuclear ubiquitin immunoreactivity of the pigmented substantia nigra neurons in the midbrain was induced by severe stress in fires.

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“…30 Bona et al 31 found that interleukin-1␤ and tumor necrosis factor-␣ were the first inflammatory cytokines expressed after hypoxia-ischemia in immature rats, followed by ␣-chemokines, ␤-chemokines, and finally neutrophils within vessels and brain parenchyma. In another developmental study, after intracerebral administration of interleukin-1␤, upregulation of chemokines and invasion of neutrophils were greater in young than in adult rats.…”

Section: Discussionmentioning

confidence: 99%

New Pediatric Model of Ischemic Stroke in Infant Piglets by Photothrombosis

Kuluz

Prado

et al. 2007

Stroke

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Background and Purpose-The etiology and pathophysiology of acute ischemic stroke in children differ greatly from those in adults. The purpose of this study was to establish a new pediatric model of ischemic stroke in infant piglets for use in future studies of the response of the developing brain to focal ischemic injury. Methods-Ischemic stroke was produced in male infant piglets (2 to 4 weeks old) by photothrombotic occlusion of the middle cerebral artery. Regional cerebral blood flow was measured with radiolabeled microspheres up to 4 hours after occlusion. Early histopathology, including caspase-3 immunohistochemistry for apoptosis, was examined 4 hours after ischemia. The nature of the thrombus and its interaction with vascular endothelium were assessed by electron microscopy. Results-Severe ischemia (0 to 15 mL/100 g per min) occurred rapidly in 1.4Ϯ0.2 g of tissue at 15 minutes and increased to 2.4Ϯ0.7 g at 4 hours. Similarly, moderate ischemia (16 to 30 mL/100 g per min) was measured in 1.2Ϯ0.3 g of tissue at 15 minutes and increased to 2.0Ϯ0.6 g at 4 hours. These regional cerebral blood flow values represent ischemic levels of blood flow in 20% to 25% of the volume of the ischemic hemisphere at 4 hours after ischemia. Ischemic infarction occurred in both gray and white matter, and cerebral microvessels in the ischemic hemisphere contained large numbers of inflammatory leukocytes. Caspase-3-positive cells were few in number and were found in the periphery of the infarct; cell death appeared to occur primarily by necrosis rather than apoptosis at 4 hours. Electron microscopy revealed a pure platelet thrombus firmly attached to the vascular endothelium, which in some areas appeared to be detached from the basement membrane. Conclusions-Ischemic stroke can be produced in infant piglets by middle cerebral artery photothrombosis. The stroke involved both gray and white matter and exhibited a robust inflammatory component. The mean infarct volume determined histopathologically amounted to 9.6Ϯ2.4% of the affected (ipsilateral) hemisphere, which was correlated well with the mass equivalent of tissue (12.0Ϯ3.5%), in which severe declines in regional cerebral blood flow were observed at 4 hours.

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A quantitative immunohistochemical study on the time-dependent course of acute inflammatory cellular response to human brain injury

Cited by 75 publications

References 17 publications

No stress - no whiplash?

No stress - no whiplash?

Intranuclear ubiquitin immunoreactivity in the pigmented neurons of the substantia nigra in fire fatalities

New Pediatric Model of Ischemic Stroke in Infant Piglets by Photothrombosis

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