Brain-Stem Injury and Long Survival—a Forensic Analysis

1983 ◽  
pp. 109-114 ◽  
Author(s):  
H. Bratzke
Keyword(s):  
Brain Stem ◽  
Forensic Analysis ◽  
Long Survival ◽  
Brain Stem Injury

Evaluation of brain-stem dysfunction following severe fluid-percussion head injury to the cat

1991 ◽  
Vol 74 (2) ◽  
pp. 270-277 ◽  
Author(s):  
Katsuji Shima ◽  
Anthony Marmarou
Keyword(s):  
Brain Stem ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Brain Stem Injury ◽  
Group 2 ◽  
High Level ◽  
Subarachnoid Hemorrhages ◽  
Fine Print ◽  
Group 1

✓ The degree of brain-stem dysfunction associated with high-level fluid-percussion injury (3.0 to 3.8 atm) was investigated in anesthetized cats. Measurements were made of the animals' intracranial pressure (ICP), pressure-volume index (PVI), far-field brain-stem auditory evoked responses (BAER's), and cerebral blood flow (CBF). The animals were classified into two groups based on the severity of neuropathological damage to the brain stem after trauma: Group 1 had mild intraparenchymal and subarachnoid hemorrhages and Group 2 had severe intraparenchymal and subarachnoid hemorrhages. The ICP values in Group 1 were insignificantly lower than those in Group 2, while the PVI values in Group 2 were clearly lower (p < 0.05). Immediately after the injury, peaks II, III, and IV of the BAER's demonstrated a transitory and marked suppression. One Group 1 and two Group 2 animals showed the disappearance of peak V. In Group 1, the latencies of peak II, III, and IV gradually increased until 60 to 150 minutes postinjury, then returned to 95% of baseline value at 8 hours; however, the animals in Group 2 showed poor recovery of latencies. Two hours after brain injury, the CBF decreased to 40% of the preinjury measurement in both groups (p < 0.001). In contrast to Group 2, the CBF in Group 1 returned to 86.8% of the preinjury measurement by 8 hours following the injury. Changes in PVI, BAER, and CBF correlated well with the degree of brain-stem injury following severe head injury'- These data indicate that high-level fluid-percussion injury (> 3.0 atm) is predominantly a model of brain-stem injury.

Some syndromes of brain stem injury in dogs

1935 ◽  
Vol 31 (3-4) ◽  
pp. 496-500
Author(s):  
I. Ya. Churaev
Keyword(s):  
Brain Stem ◽  
Severe Damage ◽  
Decerebrate Rigidity ◽  
Brain Stem Injury ◽  
The Brain

Experimenting on the brainstem in a dog to obtain decerebrated rigidity, I noticed a variety of other symptoms that occur with decerebration and present either with decerebrate rigidity, or in cases of severe damage without it. It seemed that the description of these symptoms, related to certain levels of damage to the brain stem, might be of interest, since the symptomatology of injuries and diseases of the brain stem, despite its richness, still cannot be considered exhausted.

Fetal heart rate variability and brain stem injury after asphyxia in preterm fetal sheep

2004 ◽  
Vol 287 (4) ◽  
pp. R925-R933 ◽  
Author(s):  
Sherly George ◽  
Alistair J. Gunn ◽  
Jenny A. Westgate ◽  
Christine Brabyn ◽  
Jian Guan ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Brain Stem ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Epileptiform Activity ◽  
Fetal Sheep ◽  
Fetal Movements ◽  
Brain Stem Injury ◽  
Fetal Heart Rate Variability

This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 of gestation (91 ± 1 days, term is 147 days) were exposed to either sham occlusion ( n = 10) or to complete umbilical cord occlusion for either 20 ( n = 7) or 30 min ( n = 10). Cord occlusion led to a transient increase in FHRV with abrupt body movements that resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion related to abnormal atrial activity. After reperfusion, FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first 4 h of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background, which was associated with abnormal fetal movements. As the epileptiform activity resolved, FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brain stem injury in the 30 min group but not in the 20 min group. In conclusion, during early recovery from asphyxia, epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brain stem injury.

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