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OBJECTIVE: To explore the content change of neurofilament (NF) protein subunits in the experimental brain diffuse axonal injury (DAI) by lateral head rotation. METHODS: Twenty-four Sprague Dawley (SD) rats were equally divided into three injury groups (2 h, 12 h, and 24 h post injury) and one control group. The models of DAI were made in the injury groups by lateral head rotation. Western blotting technique was used to measure the content of NF68 (a kind of NF protein subunit) in the brainstem tissues among all the injured and control rats. The NF68 immunohistochemical staining was used in another six SD rats in order to observe the morphological changes in DAI. RESULTS: The NF68 content in the brainstem tended to decrease at 2 h post injury, decreased significantly at 12 h and continued its decrease at 24 h. NF56 and NF52, as the breakdown products of NF68, had a tendency to increase at 2-12 h after the injury, and amounted to a significantly higher level at 24 h. Microscopically, there were a lot of swelling neuronal axons in the ventral part of the medullar oblongata at 2 h after the injury. Some axons were disconnected, and axonal retraction balls formed on their proximal end. CONCLUSIONS: There is an occurrence of phosphorolysis within the brainstem in DAI by lateral head rotation. These reactions cause the breakdown of NF68, which results in the decrease of NF68 in content. It suggests that the breakdown of neurofilament protein subunits is an important reason for structur al destroy of neurofilaments in DAI.
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OBJECTIVE: Exploring the intra-axonal overloading of calcium ion (Ca(2+)) in brain diffuse axonal injury (DAI) and the therapeutic effect of calcium antagonist(Nimotop) on DAI. METHODS: Fourteen SD rats were divided into injury group, treatment group and control group. The DAI model of rats was produced by using a head-instant-axial-rotation device. Tissues from the medulla oblongata of rats were taken 2-24 h post-injury and processed for electron microscopic observation by a cytochemical technique for calcium ion. RESULTS: In the injured rats there was evidence of local disruption of myelin sheath,lucent spaces between myelin sheath lamellae, separation of axolemma from the inner layer of myelin sheath, peripheral accumulation of organellae, intra-axonal formation of vacuoles and reduction of mitochondria. A large number of fine calcium deposits were seen on the affected myelin sheath. The severity of the myelin sheath lesion was related positively to the number of calcium deposits on it. In the later post-injury period the coarse calcium particles appeared within the damaged axon. Neuronal somas and microvascular endotheliums showed a lot of vacuoles and some fine calcium deposits. Many microvilli formed on the luminal aspect of endothelium. In the treatment group myelin sheath tended to be injured locally, and axoplasmic mitochondria were nearly normal in number, structure, and distribution. Few calcium deposits were found in axons. Vacuolization was obviously reduced in neuronal soma and endothelium. CONCLUSIONS: In DAI there exists an intra-axonal overloading of calcium ion, which is a key factor to the occurrence and development of DAI. Early use of Nimotop can alleviate DAI.
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OBJECTIVE: To study the changes of brain TXA(2) and PGI(2) levels in a new rodent model of impact acceleration diffuse brain injury with hypotention and hypoxia and the effect of diaspirin cross linked hemoglobin solution (DCLHb) on brain TXA(2) and PGI(2) levels. METHODS: Thirty-two male SD rats were randomized into sham, head injury alone, head injury with secondary insults and injury with insults followed by DCLHb administration groups. Animals were physiologically monitored throughout the experiment and the prostanoids were measured via radioimmunoassay (RIA). RESULTS: There were no changes in TXB(2) and 6-keto-PGF1alpha (stable metabolites of TXA(2) and PGI(2)) levels in injury alone group while TXB(2) level in secondary insults group elevated significantly and both TXB(2) and 6-keto-PGF1alpha levels in injury with insults followed by DCLHb administration augmented significantly in comparison with the corresponding value of sham at 4 h postimpact. CONCLUSIONS: The only increase in TXA(2) level in secondary insults rats suggests that there may be both thrombotic episodes and vasoconstriction leading to focal increase in micro-circulatory resistance which contributes to a decreased focal cerebral blood flow (CBF). And it is hypothesed that DCLHb may exert its protective properties through increasing PGI(2) production in injured brain by affecting CBF and cerebral perfusion pressure (CPP).
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OBJECTIVE: To improve the outcome of treatment in patients with craniocerebral firearm wound. METHODS: Prospectively and retrospectively reviewed a series of 93 patients presented to the Xi-Jing Hospital of Fourth Military Medical University with a diagnosis of craniocerebral firearm wound during a period of 27 years from July 1970 to July 1997. All the patients had acute craniocerebral firearm wound. Of these, it consisted of 81 males (87.1%) and 12 females (12.9%) ranging from 3 months to 58 years in age (median 24.6 years). The lesion included 16 tangential wounds, 58 tubular wounds and 19 through-and-through wounds. The cases were urgent and in serious and unstable condition. All the patients underwent surgical intervention and aggressive perioperative management in the neurosurgical intensive care, including resuscitative protocols. RESULTS: After emergency treatment and operation, 9 cases died (9.7%). Follow-up studies at three months postoperative showed that 56 cases (66.7%) had made good recovery. Rates of moderate disability, severe disability or vegetative state in this series were 19.0%, 10.7% and 3.6%, respectively. Long term follow-up studies (median 5.5 years) found that 42 (50.0%) were capable of resuming their occupation. CONCLUSIONS: Craniocerebral firearm wounds are often severe, needing urgent treatment for the patients. Timely, proper and thorough initial debridement are crucial for avoiding rapid neurological deterioration.
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74 cases of the aged severe craniocerebral injury were presented in this paper, which accounts for 11.9% of the severe craniocerebral injury for the period. Among them, 28 cases died with a morta-lity of 37.8%. The mortality amounts to 51.4% in intracranial hematoma cases. 5 cases over 70 years all died. The reaction capacity becomes lower in old people, so that in craniocerebral injury the early clinical manifestations are difficult to represent the truth.Close observation and the early accurate diag-nosis are rather important. Attention should be paid to the multiple injuries and severe medical con-ditions. Some factors such as early clearance of the intracranial hematoma and prevention of com-plications and hypotension during an operation may reduce the mortality.Prognosis may be affected by such factors as the severity of the primary, injury, the compound injuty, complications, age and the deficiency in cerebral blood supply after cranio-cerebral injury.
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The experience in the management of 108 cases of deeply situated meningiomas is presented. Complete removal of the tumor has been possible in 83 cases (76.9%), partial resection in 22 cases (20.3%). The surgical results were excellent in 72.2% and fair in 16.7%. Early diagnosis and an attempt to remove completely of such tumors should always be considered as the treatment of choice. In order to reach this goal, we propose:(a)wide exposure, induced hypotension, hypothermia, interruption of the blood supply at the base of the tumor, and careful hemos-tasis are essential; (b) in addition, microsurgical dissection to avoid injury of the neighbouring important structures as well as vital areas of the brain are mandatory. The removal of an unusual giant mening-ioma arising in the medial aspect of the sphenoid ridge illustrated these points well. The tumor was13?10?8cm in size and 864g in weight. The patient recovered uneventfully and his general condition has remained good for years. Recent CT scan showed no recurrence.