[Case study reports. 20. (Society for the Study of Scientific Nursing)].
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Biomedical subjects
Publications and source records attributed to Y Yanagida.
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Fracture of the cervical spine in a patient with ankylosing spondylitis is presented. A 43-year-old male was involved in a fight when drinking. He received blows to his face and the lower jaw, and fell backward on the street and died. The postmortem examination showed abrasions and subcutaneous hemorrhages on the face and the lower jaw. A transverse fracture was observed through the intervertebral disc space between the fifth and sixth cervical vertebrae. The cervical spinal cord was completely ruptured at the fracture site. Ossification of the supporting ligaments and anterior surface of dics were found. The spine was bony ankylosed. The alcohol levels of blood and urine were 2.95 and 3.84 mg/ml, respectively. The cause of death was paralysis of respiration. The victim had suffered from the ankylosing spondylitis for many years. His neck had no mobility. The X-ray films taken at age 42 showed complete ankylosis of the spine, so-called "bamboo" spine. It seemed that the blow to his face and the lower jaw caused hyperextension of the neck and easily caused the cervical fracture because of the loss of flexibility and fragility from osteoporosis in the ankylosed spine.
The victim, 52 year old man, was thrust down and hit his left occiput against the concrete floor. He was hospitalised and his comatose state continued to the death. On admission, blood pressure was 212/110 mmHg and the computed tomography scan of the head showed only an extensive right subdural hematoma. But the intracerebral hemorrhages in the right frontal, temporal and parietal lobes were recognized 10.5 hours after the trauma. A subdural hematoma was evacuated by operation on the second hospital day. The intracerebellar hemorrhage also appeared 16 hours after the trauma. Blood pressure fluctuated between 160/80 and 200/110 mmHg. The photo of CT scan at 38.5 hours after the trauma showed little subdural hematoma and new intracerebral hemorrhage located in the left temporal lobe. On the third hospital day, he was equipped with a respirator and blood pressure was between 132/84 and 242/100 mmHg. The reaction of the pupils to light disappeared on the 8th hospital day. Blood pressure gradually decreased on the 9th and 10th hospital days and he died on the 11th day. Autopsy revealed a bruise in the left occiput, a linear fracture in the frontal and left parietal bones and a small amount of subdural hematoma on the surface of the right cerebral hemisphere. Cortical contusions were found in the right frontal, the both temporal and the left parietal lobes. Intracerebral hemorrhages were found in the right frontal, the both temporal and the right parietal lobes. Intracerebellar hemorrhage was also found. Cardiac hypertrophy and atherosclerosis of the aorta were recognized. We thought that small hemorrhages which were not clearly detectable by CT scan immediately after injury may have developed into massive intracerebral and intracerebellar hemorrhages due to high blood pressure after a hospitalization.
A very rare case of severe calcification in brain is reported. A 49-year-old man was hit and run by a motorcar in acrossing a road on foot, and he died 1 hour later in an emergency hospital. Medico-legal autopsy was done at 5 hours after his death. The cause of death was cerebral contusion caused by a struck on partieto-occipital region. Unusually severe calcification was observed in the right and left cerebral hemispheres, especially basal ganglia, in the border areas between grey and white matters of frontal, parietal and occipital lobes, as well as in the cerebellar nucleus, cortex and medulla. Histological examination showed severe multiple calcification in the brain tissue. Dispersed deposit of pseudocalcium-Ca and edema were observed around the calcifications. Proliferation of glia cells and decrease of nerve cells were also noted. In his past history, he began to speak distinctly and to stagger since 8 years ago. Three years ago, he collided with guardrail while driving his motorcycle, and he was hospitalized. Calcification in the brain was already revealed in the roentogenographic examination. In the laboratory findings, the data of serum calcium, serum phosphorus and Ellsworth-Haward test were normal. The antibody of toxoplasma, however, showed high level more than X 1,024. After he was discharged, dementia, instability of trunk and dysarthria still continued, and he used to across a crowded road unconcernedly. The cause of the calcification might be suspected to be toxoplasmosis, although neither trophozoites, cysts nor oocysts were found in the brain tissue.
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Tizanidine behaved as the partial agonist on the alpha 1-adrenoceptor in high doses (10(-6) -10(-4)M) and as the alpha 2-adrenoceptor agonist in low doses (3 X 10(-9) - 10(-6)M). Tizanidine is about one-third as potent as clonidine in alpha 2-agonistic effect
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An impact incurred by the movable head may bring about a change in intracranial pressure and this change may play an important part in the occurrence of the cerebral contusion. We have carried out the following experiments to determine whether the intracranial pressure change was attributed to an accelerated motion of the head or to a skull deformation. In the blow experiment in which the head was accelerated, a positive peak in the intracranial pressure was recorded immediately after impact at the impact site and a negative one at a site opposite the impact. In the one in which the skull could be deformed, the intracranial pressure curves at both sites contained harmonics. The modal analysis revealed an inbending in the frontal and occipital regions of the skull and an outbending in the parietal and temporal regions immediately after impact, followed by a reverse deformation. Regarding the intracranial pressure change, positive pressures were recorded in the frontal and occipital regions immediately after impact, followed by a negative one. This study demonstrated that the positive and negative peaks were caused by the accelerated motion of the head, and that the curve of the intracranial pressure changes contained harmonics which were caused by the deformation of the skull.
In cases of a severe head injury caused by a fall, coup contusions are either absent or very minor, in contrast to presence of extensive contre-coup damage. In cases of a severe blow to head, however, the reverse occurs, with contre-coup lesions a rarity and coup damage extensive. To investigate this further, head injuries caused by a 'blow' or a 'fall' have been studied, using physical human models of the head and neck, both filled with distilled, degassed water and fixed onto a dummy torso. An impact of a constant magnitude was applied to the midoccipital region in 'blow' and 'fall' experiments, and the acceleration of the head and changes in the intracranial pressure were measured, with the resulting data analyzed by a computer. In both experiments, the peak amplitude of the acceleration pulse were almost the same. Similarly, the intracranial pressure curve at the impact site consisted of a positive pulse that hardly differed, nor did the peak amplitude of that pulse vary significantly. In the 'blow' experiment, however, the intracranial pressure curve at the site opposite the impact consisted of a negative pulse, whereas in the 'fall' experiment, the intracranial pressure recorded at the same area was negative but of a longer duration, with an absolute value that was slightly greater. Our results indicate that an impact to the head triggers a different response in the intracranial space, dependent on whether that impact force was caused by a 'blow' or a 'fall'.