Epistaxis complicating a severe craniofacial injury is not unusual, but in most cases bleeding is easily controlled by nasal packs. On the other hand, epistaxis as a major manifestation of traumatic aneurysm of the internal carotid artery is reported to be rare. When this occurs, however, prognosis is grave and the treatment creates a perplexing nenrosurgical problem.In the case of penetrating injury involving the head and face, the correct diagnosis of the source of bleeding is usually made. When the epistaxis occurs weeks after the closed head injury, however, its direct relation to the previous injury is often not so apparent and easily escapes the attention of both patient and physician. In fact, causal relationship between preceding trauma and present epistaxis is only occasionally identified when the patient is first seen with an epistaxis from a traumatic aneurysm of the internal carotid artery.We have treated four consecutive cases of traumatic aneurysm of the internal carotid artery. Two of them came under our care in a one month period. From this experience, we are inclined to believe that traumatic aneurysm of the internal carotid artery is less rare than previous reports would indicate. It is this belief that prompted the present article.In all four cases the aneurysm was verified either by carotid angiography or at autopsy, or both. In three of them, severe recurrent epistaxis was observed. In the remaining one, delayed epistaxis was absent but this ease is of particular interest as the aneurysm was associated with a homolateral carotieocavernous fistula and both of them were followed up by means of repeat angiographic studies over several months.
Report of CasesCase I: Tra]]ic accident. Epidural haematoma evacuated. Severe ~'ecurrent epistaxis. Exsanguination. Autopsy. G. M., a 19-year-old man, was involved in a traffic accident. A depressed fracture in the left frontal region, linear fractures in the right frontal and Act~ Neurochirurgica, Vol. XVII, Fast. 3 II
We have examined two patients with posterior fossa lesions. Although they showed a similar tonic posture, one was thought to be epileptic and the other not.The first case was a two-year-old boy. He was admitted to Nagasaki University Hospital because o€ a large head and he was diagnosed as a Dandy-Walker cyst. The boy was stuporous and showed an opisthotonic posture all day long and the deep reflexes were hyperactive.The attacks occurred 2-3 times a day. He suddenly developed a decerebrated posture superimposed upon opisthotonus. In each attack, the hands were pronated and the neck and back were hyperextended which lasted two or three minutes. During the attacks, he was thought to fall into unconsciousness and a gradual increase of the respiratory rate was also observed at that time. The EEG was characteristic. In the interictal stage, slow wave bursts, slow spikes and slow spike-and-waves were observed at all leads. In contrast, during each attack, the EEG mainly consisted of diffuse low voltage fast activity (desynchronization), suggesting that the discharging focus was in the midbrain reticular formation.After an operation of the ventriculoperitoneal shunt, he regained consciousness and the attacks increased markedly, probably because of an occurrence of the transtentori-a1 upward herniation.During the attacks, the EEG also revealed a low voltage fast pattern. Then, by adding the cyst-peritoneal shunt, such decerebrated attacks disappeared and the opisthotonic posture also improved. The EEG recorded at that time showed mainly slow wave activity but neither spikes nor low voltage fast activities.The second case was a 10-year-old girl with Lt-cerebellopontine glioma. Three months after the operation, she possessed the opisthotonic posture, and had often the general tonic spasm. But she clearly remained in a consciousness state. The EEG showed almost normal activity even at the time of increased tonic spasm.In conclusion, the terms decerebrate, opisthotonic, tonic mesencephalic as well as cerebellar seizure (fit) have been dropped from the international classification of epilepsy because of the fact that they had nothing to do with epileptic discharges. In our first case, however, the EEG strongly suggested that his decerebrate attacks had been caused by the mesencephalic discharging lesion. Included were two different mechanisms under the name of tonic mesencephalic seizure ( Penfield and Jasper), the first true in epileptic nature and the other not epileptic.
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