Cases reported "Brain Concussion"

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1/3. Blunt basal head trauma: aspects of unconsciousness.

    Two cases of street violence directed to the skull base level and transverse to the cervical axis are described. No skeletal damage. The violence resulted in the so-called "traumatic subarachnoid haemorrhage", an often used, unspecified forensic "diagnosis"; it was here revealed to be due to rupture of the wall of the posterior inferior cerebellar artery (p.i.c.a). However, this was only one of the possible explanations for the acute symptoms of unconsciousness (concussion) and almost immediate death. The careful examination of these two cases and of a series of control cases revealed that at the trauma, stress and strain may have occurred to arterial branches serving as feeding perforant vessels to the medulla oblongata; in these cases they were coursing directly from the p.i.c.a. region.--The type of direct impact has often been regarded as mild! However, its location suboccipitally as in these cases can become dangerous. The resulting direct or indirect deficit of brain stem functions are discussed in these cases as well as "concussion-related symptoms" resulting after other types of head and neck injury.
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2/3. Kinesigenic choreoathetosis due to brain injury.

    This uncommon paroxysmal movement disorder featuring attacks of dystonic spasm with athetoid posturing is usually of idiopathic nature, often familial and starting in childhood. There are a few reported examples due to cerebral pathology, and only four previous cases due to brain trauma. We report here a 21 year old man with left-sided motor spasms, choreoathetoid in type, which were clearly caused by a right frontal penetrating injury with contusion and haemorrhage. The attacks were relieved by phenytoin therapy. In this case, it seems that the post-traumatic paroxysmal kinesigenic choreoathetosis may be a form of reflex epilepsy.
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3/3. Clinicopathological study of acute subdural haematoma in the chronic healing stage. Clinical, histological and ultrastructural comparisons with chronic subdural haematoma.

    Seven cases of acute subdural haematoma in the chronic healing stage, were studied clinicopathologically. Operation was not performed until 17-30 days after major trauma, and revealed subdural granulation tissue of irregular thickness, but no visible inner membranes. Although this capsule contained blood pigment and numerous macrophages, new haemorrhagic foci or eosinophilic infiltrations were extremely rare. Capsular vessels generally had thick vascular walls, distinct basement membranes and tight endothelial junctions. Perivascular blood substance was presumably not secondary haemorrhage from these vessels, but residue from the acute subdural haematoma itself. The possibility of transition from this haematoma to chronic subdural haematoma is discussed.
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