[Role of echoencephalography in the diagnosis of brain concussion].
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This study examined physiological and histopathological changes in the cat produced by a new experimental fluid injury device. Spontaneously breathing (N = 14) and artificially ventilated (N = 45) cats were subjected to systemically varied magnitudes of fluid percussion brain injury. Within certain injury ranges, increasing magnitudes of fluid percussion injury produced increasing durations of apnea, as well as greater transient increases in mean arterial blood pressure, intracranial pressure and cerebral perfusion pressure. Acute increases in intracranial pressure may have been related to cerebral vasodilatation produced by the systemic hypertension following brain injury. Injuries associated with pressure transients greater than 10 atm ms produced concussive responses, including irreversible apnea in spontaneously breathing cats and temporary pupillary dilatation, increases in heart rate and mean arterial blood pressure in artificially ventilated cats. Injuries greater than 39 atm ms frequently produced histopathological and physiological indices of significant irreversible brain damage, including fixed and dilated pupils, systemic cardiovascular hypotension and deteriorating blood gases. Injury magnitudes less than 20 atm ms did not produce macroscopic evidence of histopathology, intermediate injury ranges produced increasing evidence of subarachnoid and petechial hemorrhage while injury levels greater than 40 atm ms frequently produced significant histopathology including massive hematomas. Injury greater than 10 atm ms resulted in opening of the blood-brain barrier, as assessed by extravasation of horseradish peroxidase. Injury greater than 19 atm ms produced suppression of EEG amplitudes which did not recover for up to 40 minutes after injury. These data provide detailed information on the physiological and histopathological consequences of fluid percussion injury in the cat and indicate that this modified fluid percussion apparatus can produce graded levels of brain injury similar to those previously reported for fluid percussion injury.
This study presents a new device for producing experimental, concussive head injury together with a detailed description of biomechanical features of fluid percussion brain injury in the cat. Anaesthetized cats were subjected to multiple (N = 3) or single injuries (N = 87). The variables studied in repeated injury experiments included the volume of fluid injected intracranially, rate of fluid flow, and the associated pressure transients recorded extracranially in the injury device and intracranially at supratentorial and infratentorial sites. Peak fluid flow increased with increasing volumes of fluid loaded intracranially. Extracranial pressure peaks and durations increased when volume loading was increased. Extracranial and intracranial pressure transients were similar at all recording sites. The form of pressure transients recorded in single injury experiments was similar to that recorded in multiple injury experiments. In single injury experiments, the extracranial pressure peaks and durations also increased with increased intracranial fluid volume loading. The slopes describing the relationships between intracranial volume loading and extracranial pressure transients were significantly different in single and multiple injury experiments. Details of the design and use of the head injury device are also discussed.
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