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Thomas W. Langfitt and Neal F. Kassell

exaggerated. 11, 16 Furthermore, marked alterations in brain volume of unknown etiology have frequently been described and usually are manifested by a rapid change in cerebrospinal fluid pressure or sudden swelling of the brain at the time of craniotomy. This has been observed following severe head trauma, 2, 5, 10 in patients with intracranial neoplasms, 1, 2, 10, 11, 16 hydrocephalus, 8 and pseudotumor cerebri. 4, 5 We have also seen rapid fluctuations in intracranial pressure from 10 to 90 mm. Hg in patients following spontaneous subarachnoid hemorrhage. 14

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Hiroo Johshita, Neal F. Kassell, Tomio Sasaki and Hisayuki Ogawa

changes in microcirculation after SAH, stereological parameters 37 including volume density (in cu mm/cu mm), surface density (sq mm/cu mm), and numerical density (no./cu mm) of Evans blue-filled capillaries were computed by areaperimetry analysis, using a Zeiss Videoplan system equipped with a stereology program. The minimum intercapillary distance ( µ m) 2 and minimum capillary diameter ( µ m) were also measured in the same fields. Vessels with minimum diameters of more than 10 µ m were excluded from the data. An average of the pooled data for each parameter was

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Stephen J. Monteith, Neal F. Kassell, Oded Goren and Sagi Harnof

associated decreased cerebral blood flow, as well as release of toxic metabolites and free radical generation from breakdown of blood products. Ischemia ensues, cell metabolism breaks down, and cells swell and die, resulting in further neurological deficit after the initial insult. The clot volume and clinical status of the patient has clearly been shown to be a valuable predictor of outcome. Broderick et al. 1 demonstrated that hemorrhage volume (0–29 cm 3 , 30–60 cm 3 , and 61 cm 3 or more), calculated by an ellipsoid method (4/3 × πabc, where a, b, and c are the 3

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Tomikatsu Toyoda, Neal F. Kassell and Kevin S. Lee

ischemia. 12, 35, 62 In the present study we examined the possibility that immunostimulant preconditioning with DPL can induce protection against ischemic neuronal injury in the brain. Using a reproducible model of transient focal ischemia in this study, we analyzed the effects of DPL preconditioning on infarction volume and MPO activity (a marker of neutrophil infiltration). In addition, the endogenous activity of SOD was determined after DPL conditioning because this antioxidant is thought to play a role in the elaboration of other forms of ischemic tolerance. 44, 54

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Thomas W. Langfitt, James D. Weinstein, Neal F. Kassell and L. John Gagliardi

ventricle. The volume of saline injected into the balloon was always less than 1.0 cc. and rarely exceeded 0.5 cc. The relation of extradural to subarachnoidal pressure was investigated by inserting a steel bolt into the extradural space over the cerebral hemisphere. The bolt is hollowed out and needles are inserted through a diaphragm in the head of the bolt for injection of fluids into the extradural space and for recording of pressure. The bolt, which is self-tapping, is screwed into place through a trephine hole in the skull, and a gasket between the head of the

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Thomas W. Langfitt, Howard M. Tannanbaum and Neal F. Kassell

that the rise in intracranial pressure produced by expansion of an intracranial mass causes cerebral vasodilatation. The vasodilatation increases cerebral blood volume and produces a further rise in intracranial pressure. As this process continues, a very great increase in intracranial pressure may occur rapidly due to intense cerebrovascular congestion. As the difference between the arterial and intracranial pressures decreases, cerebral blood flow falls, and irreversible cerebrovascular dilatation ultimately occurs due to ischemic vasomotor paralysis. 10, 11 The

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David J. Boarini, Neal F. Kassell and Hans C. Coester

dividing the cardiac output by the animal's weight. Cardiac work was calculated by multiplying the difference between the mean arterial blood pressure (MABP) and the left ventricle end-diastolic pressure by the stroke volume multiplied by 1.33 × 10 −3 . Cerebral metabolic rate of oxygen (CMRO 2 ) was estimated by multiplying the difference between the arterial and sagittal sinus oxygen content by the mean cerebral hemisphere blood flow. Cerebral perfusion pressure was calculated as the difference between the MABP and sagittal sinus pressure. Cerebral vascular resistance

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Transmission of Increased Intracranial Pressure

I. Within the Craniospinal Axis

Thomas W. Langfitt, James D. Weinstein and Neal F. Kassell

pressure fell below the supratentorial pressure during supratentorial injection of fluid. The development of a progressive obstruction of the incisura is illustrated in Fig. 1 . Several small injections, to a volume of 2.0 cc., had been made into an extradural balloon prior to injection in ① where there is still full communication of pressure to the cisterna magna and lumbar subarachnoidal space. In ② the peak of the pressure in the cisterna magna fell below the supratentorial pressure, and in ③ a 15 mm. Hg differential had developed. In ④ the increase of pressure

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David W. Beck, Neal F. Kassell and Charles G. Drake

, occurring in between 0% and 4% of cases in published series. 1, 2, 5 In all reported instances, there was intracranial extension of the tumor large enough either to elevate the ICP by producing mass effect or to obstruct CSF pathways producing hydrocephalus. In our case, there was no intracranial mass effect. We propose that the direct shunting of high-pressure arterial blood, which refluxed into the major venous drainage system, impaired venous drainage, thereby increasing cerebral blood volume and ICP. Furthermore, the elevated venous pressure probably also impaired

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Neal F. Kassell, David J. Boarini, Julie J. Olin and James A. Sprowell

content of arterial and cerebral venous (sagittal sinus) blood. Cardiac index was estimated by dividing the cardiac output by the animal's weight. Cardiac work was calculated by multiplying the difference between the mean arterial and left ventricle end diastolic pressures by the stroke volume × 1.33 × 10 −3 . Cerebral metabolic rate of oxygen usage (CMRO 2 ) was estimated by multiplying the difference between the arterial and sagittal sinus oxygen content by the mean cerebral hemisphere blood flow. Cerebral perfusion pressure was calculated as the difference between