Orbital Vascular Response to Acutely Increased Intracranial Pressure in the Rhesus Monkey

Vascular responses to acute intracranial hypertension

“…The normal SSP of about 4 mm Hg as seen in the present series and by Hedges (1963), is slightly lower than the normal CSFP (Weed and Hughson, 1921).…”

“…Ryder, Espey, Kristoff, and Evans (1951), on suddenly raising the CSFP in rhesus monkeys, also found a fall of pressure in the sigmoid sinus and considered the latter to be dependent upon the cardiac output. Hedges (1963), on raising the CSFP to 200 to 400 mm water in five experiments on rhesus monkeys, recorded no change in the SSP in two, a rise in one; no mention is made of the response in the remaining two. The effects of the raised CSFP on the SSP seen in the 26 rhesus monkeys of the present series are shown in Fig.…”

“…The BP may be affected when the CSFP reaches the level of (a) the diastolic BP (Cannon, 1901;Eyster, 1906;Eyster et al, 1909;Howe, 1927;Munro, 1927;Weed, 1929;Wolff and Forbes, 1929;Wilson, 1932;Fremont-Smith and Merritt, 1933;Masserman, 1934; and others), (b) the systolic BP (Cushing, 1901;Wright, 1938;Weinstein, Langfitt, and Kassell, 1964; and others), or (c) the mean BP (Eyster et al, 1909;Howe, 1927;Munro, 1927;Browder and Meyers, 1938; and others). On raising the CSFP to about 40 mm Hg experimentally, no response in the BP was detected by Weed and Flexner (1933), Bedford (1942), and Hedges (1963). Cushing (1903) and Janeway (1904) regarded the extent of the rise of BP as an indication of the degree ofcompression ofthe brain.…”

“…We are of the opinion that the important factor responsible for this is the increased venous pressure in the cerebral veins, the latter being a compensatory mechanism to counteract the venous compression by the raised CSFP. Hedges (1963) stated that the SSP responses to the raised CSFP were unrelated to those of the ophthalmic vein pressure (OVP). In sharp contrast with that, in our series a significant correlation was seen between the SSP and the OVP in normal animals and with the raised CSFP (Hayreh and Edwards, 1971 Kornder (1919) and Hayashi (1955), from their experimental intracranial hypertension studies in dogs, concluded that the raised intracranial pressure caused a generalized rise of venous pressure; on giving atropine before the rise of the intracranial pressure no such rise of the venous pressure was seen.…”

Optical Coherence Tomography and Optic Nerve Edema

“…He proposed that impairment of orbital venous outfl ow at the level of the cavernous sinus, arterial pressure elevation, and a local hemodynamic effect within the orbit all contribute to the elevation if orbital venous pressure [ 4 ]. In 1977, in an experimental model of rhesus monkeys, Tso and Hayreh demonstrated that unlike swelling in the central nervous system, which is characterized by fl uid accumulation in glial cells and extracellular space, the primary pathologic change in papilledema is severe swelling of axons with disruption of mitochondria and neurotubules [ 5 ].…”