Vascular responses to acute intracranial hypertension

Hayreh, Sohan Singh; Edwards, John D.

doi:10.1136/jnnp.34.5.587

Cited by 21 publications

(7 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, support is given to the suggestion that the changes observed in mean arterial pressure are a feature of the initial stages of increasing intracranial pressure by the findings of other workers who observed similar changes (Hedges and Weinstein, 1964;Langfitt et al, 1966;Hekmatpanah, 1970;Goodman et al, 1972). Hayreh and Edwards (1971) noted a decrease in the arterial pressure of rhesus monkeys at low levels of intracranial pressure but, as the mean intracranial pressure increased to around 4.7 kPa (35 mmHg), they observed a slight increase in the mean arterial pressure. A decrease in diastolic pressure alone was reported by Gonzalez et al (1972) whereas Ducker and Simmons (1968) found no change in mean arterial pressure in dogs and monkeys before the onset of the SHR.…”

Section: Cardiovascular Indicesmentioning

confidence: 55%

“…Decreases in heart rate have, however, been recorded by Langfitt et al (1966) in the rhesus monkey, by Hekmatpanah (1970) in cats, and by Gonzalez et al (1972) in dogs during a gradual increase in intracranial pressure and before the appearance of systemic hypertension. In contrast, Hayreh and Edwards (1971) found a linear relationship between heart rate and CSF pressure in the rhesus monkey-as the CSF pressure increased so did the heart rate.…”

Section: Cardiovascular Indicesmentioning

confidence: 71%

See 1 more Smart Citation

Systemic vascular responses to increased intracranial pressure: 1 Effects of progressive epidural ballon expansion on intracranial pressure and systemic circulation

Fitch

1977

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

SUMMARY This paper details the results of experimental studies, on 16 dogs with artificiallyinduced intracranial space-occupying lesions, of the systemic vascular responses and the intracranial pressure changes (both in the supratentorial and infratentorial compartments) induced by increasing intracranial pressure. The changes produced were divided into two phases such that phase 1 detailed the alterations observed from the start of the balloon inflation up to the initiation of the systemic pressor response. Phase 2 recorded those alterations which occurred durig, and immediately after, the period of systemic hypertension (see Fitch et al., 1977). The changes observed during phase 1, and presented in this communication, were those of increasing intracranial pressures and decreasing mean arterial pressure and heart rate. These alterations were associated with decreases in supratentorial perfusion pressure and increases in transtentorial pressure gradient and arrhythmia index.In the classical experiments in which systemic hypertension and bradycardia were related to increased intracranial pressure, the increase in intracranial pressure was produced by the infusion of fluid into the subarachnoid space (Naunyn and Schreiber, 1881;Cushing, 1901;Kocher, 1901). Under such conditions, the increase in intracranial pressure is uniformly distributed throughout the intracranial space. For example, when this method of increasing intracranial pressure is used, the pressure in the subarachnoid space overlying the anterolateral surface of one hemisphere has been found to be equal to the pressure in the cisterna magna over the range 0-100 mmHg (Coroneos et al., 1971). In clinical practice, however, this is a rare form of increased intracranial pressure, although conditions pertaining during pneumoencephalography may approximate closely to it. Much more commonly, the clinician is concerned with alterations in intracranial pressure produced by space-occupying pathology such as tumour or haematoma. Thus, the question of the greatest interest to the clinician is that regarding the re-1 Address for correspondence and reprint requests: Dr William Fitch, University Department of Anaesthesia, Glasgow Royal Infirmary, Castle Street, Glasgow,G4 OSF, Scotland. Accepted 29 March 1977 lationship between the systemic circulatory changes and intracranial pressure when the latter is abnormal due to the effects of intracranial space-occupying pathology with concomitant distortion of intracranial structures.The following experiments were performed in order to obtain further information on the relationships existing between the systemic vascular changes noted with increasing intracranial pressure and the intracranial pressure changes found in different intracranial compartments in the presence of an intracranial mass lesion. MethodsTwo groups of investigations were carried out on anaesthetised dogs. In each animal an artificial space-occupying lesion was created by the placement of a small balloon in the extradural space. Volume changes of this...

show abstract

Section: Cardiovascular Indicesmentioning

confidence: 55%

Section: Cardiovascular Indicesmentioning

confidence: 71%

Systemic vascular responses to increased intracranial pressure: 1 Effects of progressive epidural ballon expansion on intracranial pressure and systemic circulation

Fitch

1977

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

show abstract

“…In view of that, I investigated the effect of acute elevation of intracranial pressure on the ophthalmic and systemic blood pressures in 27 rhesus monkeys, by cannulating the ophthalmic artery and vein, superior sagittal sinus at the vertex, the right jugular vein in the neck, and abdominal aorta through the femoral artery; I recorded all the pressures simultaneously, as well as the heart rate (Hayreh and Edwards 1971a,b), first at normal intracranial pressure, then by acute elevation of the intracranial pressure in steps of 5 mm Hg every five minutes to about 40–50 mmHg.…”

Section: My Studies On the Pathogenesis Of Optic Disc Edema In Raimentioning

confidence: 99%

“…This study is discussed at length elsewhere (Hayreh and Edwards 1971b). Figure 10 is an example of the findings in one animal.…”

Section: My Studies On the Pathogenesis Of Optic Disc Edema In Raimentioning

confidence: 99%

Pathogenesis of optic disc edema in raised intracranial pressure

Hayreh

2016

Progress in Retinal and Eye Research

209

178

View full text Add to dashboard Cite

Optic disc edema in raised intracranial pressure was first described in 1853. Ever since, there has been a plethora of controversial hypotheses to explain its pathogenesis. I have explored the subject comprehensively by doing basic, experimental and clinical studies. My objective was to investigate the fundamentals of the subject, to test the validity of the previous theories, and finally, based on all these studies, to find a logical explanation for the pathogenesis. My studies included the following issues pertinent to the pathogenesis of optic disc edema in raised intracranial pressure: the anatomy and blood supply of the optic nerve, the roles of the sheath of the optic nerve, of the centripetal flow of fluids along the optic nerve, of compression of the central retinal vein, and of acute intracranial hypertension and its associated effects. I found that, contrary to some previous claims, an acute rise of intracranial pressure was not quickly followed by production of optic disc edema. Then, in rhesus monkeys, I produced experimentally chronic intracranial hypertension by slowly increasing in size space-occupying lesions, in different parts of the brain. Those produced raised cerebrospinal fluid pressure (CSFP) and optic disc edema, identical to those seen in patients with elevated CSFP. Having achieved that, I investigated various aspects of optic disc edema by ophthalmoscopy, stereoscopic color fundus photography and fluorescein fundus angiography, and light microscopic, electron microscopic, horseradish peroxidase and axoplasmic transport studies, and evaluated the effect of opening the sheath of the optic nerve on the optic disc edema. This latter study showed that opening the sheath resulted in resolution of optic disc edema on the side of the sheath fenestration, in spite of high intracranial CSFP, proving that a rise of CSFP in the sheath was the essential pre-requisite for the development of optic disc edema. I also investigated optic disc edema with raised CSFP in patients, by evaluating optic disc and fundus changes by stereoscopic fundus photography and fluorescein fundus angiography. Based on the combined information from all the studies discussed above, it is clear that the pathogenesis of optic disc edema in raised intracranial pressure is a mechanical phenomenon. It is primarily due to a rise of CSFP in the optic nerve sheath, which produces axoplasmic flow stasis in the optic nerve fibers in the surface nerve fiber layer and prelaminar region of the optic nerve head. Axoplasmic flow stasis then results in swelling of the nerve fibers, and consequently of the optic disc. Swelling of the nerve fibers and of the optic disc secondarily compresses the fine, low-pressure venules in that region, resulting in venous stasis and fluid leakage; that leads to the accumulation of extracellular fluid. Contrary to the previous theories, the various vascular changes seen in optic disc edema are secondary and not primary. Thus, optic disc edema in raised CSFP is due to a combination of swollen nerve fibers an...

show abstract

“…In my editorial, my conclusion that low CSFP plays no role in optic disc cupping was based on my studies (since 1961) on optic disc structure [5], the pathogenesis of optic disc swelling in raised CSFP [3,4,6,7], other CSFP studies [8,9], and the pathogenesis of optic disc cupping in glaucoma [10][11][12][13][14][15][16], as well as on the studies of others in the published literature [2]. By contrast, the hypothesis by Berdahl and colleagues [1] that CSFP "may play an important role in the development of POAG and NTG" is drawn from only the following two studies.…”

mentioning

confidence: 99%

Cerebrospinal fluid pressure and glaucomatous optic disc cupping (response to Berdahl and colleagues)

Hayreh

2009

Graefes Arch Clin Exp Ophthalmol

View full text Add to dashboard Cite

Vascular responses to acute intracranial hypertension

Cited by 21 publications

References 52 publications

Systemic vascular responses to increased intracranial pressure: 1 Effects of progressive epidural ballon expansion on intracranial pressure and systemic circulation

Systemic vascular responses to increased intracranial pressure: 1 Effects of progressive epidural ballon expansion on intracranial pressure and systemic circulation

Pathogenesis of optic disc edema in raised intracranial pressure

Cerebrospinal fluid pressure and glaucomatous optic disc cupping (response to Berdahl and colleagues)

Contact Info

Product

Resources

About