Erwin O. Ott

Increased cerebral blood volume in benign intracranial hypertension

In two patients with benign intracranial hypertension, the regional cerebral blood volume was markedly elevated (mean of 85 percent) while regional cerebral blood flow was slightly reduced (mean of 10 percent). Reduction of cerebrospinal fluid pressure by removal of cerebrospinal fluid reduced the mean values of regional cerebral blood volume by 13 percent without significant change in regional cerebral blood flow. The abnormal regional volume and regional flow returned to normal concurrent with the clinical improvement. Venous engorgement and increased intracranial blood volume appear to play an important part in the pathophysiology of increased intracranial pressure in benign intracranial hypertension. A unified concept of the pathogenesis of benign intracranial hypertension is proposed.

Redistribution of regional cerebral blood flow after glycerol infusion in acute cerebral infarction

Article abstract Regional cerebral blood flow and blood volume were measured before and after intravenous infusion of 10 percent glycerol in normal saline in a series of 24 patients with receni. ischemic or hemorrhagic cerebral infarction. Measurements were made by serial intracarotid injection of xenon 133 and technetium 99m and by the use of the gamma camera. Regional cerebral blood flow and blood volume, prior to glycerol infusion, were reduced more in patients with hemorrhagic infarction than in those with ischemic infarction. Border zones of relative hyperemia were present in both groups. After glycerol infusion (50 g), mean serum glycerol levels rose to 33.1 millimols, cerebrospinal fluid pressure was reduced, and regional cerebral blood flow and blood volume were increased in the ischemic zone of both groups, with a redistribution of blood from the hyperemic to the ischemic zones.

Disordered cholinergic neurotransmission and dysautoregulation after acute cerebral infarction.

The possible role of displaced neurotransmitter acetylcholine (ACh) in dysautoregulation was examined after experimental regional cerebral infarction was produced by occluding the middle cerebral artery (MCA) in baboons. Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xenon using the gamma camera. Autoregulation was tested with metaraminol or angiotensin infusion and the autoregulation index (A.I.) was calculated. Acetylcholinesterase (AChE) was measured in brain tissue of noninfarcted and infarcted hemispheres. Cerebral arteriovenous (A-V) differences for cholinesterase (ChE) were also measured. Regional dysautoregulation was found in infarcted gray matter and correlated with increased AChE levels in the same zones of cortex and basal ganglia. The time course of onset of dysautoregulation correlated with increased ChE uptake by the brain. Intravenous infusion of the cholinergic neurotransmitter blocker, scopolamine, restored autoregulation to the ischemic zones. Autoregulation appears to be a myogenic reflex, influenced by neurogenic and metabolic mechanisms.

Brain Tissue Pressure Gradients in Experimental Infarction Recorded by Multiple Wick-Type Transducers1

The wick catheter, applied to brain tissue pressure measurements by BROCK (1), appears to be a reliable device to measure the regional brain tissue pressure, based on our experience of implantation of about 150 wicks in 55 experimental animals.

Regional Cerebral Blood Flow Measured by the Gamma Camera After Direct Injection of 133Xe into the Distal Stump of the Occluded Middle Cerebral Artery

Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xe concurrently with measurements of local cerebral blood flow (LCBF) after injection of 133Xe directly into the distal stump of the occluded middle cerebral artery (MCA) by the use of the gamma camera after producing experimental ischemia in baboons by occluding the MCA. Regional MCA stump pressure (rMCAP) was also measured. Regions of ischemia assessed by intracarotid injection of 133Xe correlated well with the territory of infarct defined by injection of 133Xe into the distal MCA stump. Flow values in ischemic regions obtained by direct injection of 133Xe into the MCA were 15% to 20% lower than those obtained by intracarotid injection of 133Xe. Possible explanations for these differences are discussed. During induced hypertension autoregulation in ischemic areas was abolished and paradoxical responses of LCBF and rMCAP to changes in arterial carbon dioxide tension (Paco2) were confirmed.

The Importance of “CSF Pressure-Regional Cerebral Blood Flow Dysautoregulation” in the Pathogenesis of Normal Pressure Hydrocephalus

The pathophysiology of cerebral dysfunction in normal pressure hydrocephalus (NPH) and the mechanism of clinical improvement in NPH patients who undergo cerebrospinal fluid (CSF) shunting are still unclear. The hypothesis of GREITZ (1) that cerebral circulation is adversely affected by “brain distension” in conditions like NPH and the reports of improvement of cerebral blood flow (CBF) concomittant with clinical improvement after CSF shunting (2,3,4) led us to study cerebral hemodynamics and their relationship to changes in cerebrospinal fluid pressure (CSFP) in patients with NPH and “hydrocephalus ex vacuo” due to cerebral atrophy. The primary aim of the study was to determine the existence of any abnormal cerebral hemodynamics in NPH and if so, to examine their implications in the treatment and prognosis.

Brain tissue pressure gradients in experimental infarction and space occupying lesions

Abstract Regional cerebral tissue pressures were recorded with multiple wick-type pressure transducers in 31 animals under different experimental conditions. In Group 1 infarction was produced by occlusion of the middle cerebral artery ( mca , in Group 2 iophendylate (Pantopaque R ) was injected directly into the mca , in Group 3 iophendylate was injected into the common carotid artery ( cca ), and in Group 4 one cerebral hemisphere was compressed by inflation of a balloon or injection of blood into brain tissue. Marked transient cerebral tissue pressure gradients were noted after injection of iophendylate into the mca and sometimes after injection of iophendylate into the cca . Moderate transient gradients were produced by rapid inflation of an extracerebral balloon. The slowly progressive edema caused by infarction after mca occlusion and edema caused by injection of blood in a cerebral hemisphere did not produce measurable cerebral tissue pressure gradients, despite generalized increases in intracranial pressure. The same was true if the extracerebral balloon was inflated slowly.