Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with imparied CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (CMRO2), intraventricular pressure, and lactate/pH levels in the cerebrospinal fluid (CSF) were measured in 38 patients with ruptured intracranial aneurysms between the 3rd and 13th day after subarachnoid hemorrhage (SAH). Angiography was performed following the rCBF study and the degree of vasospasm was measured on the angiograms. The patients were graded clinically according to the system of Hunt and Hess. Cerebral vasospasm significantly influenced rCBF: global reductions and focal changes (ischemia, hyperemia, and tissue peaks) were commonly associated with vasospasm. Patients with severe diffuse spasm always had global ischemia (21 +/- 5 ml/100 gm/min), and cerebral infarctions were demonstrated subsequently, The CMRO2 was more reduced than rCBF, indicating an uncoupling between flow and metabolism. This relative luxury perfusion was associated with CSF lactic acidosis and intracranial hypertension. The arteriovenous difference of oxygen was equally reduced in all categories of patients, probably due to the primary insult of SAH. The CMRO2 decreased concomitantly with arterial caliber, indicating a secondary impairment of cerebral metabolism due to vasospasm.

SUMMARY In a consecutive study comprising 41 patients with completed stroke of less than 72 hours duration, cerebral angiograpby and measurements of the regional cerebral blood flow (rCBF) were performed within 24 hours after admission. The rCBF study was done using the 133-Xenon intracarotid injection method and a 254 multi-detector camera. CT scan was done 24 hours after the rCBF study.Focal cerebral hyperemia was found in 16 patients. The study revealed 3 different types of hyperemia: Border-zone hyperemia, surrounding iscbemic areas, was seen in patients with occluded arteries on angiograpby, presumably resulting from accumulation of acid metabolites in the border-zone of acute infarcts. Postischemic hyperemia was seen in patients without occlusion, presumably due to recanalization of a prior occluded artery. Remote hyperemia was found distant from the infarcted area, presumably due to local tissue pressure on brain tissue.Cortical infarcts (10 patients) all had extensive hypereraic areas. Because the 254 detector camera has an excellent resolution in the cortical surface, our findings strongly suggest that all acute cerebral infarcts are, in fact, associated with hyperemic areas. The hyperemic areas are often extensive and vascular reactivity is commonly impaired. It is suggested that treatment aimed at reducing blood flow in hyperemic areas might improve prognosis.Stroke, Vol 12, No 5, 1981ISCHEMIC LESIONS are responsible for the neurological deficits in most patients with stroke.

The pulsatility index (PI) registreted by the transcranial doppler (TCD) was examined in relation to arterial pCO2 (paCO2) and epidural pressure (ICP). In 10 normal subjects PI was studied during variations in paCO2. In 10 neurosurgical patients with head injuries concomitant measurements of PI and ICP were obtained. The results showed a negative exponential correlation between PI and paCO2. PI changed with 3.2% pr mmHg paCO2. A positive exponential correlation between PI and ICP was observed. PI changed with 2.4% pr mmHg ICP. In the subgroup of patients with raised ICP (15 mmHg <) p

The authors measured regional cerebral 133xenon (133Xe) blood flow (rCBF), intraventricular pressure (IVP), cerebrospinal fluid (CSF) pH and lactate, systemic arterial blood pressure (SAP), and arterial blood gases during the acute phase in 23 comatose patients with severe head injuries. The IVP was kept below 45 mm Hg. The rCBF was measured repeatedly, and the response to induced hypertension and hyperventilation was tested. Most patients had reduced rCBF. No correlation was found between average CBF and clinical condition, and neither global nor regional ischemia contributed significantly to the reduced brain function. No correlation was found between CBF and IVP or CBF and cerebral perfusion pressure (CPP). The CSF lactate was elevated significantly in patients with brain-stem lesions, but not in patients with "pure" cortical lesiosn. The 133Xe clearance curves from areas of severe cortical lesions had very fast initial components called tissue peaks. The tissue peak areas correlated with areas of early veins in the angiograms, indicating a state of relative hyperemia, referred to as tissue-peak hyperemia. Tissue-peak hyperemia was found in all patients with cortical laceration or severe contusion but not in patients with brain-stem lesions without such cortical lesions. The peaks increased in number during clinical deterioration and disappeared during improvement. They could be provoked by induced hypertension and disappeared during hyperventilation. The changes in the tissue-peak areas appeared to be related to the clinical course of the cortical lesion.

Intraventricular pressure (IVP) was measured continuously by the method of Lundberg for an average period of 8 days in 52 patients with recent rupture of an intracranial saccular aneurysm. The patients were graded as follows according to the system of Hunt and Hess: 13 patients were Grades I-II, 19 patients Grades II-III, and 20 patients Grades III-V. The degree of cerebral arterial spasm was measured on angiograms taken on admission and approximately 7 days later. Drainage of ventricular cerebrospinal fluid was performed intermittently when IVP exceeded 25 mm Hg. The results showed a close correlation between changes in clinical grade and in mean IVP. Drainage improved the condition in uncomplicated cases, but was less effective or ineffective when severe vasospasm or rebleeding occurred. Lowering the IVP by drainage did not appear to increase the risk of rebleeding. In contrast to patients with no or slight spasm, patients with severe spasm had a permanently elevated IVP, even before spasm was demonstrable angiographically. A mean IVP exceeding 25 mm Hg for the whole period of monitoring was associated with a poor prognosis. Finally, indications for continuous monitoring of IVP and ventricular drainage in aneurysm patients are suggested.

Summary: Serial measurements of CBF and metabolism require mUltiple cerebral venous blood samples. Retro grade catheterization of the right internal jugular vein is easily performed at a point 2.5-3 em lateral to, and 2 em above, the medial end of the right clavicula. Complica tions are few and minor. In 1/80 (1.25%) cases the carotid