Cerebral infarction due to carotid occlusion and carbon monoxide exposure III. Influence of neck vein occlusion.

Unilateral cerebral infarcts were produced in the rat by ligation of one common carotid artery and a subsequent exposure to carbon monoxide. In animals which had undergone an additional ligation of the external jugular veins leading to a moderate increase of the cephalic venous pressure the outcome of the procedure was ameliorated significantly. Venous pressure elevation was thought to reduce the venous vascular resistance effectively by preventing the leptomeningeal veins from collapsing. Collapse of the leptomeningeal veins probably occurred during the severe carbon monoxide-induced hypotension causing a steep increase of cerebral vascular resistance.     

Cerebral infarction due to carotid occlusion and carbon monoxide exposure. I. Pathophysiological and neuropathological investigations.

Ligation of one common carotid artery and exposure to carbon monoxide has proved to be a reliable method of producing unilateral cerebral infarcts in the rat, allowing controlled experiments in any given sample size. Pathophysiological measurements in awake and narcotized rats has shown that, in contrast to hypoxic hypoxia, the carbon monoxide-induced functional anaemia (3000 ppm in room air) did not stimulate chemoreceptors, thus causing a severe systemic hypotension owing to peripheral vascular dilatation. This hypotension is likely to represent the main pathogenetic factor in this model. An inhibition of ferro-enzymes by carbon monoxide did not seem to be involved. The only cause of death was shown to be diffuse ipsilateral brain oedema with or without extra-vasation of serum proteins. The EEG, the systemic arterial pressure, rotational behaviour, and carotidal stump pressure proved to be reliable predictors of outcome.     

Cerebral bloodflow and oxygen metabolism in borderzone and territorial infarcts due to symptomatic carotid artery occlusion

It remains controversial whether borderzone infarcts are due to compromised cerebral perfusion and whether territorial infarcts are caused by artery-to-artery emboli in case of occlusion of the internal carotid artery. The present positron emission tomography study compares with normal controls, the average regional cerebral bloodflow (rCBF), regional oxygen extraction fraction (rOEF) and regional cerebral metabolic rate for oxygen (rCMRO₂) in the infarct area, the peri-infarct zone, the remaining homolateral hemisphere and in the contralateral hemisphere of 10 patients with borderzone and 17 patients with territorial infarcts, due to internal carotid artery occlusion by atherosclerosis and by cervical dissection. The steady-state technique with oxygen-15 was used. A nearly significant increase of rOEF with lowered rCBF and rCMRO₂ was observed in the peri-infarct zone of patients with territorial infarcts. In patients with borderzone infarcts rCMRO₂ was decreased in the peri-infarct zone, in the remaining homolateral hemisphere and in the contralateral hemisphere without changes in rCBF and rOEF. The present study finds no arguments that impaired cerebral perfusion is a more frequent cause of borderzone than of territorial infarcts.     

Cerebral blood flow after carotid occlusion and extracranial-intracranial bypass.

Eleven patients with occlusion of one internal carotid artery showed marked reduction of regional cerebral blood flow (rCBF) through the hemisphere on the affected side with high rCBF on the opposite side. Six of the patients had no surgery, during follow-up of 2 to 5 years. rCBF increased on both sides leaving a persisting asymmetry of rCBF. Five patients had extracranial-intracranial bypass; rCBF increased on the affected side but not on the opposite side. Asymmetry of rCBF between the hemispheres remained but was much less than in the non-operated group.     

Reperfusion strategies in stroke due to isolated cervical internal carotid artery occlusion: systematic review and treatment comparison

Neurological Sciences - Despite intravenous thrombolysis (IVT) and endovascular treatment (EVT) have been demonstrated effective in acute ischemic stroke (AIS) due to large vessel occlusions, there...     

A case of cortical blindness due to carbon monoxide poisoning

We report a case of cortical blindness occurring 7 days after acute CO poisoning with no other neurological or psychic deficits apart from denial of the blindness with visual confabulation and slight loss of retentive memory. There was scant correlation between the course of the clinical pattern, which cleared completely within 6 days, and the electroencephalographic pattern with marked and diffuse slowing, which did not recede completely during 3 months observation. CT scanning of the skull, initially within normal limits, displayed 2 weeks later a faint but diffuse hypodensity of the white substance, more marked in the occipital region, which was no longer present 80 days after the first scan.

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Sommario Viene descritto un caso di cecità corticale comparsa sette giorni dopo un 'intossicazione acuta da CO, senza altri deficit neurologici e psichici, tranne anosognosia con confabulazioni limitate alla sfera visiva e lieve deficit della memoria di fissazione. Si rileva una scarsa corrispondenza tra l'evoluzione del quadro clinico, risoltosi completamente entro il sesto giorno dall'esordio, e la persistenza di marcati rallentamenti elettroencefalografici diffusi, non completamente regrediti nei tre mesi successivi di osservazione. L'esame TC del cranio, inizialmente nella norma, evidenzia, dopo due settimane, una sfumata ipodensità diffusa della sostanza bianca, più marcata a livello occipitale, che scompare al successivo controllo effettuato dopo 80 giorni.

     

Cerebral blood flow in the evolution of infarction following unilateral carotid artery occlusion in Mongolian gerbils

Cerebral blood flow (CBF) was measured in gerbils 2, 4, 7, and 12 hours after unilateral irreversible carotid artery ligation to determine if the delayed ischemic damage to nerve terminals that occurs over 8 hours after stroke could be due to changes in CBF. [14C]butanol (4.5 mu Ci in 45 microliter 0.9% saline) was injected into the femoral vein, and cpm accumulating in the cerebrum and in a catheter inserted in the abdominal aorta were measured. CBF (ml/100 g/min, mean +/- SEM) in sham-operated control gerbils was 108.4 +/- 37.5 in the left hemisphere and 123.8 +/- 37.1 in the right. CBF in the ischemic left cerebrum was 41.0 +/- 7.7 at 2 hours (n = 7), 21.6 +/- 7.2 at 4 hours (n = 4), 26.2 +/- 4.6 at 7 hours (n = 7), and 9.7 +/- 3.1 at 12 hours (n = 6). CBF in the nonligated right hemisphere was 115.0 +/- 15.3 at 2 hours, 70.4 +/- 23.3 at 4 hours, 80.4 +/- 14.6 at 7 hours, and 50.9 +/- 20.1 at 12 hours. As expected, CBF was significantly reduced in the ischemic left cerebral hemisphere compared with the nonligated right cerebral hemisphere at each time, but CBF in the ischemic left cerebral hemisphere was also significantly lower at 12 hours than at 2 hours (p = 0.002) and at 7 hours (p = 0.014). CBF in the nonligated right cerebral hemisphere was also lower at 12 hours than at 2 hours (p = 0.02). No changes in PCO2 or blood pressure accounted for these differences.(ABSTRACT TRUNCATED AT 250 WORDS)     

Two cases of spontaneous internal carotid artery occlusion due to giant intracranial carotid artery aneurysm

Although spontaneous thrombosis of a giant intracranial aneurysm is relatively common, occlusion of its parent artery is rare. We describe two recent patients in whom the parent artery spontaneously occluded. One patient had severe stenosis of the left internal carotid artery, with delayed appearance of a faint shadow of vascular widening near the posterior clinoid process. One month later, complete occlusion of the left internal carotid artery was shown angiographically. The second patient had dysarthria and left hemiparesis, resulting in the diagnosis of a left internal carotid artery giant aneurysm. He had suffered an episode of visual disturbance of the right eye 5 years before. Angiography showed the right cervical internal carotid artery to be occluded. We believe the mechanism of parent artery occlusion in our two patients to be due first to stretching of the internal carotid artery by the enlarged aneurysm, followed by compression of the internal carotid artery by the aneurysm itself. Next, the anterior clinoid process and the optic nerve are involved, and, finally, thrombosis of the aneurysmal cavity extends into the internal carotid artery itself.     

Responses of rat brain to induced spreading depression following exposure to carbon monoxide

Until recently carbon monoxide (CO) was known only for its noxious effects. Exposure to CO results in an autoregulatory increase in cerebral blood flow (CBF). Little information is available on brain energy metabolism under low CO concentrations and on the effect of CO on the stimulated brain. In this study cortical spreading depression (SD) was induced in order to cause transient brain depolarization and increased energy demand. The multisite assembly (MSA), which contains four bundles of optical fibers for monitoring the intramitochondrial NADH redox state and tissue reflectance as well as four DC electrodes enabling measurement from four consecutive points on the cerebral cortex, was used to measure energy metabolism and the propagation of SD waves during exposure to CO. CBF in the contralateral hemisphere was measured using the laser Doppler technique. Three experimental groups of animals were examined: SD was induced during exposure to 1000 ppm CO, immediately after exposure to CO and 90 min after cessation of exposure to CO. Three control groups were also examined, in which the animals underwent the same procedures but were not exposed to CO. In all animals exposure to CO was followed by a significant increase in CBF. The greatest effect was found when SD was induced immediately after cessation of exposure to CO. SD wave frequency decreased when induced immediately after exposure to CO, whereas it increased when SD was induced 90 min after exposure. The amplitude of the NADH oxidation waves and their integral were smaller during SD induced immediately after exposure to CO. The DC potential did not change, suggesting that CO did not affect the SD initiation mechanism but rather resulted in energy depletion during recovery from SD. This study demonstrates that even at a concentration of 1000 ppm CO interferes with the metabolic activity of the brain during repolarization of the SD-induced negativity.     

Cerebral blood flow and oxygen metabolism in symptomatic internal carotid artery occlusion by (traumatic) cervical artery dissection

The present study investigates whether cerebral infarction resulting from internal carotid artery occlusion by cervical dissection is due to emboli, released from a superimposed luminal thrombus, or is due to haemodynamic failure and hypoperfusion. Ten patients with a history of stroke and with a visible cerebral infarct on computed tomographic scan, due to cervical dissection and thrombosis of the internal carotid artery, were studied with positron emission tomography in order to assess the regional cerebral blood flow (rCBF), the regional cerebral metabolic rate of oxygen (rCMRO2) and the regional oxygen extraction fraction (rOEF) in different regions of the brain. rCBF and rCMRO2 were only decreased in the infarct area but not in the peri-infarct zone or elsewhere in the brain. As rOEF was not increased in the affected cerebral hemisphere, the present study suggests artery-to-artery embolism rather than a haemodynamic event as the cause of the stroke. Use of anticoagulants thus appears to be the appropriate treatment in the acute stage.     

Blood flow and ionic responses in the awake brain due to carbon monoxide

This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The elevation in blood flow was inhibited by L-nitroarginine methyl ester, indicating that nitric oxide was responsible for the CO-induced elevation in blood flow. Exposure to 2000 ppm CO also triggered a significant decrease in pH and rise in extracellular potassium ion, possibly due to ion-pump inhibition. The amplitude of the electrocorticogram wave activity decreased, indicative of a compromise to physiological activity. These changes were not observed in rats anesthetized with pentobarbital during CO exposure, although anesthesia had no effect on the CO-induced elevation in blood flow and there was still no change in mitochondrial NADH redox level. We concluded that CO acts by separate mechanisms to alter cerebral vasoactivity and neuronal metabolic responses and that both processes are independent of hypoxic stress.     

Short-term prognosis of stroke due to occlusion of internal carotid artery based on transcranial Doppler ultrasonography.

BACKGROUND AND PURPOSE: The clinical course of stroke due to occlusion of the internal carotid artery is influenced by amount of collateral flow. We measured mean frequency shifts in the middle cerebral artery by transcranial Doppler ultrasonography to determine its prognostic value. METHODS: Patients with proven extracranial occlusion of the internal carotid artery and ipsilateral hemispheral stroke were enrolled in our study. We performed transcranial Doppler ultrasonography on 31 patients within 48 hours after the stroke onset and followed up 25 patients in 28 days. At the same time, neurological examination with quantification of neurological deficit was done. We correlated values of flow frequency shifts on the side of stroke with degree of neurological deficit at the onset and at 28 days as well as the degree of clinical improvement and the value of frequency shifts. RESULTS: We found a negative correlation between blood flow frequency shifts in the middle cerebral artery and degree of neurological deficit at the onset (Spearman rank correlation coefficient, -0.567; p less than 0.001). We also found a positive correlation between the change of the neurological deficit during follow-up and frequency shifts at the onset (Spearman rank coefficient, 0.548; p less than 0.05). CONCLUSIONS: Diminished blood flow velocity (mean frequency shift) in the area of stroke is a negative prognostic factor for the degree of neurological deficit at the onset and a negative prognostic factor for possible improvement. Knowledge of hemodynamic conditions in the stroke area may help to improve therapeutic decisions.     

Posttraumatic cerebral infarction due to progressive occlusion of the internal carotid artery after minor head injury in childhood: a case report

Purpose  

Although minor head injury in childhood is a common occurrence and usually no complications, posttraumatic cerebral infarction has rarely been reported. Such infarction is characterized by occlusion of the lateral lenticulostriate artery. The authors report an atypical case of posttraumatic occlusion of the internal carotid artery (ICA) after minor head injury in childhood.