Acute regional cerebral blood flow changes caused by severe head injuries

To evaluate the changes in cerebral blood flow (CBF) that occur immediately after head injury and the effects of different posttraumatic lesions on CBF, 61 CBF studies were obtained using the xenon-computerized tomography method in 32 severely head-injured adults (Glasgow Coma Scale score (GCS) less than or equal to 7). The measurements were made within 7 days after injury, 43% in the first 24 hours. During the 1st day, patients with an initial GCS score of 3 or 4 and no surgical mass had significantly lower flows than did those with a higher GCS score or mass lesions (p less than 0.05): in the first 1 to 4 hours, those without surgical mass lesions had a mean CBF of 27 cc/100 gm/min, which rose to 44 cc/100 gm/min by 24 hours. Patients without surgical mass lesions who died tended to have a lower global CBF than did those with better outcomes. Mass lesions were associated with a high global CBF and bihemispheric contusions with the lowest flows. By 24 hours after injury, global blood flow increased in groups that originally had low flows and decreased in those with very high initial flows, such that by 36 to 48 hours, most patients had CBF values between 32 and 55 cc/100 gm/min. Lobar, basal ganglion, and brain-stem blood flow values frequently differed by 25% or more from global averages. Brain-stem CBF varied the most but did not correlate with clinical signs of brain-stem dysfunction. Double studies were performed at two different pCO2 values in 10 patients with various posttraumatic lesions, and the CO2 vasoresponsivity was calculated. Abnormal CO2 vasoresponsivity was found with acute subdural hematomas and defuse cerebral swelling but not with epidural hematomas. In patients without surgical mass lesions, the findings suggest that CBF in the first few hours after injury is often low, followed by a hyperemic phase that peaks at 24 hours. Global CBF values vary widely depending on the type of traumatic brain injury, and brain-stem flow is often not accurately reflected by global CBF values. These findings underscore the need to define regional CBF abnormalities in victims of severe head injury if treatment is intended to prevent regional ischemia.     

The incidence of delayed traumatic intracerebral hematoma with extradural hemorrhages

After introduction of computerized tomography (CT), we experienced 22 patients with traumatic extradural and intracerebral combined hematomas, of whom 15 underwent sequential CT scans. In 14 of the 22 patients or 13 of the 15 patients whose initial CT scans were performed early, within 6 hours after injury, intracerebral hematomas developed more slowly than extradural hematomas. In ten of the 13 patients, development of intracerebral hematomas was demonstrated only after removal of extradural hematomas, and in four patients acute brain swelling was observed during surgery. Therefore it is emphasized that the incidence of post-surgical intracerebral hematoma with extradural hemorrhages is high and that acute brain swelling during surgery for extradural hematomas is largely caused by the delayed intracerebral hematomas.     

AVDO2 and EEG as indicators for treatment of post-traumatic brain swelling--experimental study.

A cat model of compression ischemia using epidural balloon inflation investigated: 1) the relationship between postischemic cerebral blood flow (CBF) and metabolism and brain swelling, 2) the use of arteriovenous oxygen difference (AVDO2) and electroencephalographic (EEG) frequency band analysis for monitoring CBF and cerebral metabolism, and 3) indications for selecting the therapy. Global ischemia was induced by brain compression, followed by rapid decompression, and AVDO2, CBF, cerebral metabolic rate for oxygen, and EEG were monitored. The animals were divided into delayed brain swelling and no swelling groups. The severity of compression ischemia influenced the recovery of CBF and cerebral metabolism. The AVDO2 and EEG reflected the CBF and cerebral metabolism. These parameters are useful in selecting the therapy for focal brain injury.     

Diffuse axonal injury and early intracranial sequelae in severe head injury.

The importance of diffuse axonal injury (DAI) and early intracranial sequelae was studied in 107 patients with diffuse and focal brain injuries. Comprehensive neuropathological study was also undertaken in 24 fatal patients. The mortality rate was clearly the highest in traumatic subarachnoid hemorrhage, followed by acute subdural hematoma, cerebral contusion with delayed hematoma formation, traumatic intracerebral hematoma, diffuse cerebral swelling, DAI with classical features, and finally nearly normal on computed tomographic scans. The mean flow velocities in the middle cerebral artery recorded by transcranial Doppler ultrasound were variable in diffuse brain injury, but commonly decreased on the hematoma side depending on increased intracranial pressure and decreased cerebral perfusion pressure in focal brain injury. Deep-seated hemorrhagic lesions did not expand in diffuse brain injury, but sizable hematoma developed within 24 hours in focal brain injury. The platelet count was significantly lower in patients with poor outcomes in focal brain injury. Histological evidence of classical DAI was found in eight (50%) of 16 cases with focal brain injury. DAI of varying severity is the common subjacent lesion in patients with severe head injury, but the final outcome varies greatly with different lesion types.     

Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries

OBJECT: The edema associated with brain swelling after traumatic brain injury (TBI) has been thought to be vasogenic in origin, but the results of previous laboratory studies by the authors have shown that a cellular form of edema is mainly responsible for brain swelling after TBI. In this study the authors used magnetic resonance (MR) imaging techniques to identify the type of edema that occurs in patients with TBI. METHODS: Diffusion-weighted MR imaging was used to evaluate the apparent diffusion coefficient (ADC) in 44 patients with TBI (Glasgow Coma Scale Score < 8) and in eight healthy volunteers. Higher ADC values have been associated with vasogenic edema, and lower ADC values with a predominantly cellular form of edema. Regional measurements of ADC in patients with focal and diffuse injury were computed. The water content of brain tissue was also assessed in absolute terms by using MR imaging to measure the percentage of water per gram of tissue. Cerebral blood flow (CBF) was measured using stable Xe-computerized tomography (CT) studies to rule out ischemia as a cause of cellular edema. The mean ADC value in the healthy volunteers was 0.82 +/- 0.05 x 10(-3) mm2/second. The ADC values in the patients with diffuse brain injury without swelling were close to the mean for the healthy volunteers. In contrast, the patients with brain swelling had increased brain water content and low ADC values (mean 0.74 +/- 0.05 x 10(-3) mm2/second). The ADC values correlated with CT classifications. In all patients with low ADC values, the CBF values were outside the range for ischemia. CONCLUSIONS: The brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.     

Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure.

Severe head injury often causes an increase in intracranial pressure (ICP) and decreases in cerebral blood flow (CBF) and cerebral oxygen delivery (CO2del). To determine if this reduction in CBF and CO2del would produce cerebral ischemia and if this reduction would be abrogated by maintaining global cerebral perfusion pressure (CPP), we studied CPP, ICP, CBF, CO2del, cerebral oxygen extraction ratio (CO2ER), and cortical water content (CWC) in a porcine model of focal cryogenic brain injury. Fifteen mature swine were randomized to two groups. The experimental group (n = 7) had a brain lesion and was studied for 24 hours. The control group (n = 8) was instrumented only. Cryogenic injury significantly increased ICP and decreased CBF and CO2del compared with controls. There were no significant differences in CPP between the groups for the entire experiment, and the CPP was well above the ischemic threshold. The CO2ER significantly increased in the first three hours after brain injury. However, CO2ER in experimental animals tended to decrease 12 hours after brain injury and was not significantly different from that in controls. Cryogenic injury significantly increased the CWC in the lesioned hemisphere. These data indicate that focal brain injury results in persistent ischemia despite the normalization of CPP, suggesting that a significant increase in cerebral vascular resistance (CVR) occurs after brain injury. We conclude that in addition to maintenance of CPP, intervention to reduce CVR may be important in the management of brain injury.     

Computerized tomography, magnetic resonance imaging, and positron emission tomography in the study of brain trauma. Preliminary observations

Results of computerized tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), xenon-133 measurement of cerebral blood flow (CBF), and neuropsychological assessments are described in three head-injured patients. The patients were selected because they presented with intracranial hemorrhage diagnosed by CT. Two of the patients were studied acutely and again approximately 6 months later. In the acute stage, MRI was superior to CT in identifying the precise location and extent of intracranial hemorrhage and associated edema. Small subdural hematomas diagnosed on MRI were missed with CT scanning. The extent of apparent encephalomalacia in the chronic stages of injury was also better defined with MRI. Positron emission tomography showed disturbances of glucose metabolism that extended beyond the structural abnormalities demonstrated by MRI and CT; anterior temporal lobe dysfunction was particularly evident in all three patients. Regional CBF studies failed to detect a number of the abnormalities seen on MRI and CT, and even ignored the metabolic dysfunction evident on PET that should have been accompanied by changes in regional CBF. The neuropsychological studies localized frontal lesions, but did not reveal abnormalities attributable to the structural lesions and the reduced metabolism in the anterior temporal lobes.     

外伤性迟发性颅内血肿临床特点及首次CT的影像学特征分析

目的分析外伤性迟发性颅内血肿临床特点及首次CT影像学特征,早期诊断外伤性迟发性颅内血肿,提高疗效。方法回顾性分析我院2005年至2009年经CT证实的外伤性迟发性颅内血肿患者的临床资料,总结临床特点和首次CT影像学特征。结果迟发性血肿多发生在伤后3d内,额颞部好发,老年人容易发生,进行性的意识水平下降或出现新的神经系统体征往往意味着迟发性血肿;首次CT发现头皮血肿、颅骨骨折、气颅、脑挫伤、蛛网膜下腔出血、外侧裂血肿等预警征象时,要警惕迟发性血肿的发生。结论如果首次CT扫描有头皮血肿、颅骨骨折、脑挫伤、蛛网膜下腔出血、外侧裂血肿者,或颅内血肿成功清除后,但临床症状和特征未改善甚至加重者,进行性的意识水平下降者,伤后应将头部CT动态扫描作为常规检查,做到早期诊断、及时治疗。     

The effects of aortic crossclamping and resuscitation on intracranial pressure, cerebral blood flow, and cerebral water content in a model of focal brain injury and hemorrhagic shock

Aortic crossclamping (AOXC) is performed frequently in hypotensive trauma patients who may have had a head injury. The effect of AOXC on the injured brain is unknown. We studied the effect of AOXC on mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral perfusion pressure (CPP), and cerebral water content in a porcine model of focal cryogenic brain injury. Four groups of animals were studied: Group I--brain injury only; Group II--brain injury and AOXC; Group III--brain injury with hemorrhage and AOXC; and Group IV--AOXC only. Focal cryogenic grain injury increased the ICP in Groups I-III. Aortic crossclamping increased MAP, CBF, ICP, and CPP after hemorrhage in Group III. Following declamping and resuscitation there were no differences between the groups in any studied variable. Cerebral water content at the site of the focal brain injury was greater than in nonlesioned cortex but there was no significant difference between groups despite a greater positive fluid balance in hemorrhaged animals. AOXC improved perfusion to the injured brain without a significant increase in ICP. Increased MAP induced by AOXC and large fluid resuscitation appeared to have no detrimental effect on ICP, CBF, cerebral water content, or CPP in this model of brain injury.     

Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia

Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 +/- 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p less than 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF less than or equal to 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.     

Centrifugal distribution of regional cerebral blood flow and its time course in traumatic intracerebral hematomas

Cerebral blood flow (CBF) alterations following post-traumatic contusions have been demonstrated in recent papers. We evaluated regional CBF (rCBF) by means of Xenon-enhanced computerized tomography (Xe-CT) in 29 traumatic intracerebral hematomas, from 22 patients with severe head injury (GCS < or = 8). Fifty traumatic hematoma/Xe-CT CBF measurements were obtained from 39 Xe-CT studies performed during the acute phase (corresponding to the first 20 days post-injury). The rCBF was measured in three different regions of interest: the hemorrhagic core, the perihematoma edematous low-density area, and a 1-cm rim of perihematoma normal-appearing brain tissue, surrounding the edematous low-density area. We found a centrifugal improvement of rCBF as well as a decrease in the rates of CBF levels below 18 mL/100 g/min from the core to the periphery (p < 0.0001), which persisted over time. Ischemic rCBF values were detected in the perihematoma low-density area only in 24% of the traumatic hematomas. The time course of rCBF levels showed a reduced flow in the first 24 h, with a recovery of flow from day 2 to day 4, followed by another reduced flow (p < or = 0.0001) both in the perihematoma edematous low-density area and in the non-lesioned tissue. Our findings suggest that the only area with persistent ischemic values was the hemorrhagic core. Low rCBF levels seen in the perihematoma low-density area may only be ascribed partially to ischemia and can possibly recover over time. These results could encourage a surgical approach based on an early evacuation of the hemorrhagic core associated to a preservation of the surrounding edematous tissue.     

脑灌注压对创伤性脑损伤后急性脑缺血的影响

目的 观察不同脑灌注压(CPP)对创伤性脑损伤后急性脑缺血的影响.方法 实验家兔60只,随机分为正常对照组(无损伤组)、高CPP组(90～110)mm Hg、中CPP组(70～80)mm Hg、低CPP组(50～60)mm Hg、极低CPP组(35～45)mm Hg.采用Feeney's自由落体撞击法建立急性局灶性脑挫裂伤模型,伤后80 min静脉给予升压和降压药物调控血压使CPP达到设计要求,同步进行脑血流、CPP测定,并进行图像分析,且观察不同CPP下颅脑损伤后急性脑缺血动物脑含水量及神经组织超微结构改变.结果 对照组局部脑血流量(rCBF)为156.18±6.22;高CPP组实验组rCBF为140.03±17.32,中CPP组rCBF为100.46±21.37,低CPP组rCBF为86.46±10.30,极低CPP组rCBF为60.36±8.32.对照组脑含水量为(78.21±0.26)%;高CPP组实验组脑含水量为(80.15±0.52)%,中CPP组脑含水量为(80.27±0.36)%,低CPP组脑含水量为(81.18±0.62)%,极低CPP组脑含水量为(81.34±0.83)%.实验组脑组织含水量高于对照组(P<0.01);实验组rCBF较对照组明显降低,差异有统计学意义(P<0.01);高CPP组rCBF明显高于低CPP组及极低CPP组,差异有统计学意义(P<0.01);中CPP组rCBF虽低于对照组及高CPP组,而高于低CPP组及极低CPP组,但组间比较筹异无统计学意义(P>0.05).低CPP组及极低CPP组脑含水量、超微结构较对照组差异有统计学意义(P<0.05).结论 在缺血急性期及时有效地改善脑循环、恢复脑供血是阻止脑缺血发展成为脑组织不可逆损伤的重要环节.     

Posttraumatic diffuse cerebral lesions. Relationship between clinical course, CT findings and ICP.

One hundred and fifty patients with posttraumatic diffuse cerebral lesions were reviewed. Criteria of inclusion were immediate coma and CT appearance of diffuse lesions, that were classified as follows: (a) Diffuse axonal injury (70 cases): patients with normal CT scan (50 cases) and patients with shearing injury (focal hemorrhages in corpus callosum, basal ganglia and brain stem; gliding contusions) (20 cases); (b) Diffuse brain swelling (80 cases): reduced or absent lateral ventricles, absence of 3rd ventricle and basal cisterns. Many of these patients had either subarachnoid haemorrhage or subdural blood effusion. Clinical course and mortality rate were in a ranking order in the considered groups. Patients with normal CT had a less severe coma and a better outcome than patients with shearing injury and diffuse brain swelling. There was evidence of high intracranial pressure in 75% of the patients with brain swelling, whereas no patient with normal CT had ICP elevation. Diffuse axonal injury represents a primary posttraumatic diffuse lesion. Secondary vascular involvement, due to hypoxia, shock and other unknown causes, is responsible for the appearance of vasoparesis, hyperemia and diffuse brain swelling.     

Selection of patients for extra-intracranial arterial bypass surgery based on rCBF measurements.

Extracranial intracranial arterial anastomosis is gaining acceptance as a form of treatment in selected cases with ischemic cerebrovascular disease. To establish indications for this operation and to provide an objective assessment of postoperative results, regional cerebral blood flow (rCBF) studies were performed in 110 patients with cerebrovascular insufficiency considered for extra-intracranial bypass surgery. The 133Xe intracarotid injection method with 16 externally placed detectors was used for measuring rCBF. Postoperatively, rCBF was measured in 40 patients. From these results our present criteria for surgery have evolved. The probability of a good postoperative result is best in patients who showed focal cerebral ischemia or a moderate general reduction of CBF with an additional ischemic focus. The operation is contraindicated in patients with either normal or severely reduced CBF values (less than 60% of normal).     

Cerebral oxygen consumption and ischemia in traumatic brain injury

AIM: Clinical and experimental studies have shown a reduction of cerebral blood flow (CBF) and metabolic alterations following traumatic brain injury (TBI). The incidence of ischemia and the meaning of post-traumatic metabolic alterations are still unclear. METHODS: Revision of CBF and metabolic changes following TBI based on the literature and on our clinical experience. RESULTS: Cerebral ischemia and metabolic alterations are part of the secondary insults/damage leading to an increased damage following TBI. Global ischemia occurs early following TBI as shown by CBF measurements and by greater values of arterio-jugular difference of oxygen (AJDO(2)) during the 1(st) 24 hours postinjury. Post-traumatic ischemia should be defined based on the relationships between CBF and on the metabolic requirements of the brain. Regional ischemia occurs more frequently than global ischemia as shown by regional monitoring of cerebral oxygenation. Following TBI there is a transient phase of increased glycolitic activity followed by a more prolonged phase of reduced metabolic rate of glucose (CMRglc) and oxygen (CMRO(2)). The extent of CMRO(2) reduction is a marker of injury severity and it is associated with unfavorable outcome. CONCLUSION: Cerebral ischemia occurs following TBI and should be defined based on CBF value and the metabolic needs of the brain. Global monitoring of cerebral oxygenation adequacy should be combined with regional monitoring. The meaning of high AJDO(2) values should be reconsidered: if they can highlights potential ischemia they are also showing a still living brain with a partially preserved oxygen extraction capability.     

Focal cerebral hyperemia in postconcussive amnesia.

Transient amnesia caused by minor head injury is commonly encountered in daily neurosurgical practice, but the mechanism of such amnesia has not been extensively studied. We measured the regional cerebral blood flow (rCBF) of patients with postconcussive amnesia with Xe/CT CBF to examine whether a focal disturbance of CBF exists. The Xe/CT CBF study was performed in eight patients with closed head injury without organic cerebral lesion while they were suffering from posttraumatic amnesia (concussion group). The time interval between accident and CBF measurement was less than 2 h in three patients, 5-6 h in two, 8-9 h in two, and 18 in one. The results were compared with those of nine normal volunteers and eight other age-matched patients who recovered without any neurological deficit despite the presence of hemorrhagic regions (mild hemorrhage group). The rCBF of the concussion group was significantly elevated in the bilateral mesial temporal cortex in comparison to the normal group. The rCBF in the mild hemorrhage group was lower than that of normal controls in all regions. The analysis of right-left difference in CBF indicated that there was significant asymmetry (right > left) in the frontal and temporal cortex in the concussion group, but not in the normal and mild hemorrhage group. This Xe/CT CBF study in acute stages of cerebral concussion, in which patients were amnestic, detected focal cerebral hyperemia. Such hyperemia in regions closely related to human memory function may be the result of vasoparalysis or the compensatory activation of memory circuits after denervation injury.     

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.     

小鼠局灶性脑缺血的脑血流动力学和脑损害的评价

目的　建立一种可靠的小鼠脑缺血模型,了解永久性和暂时性阻断血管后的脑病理生理变化。方法　 Ｃ Ｄ１ 小鼠,单侧大脑中动脉线栓阻断,监测脑血流,测量梗塞体积和血脑屏障破坏程度。结果　小鼠均出现成熟缺血核心区和半暗区。不同缺血／ 再灌注时间产生不同缺血损害和血脑屏障破坏,但有时限。结论　建立了一种可靠、复制性强的小鼠局灶性缺血模型。血脑屏障破坏在缺血损害中起重要作用。短时间缺血后的再灌注能减轻缺血性脑损害。     

Brain specific gravity and CT scan density measurements after human head injury

White matter specific gravity was measured using the microgravimetric method in 20 comatose patients with diffuse head injury who were undergoing intracranial pressure (ICP) monitoring, and in 19 patients with focal injuries who were undergoing evacuation of contusions or intracerebral hematomas. Computerized tomography (CT) density readings were obtained for each site of white matter sampling by locating the sampling site on the preoperative CT scan. A significant correlation was found between the specific gravity values and the CT density numbers (r = 0.775; p less than 0.001). Patients with focal injuries demonstrated reduced perifocal specific gravity, suggesting brain edema. The mean specific gravity in patients with diffuse injury was within the normal range. In 10 of 12 patients in whom the specific gravity was above the normal range, the CT density was also above the normal range. These data suggest that cerebral vascular engorgement is the cause of the high specific gravity. Six (60%) of this small subgroup of 10 patients also demonstrated a high ICP.     

Xenon-enhanced computed tomographic measurement of cerebral blood flow in patients with chronic subdural hematomas

We compared clinical symptoms with extent of brain shift on computed tomographic (CT) scans and quantitative and three-dimensional measurements of cerebral blood flow (CBF) on xenon-enhanced CT scans in 10 patients with chronic subdural hematomas. Five patients had only headache and minimal or no brain shift on a CT scan. The other five had hemiparesis and/or mental disturbance in addition to headache and moderate or severe brain shift on a CT scan. The mean hemispheric CBF decreased about 7% in patients with headache and about 35% in patients with hemiparesis and/or mental disturbance. It decreased also on the side without the hematoma. The CBF reduction was always more pronounced in the putamen and thalamus than in the cortex. On the contrary, the cortex CBF was mostly preserved or even elevated in both groups of patients. We speculate that CBF reduction in patients with a chronic subdural hematoma occurs initially in central cerebral areas like the basal ganglia and thalamus, and then extends to the entire hemisphere including the cortex as brain compression and displacement progress. Central cerebral area involvement might be more responsible for clinical symptoms than the cortex.