Regional cerebral blood flow and metabolism in chronic subdural hematoma

There are two hypotheses on how chronic subdural hematoma causes hemiparesis and other focal neurologic symptoms without, in most cases, leaving permanent neurologic deficits. One hypothesis is that the reduced regional cerebral blood flow (rCBF) caused by either compression or distortion of the local or remote brain tissue is responsible for hemiparesis. The other hypothesis is that the reduction in rCBF alone is not sufficient to cause permanent hemiparesis.     

Relation of regional cerebral blood flow to hemiparesis in chronic subdural hematoma

To investigate the causative mechanism of hemiparesis in chronic subdural hematoma, 38 patients with unilateral chronic subdural hematoma were studied on the relationship between their clinical manifestations and regional cerebral blood flow measured with 133xenon inhalation (16 detectors on each side of the head, Initial Slope Index). Twenty-five patients with hemiparesis (hemiparesis group) and 13 patients with headaches only and without any neurological deficits (headache group) were examined before surgery for chronic subdural hematoma. Among the hemiparesis patients, 15 were examined after surgery. Preoperative regional cerebral blood flow values in the headache group were normal in all regions bilaterally and showed no significant regional difference in one hemisphere or interhemispheric difference between the corresponding regions in both hemispheres, whereas preoperative regional cerebral blood flow values in the hemiparesis group were generally around the lower limit of the age-matched normal value and were subnormal in some areas, and the regional cerebral blood flow values were significantly lower on the hematoma side than on the intact side in most regions. The rolandic region especially showed the lowest regional cerebral blood flow value of 32.3 in the Initial Slope Index on average and the most significant interhemispheric differences of regional cerebral blood flow. Such a preoperative reduction of regional cerebral blood flow in the hemiparesis group normalized along with clinical improvement after evacuation of the hematoma. It was suggested that localized cerebral blood flow reduction at the rolandic cortical region under the hematoma might be one of the causative factors of hemiparesis in chronic subdural hematoma.     

Clinical features of chronic subdural hematoma: neuropsychiatric and neuropsychologic changes in patients with chronic subdural hematoma

This article provides a background review of the cognitive and behavioral symptoms associated with chronic subdural hematoma (CSH). The areas addressed include the initial cognitive and behavioral symptom presentation, lateralization and localizing signs, differences between older and younger patients, and differential diagnosis. Although it is clear that behavioral and cognitive abnormalities are seen in CSH, further work is needed to objectively clarify the range of symptoms and signs.     

Local cerebral blood flow mapping before and after removal of acute subdural hematoma in the rat.

The cause of hemispheric swelling and high intracranial pressure after acute subdural hematoma is unknown, yet this is a major cause of death related to this condition. To investigate whether vascular engorgement is the cause of this form of hemisphere swelling, we have autoradiographically mapped regional cerebral blood flow before and after removal of acute subdural hematoma in a rat model. Hyperemia was patchy and infrequent. The major cause of the significant hemisphere swelling seen after hematoma removal was enlargement of the zone of focal tissue ischemia and edema under the hematoma.     

Coagulopathy in chronic subdural hematoma.

Coagulation factors were studied in 30 fluids aspirated from 25 patients with chronic subdural hematoma. Compared with the normal range for plasma, the hematoma fluids demonstrated a marked reduction in factors II, V, VII, VIII, and X, moderate reduction of factors IX and XI, and slight reduction of XII. Factor VII and IX inhibitors were not present or negligible. Activated protein C and antithrombin III were decreased and fibrinopeptide A was markedly increased. No case had a basic disorder causing these abnormal data spontaneously. The decrease in activated protein C possibly caused the marked reduction of factor VIII, therefore the intrinsic and extrinsic clotting pathways were affected differently. The results show excessive activation of coagulation, predominantly via the extrinsic clotting pathway in hematoma, suggesting its importance in the growth of chronic subdural hematoma.     

Calcified chronic spinal subdural hematoma demonstrated by computed tomography

Spinal subdural hematoma is a rare clinical condition that may result in spinal cord compression. The authors present a patient with chronic calcified spinal subdural hematoma demonstrated by computerized tomography. Surgical removal resulted in clinical improvement.     

Contralateral development of chronic subdural hematoma after evacuation of chronic subdural hematoma. A case report

Contralateral acute complications such as acute epi/subdural hematomas can be encountered after evacuation of a chronic subdural hematoma, though they are rare. We found only one case of chronic subdural hematoma following the surgery for contralateral chronic subdural hematoma, have been published in English language literature. A 73-year-old male admitted to our hospital with a right-sided subdural hematoma. The subdural hematoma was evacuated through a burr-hole. A left-sided subdural higroma appeared after operation and turned into classical subdural hematoma in the course of time. After evacuation of contralateral chronic subdural hematoma, the patient recovered completely. All stages of the development of contralateral chronic subdural hematomas were shown by serial computed tomograms. It was suggested that traumatic chronic subdural hematomas develop from mostly subdural higromas. If contralateral subdural higroma is seen after surgical evacuation of a chronic subdural hematoma, the possibility of development of contralateral chronic subdural hematoma must be kept on mind.     

Pressure changes within a chronic subdural hematoma during hemodialysis

Spontaneous intracranial hemorrhage is not an infrequent complication of systemic anticoagulation, as occurs in hemodialysis. The neurological symptoms of subdural hematoma may be similar to those of dialysis disequilibrium. The pressure within a subdural fluid collection was monitored in a patient undergoing hemodialysis. The patient was known to become unresponsive during previous dialysis treatments. The initial pressure within the subdural cavity was measured to be -10.0 cm H2O prior to dialysis. The pressure within the collection decreased to a minimum value of -19.4 cm H2O during dialysis and stabilized at -16.4 cm H2O at the termination of dialysis. The neurological status changed subjectively during the procedure, with the patient becoming unresponsive to verbal stimuli as the intracranial pressure reached a minimum. These findings represent a syndrome similar to aliquorrhea, or low cerebrospinal fluid pressure within an otherwise asymptomatic subdural hematoma. Previously only increased intracranial pressure has been reported with hemodialysis.     

Failure of cerebral blood flow-metabolism coupling after acute subdural hematoma in the rat.

We have used a recently introduced cerebral blood flow tracer, technetium-99-DL-hexamethylpropylene amine oxime, to map regional cerebral blood flow simultaneously with measurements of glucose metabolism ([14C]-2-deoxyglucose technique) using autoradiography. The technique was used to compare the acute effects of middle cerebral artery occlusion with the more complex events that occur after induction of an acute subdural hematoma (SDH) in the rat. Previous studies with this SDH model have shown that an infarction is induced in the cortex under the hematoma. In both models, the core of the infarct zone was associated with a reduction in both flow and metabolism to less than 15% of control values. In both models, the infarct core was surrounded by a band of tissue in which glucose metabolism increases by 60 to 70% and blood flow is reduced by the same amount. Global blood flow after the SDH was reduced by 14%, but remained unchanged after middle cerebral artery occlusion. In the hippocampus, a massive increase in metabolism (up to 157%) after SDH was accompanied by a paradoxical decrease in blood flow (32%). This discrepancy between blood flow and metabolism indicates loss of flow-metabolism coupling and provides a mechanism for infarct recruitment and delayed hippocampal damage after SDH.     

Cardiovascualr changes with acute subdural hematoma.

Of 100 consecutive patients with acute subdural hematoma, 53 survived. Blood pressure and heart rate changes were not reliable indicators of increased intracranial pressure or cerebral disaster. Electrocardiographic changes in these patients were dramatic. Forty-one patients developed a new cardiac arrhythmia. Increased intracranial pressure and brain lesions adversely affect the heart. These effects must be recognized and appropriately treated.     

Physiopathology of chronic subdural hematoma

Coagulation, fibrinolysis and kinin-kallicrein system disorders could explain chronic subdural hematoma pathophysiology. The marked decrease in antithrombin III in the hematoma suggest that the decreased levels of clotting factors were caused by excessive coagulation resulting in clotting factors consumption. The decrease in alpha 2-antiplasmin with the increase of fibrin degradation products suggest that hyperfibrinolytic activity of the subdural hematoma. Coagulation and fibrinolysis disorders could explain repetitive hemorrhages from the outer membrane, which cause progressive enlargement of the hematoma. Kinin-kallicrein system disorders raise the hemorrhage by its action on the outer membrane. Nowadays, the earliest osmotic theory should reasonably be abandoned.     

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.