1975
DOI: 10.1111/j.1600-0404.1975.tb07604.x
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Regional Cerebral Blood Flow in Patients With Chronic Subdural Hematomas

Abstract: Cerebral blood flow (CBF) was measured by the intra-arterial 133Xenon method in seven patients, aged 55 to 76 years, with chronic subdural hematomas. Before operation, CBF was reduced to an average of 31 ml/100g/min, range 24-38 ml/100g/min. One to 3 weeks after operation, when all had improved, CBF averaged 38 ml/100g/min, range 34-43 ml/100g/min. The reduction of CBF was probably secondary to a reduced metabolic demand. Clinical improvement continued for months after operation.

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Cited by 50 publications
(19 citation statements)
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“…Pathophysiologic mechanisms, though requiring further elucidation, are responsible in the occurrence of seizures after CSDH, including (1) development of a space-occupying lesion with mass effect, inducing reduced cerebral blood flow that may be involved in immediate seizures [22]; (2) a variety of surgical techniques or unpredicted brain insults may be present individually or together, which may provoke early seizures [5]; and (3) late-onset seizures can theoretically be due to gliosis from previous cortical injury or the presence of hematoma capsules [18].…”
Section: Discussionmentioning
confidence: 99%
“…Pathophysiologic mechanisms, though requiring further elucidation, are responsible in the occurrence of seizures after CSDH, including (1) development of a space-occupying lesion with mass effect, inducing reduced cerebral blood flow that may be involved in immediate seizures [22]; (2) a variety of surgical techniques or unpredicted brain insults may be present individually or together, which may provoke early seizures [5]; and (3) late-onset seizures can theoretically be due to gliosis from previous cortical injury or the presence of hematoma capsules [18].…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, the pathophysiology of epileptogenesis in these patients is incompletely known, but is thought to be biphasic, with 1) early and 2) late post traumatic epilepsy (PTE) (Agrawal et al 2006). One hypothesis states that in the immediate peri-injury period, brain swelling, cerebral ischemia and the release of excitatory amino acids and other toxins precipitate neuronal damage (Agrawal et al 2006; Brodersen and Gjerris 1975). Comparatively, in the late post injury period, an excess of extracorpuscular hemoglobin facilitates the creation of cytotoxic hydroxyls, reactive oxygen species moieties and glutamate accumulation (Payan et al 1970).…”
Section: Introductionmentioning
confidence: 99%
“…Aspects of the epidemiology, histology, and pathophysiology of these haematomas have been reported in several papers (Putnam and Cushing, 1925;Weir, 1971; Brodersen and Gjerris, 1975;. However, with the exception of two communications (McKissock et al, 1960;Loew and Kivelitz, 1976), relatively little attention has been paid to the clinical presentation, diagnostic investigations, and prognosis.…”
mentioning
confidence: 99%