In this report the authors describe a noninvasive transcranial method of determining the flow velocities in the basal cerebral arteries. Placement of the probe of a range-gated ultrasound Doppler instrument in the temporal area just above the zygomatic arch allowed the velocities in the middle cerebral artery (MCA) to be determined from the Doppler signals. The flow velocities in the proximal anterior (ACA) and posterior (PCA) cerebral arteries were also recorded at steady state and during test compression of the common carotid arteries. An investigation of 50 healthy subjects by this transcranial Doppler method revealed that the velocity in the MCA, ACA, and PCA was 62 +/- 12, 51 +/0 12, and 44 +/- 11 cm/sec, respectively. This method is of particular value for the detection of vasospasm following subarachnoid hemorrhage and for evaluating the cerebral circulation in occlusive disease of the carotid and vertebral arteries.
✓ Present knowledge of the still controversial pathogenetic, ultrastructural, diagnostic, and treatment aspects of chronic subdural hematomas is reviewed.
The end-tidal carbon dioxide partial pressure (PCO2) response curves for the flow velocity in the middle cerebral artery were studied in 31 normal subjects with transcranial Doppler techniques. An exponential curve with an exponent of 0.034 mm Hg-1 was found to be a good fit to the recorded data. By means of this relationship, recordings of flow velocity in cerebral arteries can be normalized to a standard value of PCO2. Physiological aspects of cerebrovascular reactivity to PCO2 and the clinical implications of the PCO2 response curve are discussed. The normal material provides a reference for assessing pathological responses.
A consecutive series of 32 adult patients with chronic subdural hematoma was studied in respect to postoperative cerebral reexpansion (reduction in diameter of the subdural space) after burr-hole craniostomy and closed-system drainage. Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. Our study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly.
A consecutive series of 21 adult patients with chronic subdural hematoma was studied in respect to postoperative resolution of subdural collections and clinical improvement after burr hole evacuation without subdural drainage. This series was compared to a previously studied series of patients with chronic subdural hematoma in whom postoperative closed system drainage had been installed. Using the identical protocol for treatment and postoperative follow-up, we obtained identical results with respect to time-related neurological improvement and persistence of subdural collections in the undrained and drained series, except that the steadily progressive clinical improvement during the early postoperative phase (24 hours) in all cases of the drained series was not universal in the undrained cases. Our study suggests that, to avoid the possibility of early postoperative clinical deterioration, burr hole craniostomy and closed system drainage is advisable. We think that subdural drainage is not necessary when the installation of the drainage system seems to be technically difficult, as it may be in cases with considerable perioperative cortical expansion.
The use of dental processing software for computed tomography (CT) data (Dentascan) is described on postmortem (pm) CT data for the purpose of pm identification. The software allows reconstructing reformatted images comparable to conventional panoramic dental radiographs by defining a curved reconstruction line along the teeth on oblique images. Three corpses that have been scanned within the virtopsy project were used to test the software for the purpose of dental identification. In every case, dental panoramic images could be reconstructed and compared to antemortem radiographs. The images showed the basic component of teeth (enamel, dentin, and pulp), the anatomic structure of the alveolar bone, missing or unerupted teeth as well as restorations of the teeth that could be used for identification. When streak artifacts due to metal-containing dental work reduced image quality, it was still necessary to perform pm conventional radiographs for comparison of the detailed shape of the restoration. Dental identification or a dental profiling seems to become possible in a noninvasive manner using the Dentascan software.
Eleven cases of cerebral cavernous angiomas (cavernomas) were observed within a period of 3 years. Two patients presented with cerebral hemorrhage, five with epilepsy, three each with a progressive focal neurological deficit, and one with papilledema. The unruptured lesions had a heterogeneous density on computed tomography with relatively little contrast enhancement. Two lesions contained major cysts. In one of these cases, the cyst measured 5.5 cm in diameter, had an enhancing membrane, and was surrounded by brain edema. Angiography did not show hypervascularity in any instance. During exploration and histological processing, special attention was paid to signs of previous silent hemorrhages and to the degree of encapsulation of the lesion. Iron deposits (signs of previous hemorrhages) were seen to varying degrees inside all cavernomas as well as in the surrounding gliotic cerebrum, and a causal relation between iron deposits and epileptic seizures seems likely. Encapsulation was minimal with the ruptured cavernomas and particularly prominent with the cystic lesions. The membrane of the giant cystic lesion with peripheral brain edema had a histological structure similar to that of the membranes of chronic subdural hematomas. It is suggested that continuous growth of cavernoma cysts is the result of recurrent hemorrhages from sinusoids of the malformation and from the neocapillary network of the cyst membranes.
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