Cardiovascular effects of experimental head injury in the monkey.
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Angiography↗
Biomedical subjects
E S Flamm
Publications and source records attributed to E S Flamm.
Temporal correspondence of intracranial, cochlear and scalp-recorded human auditory nerve action potentials.
Conventional, vertex-ipsilateral ear records ('A'), as well as 3-channel Lissajous' trajectories (3-CLTs) of auditory brain-stem evoked potentials (ABEPs) were recorded from the scalp simultaneously with tympanic membrane electrocochleograms ('TME') and auditory nerve compound action potentials ('8-AP') recorded intracranially using a wick electrode on the auditory nerve between the internal auditory meatus and the brain-stem. The recordings were made during surgical procedures exposing the auditory nerve. The peak latency recorded from 'TME' corresponded to trajectory amplitude peak 'a' of 3-CLT and to peak 'I' of the 'A' channel ABEP. Peak latency of '8-AP' was slightly longer than the latency of peak 'II' of 'A' when '8-AP' was recorded from the root entry zone and the same or shorter when recorded from the nerve trunk. '8-AP' peak latency was shorter than trajectory amplitude peak 'b' of 3-CLT regardless of where the wick electrode was along the nerve. Peak latencies from all recording sites clustered into two distinct groups--those that included N1 from 'TME,' peak 'I' of the 'A' record and trajectory amplitude peak 'a' of 3-CLT, and those that included the negative peak of '8-AP' and trajectory amplitude peak 'b' of 3-CLT, as well as peak 'II' of the 'A' record, when present. In one case, the latency of peak 'II' and trajectory amplitude peak 'b' was manipulated by changing the conductive properties of the medium surrounding the auditory nerve.(ABSTRACT TRUNCATED AT 250 WORDS)
Acoustic Stimulation↗
Experimental cerebral vasospasm and cyclic adenosine monophosphate (c-AMP).
Blood induced acute and chronic cerebral vasospasm were studied in Rhesus monkeys by serial angiography. Two vasoactive agents were evaluated. In acute spasm, phosphodiesterase inhibition by Aminophylline consistently reversed the vasospasm. This agent alone was ineffective in chronic spasm and required the addition of Isoproterenol to produce reversal of vasospasm. It is proposed that cerebral vasospasm may be associated with a decrease of intracellular c-AMP in vascular smooth muscle which can be reversed by manipulation of the enzyme pathway involved. It is further proposed that c-AMP is a basic common pathway through which adrenergic vascular reactivities are mediated.
Aminophylline↗
Extracranial aneurysms of the posterior inferior cerebellar artery.
OBJECTIVE: Extracranial aneurysms of the distal posterior inferior cerebellar artery (PICA) are extremely rare and sometimes difficult to diagnose without an adequate angiogram. We present the first series of 3 patients who were evaluated by the senior author and treated surgically. METHODS AND RESULTS: All 3 patients presented with subarachnoid hemorrhage (SAH). Clincial symptoms, included occipital headache, nuchal rigidity, abducens nerve palsy and rapid neurologic deterioration. A unilateral injection of the vertebral artery failed to show the distal contralateral PICA and the aneurysm in 1 patient. All patients underwent aneurysm clipping through a posterior fossa craniectomy and C-1 laminectomy. The aneurysms were located on the tonsillomedullary segment of the PICA, 10-12 mm below the level of the foramen magnum. CONCLUSIONS: It is important to adequately visualize the distal extent of both PICAs or these aneurysms may not be seen. Patients who present with SAH must have the entirety of both vertebral arteries evaluated to avoid missing these aneurysms. The aneurysms were located adjacent to the atlas necessitating an upper cervical laminectomy for adequate surgical exposure. In general, the patients did well postoperatively and none of the patients developed cerebral vasospasm.
Adolescent↗
The international EC/IC bypass study.
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Cerebral Revascularization↗
EC/IC Bypass Study.
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Cerebral Revascularization↗
Intracranial hemorrhage and cocaine use.
Cocaine use has increased rapidly over the past few years. This has led to an increase in the number and variety of cocaine-related conditions for which medical attention is sought. Among these have been several cases of intracranial hemorrhage. Four cases reported in the literature and 6 from our own institution are presented here. They represent different diagnoses including hemorrhage from aneurysms and arteriovenous malformations, hemorrhage into a tumor, and spontaneous hemorrhage with no underlying lesion with and without preexisting hypertension. Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. Cocaine may also cause arterial spasm. Although the pathophysiology has not been entirely resolved, the clinical significance of this association is clear. Intracranial hemorrhage should be considered in the differential diagnosis whenever a patient presents with an acute alteration in neurologic examination associated with cocaine use.
Adult↗
Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia.
Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and frontoparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2, 4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p less than 0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 mumoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Regional brain calcium changes in the rat middle cerebral artery occlusion model of ischemia.
Entry of Ca ions into ischemic neurons is believed to cause cell damage. Although several investigators have demonstrated changes in extracellular Ca ionic activity consistent with Ca movement into cells, direct and quantitative evidence for Ca entry into ischemic cells is lacking. We used atomic absorption spectroscopy to measure the regional distribution of tissue Ca contents of rat brains sampled at 2, 4, and 24 hours after middle cerebral artery occlusion (MCAo). At 4 hours after MCAo, Ca concentrations increased significantly (p less than 0.005) in the ischemic middle cerebral artery territory, i.e., the pyriform and frontoparietal cortices, but not in the surrounding brain. At 24 hours, Ca concentrations in the pyriform and frontoparietal cortex were respectively 30.79 (+/- 2.90) and 29.19 (+/- 3.28) mumol/g dry tissue wt compared with 11.9 (+/- 1.7) mumol/g in sham-occluded rats. Tissue Ca concentration changes in the parasagittal cortex and basal ganglia adjacent to the infarct site were much smaller and did not differ significantly from controls until 24 hours. In the ischemic middle cerebral artery territory, greater than 1.0 mumoles of Ca entered per gram of dry tissue weight per hour during the first 4 hours after MCAo. Linear regression analysis revealed a significant correlation (r = 0.9722) between changes in tissue Ca and water, with a slope indicating that 5.88 mumoles of Ca accompanied each milliliter of water entering the lesioned hemisphere. Such massive accumulations of Ca not only confirm Ca entry into injured cells, but indicate the presence of a remarkable Ca sink which sequestered within 24 hours more than 17 times the amount of free Ca present in the tissue before MCAo.
Animals↗
Control of cerebral vasospasm by parenteral phenoxybenzamine.
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Adrenergic alpha-Antagonists↗
Alterations of cyclic AMP in cerebral ischemia.
Cyclic AMP levels were measured in brains of 21 cats after occlusion of a middle cerebral artery by a transorbital approach. Brain samples for determination of cAMP by a protein binding radioassay were obtained from the ischemic and contralateral temporal lobes before sacrifice, 1, 3, and 24 hours after occlusion of the right middle cerebral artery. At 1 hour, no difference between the 2 sides was observed; a mean of 17.4 pmoles/mg protein was observed from the side of the occlusion and 18.9 pmoles/mg protein from the contralateral side. At 3 hours, a mean value of 8.9 pmoles/mg protein on the ischemic side and a level of 21.7 pmoles/mg protein on the contralateral side were observed. At 24 hours, the cAMP level on the ischemic side remained below the nonischemic side; the values obtained were 13.7 pmoles/mg protein compared to 27.9 pmoles/mg protein compared to 27.9 pmoles/mg protein. These changes in cAMP as early as 3 hours after the onset of ischemia, when such a lesion is reversible, may indicate that in initial step in the alteration of cellular metabolism following ischemia is due to membrane perturbation and altered production of this second messenger.
Animals↗
Free radicals in cerebral ischemia.
The possibility that cerebral ischemia may initiate a series of pathological free radical reactions within the membrane components of the CNS was investigated in the cat. The normally occurring electron transport radicals require adequate molecular oxygen for orderly transport of electrons and protons. A decrease in tissue oxygen removes the controls over the electron transport radicals, and allows them to initiate pathologic radical reactions among cell membranes such as mitochondria. Pathologic radical reactions result in multiple products, each of which may be present in too small a concentration to permit their detection at early time periods. It is possible to follow the time course, however, by the decrease of a major antioxidant as it is consumed by the pathologic radical reactions. For this reason, ascorbic acid was measured in ischemic and control brain following middle cerebral artery occlusion. There was a progressive decrease in the amount of detectable ascorbic acid ranging from 25% at 1 hour to 65% at 24 hours after occlusion. The reduction of this normally occurring antioxidant and free radical scavenger may indicate consumption of ascorbic acid in an attempt to quench pathologic free radical reactions occurring within the components of cytomembranes.
Animals↗
Preliminary experience with ultrasonic aspiration in neurosurgery.
A new instrument utilizing ultrasonic energy to fragment and aspirate normal and pathological tissue has been evaluated for neurosurgical use. The instrument has been tested in several animal models to assess its efficacy and safety. The instrument has been used clinically in 38 cases for removal of meningiomas, acoustic neurinomas, and other tumors. Future modifications and applications are discussed.
Animals↗
Comparison of MR imaging with clinical history in the identification of hemorrhage in patients with cerebral arteriovenous malformations.
Twenty-nine patients with true arteriovenous malformations as diagnosed by MR imaging or angiography were examined by MR to detect the presence of hemosiderin deposition, a marker for remote hemorrhage. The resulting information was compared with the clinical record to determine the frequency with which MR demonstrated prior hemorrhagic episodes where no clinical evidence for such episodes existed. Twenty (69%) of 29 patients with arteriovenous malformations showed evidence of acute or older hemorrhage. In four (14%) of 29 cases MR showed a hypointense signal on long TR images, suggesting hemosiderin, but no clinical history could account for prior hemorrhage. Additionally, six (21%) of 29 patients had a clinical history suggestive of acute hemorrhage, but no evidence of bleeding was found on MR. The presence of prior or current hemorrhage is critical to deciding whether to surgically resect the arteriovenous malformation or to treat it conservatively, because of the high rate of rebleeding in patients presenting with hemorrhage or those with a history of this disorder. For this reason, MR imaging has an important role in the management of patients with arteriovenous malformations.
Adolescent↗
Vasospasm secondary to ruptured aneurysm: assessment by digital intravenous angiography.
Digital intravenous angiography was used for the documentation and evaluation of cerebral vasospasm secondary to acute ruptured aneurysm. Attenuation of vessel caliber and/or generalized poor visualization of intracranial arteries and prolongation of circulation time were observed in seven patients with the acute clinical diagnosis of cerebral vasospasm. Posttreatment intravenous angiography demonstrated improvement in both arterial caliber and circulation time in six patients who responded to medical therapy for vasospasm. Digital intravenous angiography allowed repeat investigations of the intracranial vasculature safely and quickly without undue risk to the critically ill patient.
Cerebral Angiography↗