Ethical decision-making in veterinary practice.
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Biomedical subjects
Publications and source records attributed to S Mullan.
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The current members of the faculty at the University of Chicago are acutely aware of the great historic tradition they have inherited. Like all academic medical centers, they are challenged by the current socioeconomic climate, but with the vast intellectual resources of the University of Chicago and its secure place in the community, both locally and nationally, we are confident of our ability to make a continuing contribution to the development of neurosurgery.
The literature on the formation of cerebral veins is reviewed to obtain a better understanding of some cerebrovascular anomalies. Clinical observations such as the entry of the superior ophthalmic vein into the cavernous sinus through the inferior rather than the superior orbital fissure, the relative infrequency of middle cerebral vein backflow in the presence of an extensive cavernous fistula, and the relative infrequency of hemorrhage in relation to the inferior petrosal fistula all relate to the persistence of an older venous pathway. The frequent occurrence of hemorrhage in association with the superior petrosal sinus fistula and the frequent failure of the superior petrosal sinus to connect to the cavernous sinus similarly have an embryological explanation. The frequent association of the vein of Galen aneurysm and an absent or deformed straight sinus probably relates to the time at which the paired internal cerebral veins fuse into one channel. It is speculated that the origins of cerebral venous malformations (CVMs) and arteriovenous malformations (AVMs) probably relate to sequential formation and absorption of surface veins, which occur in human embryonic development mainly in the 40- to 80-mm length interval, although persistent AVM growth is possible even after birth. The frequent absence or anomaly of the middle cerebral vein and its failure to communicate with the cavernous sinus in the presence of both CVMs and AVMs are linked to the late development of that vein and to its even later connection to the cavernous sinus.
Three cases of cerebral venous malformation (CVM) are presented to demonstrate the triad that characterizes CVM: abnormal surface venous drainage, a "star-cluster" system of deep collecting veins, and a deep draining vein. Four other cases are introduced that illustrate this triad and show an additional feature, namely arterial fistulization; these cases represent arteriovenous malformations (AVMs). A final case demonstrates a CVM within an AVM. Both of these structures have a common draining vein and an identical venous core. On the basis of the cases described and of others less suitable for illustration, it is postulated that an AVM is a fistulized CVM and that both relate to a failure in the development of the cortical venous mantle. This proposition is based on the authors' observations and their assessment of the "best possible fit."
The clinical course of three patients who had combined sagittal and lateral sinus dural fistulae is described. One patient, with impending blindness and a short life span, underwent right lateral sinus thrombosis in one stage. The second patient underwent sagittal and right lateral sinus thrombosis in four stages, and her remaining lateral sinus spontaneously occluded. A small untreated fistula persists in the right lower sigmoid. The third patient underwent sagittal sinus, left lateral sinus, and left parietal sinus thrombosis in six stages. A small untreated far-anterior fistula persists. All "satellite" fistulae have spontaneously disappeared. The small asymptomatic untreated residual fistulae have no demonstrable retrograde venous drainage and, therefore, require no treatment at this time.
Evidence is presented that dural fistulae are preceded by sinus thrombosis and that their danger lies in arterialized venous pressure within the cranium or the orbit. Arterial side occlusion leads to recurrence, while venous side occlusion leads to permanent cure. Vein of Galen aneurysms embrace some features of cerebral arteriovenous malformations (AVM's), namely a reticulum, and some features of dural fistulae, namely evidence of previous sinus anomaly and direct drainage into a sinus. These aneurysms are also permanently cured by venous side thrombosis, although the dangers inherent in their reticulum demand that this be done in stages or preceded by arterial side embolization. A very limited experience with venous end occlusion of cerebral (and spinal) AVM's suggests that they, too, can be permanently cured by venous side occlusion without excision. Their reticulum demands maximum, multistage, preliminary arterial side embolization together with intraoperative hypotension during the venous occlusion stage in order to minimize intracerebral hemorrhage or swelling. Schematic models of both fistulae and malformations are presented, together with reasons why particulate embolization is safer than glue embolization. The theory is advanced that dural fistulae, vein of Galen aneurysms, and AVM's are venous- rather than arterial-based lesions, which is consistent with the experience that permanent cure has been effected by venous side occlusion without excision in all three anomalies. It is speculated that there may be a developmental link between AVM and the venous malformation, the AVM being essentially a fistulized venous malformation.
A case is presented in which a giant intracranial vertebral artery aneurysm gave rise to an associated ipsilateral posterior inferior cerebellar artery (PICA) from its waist. Proximal vertebral artery ligation at C-1 was achieved. The aneurysm filled from the opposite vertebrobasilar junction. Direct intracranial trapping of the right vertebral aneurysm was followed by successful anastomosis of the proximally sectioned right PICA to the adjacent left PICA in an end-to-end fashion.
Diet-induced atherosclerosis in rhesus monkeys was suppressed in the carotid arteries and thoracic aorta by the calcium antagonist nifedipine given orally for a period of 1 year at a dose of 10 mg b.i.d. The extent of atherosclerosis was determined by quantitative micromorphometric studies. No change in serum blood cholesterol or biochemical composition of the major vessels was detected, but the intimal area and thickness of the atherosclerotic plaques in the carotid arteries of the nifedipine group were markedly less than those found with the control group (p less than 0.05). However, no statistically significant differences were seen in the degree of atherosclerotic involvement of the other major arterial vessels. Although the mechanism is not clear, nifedipine may be useful in the treatment of carotid artery disease.
Three patients are reported with the rare combination of moyamoya disease and features of an associated arteriovenous malformation. Two of the patients developed ischemic symptoms, and the third patient presented with an intracerebral hemorrhage. All three patients fit the criteria of a stage III moyamoya syndrome on the basis of the angiographic classification described by Suzuki and Takaku. The patients were referred to this medical center following angiography with the presumptive diagnosis of arteriovenous malformation.
Morphometric and chemical changes in the arterial wall were studied after 12 months of diet-induced atherosclerosis in rhesus monkeys treated with either bilateral surgical thoracic sympathectomy or propranolol. There was a marked reduction in the progression of atherosclerosis in the carotid arteries and a moderate reduction in the disease found in the thoracic aorta of monkeys treated initially with a sympathectomy, in comparison to control monkeys fed an atherogenic diet alone. Propranolol at a dose of 40 mg/12 hrs also seemed to reduce the progression of atherosclerosis in the carotid arteries and thoracic aorta, although the differences were less dramatic. There were minimal differences in the extent of atherosclerosis in the abdominal aorta or femoral arteries of animals in either treatment group as compared with the control group. Similarly, the chemical composition of these same major vessels showed no significant differences. Therefore, in the face of severe atherogenic stimuli, chemical or surgical sympathectomy may be useful in controlling atherosclerosis in specific arterial beds.
The risk of hemorrhagic complications with anticoagulation therapy in patients following intracranial surgery has prevented investigation of the potential use of heparin in the early postoperative period. The authors have evaluated the safety of anticoagulation therapy following experimental craniotomy in male Holtzman rats. The dose and schedule of heparin administration, which elevated and maintained the activated partial thromboplastin time (APTT) within the therapeutic range of 1 1/2 to 3 X control APTT, was alternating doses of 400 and 500 IU/kg injected subcutaneously every 6 hours. This schedule was initiated 2, 4, 7, 10, and 14 days after craniotomy and was continued for 72 hours thereafter. The results demonstrated that the incidence of intracerebral hemorrhage declined as the postoperative interval prior to initiation of anticoagulation increased. If anticoagulation therapy was initiated during the first 7 postoperative days, the risk of intracerebral hemorrhage was high (mean 14.7%): however, if an additional 3 to 7 days elapsed prior to initiation of anticoagulation, the incidence of intracerebral hemorrhage dropped significantly (mean 0%) (p less than 0.05). These results suggest that anticoagulation therapy can be safely initiated 10 to 14 days after craniotomy.
Beta-Endorphin-like immunoreactivity in cerebrospinal fluid was assayed in 11 patients receiving electrical stimulation of the brain for chronic pain. Immunoreactivity increased dramatically after contrast ventriculography prior to stimulation. No further elevations were observed after stimulation. The magnitude and time course of elevations were identical after placement of electrodes either in the thalamus or in the periventricular gray matter. These results suggest that previous findings of stimulation-induced elevation of beta-endorphin-like immunoreactivity in cerebrospinal fluid are attributable to an artifact of contrast ventriculography.
Much interest has recently been focused on the possible role of the endogenous opiates in the perception of pain in humans. Several investigators have examined the levels of these substances in human cerebrospinal fluid (CSF) in attempts to identify the mechanisms by which electrical stimulation of the brain might induce analgesia. Most of these CSF samples were collected at the time of ventriculography or myelography. In the present study, the levels of beta-endorphin in the CSF of 22 patients undergoing myelography were examined before and after the injection of a contrast agent. beta-Endorphin increased an average of 356% (p less than 0.0005) 15 to 20 minutes following the injection of contrast material into the lumbar subarachnoid space. Thus, routine myelography may have a profound effect on the levels of beta-endorphin measured by radioimmunoassay in human CSF, and great care must be taken in interpreting the significance of changes seen in beta-endorphin levels in CSF collected from patients at the time of myelography or ventriculography. The effect of the injection of contrast material on beta-endorphin immunoreactivity must be distinguished from the postulated effects of any analgesia-inducing therapy.
Six adult dogs were implanted stereotaxically with chronic indwelling Medtronic platinum-tipped electrodes in the left ventromedial hypothalamic area (VMH); two dogs with electrodes placed in the subcortical white matter served as controls. Following 24 hours of food deprivation, VMH-stimulated dogs delayed their next meal for a period ranging from 1 to 18 hours. When not stimulated, however, each dog ate immediately upon receiving its food and consumed greater than average daily intake (p less than 0.005). The two control dogs ate immediately upon receiving food regardless of whether they were stimulated or not. Dogs that received 1 hour of VMH stimulation every 12 hours for 3 consecutive days maintained an average daily food intake of 35% of normal baseline levels (range 13% to 51%), and water consumption averaged 50% of baseline intake (range 29% to 67%). Both of these results were statistically significant (p less than 0.01). After cessation of stimulation, food and water intake returned to normal within 6 to 9 days, with no observable "rebound hyperphagia." The two animals that received subcortical electrodes showed no change in food or water intake with stimulation. Blood pressure, pulse, respiration, temperature, and gross behavior were not altered during or after stimulation. These results suggest that the use of electrical stimulation of the VMH may be a useful modality for regulating food intake, and deserves further examination as a potential alternative therapy for human morbid obesity.
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Fifty patients were treated for trigeminal neuralgia by percutaneous microcompression of the trigeminal ganglion. A No. 4 Fogarty balloon catheter was inserted under brief general anesthesia, using biplane fluoroscopy. This procedure is essentially a percutaneous simplication of the older Taarnhøj-Sheldon-Pudenz operation. The follow-up period ranged from 0.5 to 4.5 years. Pain recurred in 12% of cases during that time, and it is anticipated that within 5 years the recurrence rate will reach 20%, which is approximately the same rate as for the alternative established procedures. The advantages of this technique are freedom from discomfort on the part of the patient, a remarkable ease of performance on the part of the operator, absence of associated mortality, and a minimal morbidity rate.
The authors present a case of proximal myopathy secondary to epsilon-aminocaproic acid (EACA) administration. This well recognized entity does not occur immediately after institution of therapy, but follows a delay of several days and a cumulative dose. Its consequences include a spectrum of symptoms from myalgias to severe myopathy with rhabdomyolysis, myoglobinuria, and acute tubular necrosis. A presenting symptom of calf pain in a patient receiving EACA should not automatically imply deep vein thrombosis. Serial creatine phosphokinase measurements are essential in monitoring a patient undergoing EACA therapy, especially after 2 weeks of treatment and a total dose of greater than 500 gm.
Examples are presented of the use of a compression balloon to treat trigeminal neuralgia, of a dilating balloon to release a web obstruction of the internal carotid artery, of detachable balloons to seal carotid-cavernous and vertebral-venous fistulas, of a temporary occlusive balloon to aid in thrombogenic treatment of a giant aneurysm, and of a temporary occlusive balloon with double or triple-lumen capacity to assist in angiographic diagnosis and to provide reversible carotid occlusion.