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Biomedical subjects

M K Morgan

Publications and source records attributed to M K Morgan.

At least 19 recordsLinked to original sources
PubMed2004

Surgery for unruptured intracranial aneurysms in a low-volume neurosurgical unit.

OBJECTIVES: To evaluate outcomes after surgical treatment for unruptured intracranial aneurysms in a low-volume neurosurgical unit. MATERIAL AND METHODS: Consecutive patients operated during the years 1988-98 at the Department of Neurosurgery, University Hospital of North Norway, were studied retrospectively. Procedure-related complications were registered. The modified Rankin Scale and the Glasgow Outcome Scale, Extended version (GOS-E), were used for assessment of outcome. RESULTS: Thirty-six aneurysms were repaired in 32 patients during 34 surgical procedures. Surgery-related central nervous system complications occurred in eight (25%) patients. The complication rate was 35% for the first 17 procedures, and 12% for the last 17. The latter group of procedures were performed during a period of 3 years, whereas the former group was spread over a period of 8 years. A favourable outcome (GOS-E score 6-8) was reached in 27 (84%) patients. CONCLUSION: Decision-making in patients with unruptured intracranial aneurysms must be based on knowledge about institution-specific complication rates, preferably followed on a prospective basis.

Adult↗
PubMed2002

Magnesium: a useful adjunct in the prevention of cerebral vasospasm following aneurysmal subarachnoid haemorrhage.

UNLABELLED: Despite recent advances in the management of aneurysmal subarachnoid haemorrhage delayed ischaemic deficits from cerebral vasospasm remains a major cause of morbidity and mortality. As magnesium is a potent cerebral vasodilator we have introduced routine supplementation in patients presented with subarachnoid haemorrhage to determine whether there has been a reduction in the incidence of cerebral vasospasm. METHOD: All patients presented with aneurysmal subarachnoid haemorrhage from February 1997 were included except those who presented after day 5 following bleed. Identical management protocol was used except intravenous magnesium supplementation which was introduced to all patients from May 1999. Incidence of cerebral vasospasm on angiograms among the two groups was analysed. RESULTS: Seven out of 10 patients who did not receive magnesium supplement developed vasospasm requiring intra-arterial papaverine compared with 2 of 13 patients among the treated group (P<0.008). CONCLUSIONS: From our pilot study it appears that magnesium supplement has a beneficial role in the prevention of cerebral vasospasm following aneurysmal subarachnoid haemorrhage. Further studies would seem justified.

Adult↗
PubMed2001

The surgical management of contralateral anterior circulation intracranial aneurysms.

This study reviews the surgical management of contralateral anterior circulation aneurysms in patients with bilateral intracranial aneurysms repaired following a unilateral craniotomy. Between 1993 and 1999, 27 patients had 88 intracranial aneurysms repaired. Eleven patients presented following subarachnoid haemorrhage. Excluding midline aneurysms, 31 anterior circulation aneurysms were contralateral to the craniotomy and all were repaired at the same time that ipsilateral or midline aneurysms were repaired. Morbidity included one death and one case of loss of unilateral vision directly attributable to surgery and two cases of cerebral infarction due to vasospasm. No new neurological deficit or mortality could be directly attributed to the repair of a contralateral aneurysm. The repair of all accessible aneurysms, including those contralateral to the craniotomy, during one session avoids the risk of haemorrhage from incidental or unrecognised ruptured aneurysms (particularly during the aggressive treatment of vasospasm), avoids a second craniotomy, decreases overall hospitalisation and can improve visualisation of carotid-ophthalmic aneurysms.

Adult↗
PubMed2001

Spinal arteriovenous malformations: a review with case illustrations.

Spinal arteriovenous malformations are united by the existence of arteriovenous shunting but are quite heterogeneous in terms of pathology. Until recently, the pathological confusion has been such that management has been poorly understood and this is magnified by the rarity of the lesions. Type 1 AVMs, where the fistula is located in the dura, usually present with a venous hypertensive myelopathy and are relatively easily dealt with surgically. Type 2 AVMs, most closely mimicking the parenchymal AVMs of the brain, usually present with haemorrhage and may be surgically remediable but with much greater risk than the type 1 lesions. Type 3 AVMs, with a diffuse location through both the cord and extra-CNS tissue, usually present early in life with a myelopathy and are often untreatable. Type 4 AVMs, with a fistula located on the pial surface of the cord, usually present with a venous hypertensive myelopathy or subarachnoid haemorrhage, can be treated relatively easily by surgery when small but may be better treated endovascularly when the fistula is large. The purpose of this review is to summarise the current pathological, clinical and management literature with illustrative cases underscoring the important features of this heterogeneous disorder.

Adult↗
PubMed2001

Prolonged thiopentone infusion for neurosurgical emergencies: usefulness of therapeutic drug monitoring.

Serial serum thiopentone concentrations were measured during and following completion of an intravenous infusion of thiopentone in 20 patients with neurosurgical emergencies. The concentration data from a further 55 patients who had had some such measurements were reviewed retrospectively. The patients received an infusion for longer than 24 hours at a rate adjusted to maintain EEG burst suppression. The data were interpreted in terms of thiopentone pharmacokinetics and used to produce statistical models relating to clinical outcomes. In these patients, the one-month mortality rate following commencement of thiopentone treatment was 20%; the mean durations of pupillary and motor unresponsiveness following cessation of an infusion were 22 and 91 hours, respectively. Predictors of a prolonged duration of motor unresponsiveness included a prolonged duration of pupillary unresponsiveness, a low thiopentone clearance and a high maximum serum concentration of thiopentone. From pooled logistic regression, median effective serum thiopentone concentrations (EC50) were found to be 50 mg x l(-1) for recovery of pupillary responsiveness and 12 mg x l(-1) for the recovery of motor responsiveness. Because prolonged high-dose thiopentone leads to prolonged residual serum concentrations, it is difficult to distinguish the residual pharmacological effects of thiopentone from the clinical condition. This study suggests that, based on EC50 values for responses, monitoring of post-infusion serum thiopentone concentrations may help determine whether a patient's clinical state is due to residual thiopentone pharmacological effects.

Adult↗
PubMed2001

Angioplasty and stenting in the posterior cerebral circulation.

PURPOSE: To report initial experience with intracranial vertebral artery (VA) and basilar artery (BA) percutaneous transluminal angioplasty (PTA) and stenting. METHODS: Eleven patients (10 men; mean age 66 years, range 56-75) with intracranial 14 VA and 3 BA stenoses were managed from December 1997 through November 1999. All patients presented with vertebrobasilar ischemia (VBI) despite antiplatelet and anticoagulant therapy. Clinical presentations included visual disturbance (n = 8), dysarthria/dysphasia (n = 5), and vertigo (n = 5). RESULTS: Five patients underwent PTA only of 7 lesions with a mean preprocedural stenosis of 80% (range 50%-90%) that was reduced to 54% (range 30%-70%) after dilation. Six patients received 9 stents, 2 for VA dissections, 3 for tandem lesions, and 1 for a BA lesion. There were no embolic strokes. Patients were followed by clinical evaluation and personal or telephone interviews. Over a mean 18-month follow-up (range 12-35), 8 (73%) patients remained asymptomatic, while 3 (27%) had permanent deficits, 2 related to the procedure and 1 owing to distal disease CONCLUSIONS: Intracranial VA or BA angioplasty and stenting alleviated symptoms in patients with vertebrobasilar ischemia despite best medical management and may prevent stroke.

Aged↗
PubMed2000

Postoperative seizure outcome in a series of 114 patients with supratentorial arteriovenous malformations.

The incidence of de novo and ongoing postoperative seizures and factors implicated in an increased likelihood of seizures following supratentorial cerebral arteriovenous malformation (AVM) resection remain controversial. We investigated the frequency, severity and variables associated with postoperative seizures in 114 consecutive patients who underwent complete surgical excision of supratentorial AVMs at our institution. The minimal follow up period was 24 months. The incidence of seizures post-AVM surgery was 21% (less than half that found preoperatively). The incidence of postoperative seizures first manifesting >12 months post-AVM resection was 6.3%. A history of preoperative seizures was associated with an increased likelihood of multiple (> or =4) seizures >1 month post-AVM resection (chi2 = 4.38, P = 0.04). Poor functional neurological outcome at 12 months was also a risk factor for the development of > or =1 postoperative seizure using logistic regression analysis (P = 0.04, odds ratio 1.52, 95% CI 1.01-2.28). Cessation of AED therapy in all patients who remain seizure-free at 12 months post-AVM resection is appropriate due to a low risk of new seizure onset or seizure recurrence.

Adolescent↗
PubMed2000

Aggressive management of aneurysmal subarachnoid haemorrhage based on a papaverine angioplasty protocol.

The aim of this study was to analyse the results of intensive therapy unit management of aneurysmal subarachnoid haemorrhage incorporating angioplasty in the protocol. Two hundred consecutive patients were treated using a detailed protocol that included nimodipine, early aneurysm repair, and surveillance angiography. Angiography was performed on days 5 to 7 (or when the clinical state suggested the presence of vasospasm). If angiographic vasospasm was identified, irrespective of whether clinical vasospasm was present or absent, papaverine was selectively administered. In patients with vasospasm blood pressure was elevated to 160-180 mmHg and selective papaverine administration was repeated daily until vasospasm resolved. In cases requiring more frequent administration of papaverine, or in whom papaverine failed to adequately reverse spasm, balloon angioplasty was considered and for clinically refractory cases barbiturate coma was introduced. 43% of patients underwent papaverine administration and of these the average number of separate papaverine procedures was four (maximum 23). 26% of patients developed neurological deficits though to be due to vasospasm whilst 17% underwent papaverine angioplasty without clinical signs of vasospasm. Twelve patients (6%) were entered into barbiturate coma. There was a 5.5% mortality and no difference in outcome between patients who developed angiographic vasospasm and those who did not. For those developing clinical vasospasm, 71% were independent and 10% were dead at follow up compared with 84% reaching independent grades and 4% dead in those not developing clinical vasospasm. These differences failed to reach a significant difference. The average Intensive Therapy Unit stay for aneurysmal subarachnoid haemorrhage patients was 13.1 days with a mean cost to the hospital of $AUD 24,379. This protocol appears to be both a clinically and cost effective method of managing aneurysmal subarachnoid haemorrhage.

Angioplasty, Balloon↗
PubMed2000

Changing role for preoperative embolisation in the management of arteriovenous malformations of the brain.

BACKGROUND: The aim of this study was to analyse the results of the use of preoperative embolisation in the management of arteriovenous malformations of the brain at one institution between 1989 and 1999. METHODS: Two hundred and fifty consecutive cases of angiographically confirmed arteriovenous malformations underwent surgery by one surgeon. Cases of dural or spinal arteriovenous malformations have been excluded. Forty-five cases underwent preoperative embolisation. Embolisation was mostly by particulate embolic material delivered 4 to 6 days before the intended surgery. The incidence of embolisation declined from 21 cases of the first 50 arteriovenous malformation cases surgically treated to five in the last 50 cases. For arteriovenous malformations of less than 3 cm, only the first two temporal quintiles had embolised cases; six in the first and three in the second. Outcome was measured by the Modified Rankin Scale. RESULTS: By 12 months (or last follow up, if less than this time has elapsed) following surgery, 1.6% of patients had died, 2.4% had a Modified Rankin scale score of 4 or 5, 6.4% had a Modified Rankin scale score of 3, 8.4% had a Modified Rankin scale score of 2, 14.4% had a Modified Rankin scale score of 1, and 66.8% were without neurological deficit. There was no difference in outcomes in each of the temporal quintiles. The four deaths were related to intraoperative haemorrhage, ruptured aneurysm, acute myocardial infarction or unrelated infection. Angiographic cure was achieved in 244 of 246 surviving cases. The two cases with residual arteriovenous malformations underwent focussed irradiation. Permanent morbidity could be attributable to embolisation, intraoperative events (resection functional brain, arteriovenous malformation rupture, aneurysm rupture or myocardial infarction) or postoperative events (arterio-capillary-venous hypertensive syndrome or infection). Of these 29 patients 14 had undergone embolisation. Mortality and major morbidity (Modified Rankin scale score greater than 2 due to treatment) occurred in 8.8% undergoing embolisation compared with 1.9% not embolised. The cause for major morbidity in these four embolised cases was intraoperative or postoperative haemorrhage. CONCLUSIONS: These results reflect that cases selected for embolisation were those at most risk from intraoperative haemorrhage. Arteriovenous malformations that are less than 3 cm in maximal diameter should only rarely be considered for preoperative embolisation because of their low surgical morbidity. In the presence of a significant deep perforating artery contribution that cannot be effectively embolised the risks of operative haemorrhage is high irrespective of the effectiveness of embolising ancillary non-perforating arteries.

Arteriovenous Malformations↗
PubMed2000

Microsurgery for small arteriovenous malformations of the brain: results in 110 consecutive patients.

OBJECTIVE: To examine the results of surgery in 110 consecutive patients with arteriovenous malformations (AVMs) smaller than 3 cm in diameter. These results are compared with the published results of other microsurgical series as well as with results for patients treated with focused irradiation. METHODS: From January 1989 to November 1998, 121 patients with AVMs smaller than 3 cm were treated at our institution. One hundred ten patients underwent microsurgical removal of their AVMs. The presentation, preoperative neurological status, and postoperative outcome were recorded. Follow-up was complete for all surgical cases. RESULTS: Of the 110 patients, 109 (99%) had angiographically confirmed obliteration of their AVMs. Two patients (1.8%) required reoperation for residual AVM. Two (4.3%) of 46 patients with AVMs in eloquent brain areas experienced worsening of their neurological status after surgery. One (1.6%) of 64 patients was worse neurologically after removal of an AVM in a noneloquent area. CONCLUSION: Microsurgical removal is a safe and effective treatment for the majority of AVMs smaller than 3 cm in diameter. Although the treatment is accompanied by a risk of acute onset of neurological deficits, this tends to be transient in the majority of cases. Furthermore, microsurgical excision of small AVMs offers patients immediate protection from the natural history of their vascular lesions.

Adult↗
PubMed1999

Computer modelling of the cerebrospinal fluid flow dynamics of aqueduct stenosis.

As the craniospinal space is a pressure loaded system it is difficult to conceptualize and understand the flow dynamics through the ventricular system. Aqueduct stenosis compromises flow, increasing the pressure required to move cerebrospinal fluid (CSF) through the ventricles. Under normal circumstances, less than one pascal (1 Pa) of pressure is required to move a physiological flow of CSF through the aqueduct. This is too small to measure using clinical pressure transducers. A computational fluid dynamics (CFD) program, CFX, has been used to model two forms of aqueduct stenosis: simple narrowing and forking of the aqueduct. This study shows that with mild stenoses, the increase in pressure required to drive flow becomes significant (86-125 Pa), which may result in an increased transmantle pressure difference but not necessarily an increased intraventricular pressure. Severe stenoses will result in both. Wall shear stresses increase concomitantly and may contribute to local damage of the aqueduct wall and further gliosis with narrowing.

Cerebrospinal Fluid↗
PubMed1999

Barbiturate coma for severe, refractory vasospasm following subarachnoid haemorrhage.

OBJECTIVE: To document the outcome of patients treated with barbiturate coma for severe symptomatic angioplasty-resistant vasospasm. To compare mortality with that predicted by admission APACHE II score, and neurological outcome with that of historical controls treated with barbiturate coma for vasospasm, and with historical controls with delayed ischaemic deficits from vasospasm treated with nimodipine. DESIGN: Cohort study. SETTING: Neurosurgical Intensive Care Unit of tertiary referral university teaching hospital. PATIENTS: Eleven (6.7%) of 164 consecutive patients with aneurysmal SAH managed according to our protocol who were treated with thiopentone-induced burst suppression coma for severe symptomatic, angioplasty-resistant vasospasm. INTERVENTIONS: Chart, database and literature review. MEASUREMENTS AND RESULTS: All 11 patients survived to hospital discharge (mortality 0%) compared with first-day APACHE II predicted mortality of 30.6% (p=0.15). Outcome at 6 months was: good recovery 8/11 (72.7%), moderate disability 2/11 (18.2%), vegetative survival 1/11 (9.1%). Ten of 11 (90.9%) had a good neurological outcome compared with 50.6% of historical controls with delayed ischaemic deficit from vasospasm (odds ratio 9.78, 95% confidence interval 1.24-77.0, p=0.02), and 0% of previously reported patients treated with barbiturate coma for vasospasm (p < 0.01). CONCLUSION: Our results are better than previously published outcomes and suggest formal evaluation of barbiturate coma in the treatment of severe resistant symptomatic vasospasm following SAH is warranted.

APACHE↗
PubMed1999

Recurrent stenosis of common carotid-intracranial internal carotid interposition saphenous vein bypass graft caused by intimal hyperplasia and treated with endovascular stent placement. Case report and review of the literature.

Intimal hyperplasia is a well-known cause of delayed stenosis in vein bypass grafts in all types of vascular surgery. Options for treatment of stenosis in peripheral and coronary artery bypass grafts include revision surgery and the application of endovascular techniques such as balloon angioplasty and stent placement. The authors present a case of stenosis caused by intimal hyperplasia in a high-flow common carotid artery-intracranial internal carotid artery (IICA) saphenous vein interposition bypass graft that had been constructed to treat a traumatic pseudoaneurysm of the intracavernous ICA. The stenosis recurred after revision surgery and was successfully treated by endovascular stent placement in the vein graft. The literature on stent placement for vein graft stenoses is reviewed, and the authors add a report of its application to external carotid-internal carotid bypass grafts. Further study is required to define the role of endovascular techniques in the management of stenotic cerebrovascular disease.

Adult↗
PubMed1999

Delayed neurological deterioration following resection of arteriovenous malformations of the brain.

OBJECT: The aim of this study was to analyze delayed neurological deficits following surgical resection of arteriovenous malformations (AVMs). METHODS: The authors report on a consecutive series of 200 patients with angiographically proven AVMs of the brain that were surgically resected between January 1989 and June 1998. The 30-day mortality rate for patients in this series was 1%, with one death caused by AVM resection and one death attributed to basilar artery aneurysm repair following successful AVM resection. The Spetzler-Martin grading system correlated well with the difficulty of surgery. No permanent incidence of morbidity resulted from resection of Grade I or II AVMs; the percentage of patients with a significant neurological deficit due to resection was 7.8% for those with Grade III lesions and 33.3% for those with Grade IV or V AVMs. However, this grading system did not accurately predict the development of delayed neurological deficits. Ten patients (5%) developed delayed neurological deficits after recovering from anesthesia and surgery. The delayed deficit was due to hemorrhage in four of the 10 patients and all four had undergone resection of AVMs measuring at least 4 cm in diameter. An increase in blood pressure during the first 8 postoperative days precipitated hemorrhage in these patients. Edema arising as a consequence of propagated venous thrombosis (two patients) was associated with extensive venous drainage networks rather than large AVM niduses. Both hemorrhagic and edematous complications can be included under the umbrella term of "arterial-capillary-venous hypertensive syndrome" to describe the common underlying pathogenesis accurately. An additional four patients developed a delayed deficit as a result of vasospasm. Vasospasm occurred when resection had involved extensive dissection of proximal anterior and middle cerebral arteries; in such cases the incidence of vasospasm was 27%. CONCLUSIONS: On the basis of their analysis of these complications, the authors recommend strict blood pressure control for patients with lesions measuring 4 cm or more in diameter (particularly those with a deep arterial supply). Thromboprophylaxis with aspirin and heparin is prescribed for patients with extensive venous drainage networks, and prophylactic nimodipine therapy and angiographic surveillance for vasospasm are suggested for patients in whom extensive dissection of proximal anterior or middle cerebral arteries has been necessary.

Adolescent↗
PubMed1999

Outcome from treatment for spinal arteriovenous malformation.

Our knowledge of the outcome from treatment for spinal arteriovenous malformations (AVMs) is limited to a few small, anecdotal series and is thus far from complete. Furthermore, with the recent rapid evolution of our knowledge of AVM pathology, many reported cases are difficult to place in the current classification system. In general, outcome for the four classifications of AVMs are as follows: type I respond well to surgical disconnection of the arteriovenous fistula if treatment is early; type II AVMs are currently best treated by surgery but risks of a poor outcome need to be carefully considered; type III are only rarely treatable; type IVa and IVb are likely to respond well to surgery but our knowledge is limited; and type IVc are likely to fare poorly from surgery but should have a better outcome from endovascular therapy.

Arteriovenous Malformations↗
PubMed1999

Toxic effects to mink of moniliformin extracted from Fusarium fujikuroi culture material.

Acute and subacute effects of i.p. exposure to moniliformin in mink (Mustela vison) were investigated. Moniliformin was extracted from Fusarium fujikuroi culture material containing 9,174 ppm moniliformin. An acute LD50 between 2.2 and 2.8 mg moniliformin/kg bw was determined for 9-mo-old female mink. Subacute exposure to 1.5 to 3.2 mg total moniliformin/kg bw resulted in dilated (right side) hearts rounded in appearance. Statistical differences observed in serum chloride and albumin, amylase activities, spun packed-cell volumes, red blood cell counts, hemoglobin concentrations, and hematocrit values between control and moniliformin-dosed mink were considered biologically insignificant because values were within ranges reported for normal mink. Electron microscopic examination of the right ventricular free heart wall of mink receiving acute or subacute doses of moniliformin revealed ultrastructural damage to myofibers, mitochondria, nuclei, Z- and M-lines and sarcoplasmic reticula, and increased extracellular collagen deposition. These results showed that mink are among the more sensitive mammals to moniliformin and that this mycotoxin specifically targets and damages the hearts of mink.

Animals↗