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Biomedical subjects

D A Lang

Publications and source records attributed to D A Lang.

At least 55 records · Page 3Linked to original sources
PubMed1993

The suboccipital transcondylar approach to the clivus and cranio-cervical junction for ventrally placed pathology at and above the foramen magnum.

The dorsolateral suboccipital transcondylar approach for pathology anterolateral or ventral to the neuraxis around the lower clivus and brainstem was used in 10 patients with a variety of different pathological problems: Key features of the approach include exposure and mobilisation of the vertebral artery and resection of the postero-medial portion of the atlanto-occipital joint. Despite the excellent access achieved additional exposure may be required in some patients with strictly anterior pathology or a lesion above the mid-clivus.

Adult↗
PubMed1993

A simple scoring system for accurate prediction of outcome within four days of a subarachnoid haemorrhage.

This study was designed to examine the consistency of a number of easily identifiable predictive factors in assessing outcome within four days of a subarachnoid haemorrhage. Patients with a proven subarachnoid haemorrhage, aged between 15-65, of any neurological grade who had bled within 72 hours of admission, and who had undergone a CT scan within 96 hours of the ictus, were included. Three groups of patients were studied prospectively. The studies were separated in time and place. The series were similar overall but there were some variations between the three groups of patients because of alterations in referral patterns and management strategies between the series. There were significant differences in the patients' ages, grades on admission, timing of angiography, negative angiography rate and timing of operation. This did not affect overall outcome; 57%, 61% and 59% of the patients in series 1, 2 and 3 respectively making a good recovery. The proportion of patients with a poor outcome was also similar. To identify the level of risk of an individual patient within the first few days of haemorrhage, we considered a number of early predictive factors. Two emerged as strong predictors of outcome; the early neurological grade and the distribution of blood on the CT scan. We developed a simple scoring system from the first series, based on these findings, designed to predict outcome at three months. The scoring system was calculated on the basis of the distribution of blood seen on the CT scan and the patients' neurological grade on admission. Two points each were scored for interhemispheric, intraventricular, basal or intracerebral blood (excluding blood in the sylvian fissures). Patients in grade 1-3 scored -1, grade 4 scored 0, grades 5 & 6 scored +5. The scan score and grade score were summated to give the overall score. Patients were placed in risk groups (low, score -1; medium, score 0-2; high, score 3+). The scoring system was then applied prospectively to the two subsequent groups of patients. In each of the three series there was a clear correlation between the patients' scores and their outcomes but more importantly the probability of each outcome for each risk group was considered. In both the second and third series the probability of a full recovery in the low risk group was very likely--P = 0.000.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1991

Gadolinium DTPA enhanced magnetic resonance imaging in acute head injury.

We studied the effect of contrast enhancement on magnetic resonance imaging (Gadolinium DTPA Magnetic Resonance) in 10 patients with a recent head injury. The use of contrast did not increase the number of traumatic lesions identified and we did not detect evidence of altered blood brain barrier permeability in any of the 7 patients, who had a total of 27 lesions, imaged between one and 4 days after injury. Enhancement was found in each of 3 patients imaged 6 or more days after injury. These findings suggest that traumatic cortical and intraparenchymal lesions are not associated with increased cerebrovascular permeability within the first 96 hours of a head injury.

Adult↗
PubMed1990

Gadolinium-DTPA enhanced magnetic resonance imaging in human head injury.

We used low field magnetic resonance imaging and Gadolinium-DTPA to study 10 recently head injured patients. On the pre-contrast images we identified 36 abnormalities in 9 of the 10 patients. After contrast enhancement was seen in 9 of these lesions in 3 patients imaged 5-6 days after injury. Altered blood brain barrier permeability to gadolinium was not seen in 6 patients studied within 4 days of trauma. We did not identify any lesions with gadolinium that were not present on the pre-contrast images. We do not think that the routine use of contrast in head injury is justified since clinically important lesions will be present on routine sequences. However the use of gadolinium may provide information about the nature and timing of the underlying pathophysiological changes. In human head injury cytotoxic oedema occurs early and vasogenic oedema does not occur until 5-6 days after injury.

Adult↗
PubMed1989

Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial.

OBJECTIVE: To determine the efficacy of oral nimodipine in reducing cerebral infarction and poor outcomes (death and severe disability) after subarachnoid haemorrhage. DESIGN: Double blind, placebo controlled, randomised trial with three months of follow up and intention to treat analysis. To have an 80% chance with a significance level of 0.05 of detecting a 50% reduction in an incidence of cerebral infarction of 15% a minimum of 540 patients was required. SETTING: Four regional neurosurgical units in the United Kingdom. PATIENTS: In all 554 patients were recruited between June 1985 and September 1987 out of a population of 1115 patients admitted with subarachnoid haemorrhage proved by the results of lumbar puncture or computed tomography, or both. The main exclusion criterion was admission to the neurosurgical units more than 96 hours after subarachnoid haemorrhage. There were four breaks of code and no exclusions after entry. One patient was withdrawn and in 130 treatment was discontinued early. All patients were followed up for three months and were included in the analysis, except the patient who had been withdrawn. INTERVENTIONS: Placebo or nimodipine 60 mg was given orally every four hours for 21 days to 276 and 278 patients, respectively. Treatment was started within 96 hours after subarachnoid haemorrhage. END POINTS: Incidence of cerebral infarction and ischaemic neurological deficits and outcome three months after entry. MEASUREMENTS: Demographic and clinical data, including age, sex, history of hypertension and subarachnoid haemorrhage, severity of haemorrhage according to an adaptation of the Glasgow coma scale, number and site of aneurysms on angiography, and initial findings on computed tomography were measured at entry. Deterioration, defined as development of a focal sign or fall of more than one point on the Glasgow coma scale for more than six hours, was investigated by using clinical criteria and by computed tomography, by lumbar puncture, or at necropsy when appropriate. All episodes of deterioration and all patients with a three month outcome other than a good recovery were assessed by a review committee. MAIN RESULTS: Demographic and clinical data at entry were similar in the two groups. In patients given nimodipine the incidence of cerebral infarction was 22% (61/278) compared with 33% (92/276) in those given placebo, a significant reduction of 34% (95% confidence interval 13 to 50%). Poor outcomes were also significantly reduced by 40% (95% confidence interval 20 to 55%) with nimodipine (20% (55/278) in patients given nimodipine v 33% (91/278) in those given placebo). CONCLUSIONS: Oral nimodipine 60 mg four hourly is well tolerated and reduces cerebral infarction snd improves outcome after subarachnoid haemorrhage.

Administration, Oral↗
PubMed1983

Control of pulsatile insulin secretion in man.

Plasma insulin and glucose concentrations were examined in man in a basal state from central venous samples taken at 1-min intervals for up to 2.5 h. Normal subjects have insulin oscillations of mean period 14 min (significant autocorrelation, p less than 0.0001) with changes in concentration of 40% over 7 min. The pulsation frequency was stable through cholinergic, endorphin, alpha-adrenergic or beta-adrenergic blockade, or small perturbations with glucose or insulin. Stimulation of insulin secretion by intravenous glucose, tolbutamide or sodium salicylate increased the amplitude of the insulin oscillations while the frequency remained stable. Patients with a truncal vagotomy or after Whipple's operation had longer-term oscillations of 33 and 37 min periodicity (autocorrelation: p less than 0.0001), with insulin-associated glucose swings four times larger than those of normal subjects. Type 2 (non-insulin-dependent) diabetic patients had a similarly increased insulin-associated glucose swing of six times that seen in normal subjects. The hypothesis is proposed that the 14-min cycle of insulin production is controlled by a 'pacemaker' which assists glucose homeostasis. The longer 33-37-min oscillations, seen in those with denervation, may arise from a limit-cycle of the feedback loop between insulin from the B cells and glucose from the liver. The vagus may provide hierarchical control of insulin release.

Adult↗
PubMed1982

Pulsatile, synchronous basal insulin and glucagon secretion in man.

The basal plasma insulin, glucagon, and glucose concentrations of 28 normal subjects were measured at 1-min intervals for periods of 45-120 min. Regular plasma insulin and/or glucagon cycles were detected in 11 subjects by autocorrelation (mean periods 13.1 and 13.7 min, respectively). Individual plasma insulin cycles were defined in all subjects (mean period 10.7 min, amplitude 1.1 mU/L), and were associated, after averaging, with plasma glucagon (amplitude 5.5 pg/ml) and plasma glucose (0.02 mmol/L) cycles. There was a significant correlation between the amplitudes of simultaneous plasma insulin and glucagon cycles (r = 0.23, P = less than 0.05, N = 124). Cross-correlation demonstrated a delay of 2 min between the changes in plasma insulin and glucagon. No comparable oscillations in plasma pancreatic polypeptide were detected. The synchronous pulsatile secretion of glucagon and insulin may be a mechanism by which insulin's hepatic effects are limited, thereby maintaining hepatic glucose production but allowing sufficient peripheral insulin concentrations to inhibit excessive catabolism. The simultaneous pulses of insulin and glucagon may be stimulated by a pacemaker, with the A-B intercellular connections producing insulin and glucagon synchrony.

Adult↗