Biomedical subjects
B Cummins
Publications and source records attributed to B Cummins.
The ISG viewing wand: an application to atlanto-axial cervical surgery using the Le Fort I maxillary osteotomy.
Surgical access to the clivus and upper cervical spine may be facilitated by a number of approaches. The Le Fort I maxillary osteotomy has been described to give improved access to the skull base for removal of tumours and treating vertebrobasilar aneurysms. We describe a case in which the combination of a particularly high translocation of the body of C2 and poor mouth opening had precluded a standard transoral approach by restricting access to the operative field. Anterior decompression of the body of C2 was therefore performed via a maxillary down-fracture with the aid of an interactive image guidance system, the ISG Viewing Wand. The ISG Viewing Wand is a new intra-operative 3 dimensional (3D) image guidance system which has now been used in over three hundred neurosurgical cases at Frenchay Hospital, Bristol. We briefly discuss the principles of the viewing wand and describe its unique application providing anatomical navigation in upper cervical spine surgery.
Clinical characteristics of traumatic extradural hematoma: a comparison between children and adults.
In this study of 43 children who had surgery for traumatic extradural hematoma (EDH) at Frenchay Hospital, England, between 1975 and 1987, the authors attempt to outline the various clinical characteristics of EDH which are different in children (age range 1-15 years) and adults (age range 16-84 years). The results confirm that children with traumatic EDH are less likely to have injury be caused by an RTA, are less likely to remain unconscious from the time of injury to the time of the operation, and are less likely to require immediate surgery (less than 6 hours after injury). In addition, the CT scan is less likely to show in associated intradural injury, and the outcome is significantly better.
Outcome following surgical evacuation of traumatic intracranial haematomas in the elderly.
In order to determine the factors influencing outcome following craniotomy for trauma in patients over the age of 65 and to establish criteria for surgical intervention, the authors carried out a retrospective analysis of the hospital and general practice records of all head injury patients over the age of 65 who underwent a craniotomy for evacuation of a post-traumatic haematoma within 7 days of injury at Frenchay Hospital during a 10-year period (1980-89). Outcome was measured using the Glasgow Outcome Scale and patients were allotted to a good outcome group (good recovery or moderate disability but independent) or a poor outcome group (severe disability, vegetative state of death). There were 35 men and 31 women with a mean age of 72.5 years (range 65-85 years). The mortality rate was 61% and 9% of patients survived in a severely disabled or vegetative state. All 20 (30%) patients with a good outcome had a Glasgow Coma Score (GCS) of 5 or more immediately before surgery. All 18 (27%) patients with a GCS of 4 or less and all 22 (33%) patients with unilateral or bilateral pupillary dilatation had a poor outcome. Outcome was significantly worse in the older patients (75-85 years) compared with the younger patients (65-74 years) and in those patients requiring craniotomy within 24 hours of injury, but the mechanism of injury (fall or road traffic accident), the presence or absence of skull fractures and limb fractures and the pre-operative CT scan appearances did not influence outcome. This study confirms the high probability of poor outcome following surgical evacuation of traumatic intracranial haematomas for elderly head-injured patients with pupillary dilatation or extensor motor responses. Craniotomy under these circumstances is not justified.
Epilepsy related to traumatic extradural haematomas.
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Basic fibroblast growth factor in the developing bovine heart.
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A monoclonal antibody that distinguishes phospho- and dephosphorylated forms of cardiac troponin-I.
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The treatment of spondylotic cervical myelopathy by multiple subtotal vertebrectomy and fusion.
The authors report their experience in the treatment of cervical spondylotic myelopathy by multiple subtotal vertebrectomy and fusion. There were 27 cases with a mean age of 66.9 years. The clinical assessment was carried out using both the Nurick and the Japanese Orthopaedic Association (JOA) grading pre- and post-operatively at 6 months. The post-operative radiological assessment was done at 3 and 6 months. Two cases died from unrelated medical problems. There were three cases of graft dislodgement. Clinical improvement was detected in 80% of cases using the Nurick grading and in 88% of cases using the JOA scoring. No cases deteriorated neurologically after operation. Bony fusion was achieved in 96% of the surviving cases by 6 months. Multiple subtotal vertebrectomy and fusion is therefore an effective method for the treatment of cervical spondylotic myelopathy.
Release of creatine kinase-MB and cardiac specific troponin-I following percutaneous transluminal coronary angioplasty.
Up to 20% of patients undergoing successful coronary angioplasty have been shown to have a mild elevation of creatine kinase-MB (CK-MB). The purpose of this study was to investigate the relationship between clinical and angioplasty procedural variables and circulating markers for cardiac injury. We measured both CK-MB and totally cardiac-specific troponin inhibitory protein (Tn-I) in 22 patients immediately before and at an average time of 10 h 36 min following successful angioplasty. Of these patients 16 had stable angina, six had unstable angina and none had recent myocardial infarction. Four patients had minor complications associated with the procedure (prolonged chest pain, limited coronary artery dissection) but none of these patients had increases in either CK-MB or Tn-I. In two patients there was a mild increase in enzyme-activity assayed CK-MB but none of the 22 patients had significant elevation of mass-assayed CK-MB or cardiac-specific Tn-I. This study supports the view that no significant myocardial damage occurs as a result of successful coronary angioplasty irrespective of the stability of the coronary artery disease. This study confirms the known discrepancies between results obtained by immunoassay and immunoinhibition enzyme assay, due to the false-positive results which can be yielded by the latter technique.
Uptake of radioiodinated cardiac specific troponin-I antibodies in myocardial infarction.
STUDY OBJECTIVE: To examine the potential diagnostic value of the cardiac myofibrillar protein troponin-I as a target for radiolabelled antibodies in detecting heart damage, the uptake of 131I labelled polyclonal cardiac troponin-I Fab was investigated in necrotic myocardial cells in canine myocardial infarction. DESIGN: Cardiac specific troponin-I Fab was prepared by immunoaffinity chromatography and injected 5 h after coronary artery ligation. Whole body gamma camera scintigraphic images were taken after the injection, and heart slices were examined for the presence of labelled antibody. SUBJECTS: Adult dogs of either sex (n = 6) were used. MEASUREMENTS AND MAIN RESULTS: Scintigraphic whole body images at 24 and 40 h after troponin-I Fab injection showed increased 131I-localisation over the apical region of the heart which corresponded to the infarcted areas. Localisation in infarcted tissue was confirmed in isolated heart and histochemically stained heart slice images. Uptake of 131I Fab was up to 24 times greater in necrotic than in normal myocardium and was inversely related to regional blood flow as determined by 141cerium microsphere distribution. Confirmation that 131I Fab uptake was due to direct binding to troponin-I in necrotic cells was obtained by coinjection of non-immune 125I labelled Fab. CONCLUSIONS: Results indicate that troponin-I could act as a suitable target for detecting myocardial necrosis.
Management of rheumatoid neck.
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Mobility of injection drug users and transmission of HIV.
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Cardiac-specific troponin-I radioimmunoassay in the diagnosis of acute myocardial infarction.
The cardiac isotype of the myofibrillar contractile protein, troponin-I, is located specifically in the mammalian heart. A sensitive radioimmunoassay has been developed to detect human and nonhuman primate cardiac troponin-I in serum down to 10 ng/ml. Immunochemical cross reactivity with skeletal troponin-I was only 2% and was species nonspecific. Normal patient levels of cardiac troponin-I are about 10 ng/ml. In patients with acute myocardial infarction (n = 32), serum cardiac troponin-I was elevated within 4 to 6 hours, reached a mean peak level of 112 ng/ml (range 20 to 550 ng/ml) at 18 hours, and remained above normal for up to 6 to 8 days following infarction. Peak cardiac troponin-I correlated with peak creatine kinase (CK) MB isoenzyme (r = 0.75). In subjects (n = 34) with skeletal muscle damage (total CK = 338 to 5384 IU/L), cardiac troponin-I levels were not elevated above normal, although CK-MB isoenzyme was elevated in some patients. Cardiac troponin-I levels were normal or slightly elevated in patients with ischemic heart disease and were normal in patients with chest pain of noncardiac origin. Immunoassay of cardiac troponin-I could be a valuable diagnostic aid in the cardiac-specific detection of cell necrosis.
Cardiac specific troponin-I release in canine experimental myocardial infarction: development of a sensitive enzyme-linked immunoassay.
A canine model of experimental myocardial infarction has been used to investigate the release of troponin-I as a specific diagnostic indicator of cardiac necrosis. An enzyme-linked immunoassay was established to detect canine cardiac troponin-I in serum. Polyclonal antisera to cardiac troponin-I showed low cross-reactivity with skeletal muscle troponin-I which was completely removed by immunoadsorption. The cardiac specific ELISA time was 5 to 6 h. Assay sensitivity was 4 ng cardiac troponin-I/ml with an upper limit of 200 ng/ml in neat serum. Mean normal circulating levels of cardiac troponin-I were 15.6 ng/ml compared with an estimated 11 ng/ml in man [Cummins, B. et al. Am Heart J 113, 1333-1344 (1987)]. After experimental infarction, cardiac troponin-I was detectable within 4 to 6 h and peaked between 10 to 16 h post-ligation. Cardiac specific creatine kinase-MB isoenzyme was released with a similar initial time course. Mean peak cardiac troponin-I and CK-MB were elevated 6- and 10-fold respectively. Cardiac troponin-I levels were elevated for up to 200 h post-ligation compared to a maximum of 100 h for CK-MB. The prolonged time course of troponin-I release was comparable to that seen clinically [Cummins, B., et al. Am Heart J 113, 1333-1344 (1987)]. Histochemical infarct size correlated well with CK-MB but less so with troponin-I release. This may reflect the complex nature of intracellular troponin-I degradation and loss from necrotic cardiac tissue.
Hydrocephalus related to pulsion diverticulum of lateral ventricle.
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The effects of brain lesions on the contingent negative variation in neurosurgical patients.
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The contingent negative variation in cases of known brain lesions.
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