Report of FIENS activities. Foundation for International Education in Neurological Surgery.
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Foundations↗
Biomedical subjects
D F Kelly
Publications and source records attributed to D F Kelly.
Staffing at veterinary schools.
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Animals↗
Femoral neck metaphyseal osteopathy in the cat.
This paper describes 17 cats that developed an idiopathic necrosis of the femoral neck. In four cats the lesions were bilateral when they were first examined and five cats developed lesions in the other limb within five months. They were all male cats, two years old or younger, and 15 had been neutered. The initial sign was a vague lameness which typically progressed, often acutely, to a more severe lameness. Radiography demonstrated radiolucency and loss of definition within the proximal femoral metaphysis, the femoral neck. In 12 cases there was a complete radiolucent line across the femoral neck. An excision arthroplasty was carried out on all the affected hips and the lameness resolved in all cases. The clinical and radiological signs suggest a primary bone resorption with secondary fracture of the femoral neck. The lesions have some similarities with Legg-Calve-Perthes' disease, traumatic fracture of the femoral neck, canine metaphyseal osteopathy, bacterial osteomyelitis and experimental feline herpes virus osteomyelitis.
Animals↗
Heterotopic pancreas at a site of colon stricture and ulceration in a guineapig.
A one-month-old female Dunkin Hartley guineapig presented with a thin hair coat and distended abdomen. Post-mortem findings after euthanasia were a protein-rich modified peritoneal transudate and heterotopic pancreas at a site of colon stricture and ulceration. Complications of pancreatic heterotopia are well recognized in man but not in animals. The finding in this individual is probably unrelated to sudden deaths in other animals in the group.
Animals↗
Characterization of intestinal morphologic, biochemical, and ultrastructural features in gluten-sensitive Irish Setters during controlled oral gluten challenge exposure after weaning.
OBJECTIVE: To characterize histologic, biochemical, and ultrastructural changes in the intestine of Irish Setters susceptible to gluten-sensitive enteropathy (GSE) during controlled oral challenge exposure with gluten after weaning. ANIMALS: Six gluten-sensitive and 12 healthy Irish Setters and 3 healthy Greyhounds. PROCEDURE: Jejunal biopsy specimens were taken at 4 and 12 months of age from the 6 gluten-sensitive Irish Setters, which had been reared on a gluten-free diet to which a controlled dose of gluten (0.5 g/kg of body weight/d) was added. Control specimens were obtained at 4 (n = 5) and 12 (7) months of age from the healthy Irish Setters, which had been fed a conventional gluten-containing diet, and at 4 months of age from the healthy Greyhounds fed the controlled dose of gluten. The specimens were subjected to histologic and ultrastructural examinations and assay of brush border enzymes. RESULTS: Gluten-sensitive Irish Setters developed abnormalities characteristic of GSE at 4 months. Abnormalities were comparable to changes not seen previously until 12 months in dogs with GSE fed a conventional gluten-containing diet. In addition, microvilli were stunted and irregular, and a few were vesiculated and reduced in number; the glycocalyx was reduced or absent. By 12 months of age, there was improvement in morphologic and biochemical parameters, indicating partial recovery despite continued exposure to gluten. CONCLUSIONS: Relative early onset of intestinal damage, compared with that previously reported, and subsequent partial recovery suggestive of oral tolerance to gluten may be attributable to oral administration of gluten as a purified extract rather than in dietary cereal, but alternative explanations include differences in environment or genetic susceptibility to gluten.
Alkaline Phosphatase↗
Cowpox in British voles and mice.
Serosurveys indicate that bank voles, field voles and woodmice are probably reservoir hosts of cowpox virus in western Europe, although virus has not yet been isolated from these species. In this study, bank voles, field voles, woodmice and laboratory mice were shown to be susceptible to combined intradermal and subcutaneous inoculation with 3-20 plaque-forming units (pfu) of cowpox virus. Bank and field voles, but not laboratory mice, were also susceptible to combined oral and nasal inoculation with 50 pfu. Few clinical signs were seen and virus was generally recovered only from inoculation sites. Bank voles were not susceptible to injection of ectromelia virus (5000 pfu) into the skin (as described above). These results provide information on which further pathogenesis and transmission studies can be based, and support the view that the orthopoxvirus antibody detected in British wild voles and woodmice indicates infection with cowpox virus. However, further investigation of the pathogenesis of cowpox in these species is needed to understand better the epidemiology of the disease.
Administration, Intranasal↗
Pulmonary venous thrombosis in caprine Pasteurella pneumonia.
A 3-year-old Angora goat that developed acute fibrinous pleuropneumonia associated with Pasteurella haemolytica infection had thrombotic occlusion of a large pulmonary vein. Thrombosis of pulmonary capillaries occurs in pneumonic pasteurellosis, but large vessels are not commonly affected. This unusual lesion may reflect the procoagulant effect of pasteurella endotoxin on vascular endothelium. An incidental observation was the presence of myocardial-type muscle fibres in the tunica media of the pulmonary vein.
Animals↗
Heterotopic neural tissue in the pharynx of a 7-week-old kitten.
A 7-week-old male kitten had a pharyngeal mass (1 x 2 cm) causing displacement of the tongue. The surgically resected tissue was seen to be a moderately discrete subepithelial mass comprising islands of neuroglia and neurons separated by dense collagenous connective tissue. It is not known whether this mass retained any connection with the brain. Histochemical and immunohistochemical examination confirmed the presence of neurons and a pleocellular glial population, supporting a diagnosis of heterotopic neural tissue. The cat remained well 20 months after surgical treatment. Heterotopic neural tissue is well-recognized in man but has not been described in animals.
Animals↗
Zygomatic salivary cyst with mucocele formation in a cat.
An eight-year-old neutered male domestic shorthair cat had a zygomatic salivary cyst with associated mucocele formation. A fluctuating swelling developed ventral to the right eye, causing bulging of the lower eyeild, and a corresponding swelling was present in the caudal vestibule of the oral cavity. Cytological examination of the fluid obtained from aspiration of the swelling was consistent with the appearance of saliva. A tentative diagnosis of zygomatic salivary mucocele was made. Surgical exploration and resection of the swelling demonstrated the presence of a multilobular cystic zygomatic salivary gland. The histopathological appearance of the resected tissue was interpreted as an inflammatory reaction to mucus derived from a multilocular salivary cyst.
Animals↗
Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study.
Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans. The characteristics and incidence of cerebral hyperglycolysis were determined in 28 severely head injured patients using [18F]fluorodeoxyglucose-positron emission tomography (FDG-PET). The local cerebral metabolic rate of glucose (CMRG) was calculated using a standard compartmental model. In six of the 28 patients, the global cerebral metabolic rate of oxygen (CMRO2) was determined by the simultaneous measurements of arteriovenous differences of oxygen and cerebral blood flow (xenon-133). Hyperglycolysis, defined as an increase in glucose utilization that measures two standard deviations above expected levels, was documented in all six patients in whom both FDG-PET and CMRO2 determinations were made within 8 days of injury. Five additional patients were found to have localized areas of hyperglycolysis adjacent to focal mass lesions. Within the 1st week following the injury, 56% of patients studied had presumptive evidence of hyperglycolysis. The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.
Adolescent↗
Cerebral blood flow as a predictor of outcome following traumatic brain injury.
As part of a prospective study of the cerebrovascular effects of head injury, 54 moderate and severely injured patients underwent 184 133Xe-cerebral blood flow (CBF) studies to determine the relationship between the period of maximum blood flow and outcome. The lowest blood flows were observed on the day of injury (Day 0) and the highest CBFs were documented on postinjury Days 1 to 5. Patients were divided into three groups based on CBF values obtained during this period of maximum flow: Group 1 (seven patients), CBF less than 33 ml/100 g/minute on all determinations; Group 2 (13 patients), CBF both less than and greater than or equal to 33 ml/100 g/minute; and Group 3 (34 patients), CBF greater than or equal to 33 ml/100 g/minute on all measurements. For Groups 1, 2, and 3, mean CBF during Days 1 to 5 postinjury was 25.7 +/- 4, 36.5 +/- 4.2, and 49.4 +/- 9.3 ml/100 g/minute, respectively, and PaCO2 at the time of the CBF study was 31.4 +/- 6, 32.7 +/- 2.9, and 33.4 +/- 4.7 mm Hg, respectively. There were significant differences across Groups 1, 2, and 3 regarding mean age, percentage of individuals younger than 35 years of age (42.9%, 23.1%, and 76.5%, respectively), incidence of patients requiring evacuation of intradural hematomas (57.1%, 38.5%, and 17.6%, respectively) and incidence of abnormal pupils (57.1%, 61.5%, and 32.4%, respectively). Favorable neurological outcome at 6 months postinjury in Groups 1, 2, and 3 was 0%, 46.2%, and 58.8%, respectively (p < 0.05). Further analysis of patients in Group 3 revealed that of 14 with poor outcomes, six had one or more episodes of hyperemia-associated intracranial hypertension (simultaneous CBF > 55 ml/100 g/minute and ICP > 20 mm Hg). These six patients were unique in having the highest CBFs for postinjury Days 1 to 5 (mean 59.8 ml/100 g/minute) and the most severe degree of intracranial hypertension and reduced cerebral perfusion pressure (p < 0.0001). These results indicate that a phasic elevation in CBF acutely after head injury is a necessary condition for achieving functional recovery. It is postulated that for the majority of patients, this rise in blood flow results from an increase in metabolic demands in the setting of intact vasoreactivity. In a minority of individuals, however, the constellation of supranormal CBF, severe intracranial hypertension, and poor outcome indicates a state of grossly impaired vasoreactivity with uncoupling between blood flow and metabolism.
Adolescent↗
Paradoxical effects of acute ethanolism in experimental brain injury.
Acute ethanol intoxication is a frequent complicating factor in human head injury, yet its impact on neurological outcome remains poorly defined. This study was undertaken to assess the effect of varying levels of preinjury ethanol on early postinjury mortality, recovery of motor function, and degree of neural degeneration after cortical contusion injury in the rat. Adult rats were pretrained on a beam-walking task, then randomized to one of five groups: low-dose ethanol and injury (1 g/kg, 16 animals); moderate-dose ethanol and injury (2.5 g/kg, 11 animals); high-dose ethanol and injury (3 g/kg, 17 animals); no ethanol and injury (nine animals); or ethanol and sham injury (seven animals). Forty minutes after intraperitoneal injection of ethanol or saline, the rats received a pneumatic piston-induced contusion injury of the left primary motor cortex. Their beam-walking ability was assessed daily for the next 7 days. At 4 weeks postinjury, the brains were sectioned and the dimensions of the cortical lesions were determined. Preinjury ethanol administration was associated with an acute postinjury mortality rate of 29.5% (p < 0.05); the highest mortality rate (47.1%) occurred in the high-dose ethanol group, whereas no deaths occurred in the animals in the no ethanol or sham-injured groups (p < 0.01). However, injured animals receiving low- and moderate-dose ethanol had significantly less severe beam-walking impairment initially, and a more rapid return to normal beam-walking ability, compared to the no and high-dose ethanol groups (p < 0.05). Additionally, the mean lesion volumes were significantly smaller in the low- and moderate-dose ethanol treatment groups compared to the no and high-dose ethanol groups (23.2 +/- 8 mm3 and 29 +/- 6.7 mm3 vs. 52 +/- 8.8 mm3 and 53.7 +/- 10.9 mm3, respectively, p < 0.01). In this cortical contusion model, the presence of ethanol before injury appears to exert a potent neuroprotective effect when administered in low or moderate doses. This action is postulated to result from ethanol-induced inhibition of N-methyl-D-aspartate receptor-mediated excitotoxicity. The loss of neuroprotection and increased mortality rates observed with high-dose ethanol may be related to ethanol-induced hemodynamic and respiratory depression.
Acute Disease↗
Ethics consultation.
This article comprehensively addresses the composition, role, and functions of a hospital ethics committee (HEC). HECs are of particular interest to critical care specialists because they often participate in or lead such committees, extending their commitment to communication and caring beyond the borders of the intensive care unit (ICU). This article also demonstrates that a well-run ICU in a hospital with a strong HEC automatically will include many of the services that the HEC normally would provide, without the need for HEC assistance.
Committee Membership↗
Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome.
The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 +/- 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 +/- 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all < or = 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.
Adult↗
Activation of transfer RNA-guanine ribosyltransferase by protein kinase C.
Transfer RNA-guanine ribosyltransferase (TGRase) irreversibly incorporates queuine into the first position in the anticodon of four tRNA isoacceptors. Rat brain protein kinase C (PKC) was shown to stimulate rat liver TGRase activity. TGRase preparations derived from rat liver have been observed to decrease in activity over time in storage at -20 or -70 degrees C. Contamination of the samples by phosphatases was indicated by a p-nitrophenylphosphate conversion test. The addition of micromolar concentrations of the phosphatase inhibitors sodium pyrophosphate and sodium fluoride into TGRase isolation buffers resulted in a greater return of TGRase activity than without these inhibitors. Inactive TGRase preparations were reactivated to their original activity with the addition of PKC. In assays combining both TGRase and PKC enzymes, inhibitors of protein kinase C (sphingosine, staurosporine, H-7 and calphostin C) all blocked the reactivation of TGRase, whereas activators of protein kinase C (calcium, diacylglycerol and phosphatidyl serine) increased the activity of TGRase. None of the PKC modulators affected TGRase activity directly. Alkaline phosphatase, when added to assays, decreased the activity of TGRase and also blocked the reactivation of TGRase with PKC. Denaturing PAGE and autoradiography was performed on TGRase isolates that had been labelled with 32P by PKC. The resulting strong 60 kDa band (containing the major site for phosphorylation) and weak 34.5 kDa band (containing the TGRase activity) are suggested to associate to make up a 104 kDa heterodimer that comprises the TGRase enzyme. This was corroberated by native and denaturing size-exclusion chromatography. These results suggest that PKC-dependent phosphorylation of TGRase is tied to efficient enzymatic function and therefore control of the queuine modification of tRNA.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Alcohol and head injury: an issue revisited.
The pathophysiologic changes associated with acute and chronic alcohol exposure in the setting of traumatic brain injury are complex. Experimental data indicate that ethanol intoxication can exacerbate brain injury through several mechanisms including hemodynamic and respiratory depression, blood-brain barrier disruption, and derangements in hemostasis. Alcohol, however, is also a potent inhibitor of N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity, and thus is neuroprotective. In contrast to the effects of acute intoxication, chronic alcohol exposure appears to result in upregulation of NMDA receptor activity and downregulation of gamma-aminobutyric acid (GABA) receptor function. This imbalance, it is hypothesized, can result in a surge of excitotoxicity following alcohol withdrawal. Trauma-related excitotoxic cell damage may be significantly potentiated by this alcohol-induced receptor imbalance that is unmasked as withdrawal occurs. Clinical and epidemiologic investigations of alcohol and outcome after head injury have not consistently demonstrated a measurable effect from either acute or chronic alcohol use. Multiple factors including the timing of intoxication in relation to time of injury, the degree and chronicity of intoxication, as well as the influence of other secondary injury processes appear to determine the net effect of alcohol in a given individual. Further clinical and experimental investigations aimed at defining the impact of alcohol use on outcome after head injury are warranted.
Alcoholic Intoxication↗