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Biomedical subjects

E Kovalik

Publications and source records attributed to E Kovalik.

9 recordsLinked to original sources
PubMed2001

A compensatory mirror cortical mechanism for facial affect processing in schizophrenia.

When primates passively observe other subjects perform specific gestures or actions, premotor and motor cortical areas involved in the internal representation and actual execution of those actions exhibit neuronal activation. This mirror mechanism matches observation, representation, and execution, facilitating internal motor rehearsal, imitation, recognition of actions by others and their meanings, and social learning. Schizophrenic patients have deficits in processing affect displayed by other people's faces, which likely relates to the poor social adaptation and functioning seen in the condition. We hypothesized that, when correctly performing working-memory tasks requiring facial affect processing, schizophrenic patients would show relative increased activity in brain areas involved in social learning and in the internal representation of facial expressions when compared to controls. We used functional magnetic resonance imaging in schizophrenic patients and normal controls to detect relative changes of blood flow in cortical areas related to the representation of facial expressions while the subjects performed simple working-memory tasks with facial emotion diagrams or color circles as cues. We found that, when the task cues were facial expressions in contrast to color circles, the schizophrenic group exhibited increased activation of the face movement areas in motor and pre-motor cortex.

Adult↗
PubMed2000

The effects of an alpha-2 adrenergic agonist, guanfacine, on rCBF in human cortex in normal controls and subjects with focal epilepsy.

Alpha-2 noradrenergic agonists may have wide applicability in the treatment of pre-frontal cortex deficits in primates and behavioral dysfunction in man. We have undertaken this study to determine the effect of an alpha-2 agonist, guanfacine, on regional cerebral blood flow (rCBF) in humans. Three subject groups were evaluated: normal controls, subjects with frontal lobe epilepsy (FLE), and subjects with temporal lobe epilepsy (TLE). All underwent a number of PET scans using 15O-water, with half before and half after a single dose of guanfacine. A wide area of increased rCBF was seen in the frontal lobe, maximal at the central region, following guanfacine in controls and subjects with TLE. Smaller areas of decrease in rCBF were seen in the posterior temporal-occipital cortex. In the FLE group a decrease in rCBF was seen in the dorsal prefrontal cortex on the epileptogenic side with only small increases seen in the mid- to anterior temporal perisylvian areas. The ability of alpha-2 agonists to enhance performance of tasks reliant on prefrontal cortex, without improving tasks believed to rely on intact temporal-hippocampal function, may be explained by these results. Epileptogenic zones appear to create both direct and indirect changes in patterns of drug response. Further studies on the cognitive properties of these agents in humans should be encouraged.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

Gender differences in regional brain response to visceral pressure in IBS patients.

In two experiments including a total of 30 irritable bowel syndrome patients, symptom-mimicking rectal pressure stimuli elicited changes in regional neural activation as measured by positron electron tomography (PET) cerebral blood flow images. Although most stimuli were not rated as painful, rectal pressure increased regional cerebral blood flow (rCBF) in areas commonly associated with somatic pain, including the anterior cingulate, insula, prefrontal cortex, thalamus, and cerebellum. Despite similar stimulus ratings in male and female patients, regional activations were much stronger for males. In both experiments, rectal pressure activated the insula bilaterally in males but not in females. Insula activation was associated most strongly with objective visceral pressure, whereas anterior cingulate activation was associated more with correlated ratings of subjective discomfort. The insula is discussed as a visceral sensory cortex. Several possible reasons for the insula gender effect are proposed.

Adult↗
PubMed2000

Normalization of hematocrit in hemodialysis patients does not affect silent ischemia.

UNLABELLED: Transient ST-segment depression measured on ambulatory ECG monitors has been described as representing silent ischemia. Patients who demonstrate silent ischemia have been reported to show increased mortality compared to patients without silent ischemia. We undertook this study to determine if the correction of anemia in End Stage Renal Disease (ESRD) patients from (+/- = standard deviation) 30 +/- 3 to 42 +/- 3 with the use of Epoietin alfa would result in decreased silent ischemia in patients with clinically evident ischemic heart disease or congestive heart failure. METHODS: Thirty one ESRD patients with congestive heart failure or patients with clinically-evident ischemic heart disease were randomized into one of two arms. Patients in Group A had their hematocrit increased with the use of slowly escalating doses of Epoietin alfa to 42 +/- 3% and patients in Group B were maintained with a hematocrit of 30 +/- 3% throughout the course of the study. All patients had a 24 hour Holter monitor recording at baseline and at 28 weeks after randomization (when they had reached their target hematocrit). Significant silent ischemia was considered to be present if patients demonstrated at least 60 seconds of > or = 1 mm ST segment depression. RESULTS: Fifteen patients were randomized to Group A and 16 patients were randomized to Group B. The mean hematocrit increased in group A from 29.1 +/- 2.4% to 40.8 +/- 5.2% after 30 weeks. The mean hematocrit in Group B remained stable at 30 +/- 3% throughout the course of the study. Ten patients demonstrated silent ischemia at baseline. At follow up patients in group A demonstrated a mean of 1.7 +/- 4.9 minutes of ischemia compared to 1.1 +/- 3.4 minutes in group B. These were not significantly different. A similar number of patients in group A and Group B required adjustments in their anti-anginal medication during the course of the study. CONCLUSION: It is possible to increase hematocrit to near normal levels in hemodialysis with the administration of exogenous Epoietin alfa. The increase in hematocrit form 30 +/- 3% to 42 +/- 3% is not associated with a change in the level of silent ischemia these patients demonstrate.

Anemia↗
PubMed2000

Normalization of hematocrit in hemodialysis patients with cardiac disease does not increase blood pressure.

UNLABELLED: Since the earliest reports of the use of Epoetin alfa in hemodialysis patients, it has been described that Epoetin alfa may exacerbate preexisting hypertension or induce hypertension in End Stage Renal Disease (ESRD) patients not previously hypertensive. We undertook this study to determine if the correction of anemia in ESRD patients with cardiac disease from a hematocrit of 30+/-3% to 42+/-3% with the use of Epoetin alfa would result in increased blood pressure. This study was a substudy of the "Normal hematocrit Study". METHODS: Thirty-one patients were randomized into one of two arms. Patients in Group A had their hematocrit increased with the use of slowly escalating doses of Epoetin alfa to 42+/-3% and patients in Group B were maintained with a hematocrit of 30+/-3% throughout the course of the study. All patients had their blood pressure recorded with a 24 hour ambulatory BP device at study entry and at 28 weeks following randomization when they had achieved their target hematocrit. Pre-dialysis systolic and diastolic BP was also recorded. RESULTS: The mean hematocrit increased in Group A from 29.1+/-2.4% to 40.8+/-5.2% after 30 weeks. The hematocrit in Group B remained stable at 30+/-3% throughout the course of the study. There was no difference in mean daytime, mean nighttime or 24 hour systolic or diastolic blood pressure between Groups A and B at either baseline or follow-up. Neither was there a difference in mean pre-dialysis systolic or diastolic BP between Groups A or B at baseline or Follow-up. Four patients in Group A and 4 patients in Group B required an increase in their antihypertensive medication during the course of the study. CONCLUSION: It is possible to increase hematocrit to normal levels in hemodialysis with the administration of Epoetin alfa. The increase in hematocrit from 30+/-3% to 42+/-3% is not associated with increased blood pressure.

Adult↗
PubMed1998

Survival in renal vascular disease.

Renal artery stenosis (RAS) is a relatively uncommon but important potentially reversible cause of renal failure. Little is known about the natural history of ischemic renal disease secondary to RAS. In previous reports, these researchers examined the incidence and risk factors associated with RAS. The study presented here investigates the long-term follow-up of these patients, specifically the effect of RAS on 4-yr, all-cause mortality in a group of 1235 patients undergoing diagnostic cardiac catheterization and abdominal aortography. A total of 1235 consecutive patients undergoing cardiac catheterization also underwent an abdominal flush aortogram. Significant RAS was considered present if one or more renal artery had 50% or greater narrowing in luminal diameter. Four-year unadjusted survival for patients with RAS was 65% compared with 86% for patients undergoing catheterization without significant RAS. Factors associated with decreased 4-yr survival included increased age, increased serum creatinine, presence of RAS, peripheral vascular disease, congestive heart failure, diabetes, hypertension, and reduced ejection fraction. Using the Cox proportional hazards model, the factors associated with decreased 4-yr survival were the presence of significant RAS, reduced ejection fraction, elevated serum creatinine, and symptoms of congestive heart failure. These observations indicate that the presence of significant RAS is a strong independent predictor of 4-yr survival in this patient population.

Age Distribution↗
PubMed1995

Percutaneous renal biopsy of ventilated intensive care unit patients.

The etiology of acute renal failure in ventilated intensive care unit patients can be determined non-invasively in more than 80% of cases. When a pulmonary renal syndrome is suspected however it is important to obtain histological confirmation of the diagnosis prior to initiating therapy. Most text books and review articles have advocated the use of open surgical biopsy in this situation. Seven years ago we began to perform percutaneous renal biopsies on medical intensive care unit ventilated patients when a pulmonary renal syndrome was suspected as an alternative to an open surgical procedure. During this period we performed the technique on 7 patients. Adequate renal tissue was obtained in all cases. We compare the complication rate with that achieved using open surgical biopsy during the same time period. The complication rate using a percutaneous technique was similar to open renal biopsy. We believe that the previously held recommendation that percutaneous renal biopsy should not be performed on ventilated patients should be re-examined.

Acute Kidney Injury↗