Biomedical subjects

Ludwig Kramer

Publications and source records attributed to Ludwig Kramer.

6 recordsLinked to original sources

PubMed2003

Neurocognitive deficit following mitral valve surgery.

OBJECTIVE: Neurocognitive deficit is an important complication in patients undergoing open heart surgery. The aim of this prospective, contemporary study was to objectively measure neurocognitive brain function following mechanical mitral valve replacement and mitral valve repair. METHODS: Forty consecutive, unselected patients (mechanical valve replacement n=20, mean age 65+/-14; valve repair n=20, mean age 64+/-7, P=0.896) entered this prospective, contemporary study. Neurocognitive function was objectively measured by means of P300 auditory evoked potentials (peak latencies, ms) and two standard psychometric tests (Mini Mental State Examination, Trailmaking Test A (TTA)), preoperatively, 7 days and 4 months postoperatively. RESULTS: Before operation, neurocognitive brain function was comparable in both patients groups (mechanical valve replacement versus valve repair: P300 potentials 374+/-25 versus 378+/-46 ms; P=0.791 and TTA 57+/-15 versus 54+/-10 s; P=0.552). Following mechanical valve replacement, neurocognitive function continuously worsened (7 day-follow-up: P300 potentials 392+/-28, P=0.001 versus preop and TTA 65+/-17, P=0.0001; 4-month follow-up: P300 potentials 406+/-39, P=0.0004; TTA 69+/-17, P=0.0001). Interestingly, neurocognitive brain function was unaffected in patients undergoing valve repair (7-day follow-up: P300 potentials 386+/-40, P=0.890 versus preop and TTA: 53+/-10, P=0.644; 4-month follow-up: P300 potentials 374+/-36, P=0.166 and TTA 54+/-11, P=0.147). At 4-month follow-up, patients with mechanical prostheses performed worse as compared to valve repair (P300 potentials: P=0.024; TTA P=0.014). CONCLUSION: As shown by P300 auditory evoked potentials and Trailmaking Test A, there is marked neurocognitive damage related to mechanical valve replacement, whereas mitral valve repair does not affect neurocognitive function. This finding supports the beneficial effect of mitral valve repair over mechanical valve replacement in the decision-making tree of borderline cases, which are suitable for both types of procedure.

Adult↗

PubMed2002

Cognitive deficit after aortic valve replacement.

BACKGROUND: Impairment of cognitive brain function after coronary artery bypass grafting (CABG) is well known. In contrast the potential neurocognitive damage related to aortic valve replacement (AVR) is uncertain. METHODS: In this contemporary case-matched control study we followed 30 patients (mean age 70 years) receiving isolated AVR with a biological prosthesis. A cohort of sex-and age-matched patients (n = 30, mean age 70 years) receiving CABG with cardiopulmonary bypass served as controls. Cognitive brain function was measured by means of auditory evoked P300 potentials (peak latencies, ms) before the operation and 7 days and 4 months after the operation. Additionally, two standard psychometric tests (Mini-Mental State Examination and the Trailmaking Test A) were performed. RESULTS: In preoperative measures there was no difference between patients undergoing AVR and patients undergoing CABG (AVR 378 +/- 37 ms, CABG 374 +/- 32 ms, p = 0.629). One week after surgery P300 peak latencies were prolonged (impaired) in both groups compared with preoperative values (AVR 405 +/- 43 ms, p = 0.001; CABG 398 +/- 44 ms, p = 0.004). At this point of follow-up there was no difference between the groups (p = 0.607). Finally, 4 months after surgery P300 auditory evoked potentials returned to normal in the CABG group (380 +/- 24 ms, p = 0.940) while in contrast in the valve group they continued to become prolonged (worsened) compared with preoperative values (410 +/- 47 ms, p = 0.005). At this time of follow-up P300 peak latencies were prolonged in AVR patients as compared with CABG patients (p = 0.032). The Trailmaking Test A and Mini-Mental State Examination failed to discriminate any difference. CONCLUSIONS: Four-month impairment of cognitive brain function is more pronounced in patients undergoing biological AVR as compared with age-matched control patients undergoing CABG. Further studies are needed to clarify the potential pathologic mechanisms causing an ongoing cognitive impairment in patients with biological aortic valve prostheses.

Aged↗

PubMed2002

Subclinical impairment of brain function in chronic hepatitis C infection.

BACKGROUND/AIMS: Central nervous system abnormalities such as fatigue and depression occur more frequently in chronic hepatitis C virus (HCV) infection than in many other causes of chronic liver disease. The finding that fatigue is unrelated to activity of hepatitis or mode of infection could indicate an independent effect of HCV on brain function. This study tested the hypothesis of a subclinical cognitive dysfunction in HCV-infected patients. METHODS: One-hundred untreated HCV-RNA positive biopsy-proven patients were investigated by P300 event-related potentials, a sensitive electrophysiologic test of cognitive processing. Health-related quality of life and fatigue were assessed using the SF-36 questionnaire and the Fatigue Impact Scale, respectively. RESULTS: Cognitive brain function was subclinically impaired in the cohort of HCV-infected patients as indicated by significantly prolonged P300 latencies (P=0.01 for comparison to matched healthy subjects) and reduced P300 amplitudes (P<0.001, respectively). Seventeen of the 100 HCV-infected patients had P300 latencies outside the age-adjusted normal range. Abnormal P300 characteristics were not related to the degree of histologic or biochemical activity of hepatitis, severity of fatigue or mental health impairment. CONCLUSIONS: This study demonstrates that patients with HCV infection showed a slight but significant neurocognitive impairment, possibly indicating a further extrahepatic manifestation of chronic hepatitis C.

Adult↗

PubMed2002

Impaired subcortical and cortical sensory evoked potential pathways in septic patients.

OBJECTIVE: Sensory evoked potential (SEP) peak latencies were recorded in order to evaluate the incidence and severity of septic encephalopathy, testing the hypothesis that the occurrence of septic encephalopathy is more frequent than generally assumed. DESIGN: Prospective cohort study. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Sixty-eight critically ill patients were studied within 48 hrs after the development of severe sepsis (n = 41) or septic shock (n = 27). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Septic encephalopathy was defined as prolongation of SEP peak latencies beyond the upper limit of the reference range of subcortical (N13-N20 interpeak latency) and cortical SEP pathways (N20-N70 interpeak latency), as well as asymmetry of peak latencies marked by the presence of subclinical cerebral focal signs. Subcortical SEP pathways were impaired in 34% and cortical SEP pathways in 84% of all patients. The prolongation of the cortical SEP pathway correlated with the Acute Physiology and Chronic Health Evaluation III score (r = 0.23; p <.0001). SEP peak latencies did not differ in patients with severe sepsis compared with those with septic shock. Subclinical cerebral focal signs were present in 24% of the subcortical SEP pathways and in 6% of the cortical SEP pathways. CONCLUSIONS: Septic encephalopathy occurs more frequently than generally assumed, and its severity is associated with the severity of illness. The impairment of subcortical and cortical SEP pathways was not different between patients with severe sepsis and those with septic shock.

Brain Diseases↗

PubMed2002

Neurophysiological evidence of cognitive impairment in patients without hepatic encephalopathy after transjugular intrahepatic portosystemic shunts.

OBJECTIVES: We aimed to test the hypothesis that subclinical cognitive brain dysfunction in cirrhotic patients would deteriorate after a transjugular intrahepatic portosystemic shunt (TIPS) in the absence of clinically detectable hepatic encephalopathy. METHODS: Out of 49 consecutive cirrhotic patients receiving elective TIPS for recurrent variceal hemorrhage, we identified 22 patients who were not encephalopathic and had not undergone liver transplantation at 6-month follow-up and confirmed TIPS patency by Doppler ultrasound. Patients were tested before and 6 months after TIPS implantation using event-related (P300) cognitive evoked potentials, late somatosensory median nerve (N70) potentials, and standard psychometric tests (Mini-Mental State and trailmaking test A). Twenty-two age-matched healthy subjects served as controls. RESULTS: Relative to controls, patients showed significantly impaired P300 and N70 latencies and abnormal psychometric test results at baseline. Six months after the TIPS, a further impairment of P300 latency was observed (p = 0.005), whereas no relevant changes in N70 latency and psychometric test results occurred. CONCLUSIONS: In cirrhotic patients with portal hypertension, neurophysiological signs of cognitive brain dysfunction are detectable in the absence of hepatic encephalopathy. A further subclinical deterioration of cognitive processing was observed 6 months after the TIPS. These findings demonstrate an aggravation of subclinical hepatic encephalopathy after a TIPS.

Adult↗

PubMed2002

Hepatorenal syndrome.

The hepatorenal syndrome is defined as functional renal failure in advanced chronic or acute liver disease with portal hypertension. Morphologic abnormalities of the kidneys are frequently absent and tubular function is preserved. Patients with the hepatorenal syndrome are characterized by progressive splanchnic and systemic vasodilation and decreased effective arterial blood volume. Compensatory activation of vasoconstrictory systems maintains systemic hemodynamic stability but causes progressive afferent renal vasoconstriction, leading to reduction of glomerular filtration rate. Renal failure may be rapidly progressive (type I hepatorenal syndrome, frequently associated with spontaneous bacterial peritonitis) or may develop more slowly (type II). Orthotopic liver transplantation is the best current treatment and leads to a gradual recovery of renal function in the vast majority of patients. Because mortality of type I hepatorenal syndrome is excessive, supportive treatment by vasoconstrictor drugs, transjugular intrahepatic portosystemic shunt, and renal replacement therapy has been investigated to achieve stability until transplantation. The definite role of these promising developments, however, is still uncertain, emphasizing the need for large prospective multicentric investigations.

Ascites↗