Understanding central fatigue: where to go?
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Electromyography↗
Biomedical subjects
Peter Rasmussen
Publications and source records attributed to Peter Rasmussen.
Capillary-oxygenation-level-dependent near-infrared spectrometry in frontal lobe of humans.
Brain function requires oxygen and maintenance of brain capillary oxygenation is important. We evaluated how faithfully frontal lobe near-infrared spectroscopy (NIRS) follows haemoglobin saturation (SCap) and how calculated mitochondrial oxygen tension (PMitoO2) influences motor performance. Twelve healthy subjects (20 to 29 years), supine and seated, inhaled O2 air-mixtures (10% to 100%) with and without added 5% carbon dioxide and during hyperventilation. Two measures of frontal lobe oxygenation by NIRS (NIRO-200 and INVOS) were compared with capillary oxygen saturation (SCap) as calculated from the O2 content of brachial arterial and right internal jugular venous blood. At control SCap (78%+/-4%; mean+/-s.d.) was halfway between the arterial (98%+/-1%) and jugular venous oxygenation (SvO2; 61%+/-6%). Both NIRS devices monitored SCap (P<0.001) within approximately 5% as SvO2 increased from 39%+/-5% to 79%+/-7% with an increase in the transcranial ultrasound Doppler determined middle cerebral artery flow velocity from 29+/-8 to 65+/-15 cm/sec. When SCap fell below approximately 70% with reduced flow and inspired oxygen tension, PMitoO2 decreased (P<0.001) and brain lactate release increased concomitantly (P<0.001). Handgrip strength correlated with the measured (NIRS) and calculated capillary oxygenation values as well as with PMitoO2 (r>0.74; P<0.05). These results show that NIRS is an adequate cerebral capillary-oxygenation-level-dependent (COLD) measure during manipulation of cerebral blood flow or inspired oxygen tension, or both, and suggest that motor performance correlates with the frontal lobe COLD signal.
Adult↗
Beta-adrenergic receptor desensitization in man: insight into post-exercise attenuation of cardiac function.
Desensitization of the beta-adrenoreceptors (beta-AR) may contribute to a post-exercise reduction in left ventricular (LV) function. However, attenuation of the chronotropic and inotropic responses to a beta-AR agonist may depend upon alterations in parasympathetic tone. Furthermore, changes in cardiac output and LV diastolic function in response to a beta-AR agonist, pre- to post-prolonged exercise, remain unclear. Seven trained males (mean+/-s.d., age 27+/-6 years) performed 4 h of ergometer rowing. Peak heart rate (HR) and LV systolic and diastolic functional responses to incremental isoproterenol (isoprenaline) infusion (2, 4 and 6 microg kg min-1) were assessed after vagal blockade (glycopyrrolate, 1.2 mg). LV systolic function was assessed by the pressure/volume ratio (systolic blood pressure/end systolic volume) and , whilst diastolic function was evaluated as peak early and late transmitral filling velocities. Following exercise, the pressure/volume ratio decreased by 25% (P<0.05), whereas was unchanged (P>0.05). The early/late filling ratio was reduced by 36% after exercise, due to an elevation in late LV filling (P<0.01). The increase in HR response to isoproterenol infusion was blunted post-exercise at both 4 and 6 microg kg min-1 (127+/-7 and 132+/-6 beats min-1) compared with pre-exercise (138+/-8 and 141+/-12 beats min-1, P<0.05). Additionally, the pressure/volume ratio and were blunted post-exercise in response to isoproterenol (P<0.05). In contrast, diastolic function was similar before and after exercise during isoproterenol infusion (P>0.05). Desensitization of the beta-AR contributes to an attenuated left ventricular systolic but not diastolic function following prolonged exercise.
Adrenergic beta-Agonists↗
MCA Vmean and the arterial lactate-to-pyruvate ratio correlate during rhythmic handgrip.
Regulation of cerebral blood flow during physiological activation including exercise remains unknown but may be related to the arterial lactate-to-pyruvate (L/P) ratio. We evaluated whether an exercise-induced increase in middle cerebral artery mean velocity (MCA Vmean) relates to the arterial L/P ratio at two plasma lactate levels. MCA Vmean was determined by ultrasound Doppler sonography at rest, during 10 min of rhythmic handgrip exercise at approximately 65% of maximal voluntary contraction force, and during 20 min of recovery in seven healthy male volunteers during control and a approximately 15 mmol/l hyperglycemic clamp. Cerebral arteriovenous differences for metabolites were obtained by brachial artery and retrograde jugular venous catheterization. Control resting arterial lactate was 0.78 +/- 0.09 mmol/l (mean +/- SE) and pyruvate 55.7 +/- 12.0 micromol/l (L/P ratio 16.4 +/- 1.0) with a corresponding MCA Vmean of 46.7 +/- 4.5 cm/s. During rhythmic handgrip the increase in MCA Vmean to 51.2 +/- 4.6 cm/s was related to the increased L/P ratio (23.8 +/- 2.5; r2 = 0.79; P < 0.01). Hyperglycemia increased arterial lactate and pyruvate to 1.9 +/- 0.2 mmol/l and 115 +/- 4 micromol/l, respectively, but it did not significantly influence the L/P ratio or MCA Vmean at rest or during exercise. Conversely, MCA Vmean did not correlate significantly, neither to the arterial lactate nor to the pyruvate concentrations. These results support that the arterial plasma L/P ratio modulates cerebral blood flow during cerebral activation independently from the plasma glucose concentration.
Adult↗
Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise.
This study investigated the influence of environmental heat stress on ammonia (NH3) accumulation in relation to nucleotide metabolism and fatigue during intermittent exercise. Eight males performed 40 min of intermittent exercise (15 s at 306+/-22 W alternating with 15 s of unloaded cycling) followed by five 15 s all-out sprints. Control trials were conducted in a 20 degrees C environment while heat stress trials were performed at an ambient temperature of 40 degrees C. Muscle biopsies and venous blood samples were obtained at rest, after 40 min of exercise and following the maximal sprints. Following exercise with heat stress, the core and muscle temperatures peaked at 39.5+/-0.2 and 40.2+/-0.2 degrees C to be approximately 1 degrees C higher (P<0.05) than the corresponding control values. Mean power output during the five maximal sprints was reduced from 618+/-12 W in control to 558+/-14 W during the heat stress trial (P<0.05). During the hot trial, plasma NH3 increased from 31+/-2 microM at rest to 93+/-6 at 40 min and 151+/-15 microM after the maximal sprints to be 34% higher than control (P<0.05). In contrast, plasma K+ and muscle H+ accumulation were lower (P<0.05) following the maximal sprints with heat stress compared to control, while muscle glycogen, CP, ATP and IMP levels were similar across trials. In conclusion, altered levels of "classical peripheral fatiguing agents" does apparently not explain the reduced capacity for performing repeated sprints following intermittent exercise in the heat, whereas the augmented systemic NH3 response may be a factor influencing fatigue during exercise with superimposed heat stress.
Adult↗
Etomidate, transfusion, and vasospasm.
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Humans↗
Laparoscopic revision of a ventriculoperitoneal shunt.
Ventriculoperitoneal (VP) shunts are the most common treatment modality for hydrocephalus. Distal catheter malfunction represents a surgical emergency and a significant cause of procedural morbidity. We report the case of a patient with acute abdominal pain following VP shunt insertion. On examination she had a tender, irreducible bulge at the abdominal laparotomy site. Exploratory laparoscopy of the abdomen yielded no abdominal wall abnormalities. At the same time, the distal catheter was noted to be absent. The abdominal bulge was incised along the laparotomy scar and clear cerebrospinal fluid was encountered. The incision was explored and the distal catheter was coiled and knotted within the preperitoneal space. The catheter was laparoscopically returned to the peritoneal cavity. This case exemplifies the utility of laparoscopy for VP shunt revision and we present a review of laparoscopic shunt revision.
Embolization, Therapeutic↗
Balloon-assisted microvascular clipping of paraclinoid aneurysms. Technical note.
Paraclinoid aneurysms represent a significant surgical challenge. Multiple techniques have been developed to maximize the effectiveness and safety of excluding these aneurysms from the cerebral circulation. Endovascular balloons have been used for proximal control of parent arteries during the treatment of aneurysms. In this report the authors describe the technique of navigating an endovascular balloon across the neck of paraclinoid aneurysms in four patients to gain proximal control, improve the accuracy of clip placement, and reduce the risk of distal embolization of intraluminal thrombus. Six consecutive patients with giant or complex aneurysms of the ophthalmic or paraclinoid internal carotid artery that were not amenable to endovascular obliteration were retrospectively analyzed. In all six patients, the aneurysm was exposed and dissected for microsurgical clipping, and attempts were made to navigate a nondetachable, compliant silicone balloon across the neck of the aneurysm. If successfully placed, the balloon was inflated during clip placement. In four patients, the balloon was successfully navigated across the neck of the aneurysm and was inflated during clip application. Internal carotid artery tortuosity precluded navigation of the balloon into the intracranial circulation in two patients. All aneurysms were completely excluded from the parent vessel according to postoperative angiography studies. No complication occurred as a direct result of the endovascular portion of the procedure. Endovascular balloon stenting of complex paraclinoid aneurysms during microvascular clipping may provide an adjunctive therapy that facilitates safe and accurate clip placement.
Aged↗
Serum transthyretin monomer as a possible marker of blood-to-CSF barrier disruption.
The CNS is shielded from systemic influences by two separate barriers, the blood-brain barrier (BBB) and the blood-to-CSF barrier. Failure of either barrier bears profound significance in the etiology and diagnosis of several neurological diseases. Furthermore, selective opening of BBB tight junctions provides an opportunity for delivery of otherwise BBB impermeant drugs. Peripheral assessment of BBB opening can be achieved by detection in blood of brain-specific proteins that extravasate when these endothelial junctions are breached. We developed a proteomic approach to discover clusters of CNS-specific proteins with extravasation into serum that correlates with BBB openings. Protein profiles from blood samples obtained from patients undergoing iatrogenic BBB disruption (BBBD) with intra-arterial hyperosmotic mannitol were compared with pre-BBB opening serum. A low molecular weight protein (14 kDa) identified by mass spectroscopy as transthyretin (TTR) consistently correlated with BBBD. Protein gel electrophoresis and immunodetection confirmed that TTR was indeed extravasated in its monomeric form when CNS barriers were breached. The time course of TTR extravasation was compared with release from the brain of another BBB integrity marker, S-100beta (11 kDa). Kinetic analysis revealed that the appearance of S-100beta, presumably originating from perivascular astrocytic end feet, preceded extravasation of TTR by several minutes. Because TTR is localized primarily in choroid plexus and, as a soluble monomer, in CSF, we concluded that although S-100beta is a marker of BBB integrity, TTR instead may be a peripheral tracer of blood-to-cerebrospinal barrier.
Biomarkers↗
Peripheral markers of brain damage and blood-brain barrier dysfunction.
PURPOSE: Occurrence of brain damage is frequently associated with abnormal blood-brain barrier (BBB) function. Two brain-specific proteins, S100beta and neuron-specific enolase (NSE) are released systemically in a variety of neurological diseases, but S100beta levels sometimes rise in the absence of neuronal damage, suggesting that S100beta is a marker of BBB rather than neuronal damage. METHODS: We measured both proteins in the serum of patients undergoing iatrogenic BBB disruption with intrarterial mannitol, followed by chemotherapy. RESULTS: Serum S100beta increased significantly after mannitol infusion (p<0.05) while NSE did not. Furthermore, in a model of intracerebral hemorrhage, S100beta increases in CSF did not lead to serum changes at a time when the BBB was intact. Modeling of S100beta release from the CNS suggested that low (<0.34 ng/ml) serum levels of S100beta are consistent with BBB opening without CNS damage, while larger increases imply synthesis and release from presumable damaged glia. CONCLUSIONS: Thus, S100beta in serum is an early marker of BBB openings that may precede neuronal damage and may influence therapeutic strategies. Secondary, massive elevations in S100beta are indicators of prior brain damage and bear clinical significance as predictors of poor outcome or diagnostic means to differentiate extensive damage from minor, transient impairment.
Animals↗
Immediate and long-term phantom limb pain in amputees: incidence, clinical characteristics and relationship to pre-amputation limb pain.
In a prospective study 58 patients undergoing limb amputation were interviewed the day before operation about their pre-amputation limb pain and 8 days, 6 months and 2 years after limb loss about their stump and phantom limb pain. All but one patient had experienced pain in the limb prior to amputation. Pre-amputation limb pain lasted less than 1 month in 25% of patients and more than 1 month in the remaining 75% of patients. At the first examination the day before amputation 29% had no limb pain. The incidence of phantom pain 8 days, 6 months and 2 years after amputation was 72, 65 and 59%, respectively. Within the first half year after limb loss phantom pain was significantly more frequent in patients with long-lasting pre-amputation limb pain and in patients with pain in the limb immediately prior to amputation. Phantom pain and pre-amputation pain were similar in both localization and character in 36% of patients immediately after amputation but in only 10% of patients later in the course. Both the localization and character of phantom pain changed within the first half year; no further change occurred later in the course. The incidence of stump pain 8 days, 6 months and 2 years after limb loss was 57, 22 and 21%, respectively. It is suggested that preoperative limb pain plays a role in phantom pain immediately after amputation, but probably not in late persistent phantom pain.
Adult↗
Phantom limb, phantom pain and stump pain in amputees during the first 6 months following limb amputation.
The incidence and clinical picture of non-painful and painful phantom limb sensations as well as stump pain was studied in 58 patients 8 days and 6 months after limb amputation. The incidence of non-painful phantom limb, phantom pain and stump pain 8 days after surgery was 84, 72 and 57%, respectively. Six months after amputation the corresponding figures were 90, 67 and 22%, respectively. Kinaesthetic sensations (feeling of length, volume or other spatial sensation of the affected limb) were present in 85% of the patients with phantom limb both immediately after surgery and 6 months later. However, 30% noticed a clear shortening of the phantom during the follow-up period; this was usually among patients with no phantom pain. Phantom pain was significantly more frequent in patients with pain in the limb the day before amputation than in those without preoperative limb pain. Of the 67% having some phantom pain at the latest interview 50% reported that pains were decreasing. Four patients (8%), however, reported that phantom pains were worse 6 months after amputation than originally. During the follow-up period the localization of phantom pains shifted from a proximal and distal distribution to a more distal localization. While knifelike, sticking phantom pains were most common immediately after surgery, squeezing or burning types of phantom pain were usually reported later in the course. Possible mechanisms for the present findings either in periphery, spinal cord or in the brain are discussed.
Aged↗