Is the ulnar nerve damaged in 'handball goalie's elbow'?

'Handball goalie's elbow' has been defined as pain in the elbow region due to repetitive forced hyperextensions of the elbow. Goalkeepers are the players most often suffering from hyperextension trauma to the elbow in European team handball. They may complain of radiating pain or numbness in the ulnar aspect of the forearm in addition to local pain in the elbow region. To detect any injury to the ulnar nerve that could explain the symptoms, we performed a neurological and neurophysiological study in goalkeepers with elbow pain. Nine goalkeepers, with a total of 15 'handball goalie's elbow', were included in this study. Neurological examination revealed a probable ulnar nerve lesion in one player. Neurophysiological and electromyographic examinations (10 examinations) were, however, normal in all players. Handball goalkeepers with elbow problems may suffer from symptoms suggestive of ulnar nerve affection, but serious or permanent injury to the ulnar nerve with wasting or paresis is unusual.

Cerebral nitric oxide concentration and microcirculation during hypercapnia, hypoxia, and high intracranial pressure in pigs.

Intracerebral nitric oxide (NO) concentration was measured to establish the technique and to investigate the response of the NO concentration to CO(2)variations, hypoxia, and reduced cerebral perfusion pressure. An intracerebral nitric oxide sensor was used in 10 pigs. Cerebral microcirculation was measured by laser Doppler flowmetry. Five pigs received 40 mg/kg nitro-1-arginine methyl ester (L-NAME). Baseline NO concentration was 246 +/- 42 nM. Hypercapnia increased cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05). Hypoxia decreased NO concentration (P< 0.05). During high intracranial pressure, cerebral microcirculation decreased (P< 0.05) before the NO concentration decreased (P< 0.05), and after normalisation of the intracranial pressure the NO concentration increased, but more slowly than the cerebral microcirculation. L-NAME caused a decrease in cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05) to a new steady state, and L-NAME attenuated the changes in NO concentration after hypoxia (P< 0.05) and high intracranial pressure (P< 0.05). In conclusion, the electrochemical sensor appears to reliably detect changes in localised intracerebral NO concentration and seems to be a promising tool for direct measurement of this chemically unstable substance.

[Scandinavian guidelines for management of minimal, mild and moderate head injuries]. / Skandinaviske retningslinjer for håndtering av minimale, lette og moderate hodeskader.

The Scandinavian Neurotrauma Committee (SNC) was initiated by the Scandinavian Neurosurgical Society to develop evidence-based guidelines for improved care of neurotrauma patients. A MEDLINE search identified 475 papers dealing with the management of minimal, mild and moderate head injuries. Fourty-two studies presenting Class II evidence on the initial management of such injuries were reviewed and management guidelines were developed. Implementation of the Head Injury Severity Scale is advocated. Patients with minimal injuries (no loss of consciousness (LOC), Glasgow Coma Scale (GCS) score 15) can be safely discharged. Routine early CT scan is recommended in cases with mild injuries (history of LOC, GCS 14-15) and patients with normal scans may be discharged. CT scan and admission is mandatory in moderate injuries (GCS < or = 13). All patients harbouring additional risk factors should be scanned and admitted. A flow chart for clinical decision making and a Head Injury Instruction card are introduced.

Effects of hypoxia and reoxygenation with 21% and 100%-oxygen on cerebral nitric oxide concentration and microcirculation in newborn piglets.

Bioelectric sensors for continuous registration of nitric oxide (NO) concentrations in tissues provide a new tool for invasive measurement of this gaseous molecule. This study sought to validate cerebral NO measurements using an amperiometric sensor. A series of experiments in 1- to 3-day-old piglets was carried out to study the response of NO and microcirculation during hypoxia (F(i)O(2) 0.06) and reoxygenation with 100% and 21% oxygen. Two-channel laser Doppler flowmetry was performed in the forebrain cortex. Significant decreases of NO levels were observed immediately after induction of hypoxemia (p < 0.05). During reoxygenation with 21 or 100% O(2) for 30 min, NO increased significantly compared to the values at the end of hypoxia (p < 0.05). The increase of NO levels in the 100% oxygen group was greater than the increase in the 21% oxygen group (p < 0. 05). There were no significant differences between the two groups during the following 3.5 h of observation. A significant increase in CBF was found in the first 2 min of hypoxia (p < 0.05), it then continued to fall to values significantly lower than baseline values at the end of hypoxemia (p < 0.05). During reoxygenation CBF normalised and there were consistent but no significant differences between the two reoxygenation groups. We conclude that NO concentration decreased during the course of hypoxia. Hypoxia-induced cerebral hyperaemia occurred in spite of significantly lower NO concentrations. Reoxygenation with 21 or 100% O(2) restored CBF in both groups similarly, although values were higher after reoxygenation with 100% O(2) compared to air. In fact, reoxygenation with 100% O(2) led to supranormal levels of NO by contrast to 21% O(2).

Colloidal blood volume expansion during high intracranial pressure.

This study tested the hypothesis that colloidal blood volume expansion could improve the cerebral circulation during high intracranial pressure. We studied cerebrovascular haemodynamic variables during high intracranial pressure with and without colloidal blood volume expansion in 12 pigs, whereas five pigs served as controls with intracranial pressure increase twice without colloidal blood volume expansion. Cerebral blood flow was measured with ultrasonic flowmetry on the internal carotid artery, and cerebral microcirculation with laser Doppler flowmetry. High intracranial pressure was induced by infusion of artificial cerebrospinal fluid into the cisterna magna. Blood volume expansion was obtained by infusion of albumin, 1 gram/kg. Albumin infusion caused increases in internal carotid artery blood flow (P < 0.05) and cerebral perfusion pressure (P < 0.005), while cerebral microcirculation and cerebrovascular resistance was unchanged. High intracranial pressure albumin infusion caused internal carotid artery blood flow (P < 0.05) and cerebral perfusion pressure (P < 0.001) to increase compared to high intracranial pressure without albumin infusion, while cerebrovascular resistance was unchanged. Cerebral micro-circulation tended to increase, but this was not statistically significant (P = 0.07). Augmentation of the intravascular blood volume during high intracranial pressure increased the arterial inflow to the brain and possibly the cerebral microcirculation by increasing the cerebral perfusion pressure. Our results tend to support that the effect of colloidal blood volume expansion is beneficial for the cerebral circulation during high intracranial pressure.

Cerebrovascular effects of high intracranial pressure after moderate hemorrhage.

Patients with head injuries often develop increased intracranial pressure after hemorrhage. The authors studied the effect of moderate hemorrhage followed by elevated intracranial pressure on cerebrovascular variables. Cerebral blood flow in 13 pigs was measured with laser Doppler flowmetry, and cerebral venous blood gases were taken from the sagittal sinus. High intracranial pressure (80% of mean arterial pressure) was induced by infusion of artificial cerebrospinal fluid into the cisterna magna, and blood pressure was reduced by bleeding to a mean of 78% of the prebleeding values in eight pigs. Five pigs served as secondary controls. High intracranial pressure before hemorrhage caused a decrease in cerebral blood flow to 34% of the baseline values, a decrease in sagittal sinus oxygen saturation to 46%, and a decrease in cerebral perfusion pressure to 36%, but did not change cerebrovascular resistance. High intracranial pressure after hemorrhage decreased cerebral blood flow to 14% of baseline values. Sagittal sinus oxygen saturation decreased to 22%, cerebral perfusion pressure decreased to 30%, and the cerebrovascular resistance increased by 355%. The moderate hypotension after hemorrhage caused a considerable enhancement of the effects of high intracranial pressure on cerebral hemodynamics.

Effect of cerebral ischaemia on the cerebrovascular and cardiovascular response to haemorrhage.

Reports studying the combination of low blood pressure and cerebral ischaemia are few, and it remains to be determined how cerebral circulatory insufficiency modifies the cerebral perfusion and the central haemodynamic response to blood loss. We hypothesised that occlusion of arteries to the brain modifies the cerebrovascular and cardiovascular responses to blood loss. Continuous measurements of the cerebral microcirculation with laser Doppler microprobes in the cerebral cortex were performed in anaesthetised pigs during cerebral ischaemia and haemorrhagic hypotension. The response to rapid bleeding (25% of the blood volume) was recorded during normal conditions and during cerebral ischaemia induced by bilateral occlusion of the common carotid arteries. During normal conditions haemorrhage caused insignificant decreases in cerebral microcirculation. Haemorrhage during bilateral carotid artery occlusion, however, caused significantly greater changes in cerebral microcirculation and a greater posthaemorrhagic increase in cerebrovascular resistance shortly after the blood loss. Haemorrhage during bilateral carotid artery occlusion also caused greater reductions in cardiac output and arterial pressure than similar blood loss caused during normal conditions. This study showed a disproportionate decrease in cerebral blood flow with haemorrhage during bilateral carotid occlusion, caused by an immediate increase in cerebrovascular resistance. The results suggest that even a moderate blood loss in patients with impaired cerebral circulation could be dangerous, because normal compensatory mechanisms to haemorrhage are impaired.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis.

OBJECT: The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. METHODS: The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-L-arginine methyl ester (L-NAME) and in nine control animals. The L-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the L-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). CONCLUSIONS: These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

Effect of alpha-adrenergic blockade on the cerebrovascular response to increased intracranial pressure after hemorrhage.

OBJECT: In this study the authors tested the hypothesis that hemorrhagic hypotension and high intracranial pressure induce an increase in cerebrovascular resistance that is caused by sympathetic compensatory mechanisms and can be modified by alpha-adrenergic blockade. METHODS: Continuous measurements of cerebral blood flow were obtained using laser Doppler microprobes placed in the cerebral cortex in anesthetized pigs during induced hemorrhagic hypotension and high cerebrospinal fluid pressure. Eight pigs received 2 mg/kg phentolamine in 10 ml saline, and 13 pigs served as control animals. During high intracranial pressure occurring after blood loss, cerebral perfusion pressure (CPP) (p < 0.01) and cerebral blood flow (p < 0.01) decreased in both groups. Cerebrovascular resistance increased (p < 0.05) in the control group and decreased (p < 0.005) in the phentolamine-treated group. The cerebrovascular resistance was significantly lower in the phentolamine-treated group (p < 0.05) than in the control group. Cerebrovascular resistance increased at lower CPPs in the control group (linear correlation, r = 0.39, p < 0.01) and decreased with decreasing CPP in the phentolamine-treated group (linear correlation, r = 0.76, p < 0.001). CONCLUSIONS: This study shows that the deleterious effects on cerebral hemodynamics induced by blood loss in combination with high intracranial pressure are inhibited by alpha-adrenergic blockade. This suggests that these responses are caused by alpha-adrenergically mediated cerebral vasoconstriction.

Effect of hemorrhage on cerebral microcirculation during normal and high cerebrospinal fluid pressure in pigs.

Studies on cerebral blood flow during hypotension and high intracranial pressure are scarce. Accordingly, this study examines the effects of increased cerebrospinal fluid (CSF) pressure on the cerebral circulatory response to hemorrhage. Measurements of cerebral microcirculation with laser Doppler flowmetry was performed in 12 pentobarbital-anesthetized pigs during hemorrhage, with and without high CSF pressure. Arterial and CSF pressures were monitored. Laser Doppler microprobes were positioned on the brain surface and in the gray and white matter. High CSF pressure (80% of mean arterial pressure) was induced by infusion of artificial CSF into the cisterna magna in eight pigs, whereas four animals served as controls. The response to rapid arterial bleeding at normal and high CSF pressure was recorded. When CSF pressure was normal, bleeding of 15% and 25% of the total blood volume caused a drop of cerebral perfusion pressure to 73 and 71 mmHg, respectively, causing a decrease in the laser Doppler signal to 90+/-8% of the baseline value. During high CSF pressure, the cerebral perfusion pressure was 23 mmHg and the laser Doppler signal was 52+/-29% of baseline. Bleeding of 15% of blood volume reduced the laser Doppler signal to 0 (equal to postmortem values) in three pigs, and bleeding of 25% of the blood volume reduced the laser Doppler signal to 0 in seven of eight pigs. Consequently, a blood loss that is of minor importance for the cerebral microcirculation in the normal state may be deleterious to the circulation when combined with high CSF pressure.

Local variations in the cerebral microcirculatory response to hypercapnia and haemorrhage.

This study evaluates local variations of the cerebral vasomotor responses to hypercapnia and haemorrhagic hypotension in a pig model. Four laser Doppler flow probes were used in each pig. There was considerable variation in laser Doppler signals between the four probes in baseline recordings. The increases in flow after CO2 administration in 7 pigs had a mean coefficient of variation of 0.43 +/- 0.31, and the flow changes after blood loss in another 7 pigs had a mean coefficient of variation of 0.45 +/- 0.34. The range of flow changes within each animal was large; the probe with the highest CO2 response showed on the average a 273% +/- 157% larger CO2 response than the probe with the lowest CO2 response. Correspondingly, the probe with the best preserved blood flow after blood loss had on the average a flow value of 93% +/- 12% of the baseline value, while the probe that changed most with haemorrhage had a flow value of 44% +/- 24% of the baseline value. Single laser Doppler recordings have been used for the monitoring of cerebral blood flow in neurosurgical critical care, but our results suggest that a single laser Doppler flow probe is not an adequate method to monitor vasoreactivity in neurosurgical patients because flow signals from one probe may be unrepresentative for other sites in the brain.

Cardiovascular response to blood loss during high intracranial pressure.

The authors hypothesized that the combination of hemorrhage and increased intracranial pressure (ICP) has deleterious effects on cardiovascular function. The effect of blood loss during normal and increased ICP was studied in eight pigs. The mean arterial pressure (MAP), pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, and cerebrospinal fluid (CSF) pressure were measured. The regional tissue blood flow was determined with radioactive microspheres labeled with four different nuclides. High ICP (80% of MAP) was induced by infusion of artificial CSF into the cisterna magna. The response to rapid arterial bleeding of 25% of blood volume was measured. The decrease in blood flow to the intestine, skeletal muscle, and the kidneys after blood loss was significantly greater during high ICP. The decrease in blood flow to the spleen and pancreas tended to be greater during high ICP, whereas the changes in blood flow to the liver, adrenal glands, and heart muscle showed no such tendency. The fall in cardiac output and heart stroke volume after blood loss were more pronounced when the ICP was high, and the increase in systemic vascular resistance was considerably greater. These observations suggest that during high ICP the physiological protective mechanisms against blood loss are impaired in the systemic circulation, and a loss of 25% of the blood volume, normally well compensated for, may induce a state of shock.

Cerebral blood flow measured with intracerebral laser-Dopplerflow probes and radioactive microspheres.

We have measured cerebral blood flow with intracerebral laser-Doppler microprobes in pentobarbital-anesthetized pigs. We compared the results with measurements from laser-Doppler probes placed on the surface of the brain and with blood flow estimation by the radioactive microsphere method. The cerebral blood flow was varied by alterations in inspired carbon dioxide, hemorrhagic hypotension, and high cerebrospinal fluid pressure. The intracerebral probes and the surface probes showed parallel responses to variations in cerebral blood flow. The correlation was closest between surface probes and the intracerebral probes measuring from the cerebral cortex (r = 0.46; P < 0.005). The r value between laser-Doppler flowmetry and radioactive microspheres was 0.41 (P < 0.0005) for all measurements. The correlation to microspheres was best for the probes located 3 or 10 mm into the brain and poorest for the surface probe. In conclusion, intracerebral laser-Doppler flow measurements reflect changes in blood flow, and the technique appears useful for continuous estimates of cerebral blood flow.

Rhythmical fluctuations of the intracerebral microcirculation studied in pigs.

Rhythmic variations in blood flow have been observed in various vascular beds, including brain. We have characterized fluctuations of the microcirculation in different locations in the brain, and studied the response to changes in arterial carbon dioxide tension, arterial pressure, and cerebrospinal fluid pressure. Laser Doppler flowmetry was performed in 20 pentobarbital-anesthetized pigs. Flow probes were positioned on the brain surface and 3, 10, and 20 mm into the cerebral tissue. The protocol included carbon dioxide breath- ing, hemorrhagic hypotension, and infusion into the cisterna magna. Twenty-five periods of low-frequency oscillations (4.5/min) were found in 10 pigs with superimposed spindle-shaped rhythmic variations (0.5/min) of the amplitude in 7. There were no rhythmic changes in arterial pressure or intracranial pressure. Rhythmic activity was most often seen in the probe positioned 20 mm into the brain and was often seen in several probes at the same time. Animals with rhythmic oscillations before interventions had lower cerebral perfusion pressure and arterial pressure, lower heart rate, and higher laser Doppler signal than the others. Blood loss often initiatied oscillations. High intracranial pressure tended to abolish preexisting oscillations. Hypercapnia always abolished preexisting oscillations. Oscillations were more frequent if the cerebral perfusion pressure was in the low range of cerebral autoregulation, occurred more often in the cerebral locations with relatively high local flow, were most likely to be localized, and therefore probably caused by local metabolic or myogenic variations.