Increased incidence of Campylobacter jejuni-associated Guillain-Barré syndromes in the Greater Paris area.

The role of Campylobacter jejuni as the triggering agent of Guillain-Barré syndrome (GBS) has not been reassessed since the end of the 1990s in France. We report that the number of C. jejuni-related GBS cases increased continuously between 1996 and 2007 in the Paris region (mean annual increment: 7%, P = 0·007).

Tongue weakness is associated with respiratory failure in patients with severe Guillain-Barré syndrome.

OBJECTIVE: Swallowing impairment may worsen respiratory weakness and conduct to respiratory complications such as aspiration pneumonia in Guillain-Barré syndrome (GBS). We prospectively evaluate how tongue weakness could be associated to bulbar dysfunction and respiratory weakness in severe GBS patients. MEASUREMENTS AND MAIN RESULTS: Tongue strength, dysphagia and respiratory parameters were measured in 16 GBS patients at intensive care unit (ICU) admission and discharge and in seven controls. Tongue strength was decreased in the GBS patients compared with the controls. At admission, patients with dysphagia and those requiring mechanical ventilation (MV) had greater tongue weakness. All the patients with initial tongue strength <150 g required MV during ICU stay. Tongue strength correlated significantly with respiratory parameters. CONCLUSION: This study confirms the strong association between bulbar and respiratory dysfunction in GBS admitted to ICU. Tongue weakness may be present in GBS, especially during the phase of increasing paralysis, and resolves during the recovery phase. Tongue strength and indices of global and respiratory strength vary in parallel throughout the course of GBS. Further studies are needed to assess if, when used in combination with other respiratory tests, tongue strength measurement could contribute to identify patients at high risk for respiratory complications.

Measuring inspiratory muscle strength in neuromuscular disease: one test or two?

Inspiratory muscle strength monitoring is crucial in patients with neuromuscular disorders. The sniff nasal inspiratory pressure (SNIP) and maximal inspiratory pressure (P(I,max)) are usually measured. The present study investigated whether the test yielding the best value at baseline continued to yield the best value during follow-up. The present study included 25 patients with Duchenne muscular dystrophy (DMD) and 61 with myotonic muscular dystrophy (MMD). SNIP and P(I,max) were measured at baseline and then annually. At baseline, SNIP was lower than P(I,max) in 20 (80%) DMD patients and 32 (52%) MMD patients. During follow-up in DMD patients, changes in the best method always occurred from SNIP to P(I,max). In MMD patients, when SNIP was better than P(I,max) at baseline, SNIP was usually (88%) better during follow-up, whereas a better P(I,max) than SNIP at baseline was frequently (50%) followed by a shift to SNIP. Maximal inspiratory pressure may be sufficient for monitoring inspiratory muscle function in Duchenne muscular dystrophy adults. In myotonic muscular dystrophy, the marked variability in the test yielding the best value at baseline indicates a need for performance of both tests at baseline. However, when sniff nasal inspiratory pressure measurement yields the best value at baseline, using sniff nasal inspiratory pressure alone during follow-up may be appropriate.

Nocturnal mechanical ventilation for chronic hypoventilation in patients with neuromuscular and chest wall disorders.

BACKGROUND: Chronic alveolar hypoventilation is a common complication of many neuromuscular and chest wall disorders. Long-term nocturnal mechanical ventilation is increasingly used to treat it. OBJECTIVES: To examine the efficacy of nocturnal mechanical ventilation in relieving hypoventilation related symptoms and in prolonging survival in people with neuromuscular or chest wall disorders. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register, MEDLINE (from January 1966 to June 2006), and EMBASE (from January 1980 to June 2006) for randomised trials and contacted authors of trials and other experts in the field. SELECTION CRITERIA: We searched for quasi-randomised or randomised controlled trials of participants with neuromuscular or chest wall disorder-related stable chronic hypoventilation of all ages and all degrees of severity, receiving any type and any mode of nocturnal mechanical ventilation. The primary outcome measure was short-term and long-term reversal of hypoventilation related clinical symptoms and secondary outcomes were unplanned hospital admission, one year mortality, short-term and long-term reversal of daytime hypercapnia, improvement of lung function and sleep breathing disorders. DATA COLLECTION AND ANALYSIS: We identified eight randomised trials. MAIN RESULTS: The eight eligible trials included a total of 144 participants. The relative risk of 'no improvement of hypoventilation related clinical symptoms' in the short-term following nocturnal mechanical ventilation was available in only one trial with 10 participants and was not significant, 0.09 (95% confidence interval (CI) 0.01 to 1.31). The relative risk of 'no reversal of daytime hypercapnia' in the short-term following nocturnal ventilation was significant and favoured treatment, 0.37 (95% CI 0.20 to 0.65). The weighted mean difference of nocturnal mean oxygen saturation was 5.45% (95% CI 1.47 to 9.44) more improvement in participants treated with nocturnal mechanical ventilation. For most of the outcome measures there was no significant long-term difference between nocturnal mechanical ventilation and no ventilation. However, the estimated risk of death based on three studies was reduced following nocturnal ventilation, 0.62 (95% CI 0.42 to 0.91). There was considerable and significant heterogeneity between the trials possibly related to differences between the study populations. Most of the secondary outcomes were not assessed in the eligible trials. Data from two crossover trials suggested no evidence for a difference in reversal of daytime hypercapnia and sleep study parameters between volume-cycled and pressure-cycled ventilation. No data could be summarised for the comparisons between invasive and non-invasive mechanical ventilation or between intermittent positive pressure and negative pressure ventilation. AUTHORS' CONCLUSIONS: Current evidence about the therapeutic benefit of mechanical ventilation is weak, but consistent, suggesting alleviation of the symptoms of chronic hypoventilation in the short-term. In three small studies survival was prolonged mainly in participants with motor neuron diseases. With the exception of motor neuron disease, further larger randomised trials are needed to confirm long-term beneficial effects of nocturnal mechanical ventilation on quality of life, morbidity and mortality, to assess its cost-benefit ratio in neuromuscular and chest wall diseases and to compare the different types and modes of ventilation.

Intravenous immunoglobulin for Guillain-Barré syndrome.

BACKGROUND: Guillain-Barré syndrome is an acute, paralysing, inflammatory peripheral nerve disease. Intravenous immunoglobulin is beneficial in other autoimmune diseases. OBJECTIVES: We aimed to determine the efficacy of intravenous immunoglobulin for treating Guillain-Barré syndrome. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register (March 2005), MEDLINE (January 1966 to March 2005) and EMBASE (January 1980 to March 2005) using the terms 'Guillain-Barré syndrome' and 'acute polyradiculoneuritis'. SELECTION CRITERIA: We included all randomised and quasi-randomised trials. DATA COLLECTION AND ANALYSIS: Two authors independently selected papers, extracted data and assessed quality. MAIN RESULTS: Another Cochrane systematic review has shown that plasma exchange significantly hastens recovery. We found six randomised trials comparing intravenous immunoglobulin with plasma exchange. We undertook a meta-analysis of five trials involving 536, mostly adult participants who were unable to walk unaided and had been ill for less than two weeks. Our primary outcome measure was the change in a seven-grade disability scale four weeks after randomisation. The weighted mean difference of this measure was not statistically significant, being only -0.02 (95% confidence interval -0.25 to 0.20) of a disability grade more improvement in the intravenous immunoglobulin than the plasma exchange group. There were no statistically significant differences in other measures. One trial involving 249 participants compared plasma exchange followed by intravenous immunoglobulin with plasma exchange alone. Another involving 37 participants compared immunoabsorption followed by intravenous immunoglobulin with immunoabsorption alone. Neither revealed significant extra benefit from intravenous immunoglobulin. One study with 39 participants showed a trend towards more improvement with high-dose compared with low-dose intravenous immunoglobulin. Another trial with 51 children found no significant difference in outcome when the standard dose was given over two days rather than five days. Three studies including a total of 75 participants suggested that in children intravenous immunoglobulin significantly hastens recovery compared with supportive care. AUTHORS' CONCLUSIONS: In adults, there are no adequate comparisons with placebo. Randomised trials in severe disease show that intravenous immunoglobulin started within two weeks from onset hastens recovery as much as plasma exchange, which is known to be more effective than supportive care. Treatment with intravenous immunoglobulin is significantly more likely to be completed than plasma exchange. Giving intravenous immunoglobulin after plasma exchange did not confer significant extra benefit. In children, intravenous immunoglobulin probably hastens recovery compared with supportive care alone. More research is needed in mild disease and in treatment starting more than two weeks after onset of the condition. Dose-ranging studies are also needed.

[Campylobacter jejuni and cytomegalovirus (CMV) infections in patients with the Guillain-Barre syndrome]. / Infections à Campylobacter jejuni et à cytomégalovirus (CMV) associées au syndrome de Guillain-Barré (SGB).

Guillain-Barre syndrome (GBS) is a rare disease triggered by postinfectious mechanisms. The disease concerns all ages, and is widely distributed around the world. The principal risks are respiratory failure, especially during the initial phase of the disease, and persisting deficit at long term. Among the infectious known agents, Campylobacter jejuni and CMV represent more than 40% of GBS causes. The clinical presentation, and the long-term prognosis of GBS related to these two etiologies are different. The physiopathological mechanisms of the nervous attack are probably also different. There is no proof, at this time, that anti-infectious treatment can improve the prognosis. The treatment is based on the early use of immunomodulatory treatments like intravenous immunoglobulins or plasma exchanges.

[Long term domiciliary mechanical ventilation in patients with neuromuscular disease (indications, establishment and follow up)]. / Ventilation mécanique a domicile et au long cours des patients neuromusculaires (indication, mise en place et surveillance).

UNLABELLED: Neuromuscular diseases represent a heterogeneous group of pathologies which common feature is the development of a restrictive ventilatory failure. BACKGROUND: Respiratory insufficiency of neuromuscular origin manifests itself by functional symptoms that must be carefully searched for in the history, such as headaches, sleep disorders, or dyspnoea of effort, sometimes very mild, or in severe cases associated with orthopnoea. Follow up should be multi-disciplinary. On the respiratory level regular measurement of blood gases, vital capacity, maximum inspiratory and expiratory pressures as well as sleep studies, will detect the criteria for mechanical ventilation (hypercarbia > 45 mm Hg, nocturnal desaturation < 88%, vital capacity < 60%, PImax < 60 cm H2O). STATE OF THE ART: The establishment of mechanical ventilation is a major decision for patients with neuromuscular disease because of the important physical, psychological, social and sometimes financial consequences. The patients and their family must be instructed precisely in order to obtain the best possible observation and compliance. The establishment requires a stay in hospital of several days to optimise the choice of ventilator, its settings, and connections. The link with the organisation managing the domiciliary ventilation is fundamental in ensuring follow up after discharge from hospital. Techniques of cough assistance must be taught to each neuromuscular patient requiring mechanical ventilation. CONCLUSION: Ventilation of neuromuscular patients requires careful evaluation of the indications and rigorous follow up by a multidisciplinary team with wide experience of this type of disease.

Dantrolene--a new therapeutic approach to the neuroleptic malignant syndrome.

The Neuroleptic Malignant Syndrome (NMS) is a rare but severe affection (spontaneous mortality 30 to 50 per cent), associating fever, hypertonia with myolysis, and respiratory impairment. Its mechanism remains debatable: The origin of the hypertonia might be central (as phenothiazines and butyrophenones induce a blockade of dopaminergic receptors in the hypothalamus) or it might be muscular (with an impairment of the sarcoplasmic reticulum uptake of calcium in a genetically abnormal muscle, as is proven in malignant hyperthermia). Whatever the actual mechanism, the oral or intravenous administration of sodium dantrolene, a peripheral muscle relaxant agent which does not affect the neuromuscular transmission but prevents the calcium-dependent contraction of actin and myosine, has proved to be effective in three recent cases of NMS.

Matrix metalloproteinase-9 is increased and correlates with severity in Guillain-Barré syndrome.

OBJECTIVE: To study the expression and activity of matrix metalloproteinases (MMPs) MMP-2 (72-kd type IV collagenase, gelatinase A), MMP-3 (58-kd stromelysin-1), and MMP-9 (92-kd type IV collagenase, gelatinase B) and tissue inhibitors of MPs (TIMP) in patients with Guillain-Barre syndrome (GBS). BACKGROUND: MMPs are able to proteolysis of basement membranes and other matrix components, promoting transmigration of inflammatory cells from circulation to nerve tissue. METHODS: Twenty-five patients with GBS were analyzed according to the phase of the disease, i.e., progression, plateau, early recovery, and late recovery. Determinations of MMP-2, MMP-3, MMP-9, and TIMP-1 were performed using ELISA, zymography, and immunocytochemistry in circulation or peripheral nerve. RESULTS: MMP-9 plasma levels were increased in 67% of patients on admission and decreased from progression to late recovery (p < 0.002). During the course of GBS, MMP-9 was progressively balanced by its inhibitor TIMP-1, as assessed by the MMP-9/TIMP-1 ratio. MMP-9 and TIMP-1 plasma levels and the MMP-9/TIMP-1 ratio correlated positively with disability. MMP-2 expression was similar to controls. MMP-3 activity was not detected, and plasma levels were not different from those in controls. Positive MMP-9 immunolabeling was 51 +/- 11% of circulating lymphocytes. It was observed in some endothelial cells and mononuclear cells adherent to the endothelium and close to myelinated fibers. CONCLUSIONS: Circulating matrix metalloproteinases (MMP-9) correlates with disease severity in Guillain-Barré syndrome (GBS). MMP-9 likely represents an important molecule in the pathogenesis of GBS and therefore could represent an interesting therapeutic target.

MMP-9 correlates with electrophysiologic abnormalities in Guillain-Barré syndrome.

To investigate the role of MMP-9 in Guillain-Barré syndrome, the authors correlated electrophysiologic abnormalities and MMP-9 plasma levels in a series of 21 patients. MMP-9 plasma levels were higher in the demyelinating group than in the nondemyelinating group, and in patients with high CSF protein level. Increase of MMP-9 circulating levels correlated with the increase of F waves latencies, reduction of CMAP amplitude, and decrease of nerve conduction velocities. Circulating MMP-9 may contribute to the peripheral nerve dysfunction of demyelinating Guillain-Barré syndrome.

IFN-beta decreases adhesion and transmigration capacities of lymphocytes in Guillain-Barré syndrome.

The adhesion capacities, transmigration capacities, and integrin expression of lymphocytes from patients with Guillain-Barré syndrome incubated with interferon-beta were studied. Interferon-beta induced a dose-dependent inhibition of lymphocyte adhesion to recombinant vascular adhesion molecule-1 (p < 0.0001) and recombinant intercellular adhesion molecule-1 (rICAM-1) (p < 0.01) without modulation of very late activation molecule-4 and lymphocyte function-associated antigen-1 expressions and a dose-dependent decrease of lymphocyte transmigration across fibronectin (p < 0.0001). Inhibition of adhesion to rICAM-1 was similar after long (18 hours) or short (5 minutes) incubation time. These results support the potential therapeutic benefit of interferon-beta in Guillain-Barré syndrome.

Circulating tumor necrosis factor (TNF)-alpha and soluble TNF-alpha receptors in patients with Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is an inflammatory disorder that may implicate proinflammatory cytokines such as TNF-alpha in its pathogenesis. We determined serum levels of TNF-alpha and the specific antagonists sTNF-Rs p55 and p75 in 24 patients with GBS at days 1, 15 and 30 of hospitalization. Patients were in the progression phase of the disease at day 1, and in the recovery phase at day 30. They were classified as able to walk (stage A), confined to bed (B), or under assisted ventilation (C). All patients underwent plasma exchange within day 1-12. At day 1, TNF-alpha levels were elevated in 15/24 patients, and sTNF-Rs were elevated in 21/23. TNF-alpha levels had not decreased at day 15, and dropped at day 30 (p < 0.04), whereas sTNF-R p55 remained elevated at day 15 and day 30. The TNF-alpha/sTNF-Rs ratio, estimating active TNF-alpha unbound to sTNF-Rs, decreased from day 1 to day 30 (p < 0.05). A positive correlation was found between disease severity and sTNF-R serum levels (p < 0.01). In conclusion, elevated circulating sTNF-Rs assesses activation of the TNF-alpha system in almost all patients with GBS and correlates positively with disease severity. Drop of TNF-alpha contrasting with sustained elevation of sTNF-R p55 during recovery suggests that sTNF-R p55 may be important in the fading of the neural inflammatory effect of TNF-alpha in GBS.

Monocyte chemoattractant protein 1 and chemokine receptor CCR2 productions in Guillain-Barré syndrome and experimental autoimmune neuritis.

Infiltration of activated lymphocytes and monocytes is a key phenomenon in the pathogenesis of Guillain-Barré syndrome (GBS) and experimental autoimmune neuritis (EAN). To investigate the role of chemokines, we determined the blood and nerve tissue expression of monocyte chemoattractant protein 1 (MCP-1), a major chemoattractant of monocytes and activated lymphocytes, and its receptor CCR2 in GBS and EAN. MCP-1 circulating levels (ng/ml) in GBS were increased at the time of progression, peaked at the time of plateau and normalized with recovery. MCP-1 circulating levels were the highest in the most disabled patients. The number of circulating CCR2 positive cells was lower in patients with GBS than in healthy subjects (p<0.004). In GBS, MCP-1 expression was observed in epineurial and endoneurial vessels, on infiltrating cells, Schwann cells and in the endoneurial extracellular matrix. Some CCR2 positive cells were observed in nerve biopsies of GBS patients. In EAN, a slight positivity for MCP-1 was observed in the sciatic nerve. There was no circulating CCR2 positive cells. However, at the time of plateau, a conspicuous infiltration of CCR2 positive cells was observed in the sciatic nerve that was no longer observed at the time of recovery. These results suggest that MCP-1 and CCR2 may participate to the recruitment of circulating mononuclear cells in nerve tissue in EAN and GBS.

Inhibition of the adhesion step of leukodiapedesis: a critical event in the recovery of Guillain-Barré syndrome associated with accumulation of proteolytically active lymphocytes in blood.

Intraneural inflammation, that reflects emigration of immune cells from blood to nerve tissue, is a critical event in Guillain-Barré syndrome pathogenesis. To investigate the adhesion and transmigration phases of leukodiapedesis, we determined in a series of patients with GBS: (1) circulating levels of soluble forms of adhesion molecules (sICAM-1 and sVCAM-1); (2) attachment capacities of circulating lymphocytes to rICAM-1 and rVCAM-1; (3) fibronectin-penetrating capacities of circulating lymphocytes; and (4) lymphocyte intracellular concentrations of MMP-9 at the different phases of GBS and in healthy controls. Circulating levels of sVCAM-1 and sICAM-1 were above normal values at the time of progression, markedly increased at the time of plateau (sVCAM-1: P<0.03; sICAM-1: P<0.02), and tended to normalize during recovery. The percentage of cells with attachment capacities to rVCAM-1 and to rICAM-1 decreased from progression to recovery by 30 and 31%, respectively (P<0.02). The number of circulating lymphocytes with fibronectin penetrating capacities was lower than controls at the time of progression (P<0.01), then progressively increased to reach values higher than controls at the time of late recovery (P<0.02). Cellular concentrations of MMP-9 in circulating lymphocytes paralleled their fibronectin penetrating capacities. These results suggest early emigration of lymphocytes into nerve, followed by shedding of adhesion molecules from endothelium, and late decrease of lymphocyte adhesion capacities. Plateau and recovery are associated with accumulation in the vascular compartment of still proteolytically active lymphocytes that can no longer adhere to endothelial cells. Modulation of the adhesion step of leukodiapedesis may be crucially involved in the switch from progression to plateau of GBS.

Cost analysis of plasma-exchange therapy for the treatment of Guillain-Barré syndrome. French Cooperative Group on Plasma Exchange in Guillain-Barré Syndrome.

OBJECTIVE: To undertake a cost analysis of therapeutic strategies with plasma exchange (PE) for the treatment of patients with Guillain-Barré syndrome. DESIGN: A randomized clinical trial including 556 patients with Guillain-Barré syndrome. We demonstrated that in the group with mild disease (walking possible) two PEs were more effective than none in shortening the time to beginning motor recovery. In the groups with moderate disease (walking impossible) and or severe disease (mechanically ventilated patients) four sessions were more effective than two and no more effective than six in shortening the time to recovery of walking with assistance and for the recovery rate of full muscle strength within 1 year. Data on outcomes and costs was collected. Complete cost data were available on 546 from the 556 patients of the trial. Costs were estimated from the viewpoint of the healthcare system and computed over a 1-year period. Because the analysis of medical outcomes did not show any difference regarding mortality but only on intermediate short-term and long-term outcomes, we carried out a cost minimization analysis. RESULTS: In two groups a dominant strategy appeared, with greater efficacy and lower costs in the two-PE arm for the mild group: 21,353 euros vs. 38,753 euros and in the four-PE arm in the moderate group: 59,480 euros vs. 80,737 euros. In the severe group four PEs were as efficient and somewhat less expensive than six: 57,621 vs. 61,056 euros. CONCLUSION: The treatment of Guillain-Barré syndrome by PE at the onset of disease appears to have medical justification. The least expensive strategies are either more or equally efficient as more expensive strategies.

Membrane oxygenators for acute respiratory insufficiency. Clinical use in 11 patients.

Extracorporeal circulation with a membrane oxygenator (ECMO) was used in 11 patients with acute respiratory insufficiency who did not respond to conventional treatment. By pass was veno-arterial in every case, seven times with femoral artery return, three times with axillary artery return, and once with both femoral and axillary return. Five patients died on ECMO. Six patients were taken off ECMO and two of them are long-term survivors. In nine cases ECMO allowed short-term control of respiratory failure. The respective roles of oxygen supply from ECMO and the haemodynamic changes incurred by its use are discussed. Although use of ECMO for long periods seems less hazardous now, present results are restricted by the lack of therapy for the underlying pulmonary lesions.

Critical incidents related to invasive mechanical ventilation in the ICU: preliminary descriptive study.

OBJECTIVES: To establish a preliminary list of critical incidents (CIs) associated with mechanical ventilation and to describe a CI reporting method. DESIGN: A list of CIs was established based on a consensus among ICU caregivers. The list was compared to CIs collected prospectively during a predefined study period. SETTING: The clinical observations were conducted in two intensive care units. PATIENTS: All patients receiving mechanical ventilation were included. MEASUREMENTS AND RESULTS: The list of CIs included death and 62 other CI types categorized as immediately life-threatening, secondarily life-threatening, or non-life-threatening. The observational study identified 527 CIs in 137 patients. Virtually all non-life-threatening CIs were ascribed to failure to comply with safety rules or to equipment failure and 40% of life-threatening CIs to the course of the disease or to patient-related factors. The match between CI types on the list and CI types observed in the ICUs was excellent. CONCLUSIONS: Use of our reporting method to create a CI database in a multicenter study including ICUs with varying recruitment patterns may help to identify markers suitable for routine continuous use as part of a quality-assurance program.

Acute carbon monoxide intoxication and hyperbaric oxygen in pregnancy.

Modalities of oxygen therapy for pregnant women intoxicated with carbon monoxide (CO) are ill defined. Hyperbaric oxygen (HBO) is presumed to be hazardous to the pregnancy. On the other hand CO entails anoxic injuries in the mother and fetus. We have entered 44 pregnant women who sustained an acute carbon monoxide poisoning at home, into a prospective study in order to assess HBO tolerance. They were treated within 5.3 +/- 3.7 h (range: 1-12) of the intoxication with a combination of 2 h of HBO at a pressure of 2 atmospheres absolute (ATA) and 4 h of normobaric oxygen, irrespective of the clinical severity of the intoxication and of the age of pregnancy. Six patients were lost to obstetric follow-up. Only 2 patients sustained a spontaneous abortion: 1 within 12 h and 1 within 15 days of the intoxication. Thirty-four women gave birth to normal newborns. Finally 1 elected to undergo abortion for reasons unrelated to the intoxication and 1 gave birth to a baby with Down's syndrome. There is no evidence that HBO was involved with either abortion of our study. We conclude that HBO may be carried out in pregnant women acutely intoxicated with carbon monoxide.

Adult maltase acid deficiency myopathy: treatment with long-term home mechanical ventilation.

We report a study of an adult with a maltase acid deficiency myopathy. A restrictive respiratory syndrome due to respiratory muscle weakness is associated with paralysis of other muscular groups. In 1982 the patient presented with an alveolar hypoventilation, and mechanical ventilation was required after acute respiratory failure. The patient has received nocturnal mechanical ventilation by tracheostomy at home for 5 years. His clinical status gradually improved in parallel to amelioration of his respiratory condition. Functional respiratory tests improved: initial hypoxia-hypercapnia disappeared, vital capacity increased. The possible mechanisms underlying the improvement are discussed. Increase in pulmonary compliance is an argument to explain the functional improvement observed. Ventilatory response to carbon dioxide was abnormal whereas the ventilatory response to exercise and maxima minute ventilation test were normal. Results are consistent with a respiratory control impairment. The role of mechanical ventilation is difficult to assess in the improvement we observed.

Kinetics of elimination and acute consequences of cerebral air embolism.

The pathophysiology of arterial air embolism inducing brain injuries remains unclear. Previous experiments demonstrated the usefulness of computed tomography (CT) in the detection of air emboli in canine brain. This canine study investigates CT's ability to detect small air bubbles and to determine the kinetics of air elimination from cerebral arteries and its relationship with clinical, electroencephalographic (EEG), and histological manifestations. CT detects small air embolism, and intracerebral air volume strongly correlates with injected air dose (r2 = 0.86, p = 2 x 10(-3)). Air clearance time significantly depends on intracerebral air volume (r2 = 0.86, p = 0.04) and on the number of bubbles (r2 = 0.71, p = 0.03), whereas half-life of air elimination does not. No relationship was found between injected air dose, air clearance time, intracerebral volume of air, and clinical, EEG, and histological findings. The data indicate that CT accurately detects small air bubbles in the early course of cerebral air embolism, that air elimination from cerebral arteries follows a first-order compartment model, and that early CT findings do not correlate with clinical, EEG, and histological manifestations.