Acute headache at emergency department: reversible cerebral vasoconstriction syndrome complicated by subarachnoid haemorrhage and cerebral infarction.

Introduction. Reversible cerebral vasoconstriction syndrome is becoming widely accepted as a rare cause of both ischemic and haemorrhagic stroke and should be evocated in case of thunderclap headaches associated with stroke. We present the case of a patient with ischemic stroke associated with cortical subarachnoid haemorrhage (cSAH) and reversible diffuse arteries narrowing, leading to the diagnosis of reversible vasoconstriction syndrome. Case Report. A 48-year-old woman came to the emergency department because of an unusual thunderclap headache. The computed tomography of the brain completed by CT-angiography was unremarkable. Eleven days later, she was readmitted because of a left hemianopsia. One day after her admission, she developed a sudden left hemiparesis. The brain MRI showed ischemic lesions in the right frontal and occipital lobe and diffuse cSAH. The angiography showed vasoconstriction of the right anterior cerebral artery and stenosis of both middle cerebral arteries. Nimodipine treatment was initiated and vasoconstriction completely regressed on day 16 after the first headache. Conclusion. Our case shows a severe reversible cerebral vasoconstriction syndrome where both haemorrhagic and ischemic complications were present at the same time. The history we reported shows that reversible cerebral vasoconstriction syndrome is still underrecognized, in particular in general emergency departments.

[Interaction brain-lungs]. / Interaction cerveau-poumon.

The brain and the lungs interact early and rapidly when hit by a disease process. Often well tolerated by the healthy brain, an impaired respiratory function may deteriorate further a "sick" brain. Hypoxemia is a prognostic factor in the brain-injured patients. At the opposite, an acute brain damage early impacts the lung function. Local brain inflammation spreads rapidly to the lung. It initiates an immunological process weakening the lungs and increasing its susceptibility to infection and mechanical ventilation. Sometimes this process is preceded by a swelling lesion, known as neurogenic pulmonary oedema, resulting from an sympathetic overstimulation which usually follows an intense and brutal surge of intracranial pressure. The management of brain-injured patients has to be directed toward the protection of both the brain and lung. Neuronal preservation is crucial, because of the lack of regenerative potential in the brain, unlike the lung. A compromise must be obtained between the cerebral and pulmonary treatments although they may conflict in some situations.

[Superior vena cava syndrome: cause of secondary raise of intracranial pressure after traumatic brain injury]. / Syndrome cave supérieur: une cause secondaire d'élévation de la pression intracrânienne après traumatisme crânien grave.

A 41-year-old male is admitted for cranial trauma, having fallen from his own height. His state of extreme agitation imposes sedation, intubation and mechanical ventilation. A CT-scan reveals acute right hemispheric subdural haematoma, with discrete midline shift, and diffuse cerebral oedema. ICP-monitoring reveals severely increased intracranial pressure, which is responsive to routine medical neuroprotective treatment. Ten days after admission, sedation and neuroprotective treatment is gradually withdrawn. At the end of the second week, a secondary ascent in ICP is observed. The presence of a right subclavian central venous line, in combination with the strong inflammatory response and septic state of the patient, has caused bilateral thrombosis of subclavian and internal jugular veins. This superior vena cava syndrome (SVCS) impedes cerebral venous drainage, thus raising ICP. Within a few days of anticoagulant therapy, SVCS resolved. Impeded cerebral venous drainage is often forgotten or ignored as a cause of secondary elevated ICP. In face of persisting or recurring raised ICP and cerebral oedema, or apparition of communicant hydrocephalus, cerebral venous drainage should be investigated.

[Sedation and analgesia for the brain-injured patient]. / La sédation-analgésie du patient cérébrolésé.

Sedation-analgesia occupies an essential place in the specific therapeutic arsenal of the brain-injured patients. The maintenance of the perfusion of the brain, its relaxation and its protection are the fundamental objectives whose finality is to avoid the extension of the lesions and to preserve the neuronal capital. Sedation is instituted when patients are severely agitated or present a deterioration of their state of consciousness (GCS< or =8). Under cover of mechanical ventilation, sedation is the first line treatment of intracranial hypertension, a common pathway of various acute brain diseases of traumatic, vascular or other origin. The use of the combination of hypnotic and opioids is the rule. The combined action of these two classes reinforces and improves their sedative effects. Midazolam is the 2 benzodiazepine of reference. Propofol is more and more frequently added to the combination of hypnotic and opioids. The "propofol infusion syndrome" is a severe limitation to its long term administration in particular among patients presenting a severe septic or inflammatory state. Propofol will be imperatively stopped in the event of metabolic acidosis, rhabdomyolysis, acute renal insufficiency, hyperkaliemia or increase in the blood triglyceride levels. The use of thiopental is restricted to the most severe cases. Its use as a monotherapy at high doses is abandoned to the profit of a co-administration with midazolam or even with the combination of midazolam and propofol. Thiopental overdose is very frequent in the event of associated hypothermia. Etomidate does not have its place apart from induction in fast sequence. The neuro-protective effects of ketamine require to be demonstrated in man before being recommended routinely. Withdrawal of sedation can be responsible for a state of agitation which can be controlled by neuroleptics.

[Endovascular treatment of vasospasm following subarachnoid aneurysmal haemorrhage]. / Traitements endovasculaires du vasospasme de l'hémorragie méningée anévrysmale.

An endovascular treatment of vasospasm following a subarachnoid aneurysmal haemorrhage is to be implemented if the patient presents clinical or biological symptoms arguing for brain ischemia in conjunction with increased Doppler velocities despite well controlled systemic haemodynamic. Treatment might be either pharmacological or haemodynamic. Calcium and phosphodiesterase inhibitors can be administered. The former could also provide a neuroprotective effect as compared to the latter. In Europe, nimodipine is widely used whereas nicardipine and verapamil are the major molecules administered in North America where iv nimodipine is not FDA approved. Papaverine is less used nowadays because of its short duration of action and of the risk of aggravation of raised intracranial pressure. Balloon angioplasty has a long lasting effect but can be applied only to proximal spasm. Complications of its use are rare but life threatening. In some cases, both the pharmacological approach and the mechanical approach are used in combination.

[On the difficulty of Traumatic brain injured patients end-of-life decisions]. / Traumatisés crâniens graves: jusqu'où aller?

Traumatic brain injury occurs abruptly, involves multiple specialized teams, solicits the health care system in its emergency dimension and engages the well being of the patient and his relatives for a life time period. Clinicians are faced with issues of uppermost importance: medical issues such as predicting long term neurological outcome of the comatose patient, ethical issues because of the influence of intensive care on the long term survival of patients in vegetative and minimally conscious state, legal issues as the consequence of the current law which has set a new concept of proportionality of care, social issues as the result of the very high cost of these pathologies. This review will focus on the brain explorations that are required such as CT scan, evoked potentials, electroencephalography, magnetic resonance imaging and magnetic resonance spectroscopy to provide to the clinician a multimodal assessment of the brain state to predict outcome of coma. Such assessment is mandatory to answer the crucial question of proportionality of care in these patients. However, these techniques need further validation on large series of patients before being useful on clinical practice.

Massive stroke in a patient with pituitary apoplexy, cervical carotid artery stenosis and hypotension.

We report a case of massive cerebral infarct in the early stage of pituitary apoplexy. The case is unique because the stroke was delayed and occurred only after the patient developed severe arterial hypotension superimposed on a tandem internal carotid artery stenosis by both the sellar mass on the siphon and an unknown homolateral atheromatous cervical lesion. Illustrated with MRI and specifically by diffusion-weighted imaging, this case reinforces the idea that a low apparent diffusion coefficient in a non-enhancing sellar mass may indicate the presence of pituitary apoplexy and help in the early adequate management of such patients.

The relationship of intracranial pressure Lundberg waves to electroencephalograph fluctuations in patients with severe head trauma.

Lundberg (or B) waves, defined as repetitive changes in intracranial pressure (ICP) occurring at frequencies of 0.5 to 2 waves/min, have been attributed to cerebral blood flow fluctuations induced by central nervous system pace-makers or cerebral pressure autoregulation. We prospectively recorded and digitalized at a frequency rate of 10 Hz (AcqKnowledge software) the following parameters in 6 brain injured patients: mean arterial pressure, heart rate, ICP, mean flow velocity of the middle cerebral artery (MFVMCA) (transcranial Doppler WAKI) and left and right spectral edge frequency (SEFl, SEFr) of continuous electroencephalogram (EEG) recordings (Philips technologies). All patients were sedated using a combination of sufentanil and midazolam and mechanically ventilated. Cerebral electrical activity (oscillations of SEF at a mean frequency of 26+/-9 mHz) and MFVMCA fluctuations were found strongly correlated with the intracranial Lundberg B waves (mean frequency 23+/-7 mHz). These result support the existence of a neuropacemaker at the origin of the Lundberg B waves. The change in cerebral electrical activity, resulting from cerebral pacemakers, could increase cerebral metabolic rate of oxygen (CMRO2) and thus lead to an increase in cerebral blood flow and secondarily of ICP through a change in cerebral blood volume.

A computed tomographic scan assessment of endotracheal suctioning-induced bronchoconstriction in ventilated sheep.

This study was directed at assessing changes in bronchial cross-sectional surface areas (BCSA) and in respiratory resistance induced by endotracheal suctioning in nine anesthetized sheep. Cardiorespiratory parameters (Swan-Ganz catheter), respiratory resistance (inspiratory occlusion technique), BCSA, and lung aeration (computed tomography) were studied at baseline, during endotracheal suctioning, and after 20 consecutive hyperinflations. Measurements performed initially at an inspired oxygen fraction (FI(O(2))) of 0.3 were repeated at an FI(O(2)) of 1.0. At an FI(O(2)) of 0.3, endotracheal suctioning resulted in atelectasis, a reduction in BCSA of 29 +/- 23% (mean +/- SD), a decrease in arterial oxygen saturation from 95 +/- 3% to 87 +/- 12% (p = 0.02), an increase in venous admixture from 19 +/- 10% to 31 +/- 19% (p = 0. 006), and an increase in lung tissue resistance (DR(rs)) (p = 0. 0003). At an FI(O(2)) of 1.0, despite an extension of atelectasis and an increase in pulmonary shunt from 19 +/- 5% to 36 +/- 2% (p < 0.0001), arterial O(2) desaturation was prevented and BCSA decreased by only 7 +/- 32%. A recruitment maneuver after endotracheal suctioning entirely reversed the suctioning-induced increase in DR(rs) and atelectasis. In three lidocaine-pretreated sheep, the endotracheal suctioning-induced reduction of BCSA was entirely prevented. These data suggest that the endotracheal suctioning-induced decrease in BCSA is related to atelectasis and bronchoconstriction. Both effects can be reversed by hyperoxygenation maneuver before suctioning in combination with recruitment maneuver after suctioning.

Intra-operative direct electrical stimulations of the central nervous system: the Salpêtrière experience with 60 patients.

Indications of surgical treatment for lesions in the central nervous system depend on the risk of a definitive neurological deficit, related to the benefit of resection. Detection of eloquent areas is then necessary because of major individual variability. Neuro-imaging functional techniques are in development and are beginning to be efficient for cortical sensorymotor mapping, but still lack sensitivity and specificity for language mapping, and remain unable to give real-time data during surgery and to perform sub-cortical mapping. The more precise and reliable method of functional mapping is represented by the intra-operative direct electrical stimulations (DES), which allow identification and preservation of essential pathways for motricity, sensibility and language, at each level of the central nervous system (cortico-subcortical). We report our experience of DES in the surgery of tumours and vascular malformations located in supra-tentorial brain eloquent areas, with a consecutive series of 60 patients operated on under general or local anaesthesia, from November 1996 until May 1999 in our department at La Salpêtrière Hospital. Presenting symptoms in the 60 subjects (39 males, 21 females, mean age: 45 years) were seizures in 37 cases with normal clinical examination, and mild neurological deficit in 29 cases. MRI showed 60 supra-tentorial brain lesions: 30 precentral, 12 postcentral, 14 perisylvian in the dominant hemisphere, 4 deep-seated. All subjects underwent surgical resection using DES, with supratentorial cortico-subcortical mapping under general anaesthesia for motor areas detection in 43 cases and under local anaesthesia for sensori-motor and/or language tasks in 17 cases. The final histological diagnosis was 44 gliomas (31 low-grade and 13 high-grade), 9 metastasis, 3 cavernomas, 4 arteriovenous malformations (AVM). Resection was total or subtotal in 52 cases (87%) and partial in 8 cases (13%). 29 patients had no post-operative deficit, while the other 31 patients were impaired post-operatively, with in all cases, except 3, a complete recovery delayed for 15 days to 3 months (overall morbidity: 5%). The median follow up was 14 months. Intra-operative direct electrical stimulations of the central nervous system constitute a reliable, precise and safe method, allowing the realization of a functional mapping useful for all operations of lesions located in eloquent areas. This technique allows a minimization of definitive post-operative neurological deficit, and concurrently an improvement in the quality of resection.

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose-response study.

BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (QVA/QT), and a dose-dependent increase in PaO2/FiO2 (P

Dose-response curves of inhaled nitric oxide with and without intravenous almitrine in nitric oxide-responding patients with acute respiratory distress syndrome.

BACKGROUND: Inhaled nitric oxide, a selective pulmonary vasodilator, in combination with intravenous almitrine, a selective pulmonary vasoconstrictor, markedly improves arterial oxygenation in 50-60% of patients with acute lung injury. The goal of this study was to assess dose response of inhaled nitric oxide with and without almitrine in patients with acute respiratory distress syndrome responding to nitric oxide. METHODS: Six critically ill patients (aged 44 +/- 7 yr) were studied during early stage of their acute respiratory failure (Murray score: 2.6 +/- 0.1). All responded to 15 parts per million (ppm) of inhaled nitric oxide by an increase in Pao2 of at least 40 mmHg at FIo2 1. Hemodynamic and respiratory parameters were recorded continuously from pulmonary artery and systemic catheters. Inspiratory, expiratory, and mean intratracheal nitric oxide concentrations were monitored continuously using a fast response time chemiluminescence apparatus (NOX 4000, Sérès, Aix-en-provence, France). On day 1, 6 inspiratory concentrations of nitric oxide were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, and 45 ppm to determine the dose response of inhaled nitric oxide on Pao2, pulmonary shunt, mean pulmonary artery pressure, and pulmonary vascular resistance index. On day 2, a continuous intravenous infusion of almitrine at a dose of 16 micrograms.kg-1.min-1 was administered and dose response to inhaled nitrix oxide was repeated according to the same protocol as during day 1. A constant FIo2 of 0.85 was used throughout the study. RESULTS: Nitric oxide induced a dose-dependent increase in Pao2 for inspiratory nitric oxide concentrations ranging between 0.15 and 1.5 ppm. Almitrine increased Pao2/FIo2 from 161 +/- 30 to 251 +/- 45 mmHg (P < 0.001) and pulmonary vascular resistance index from 455 +/- 185 to 527 +/- 176 dyn.s.cm-5.m2 (P < 0.05), and decreased pulmonary shunt (Qs/QT) from 35 +/- 2 to 33 +/- 3% (P < 0.001). During almitrine combined with nitric oxide, a dose-dependent increase in Pao2 was observed for inspiratory nitric oxide concentrations ranging between 0.15 and 1.5 ppm. Almitrine plus nitric oxide 1.5 ppm increased Pao2/FIo2 from 161 +/- 30 to 355 +/- 36 mmHg (P < 0.001), decreased Qs/QT from 35 +/- 2 to 24 +/- 2% (P < 0.001), pulmonary vascular resistance index from 455 +/- 185 to 385 +/- 138 dyn.s.cm-5.m2 (P < 0.05), and mean pulmonary artery pressure from 31 +/- 4 to 28 +/- 4 mmHg (P < 0.001). CONCLUSIONS: In 6 patients with early acute respiratory distress syndrome and highly responsive to inhaled nitrix oxide, the administration of intravenous almitrine at a concentration of 16 micrograms.kg-1.min-1 induced an additional increase in Pao2. Dose response of nitric oxide was not changed by the administration of almitrine and a plateau effect was observed at inspiratory nitric oxide concentrations of 1.5 ppm.