1/27. Correlation between jugular bulb oxygen saturation and partial pressure of brain tissue oxygen during CO2 and O2 reactivity tests in severely head-injured patients.PURPOSE: To correlate the jugular bulb oxygen saturation (SjvO2) and brain tissue oxygen pressure (PbtO2) during carbon dioxide (CO2) and oxygen (O2) reactivity tests in severely head-injured patients. methods AND RESULTS: In nine patients (7 men, 2 women, age: 26 /- 6.5 years, GCS of 6.5 /- 2.9), a polarographic microcatheter (Clark-type) was inserted into nonlesioned white matter (frontal lobe). PbtO2 and SjvO2 were monitored simultaneously and cerebral vasoreactivity to CO2 and O2 was tested on days three, five and seven after injury. Simultaneous measurements of vasoreactivity by transcranial Doppler (TCD) were undertaken. A total of twenty-one CO2 and O2 reactivity tests were performed. Critical values of PbtO2 (< 15 mm Hg) during induced hyperventilation could be observed four times in two patients. High PbtO2 values up to 80 mm Hg were observed during hyperoxygenation (FiO2 100%). CO2 vasoreactivity by means of PbtO2 was absent in four tests in which measurements by TCD showed intact responses. A stronger correlation between SjvO2 and PbtO2 during the O2 reactivity tests was observed (r = 0.6, p < 0.001), in comparison to values obtained during the CO2 reactivity tests (r = 0.33, p < 0.001). In addition, there was no statistically significant correlation (r = 0.22, p = 0.26) between CO2 reactivity values measured by TCD (4.5 /- 5.7%) and PbtO2 (3 /- 2.8%). CONCLUSIONS: Correlation between SjvO2 and PbtO2 during CO2 reactivity test is low, even if significant differences between normo- and hyperventilation values are present. In comparison to SjvO2, monitoring of PbtO2 might more accurately detect possible focal ischaemic events during rapidly induced hyperventilation in severely head-injured patients. The CO2 vasoreactivity by means of changes in Vm MCA seems to be higher in comparison to changes of PbtO2. These observations lead to the hypothesis that vasoreactivity measured by TCD overestimates the cerebrovascular response to CO2.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/27. Central hyperventilation related to administration of topiramate.Topiramate is a recently released antiepileptic agent used in the treatment of patients with refractory seizure disorders. In addition to its antiepileptogenic activities, it results in inhibition of carbonic anhydrase isoenzymes II and IV, which are present in the central nervous system. A 15-year-old female who presented with hyperpnea and primary respiratory alkalosis is reported. Other possible etiologies of the central hyperventilation syndrome were excluded. The problem resolved within 24 hours after discontinuing topiramate.- - - - - - - - - - ranking = 0.44011677357872keywords = central nervous system, nervous system (Clic here for more details about this article) |
3/27. Central neurogenic hyperventilation with primary cerebral lymphoma: a case report.We report a case of a bright, alert patient with central neurogenic hyperventilation (CNH) associated with cerebral malignant lymphoma. CNH is a syndrome comprising normal or elevated arterial oxygen tension, decreased arterial carbon dioxide tension, and respiratory alkalosis in the absence of cardiac or pulmonary disease that stimulates a compensatory hyperpnea. A-72-year-old man with recurrent central nervous system lymphoma presented with hyperpnea. showing a respiratory rate over 30 per minute. He was fully awake and conscious. Routine laboratory studies and chest X-ray were normal, but arterial blood gas examination on room air showed respiratory alkalosis, regardless of wakefulness or sleep. pulmonary infarction was denied by pulmonary flow scintigram. Rebreathing from a paper bag, intravenous administration of diazepam, and oxygen inhalation failed to alter the respiratory pattern. brain MRI demonstrated two mildly enhanced lesions within the left side of the medulla oblongata and right side of the pons. CNH is rare in patients with normal consciousness. It seems to be caused by brainstem injury that includes the respiratory center.- - - - - - - - - - ranking = 0.64011677357872keywords = central nervous system, brain, nervous system (Clic here for more details about this article) |
4/27. Chronic meningitis presenting with acute obstructive hydrocephalus.A previously healthy 24-year-old woman presented to the Emergency Department unresponsive with a glasgow coma scale score of 4 and evidence of brainstem herniation. She was intubated and hyperventilated. Computed axial tomography scan of the brain demonstrated four-chamber hydrocephalus. Continued hyperventilation and mannitol diuresis were sufficient to arrest the impending herniation while emergent ventriculostomy was arranged. The patient recovered without sequelae and ultimately received a diagnosis of chronic idiopathic meningitis. This case highlights a rarely diagnosed disorder that presented with an acutely life threatening condition.- - - - - - - - - - ranking = 0.4keywords = brain (Clic here for more details about this article) |
5/27. A case of adversive seizures induced by hyperventilation.We report a case of adversive seizures featuring neck rotation and conjugate deviation induced by the hyperventilation maneuver. At the age of 6 years the patient suffered from conjugate deviation to the left. She herself felt no symptoms other than oculomotor symptoms. hyperventilation induced an adversive seizure and ictal EEG showed sharp waves in the right frontal, central, and parietal areas. No brain image showed abnormal findings. Zonisamide completely attenuated her attacks. It is well known that hyperventilation induces absence seizures, and it has been reported that hyperventilation can induce complex partial seizures. However, no previous reports have described patients diagnosed as having adversive seizures with conjugate deviation induced by hyperventilation. We report the present case because, although its epileptogenesis is unknown, the patient is a rare case not only clinically but also electrophysiologically.- - - - - - - - - - ranking = 0.2keywords = brain (Clic here for more details about this article) |
6/27. Widespread reduction of regional cerebral blood flow during hyperventilation-induced EEG slowing ('buildup'). observation from subtraction of brain imaging with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime.To study the pathophysiological mechanisms of hyperventilation-induced EEG showing, i.e., the so-called 'buildup' phenomenon, changes in regional cerebral blood flow (rCBF) were investigated before and during the phenomenon in a 16-year-old woman with headache, thought to be of neurotic origin, by subtraction technique of brain images with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime (99mTc-HMPAO). The tracer uptake during buildup decreased by 31-42% as compared to baseline values at rest before buildup in all of the measured regions, reflecting a widespread reduction in rCBF. Gas analyses of arterial blood collected during buildup showed a decrease in PaCO2, and increases in PaO2 and pH with a slight decrease in blood pressure and an increase in pulse rate. These results directly demonstrate a close correlation between the hyperventilation-induced EEG and rCBF changes, suggesting that the buildup phenomenon results from cerebral ischemic change, presumably due to cerebral vasoconstriction caused by the PaCO2 decrease.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
7/27. Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injury.The authors measured regional cerebral 133xenon (133Xe) blood flow (rCBF), intraventricular pressure (IVP), cerebrospinal fluid (CSF) pH and lactate, systemic arterial blood pressure (SAP), and arterial blood gases during the acute phase in 23 comatose patients with severe head injuries. The IVP was kept below 45 mm Hg. The rCBF was measured repeatedly, and the response to induced hypertension and hyperventilation was tested. Most patients had reduced rCBF. No correlation was found between average CBF and clinical condition, and neither global nor regional ischemia contributed significantly to the reduced brain function. No correlation was found between CBF and IVP or CBF and cerebral perfusion pressure (CPP). The CSF lactate was elevated significantly in patients with brain-stem lesions, but not in patients with "pure" cortical lesiosn. The 133Xe clearance curves from areas of severe cortical lesions had very fast initial components called tissue peaks. The tissue peak areas correlated with areas of early veins in the angiograms, indicating a state of relative hyperemia, referred to as tissue-peak hyperemia. Tissue-peak hyperemia was found in all patients with cortical laceration or severe contusion but not in patients with brain-stem lesions without such cortical lesions. The peaks increased in number during clinical deterioration and disappeared during improvement. They could be provoked by induced hypertension and disappeared during hyperventilation. The changes in the tissue-peak areas appeared to be related to the clinical course of the cortical lesion.- - - - - - - - - - ranking = 0.6keywords = brain (Clic here for more details about this article) |
8/27. Central neurogenic hyperventilation in a conscious child associated with glioblastoma multiforme.Central neurogenic hyperventilation refers to progressive tachypnea leading to hypocarbia and respiratory alkalosis caused by cortical disorders, initially reported in comatose patients with mainly pontine infarction. Central neurogenic hyperventilation in conscious patients is even rarer, numbering around 30 reported cases including seven children, mainly associated with infiltrative gliomas and lymphomas of the brainstem and pons. We report the evolution of central neurogenic hyperventilation in a conscious child associated with an infiltrative glioblastoma multiforme diagnosed 1 year before admission. He presented with progressive tachypnea and dyspnea of 1 week duration. On examination he was fully alert and aware of his respiratory disorder. respiratory rate was 56 breaths per minute using accessory respiratory muscles. hyperventilation was unchanged during sleep. Arterial blood gases disclosed marked hypocarbia: Pco(2) of 8 mm Hg resulting in severe respiratory alkalosis at pH of 7.8. Central neurogenic hyperventilation was therefore suggested after exclusion of other respiratory or cardiac disorders. The exaggerated tachypnea persisted along with respiratory alkalosis. Over a period of 2 months his overall state markedly deteriorated; he lapsed into coma, and finally succumbed after involvement of medullary cardiovascular centers. Although extremely rare in the pediatric age group, central neurogenic hyperventilation should be suspected in any alert child presenting with unexplained increasing tachypnea and hypocarbia leading to respiratory alkalosis. The evolution of such a disorder may be an alarming sign of ensuing deterioration in patients with tumors of the brainstem and medulla before cardiovascular derangement.- - - - - - - - - - ranking = 0.4keywords = brain (Clic here for more details about this article) |
9/27. Malignant lymphoma of the central nervous system presenting with central neurogenic hyperventilation. Case report.The case is described of a 72-year-old woman who presented with a progressive right hemiparesis and central neurogenic hyperventilation. Pathological and radiological studies revealed diffuse infiltration of a malignant lymphoma into the entire central nervous system and the upper spinal cord. The authors review 12 cases of tumor-induced central neurogenic hyperventilation and discuss the pathophysiology of this condition.- - - - - - - - - - ranking = 2.2005838678936keywords = central nervous system, nervous system (Clic here for more details about this article) |
10/27. Central neurogenic hyperventilation in a conscious man with CSF dissemination from a pineal glioblastoma.A 40-year old conscious man developed central neurogenic hyperventilation (CNH). He had tumor dissemination to the brainstem 10 months after undergoing partial removal of a pineal glioblastoma. To the best of our knowledge, this is the first report of CNH caused by the cerebrospinal fluid dissemination of a tumor. The authors suggest that multiple lesions from an infiltrative tumor in the brainstem may give rise to CNH and further our understanding of the pathogenesis of CNH.- - - - - - - - - - ranking = 0.4keywords = brain (Clic here for more details about this article) |
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