Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegration of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit.
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PMID:Cerebrovascular regulation and vasoneuronal coupling. 769

Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine's curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial nerves' dysfunctions and a slight right-sided hemiparesis. An acute brainstem ischemia was diagnosed and treated immediately with high-dose heparin. Cerebral angiography revealed a proximal occlusion of the left vertebral artery but a normal right vertebral artery and a hyperplastic right posterior inferior cerebellar artery. Cranial Computed Tomography and MRI scan demonstrated multiple ischemic lesions in the posterior circulation. During a 4-week treatment course the patient underwent six episodes of acute severe hypoxia and hypercapnia requiring orotracheal intubation twice and manual ventilation by air mask over a few minutes for four times after a tracheostomy had been performed. Twice a short-term episode of hypothalamic Diabetes insipidus was observed following hypoventilation. We conclude that both Ondine's curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia.
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PMID:Ondine's curse in association with diabetes insipidus following transient vertebrobasilar ischemia. 1053 7

Respiratory insufficiency appearing during chronic lung diseases leads to hypoxemia, hypercapnia, acidosis, right ventricular failure and secondary polyglobulia. These disturbances lead to respiratory encephalopathy which is characterized by the appearance of various types of neurological syndromes. We present here the case of a patient suffering from chronic spastic bronchitis accompanied by pulmonary emphysema, whose consciousness disturbances, a generalized epileptic seizure and hemiparesis were connected with his respiratory insufficiency intensifying during the basic disease. Removal of metabolic disturbances caused by respiratory insufficiency has a key role in preventing secondary neurological syndromes.
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PMID:[A case of hypoxic encephalopathy in the course of chronic spastic bronchitis and pulmonary emphysema]. 1110 77

Moya moya is a progressive cerebral occlusive vasculopathy, rare in European countries. We describe a case of a young woman with right-hand side hemiparesis, mixed expressive aphasia, organic psychosyndrome and cognitive malfunction. Detailed imaging methods displayed bilateral stenosis of the internal carotid artery, bilateral ischemic cerebral changes and bilateral perfusion deficit, which guided us to the final diagnosis. Before the bypass surgery, cerebrovascular reserve capacity (vasoreactivity), by the brain single photon emission tomography and hypercapnia, were assessed and the lower cerebrovascular reserve was demonstrated. Bilateral bypass surgery with extracranial-intracranial anastomosis, improved the neurological deficit. Diagnosis was confirmed by histological examination of the vessel wall specimen.
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PMID:Brain single photon emission tomography and hypercapnia test in testing cerebrovascular reserve capacity, in Moya moya disease. 1908 64

Genetic mutations of sporadic hemiplegic migraine (SHM) are mostly unknown. SHM pathophysiology relies on cortical spreading depression (CSD), which might be responsible for ischemic brain infarction. Cystic fibrosis (CF) is caused by a monogenic mutation of the chlorine transmembrane conductance regulator (CFTR), possibly altering brain excitability. We describe the case of a patient with CF, who had a migrainous stroke during an SHM attack. A 32-year-old Caucasian male was diagnosed with CF, with heterozygotic delta F508/unknown CFTR mutation. The patient experiences bouts of coughing sometimes triggering SHM attacks with visual phosphenes, aphasia, right-sided paresthesia, and hemiparesis. He had a 48-hour hemiparesis triggered by a bout of coughing with hemoptysis, loss of consciousness, and severe hypoxia-hypercapnia. MRI demonstrated transient diffusion hyperintensity in the left frontal-parietal-occipital regions resulting in a permanent infarction in the primary motor area. Later, a brain perfusion SPECT showed persistent diffuse hypoperfusion in the territories involved in diffusion-weighted imaging alteration. Migrainous infarction, depending on the co-occurrence of 2 strictly related phenomena, CSD and hypoxia, appears to be the most plausible explanation. Brain SPECT hypoperfusion suggests a more extensive permanent neuronal loss in territories affected by aura. CF may be then a risk factor for hemiplegic migraine and stroke since bouts of coughing can facilitate brain hypoxia, triggering auras.
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PMID:Migrainous Infarction in a Patient With Sporadic Hemiplegic Migraine and Cystic Fibrosis: A 99mTc-HMPAO Brain SPECT Study. 3062 50