Cases reported "Hyperemia"

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1/6. Objective assessment of autonomic signs during triggered first division trigeminal neuralgia.

    A total of 26 episodes of V-1 trigeminal neuralgia attacks have been recorded in two female patients. Autonomic phenomena were assessed according to a semiquantitative scale. Attacks lasted 17 /- 5 s. Mild lacrimation without conjunctival hyperaemia, rhinorrhea or ptosis was observed, even in relatively long lasting episodes. This is in clear contradiction with SUNCT (shortlasting, unilateral, neuralgiform headache with conjunctival injection, tearing and rhinorrhea) attacks that are always dramatically accompanied by both lacrimation and conjunctival injection of the symptomatic side from the very onset of symptoms. carbamazepine provided complete and sustained relief of symptoms in both patients. Herein we will show differential autonomic features of V-1 trigeminal neuralgia vs. SUNCT that will both aid the clinician to distinguish both syndromes and stress that both entities are nosologicaly different.
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keywords = episode
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2/6. hyperemia and impaired cerebral autoregulation in a surgical patient with diabetic ketoacidosis.

    PURPOSE: We describe cerebral hyperemia and impaired cerebral autoregulation documented with transcranial Doppler (TCD) ultrasonography in an adult patient with diabetic ketoacidosis (DKA) and sepsis presenting for surgery. CLINICAL FEATURES: middle cerebral artery flow velocity was increased relative to PaCO(2) (Vmca 52 cm.sec(-1); PaCO(2) 22 mmHg) and the autoregulatory index (ARI) was 0 prior to surgery. Twenty hours after admission and treatment, cerebral hyperemia resolved (Vmca 52 cm.sec(-1) ; PaCO(2) 35 mmHg) and cerebral autoregulation returned to normal (ARI 0.91). CONCLUSION: To our knowledge, this is the first description of impaired cerebral autoregulation in adult DKA. Our observations suggest a relationship between cerebral hyperemia and impaired cerebral autoregulation in DKA.
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ranking = 8.3841793377554
keywords = acidosis
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3/6. thallium-201 uptake in variant angina: probable demonstration of myocardial reactive hyperemia in man.

    Myocardial thallium scintigraphy was performed in four subjects with variant angina and in one subject with isolated, fixed coronary obstruction. Three subjects with variant angina had short episodes of ischemic ST-segment elevation that lasted 20--100 seconds. thallium scintigrams demonstrated excess uptake in regions judged to be ischemic by angiographic and electrocardiographic criteria. Two subjects, one with variant angina and the other with a fixed coronary lesion, had prolonged episodes of ischemia that lasted 390--900 seconds. Both had reduced thallium uptake in the ischemic regions. We conclude that myocardial reactive hyperemia is the cause of excess thallium uptake in patients with variant angina who have short episodes of myocardial ischemia.
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ranking = 1.5
keywords = episode
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4/6. Cerebral hyperemia in MELAS.

    BACKGROUND: The pathophysiology of stroke-like episodes in MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is uncertain. CASE DESCRIPTION: We studied a 24-year-old man with MELAS who had fluent aphasia and right hemianopia. magnetic resonance imaging and computed tomography showed a large infarction in the parietal, temporal, and occipital lobes. We performed serial planar 133Xe regional cerebral blood flow studies and single-photon emission computed tomography. Fifteen and 26 days after the stroke-like episode, there was generalized hyperperfusion, highest in infarcted areas. Four and 8 months after the stroke-like episode, the brain was still hyperemic, with highest flow in noninfarcted tissue. Reactivity to CO2 was less than normal within the infarct at 26 days but improved thereafter. In the noninfarcted region, vasomotor reactivity was impared at 4 months, when resting flows were at their peak. CONCLUSIONS: We observed generalized cerebral hyperemia and fluctuating CO2 reactivity in MELAS, possibly a consequence of local lactic acid production. In addition, this case suggests that nonquantitative functional imaging may be misleading in MELAS.
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ranking = 16282.161970303
keywords = stroke-like episode, stroke-like, acidosis, episode
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5/6. Cerebral blood flow and oxygen metabolism before and after a stroke-like episode in patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).

    Cerebral blood flow and oxygen metabolism were examined in two patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) using positron emission tomography (PET). Regional cerebral blood flow (rCBF), regional cerebral oxygen metabolic rate (rCMRO2) and regional oxygen extraction fraction (rOEF) were determined with the steady-state technique using oxygen-15-labeled tracers (15O2, C15O2 and C15O). Case 1, a 45-year-old woman, presented with abrupt onset of fluent aphasia. T2-weighted magnetic resonance imaging (MRI) showed a high signal intensity lesion in the left temporoparietal region. The first PET study on day 16 showed increased rCBF and decreased rCMRO2 in the temporal region. In the second PET study, on day 35, rCBF in the temporal region had decreased. Case 2 was a 19-year-old male; the second son of Case 1. He complained of transient blurring of vision, and then generalized tonic-clonic convulsion occurred. A PET study six days before this stroke-like episode demonstrated increased rCBF in both frontal lobes and putamen, where MRI showed lesions after the episode. Focal hyperemia of the lesion antedated and lasted for at least sixteen days after the stroke-like episode in these MELAS patients. These stroke-like episodes appear to be the result of metabolic dysfunction in neural tissue, although the role of an ischemic vascular event cannot be ruled out.
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ranking = 48850.339582644
keywords = stroke-like episode, stroke-like, acidosis, episode
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6/6. Combined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be?

    We describe a patient with combined meningococcal septicemia and meningitis, cerebral edema and acute respiratory distress syndrome, in whom we balanced the conflicting carbon dioxide strategies for optimal pulmonary and neurological management using jugular oxygen saturation (SjvO2) monitoring to identify the upper limit of "tolerable" hypercapnia. Our observations suggest that significant acidosis was not well tolerated; however, cautious induction of pH down to 7.32 and an arterial carbon dioxide tension (PaCO2) < 5.9 kPa was tolerated acutely without significant cerebral hyperemia. Moreover, with the development of metabolic compensation and normal pH, higher levels of PaCO2 could be permitted. In similar cerebro-pulmonary circumstances we suggest that these findings warrant consideration. Alternatively, invasive monitoring of SjvO2 could be undertaken so that patient-specific criteria for permissive hypercapnia can be determined.
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ranking = 1.6768358675511
keywords = acidosis
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