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 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From the literature and our own experience, 11 cases of hemorrhage or infarction of a pituitary adenoma associated with cardiac surgery have been identified over a 13-year period. Males outnumbered females by 10 to 1. Symptoms observed were headache, lethargy, confusion, obtundation, unilateral ptosis, meiosis, and opthalmoplegia involving cranial nerves III, IV, and VI, visual field deficits, and hemiparesis. Diagnosis in most recent cases has been confirmed with computerized tomography or magnetic resonance imaging. All patients received adrenocortical steroid therapy initially. Eight patients underwent transsphenoidal hypophysectomy and all survived. One patient underwent decompression craniotomy and died. Intracranial surgery was deferred in 1 patient who survived and in another who died of a massive stroke. Residual neurological deficits were noted to be either absent, minimal, or resolving in 7 of the 9 patients who survived their initial hospitalization. While numerous mechanisms have been proposed to explain the hemorrhage and necrosis of a pituitary adenoma during heart surgery, no direct cause has been clearly identified. Surgical treatment is commonly necessary since untreated pituitary apoplexy is often fatal. Transsphenoidal hypophysectomy with decompression is the preferred method of treatment with a low perioperative mortality and fairly good long-term prognosis.
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PMID:Pituitary adenomas complicating cardiac surgery: summary and review of 11 cases. 777 76

Seventy-nine patients admitted in the neurological Intensive care unit because of severe disturbances of consciousness has been evaluated. Protocol based on previous experiences in evaluation of unconsciousness patients was used. Forty-four patients died and thirty-five survived. In 46 patients cause of illness was intracerebral hemorrhage. In 44 of them the cause of hemorrhage was arterial hypertension and in two of them rupture of a-v malformation. The majority of patients actually 41 of them showed hemispheral localization of intracerebral hematoma and five subtentorial. Pontien hemorrhages was found in three and cerebellar in two patients. In majority of 24 patients with hemispheral localization of intracerebral hematoma who showed progressive deterioration of consciousness the signs of descendent transtentorial herniation were found. The symptoms of uncal herniation were rare. In three patients with subtentorial localization of intracerebral hematoma who died signs of upward transtentorial herniation were observed. In 16 patients with ischemic cerebrovascular accident who showed disturbances of the consciousness at the admittance or soon after, nine patients died and seven survived. The cause of their condition were great hemispheral, smaller brain stem ischemic lesion, or deterioration of consciousness was related to the somatic illness. Patients with great ischemic lesions showed similar course of consciousness deterioration as it was observed in patients with hemispherical intracerebral hematomas with difference that biphasic course of illness characterized with temporary stagnation or even slight improvement of patients condition and than secondary progression of deterioration was seen only in patients with intracerebral hematoma, probably because of secondary ischemic complications. Ten patients were admitted because of subarachnoidal and two of them because of intraventricular hemorrhage. Six of them died and four survived. These patients has rupture of great sacular aneurysm with fast development of high intracranial pressure. In two of them the cause of death was rerupture of aneurysm. Stuporous patient with hemispheral neoplasm showed development of descendent transtentorial herniation which was stopped by anti oedematous and corticosteroid therapy. Comatose patient with brisk response on oculocephalic stimulation and normal papillary light reflexes was suspected on intoxication rather than structural brain lesion. He recovered by diuretics and forced rehydratation. After becoming conscious barbiturate intoxication was confirmed. Three patients were admitted in coma because of poisoning with CO, two patients died. Two patients admitted in epileptic status showed late diencephalic state of coma and they survived after anti epileptics and antioedematous treatment.
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PMID:[Disorders of consciousness as a manifestation of neurologic disease]. 864 54

Iron deficiency is a common pediatric problem affecting 20%-25% of the world's infants. Most commonly causing anemia, iron deficiency is also implicated in such neurologic sequelae as irritability, lethargy, headaches, developmental delay, and infrequently papilledema, pseudotumor cerebri, and cranial nerve abnormalities. Rarely has iron deficiency been recognized as a significant cause of stroke in the adult or pediatric populations. We report a series of 6 children, 6 to 18 months of age, who presented with an ischemic stroke or venous thrombosis after a viral prodrome. All patients had iron deficiency as a consistent finding among the group, and other known etiologies of childhood stroke were excluded. These patients provide evidence of a strong association between iron deficiency and ischemic events in children between 6 and 18 months of age.
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PMID:Iron deficiency: a cause of stroke in infants and children. 904 2

We hypothesized that plasma nitric oxide (NO), generated via inducible NO synthase (iNOS) or endothelial constitutive NO synthase and measured via its by-products NO2- and NO3- (NO2- + NO3- = NOx) would increase and remain elevated during chronic peritoneal sepsis. We further hypothesized that treatment with aminoguanidine (AG; 50 mg/kg), a selective iNOS inhibitor, would decrease NO production and alter blood flow. Sprague Dawley rats were randomized to septic and nonseptic groups. Septic rats received an intraperitoneal cecal slurry (200 mg of cecal material/5 mL 5% dextrose-H2O/kg); control rats received sterile 5% dextrose-H2O (5 mL/kg) only. Plasma NOx and hemodynamics were measured 0, 4, 12, 24, and 48 h after sepsis or sham induction. We also examined the effect of AG, an iNOS inhibitor, on plasma NOx levels and tissue blood flow at 24 h. Septic rats uniformly displayed signs of sepsis, including lethargy, piloerection, and diarrhea. NOx levels were significantly elevated compared with controls at 4, 12, 24, and 48 h (p < or = .05). Septic rats also demonstrated hypotension (t = 12, 24, and 48 h) and tachycardia (t = 4, 12, 24, and 48 h). The infusion of AG (50 mg/kg intravenously for 30 min) at 24 h significantly decreased plasma NOx in septic animals. Plasma NOx concentrations returned to basal levels by 90 min after infusion of AG. In addition, blood flow studies demonstrated that AG treatment in nonseptic rats resulted in a significant decrease in blood flow to the stomach, skin, and adipose tissue, whereas AG infusion did not significantly alter the regional perfusion profile in septic animals. Furthermore, treatment with AG did not significantly alter mean arterial pressure in either group; however, nonseptic animals exhibited a decrease in stroke volume, and septic animals demonstrated an increase in heart rate. In contrast to the rise and fall of NOx levels in endotoxemia, this study demonstrates that the initial rise is sustained during 48 h of peritoneal sepsis. This sustained increase in NOx levels in this model correlated with the observable signs of systemic infection and may relate to enhanced iNOS activity. AG infusion demonstrated variable effects on regional tissue blood flow profiles in septic and nonseptic animals and attenuated the increase in plasma NOx levels in septic animals, an index of iNOS activity.
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PMID:Effect of aminoguanidine on plasma nitric oxide by-products and blood flow during chronic peritoneal sepsis. 956 58

Pituitary apoplexy usually presents with acute neuro-ophthalmological complications that require urgent neurosurgical intervention. We present a case of pituitary apoplexy following aortocoronary bypass surgery that was asymptomatic until the patient presented with features of hormonal deficiency three months later. Only one case of pituitary apoplexy has been described in the literature following cardiac surgery that did not require operative intervention. We discuss the aetiology of pituitary apoplexy and the possible mechanisms for such an event after cardiac surgery. Although this is rare, any unusual feature after operation such as lethargy or erectile dysfunction should remind us of hypopituitarism.
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PMID:Asymptomatic pituitary apoplexy after aortocoronary bypass surgery. 1069 9

Cerebral venous thrombosis is an important cause of stroke in children. Understanding the natural history of the disease is essential for rational application of new interventions. We retrospectively identified 31 children with cerebral venous thrombosis confirmed by head computed tomography (4 patients) or by magnetic resonance imaging (27 patients). Risk factors, clinical and radiographic features, and neurologic outcomes were analyzed. There were 21 males and 10 females aged 1 day to 13 years (median 14 days). Nineteen (61%) were neonates. The most common risk factors included mastoiditis, persistent pulmonary hypertension, cardiac malformation, and dehydration. The chief clinical features were seizures, fever, respiratory distress, and lethargy. Fifteen patients had infarctions (8 hemorrhagic, 7 ischemic). Protein C and antithrombin III deficiency were the most common coagulopathies among 14 tested patients. On discharge, 11 patients were normal, 17 had residual deficits, and 2 patients died. Twenty-seven patients were followed from 1 month to 12 years (mean 22 months). At follow-up, 11 patients were normal, and 13 patients had development delay. One had residual hemiparesis and cortical visual impairment. Two had other deficits. Neonatal cerebral venous thrombosis is probably more common than previously thought, and outcomes are worse in this group. All children with cerebral venous thrombosis should be tested for coagulation disorders.
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PMID:Cerebral venous thrombosis in children. 1151 Sep 28

John Cheyne (1777-1836), a Scotsman born in Leith, graduated at Edinburgh University but spent most of his career in Dublin. He was professor of medicine (1813-19) at the Royal College of Surgeons in Ireland, physician to the House of Industry Hospitals and co-founder of the Dublin Hospital Reports in which his celebrated account of a patient with irregular breathing was described in 1818. His Essay on hydrocephalus acutus (1808) and Cases of apoplexy and lethargy (1812), important nineteenth-century contributions to neuropathology are considered here in detail. Towards the end of his life he was afflicted by depression and his posthumously-published Essays on the partial derangement of the mind (1843) was written as a therapeutic exercise.
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PMID:John Cheyne's classic monographs. 1161 12

Addisonian crisis, also commonly referred to as adrenal crisis, occurs when the cortisol produced by the adrenal glands is insufficient to meet the body's acute needs. The symptoms are nonspecific and can mimic other processes, such as sepsis. Hypotension, lethargy, and fever can all be presenting signs. Secondary addisonian crisis can also result from pituitary apoplexy. Pituitary apoplexy usually occurs as hemorrhagic or ischemic necrosis in the presence of a pre-existing pituitary adenoma, and is a rare sequela of surgery. The symptoms of pituitary apoplexy are typically impressive and are relieved by urgent transsphenoidal decompression. Hypopituitarism resulting from pituitary apoplexy can be treated with exogenous hormones. The case presented herein illustrates occult pituitary apoplexy that occurred after on-pump coronary artery bypass grafting. In this patient, the initial signs of addisonian crisis were overlooked; however, once recognized, they were reduced dramatically with standard stress-dose cortisone. A suprasellar mass with a cystic component was found on magnetic resonance imaging. The hemorrhagic pituitary gland was treated by transsphenoidal decompression, which relieved the patient's bitemporal hemianopia and 6th-nerve palsy.
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PMID:Pituitary apoplexy presenting as Addisonian crisis after coronary artery bypass grafting. 1222 22

We report continuous bilateral intracranial pressure (ICP) monitoring immediately after transtentorial herniation in a patient with massive cerebral infarction to: 1) determine presence and time course of compartmental ICP differences, and 2) to study effects of therapy on both hemispheres. A 55-year-old man admitted with watershed infarctions in the left anterior-middle-posterior cerebral arteries distribution. Initial investigations demonstrated highly narrowed left extracranial internal carotid artery. Eight days later he developed unexplained lethargy and anisocoria. Head computerized tomography (CT) showed massive left hemispheric infarction, edema, and midline shift. Bilateral subarachnoid bolts demonstrated equally elevated ICP in both hemispheres. Hyperventilation and osmotic therapy produced near-identical ICP reduction bilaterally with resolution of anisocoria. Later, plateau waves and autonomic instability developed. Shortly before loss of brainstem function, interhemispheric ICP gradients (left greater than right) of 30-40 mm Hg developed. Intracranial pressure did not equalize prior to brain death determination. Bilateral ICP monitoring did not reveal an interhemispheric ICP gradient soon after transtentorial herniation in massive MCA infarction. The presence of interhemispheric ICP gradients in massive stroke remains unproven and further clinical study is necessary.
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PMID:Interhemispheric intracranial pressure gradients in massive cerebral infarction. 1235 87

Experimental occlusion of the middle cerebral artery and the reduction of cerebral blood flow (CBF) below 15 ml/100 gm/per minute cause failure of the somatosensory evoked response and lethargy of cortical neurones. Increase of CBF to normal value normalises the bioelectrical activity within the "penumbra"--the zone surrounding the necrotic area. In this "risk zone" neurones can survive only a few hours. So the penumbra is a "therapeutic window" in which therapy can save some neurones from death. However, if decrease of CBF is continued, numerous cells within the penumbra gradually die. The phenomenon of the penumbra, based on experiments, was applied to human ischaemic stroke; however great differences between experimental and human brain ischaemia do exist. The human course of disease and the size of necrotic lesion depend on numerous additional factors. The three very important critical values of CBF which decrease in human brain ischaemia are difficult to examine. New imaging methods play a great diagnostic role in searching for the penumbra, but their diagnostic possibilities and results are limited. In the short-time duration of the therapeutic window both CT and MRI often do not indicate ischaemic lesion. So, it is not known whether the penumbra is present or not. Conclusive estimation of MRI diffusion-weighted imaging and perfusion-imaging and of their coefficient is impossible to obtain in the time exceeding the "therapeutic window'" Numerous additional various diseases and compensatory vascular mechanisms influence the necrotic zone in human focal ischaemia. Probably for this reason a difficulty in the estimation of the penumbra in human is observed. So, it seems that the penumbra--the therapeutic window or risk zone--in human probably occurs only in some cases. It may be one of numerous reasons for the limited effectiveness of ischaemic stroke therapy. It is not known when the penumbra is overspread with oedema, which always appears to a greater or a lesser degree. Maybe the efforts of experimental investigators, physicians and pharmacologists should also be taken into consideration to find drugs decreasing oedema and BBB permeability.
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PMID:Experimental and human ischaemia: is the penumbra present in human ischaemic stroke? 1257 78


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