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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiography was employed to measure the serial effects of jogging on resting left ventricular dimensions and function. Twelve men were exercised (mean age 36.8 yr) and 10 served as controls (mean age 34.8 yr). Increases of 14 and 18% were observed for predicted aerobic capacity in the training group (TG) after 3 and 6 mo of training, respectively; the control group (CG) displayed a small detraining effect. Echocardiographic findings included a significant (P less than 0.05) reduction in resting heart rate and a moderate increase in stroke volume (SV) in the TG compared to the CG. The increased SV appeared to be due to increased end-diastolic dimensions (LVIDd, LVEDV), secondary to greater ventricular filling rather than a more vigorous ventricular contraction. Posterior wall thickness, septal thickness, and calculated left ventricular muscle mass were not significantly increased in the TG compared to CG after either 3 or 6 mo training. It was concluded that left ventricular structure and resting contractile status are not altered by 6 mo of jogging training in healthy, previously sedentary men.
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PMID:Effects of endurance training on left ventricular dimensions in healthy men. 46 62

A clinical method for noninvasive measurement of regional cerebral blood flow (rCBF) and blood volume (rCBV) is described, based on Obrist's 10 minute, desaturation method after 1 minute inhalation of 133Xe. Sixteen collimated probes are placed over both hemispheres and brain stem-cerebellar regions. End-tidal 133Xe curves are used for correction of recirculation. KEV discriminators are set to record gamma and x-ray activity separately. Values are printed out automatically by a computer on a brain map. Extracerebral contamination is reduced by 1) computing curves from gamma activity, 2) applying pressure on the scalp beneath the probes, 3) 1 minute inhalation of 133Xe and recording desaturation curves for 10 minutes, thereby minimizing slow clearance from extracranial tissues. Normal values for both fast and slow compartments are reproducible and are in good agreement with the carotid injection method. The speech dominant hemishpere has higher flow than the right under conditions described. Posterior portions of the cranium over the cerebellum and brain stem appear to have higher flow gray values than the cerebral cortex. Gray matter flow decreases with advancing age.
Stroke
PMID:Improved method for noninvasive measurement of regional cerebral blood flow by 133Xenon inhalation. Part I: description of method and normal values obtained in healthy volunteers. 64 14

To better characterize the cardiac structural and functional changes that are associated with aging, Doppler-echocardiography was performed on 23 young (mean age, 25 years) and 30 old (mean age, 70 years) healthy normotensive subjects. Left ventricular cavity dimensions and wall thickness were determined and left ventricular mass index was calculated from M-mode echocardiograms. Stroke volume was calculated from Doppler-measured aortic flow. Diastolic filling was evaluated by pulsed Doppler echocardiography of mitral inflow. Posterior wall thickness (1.0 vs 0.8 cm, p less than 0.05) and relative wall thickness (0.42 vs 0.35, p less than .05) were significantly greater in the elderly subjects compared with the younger subjects. Left ventricular mass index increased on average 0.25 gm/m2/yr but was not significantly increased in the elderly compared with the younger subjects (89 vs 77 gm/m2). Shortening fraction and stroke volume did not differ between the two groups. Diastolic filling was dramatically altered with aging, and the elderly subjects demonstrated a doubling of percent atrial contribution (37% vs 19%, p less than 0.0001) and halving of peak early-to-peak atrial velocity ratio (0.85 vs 1.77, p less than .01).
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PMID:Effects of aging on left ventricular structure and function. 182 40

We describe a woman with metastatic small cell carcinoma of the lung who presented with pituitary apoplexy and hyperprolactinemia. Within seventeen months she developed florid Cushing's syndrome with anasarca, hyperpigmentation, hypertension with marked hypercortisolemia (not suppressible with 8 mg dexamethasone), elevated serum ACTH, hypokalemic metabolic alkalosis, and multiple hepatic metastases. This picture suggested the presence of ectopic ACTH syndrome. She died 26 months after the episode of pituitary apoplexy. Primary small cell carcinoma of the lung was diagnosed post-mortem. Metastases were present in the left lung, regional lymph nodes, heart, liver, bone marrow, sphenoid bone, anterior pituitary and pituitary capsule. Posterior pituitary was normal. There was no evidence of pituitary hyperplasia, of adenoma or of primary pituitary carcinoma. The results suggest the presence of a primary ACTH-producing small cell carcinoma of the lung that metastasized to the parasellar sphenoid bone and then extended to the anterior pituitary and dura to mimic a primary intrasellar cause of pituitary apoplexy and Cushing's syndrome. The case demonstrates how difficult it may be to diagnose the etiology of Cushing's syndrome and it emphasizes a unique variation in the presentation of small cell carcinoma of the lung.
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PMID:Metastatic small cell carcinoma of the lung presenting as pituitary apoplexy and Cushing's syndrome. 608 26

Posterior circulation in 82 children of "moyamoya" disease are studied. Two aspects of "moyamoya" disease, (ie; occlusive lesion of cerebral vessels and the development of abnormal vascular network as collateral channel,) are also detected in the vertebrobasilar system. Among 82 cases, 49 cases showed the occlusion of posterior cerebral artery at their quadrigeminal segment. Twenty-three showed the more proximal occlusive lesions. Vertebral artery occlusion were found in 3 cases. As the occlusive lesion progresses, abnormal vascular network at the posterior portion of skull base developed. This network consists mainly of thalamogeniculate artery, posterior choroidal artery, and also of other thalamoperforators. Visual field defect as an ischemic symptom of occipital lobe was detected in 9 cases (11%). Superficial temporal artery-middle cerebral artery anastomosis and encephalo-myo-synangiosis (temporal muscle graft), which were not considered to be so effective to the ischemia of the posterior circulation, were shown to exert indirect redistribution effect upon the vertebrobasilar system. However, this effect is such an indirect one that these surgical treatments cannot prevent the occurrence of ischemic stroke in the vertebrobasilar system. For this purpose, omentum transplantation to the occipital lobe may be needed as a method of direct revascularization.
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PMID:[Study on the vertebro-basilar system in "moyamoya" disease]. 674 16

The contribution of atrial systole in the left ventricular (LV) function and the effects of oral digoxin maintenance therapy on the LV function were evaluated noninvasively in patients who had artificial pacemakers but no clinical manifestation of congestive heart failure (NYHA Class I). Diastolic dimension (Dd), ejection time (ET), and stroke volume were constant in 8 patients without P waves on their electrocardiograms, but in 20 patients with P waves they were variable from beat to beat because of the variation of the PR intervals which caused them to reach their maximum values when the PR intervals were 160 to 200 msec. Ten out of the 28 patients were given 0.25 mg of digoxin daily for 10 days. Dd did not change significantly, but the ET and the systolic dimension were significantly shortened (P < 0.001). Posterior wall excursion, ejection fraction, and mean posterior wall velocity were significantly increased (P < 0.001). It is concluded that (1) atrial contraction is important to the LV function in patients with artificial pacemakers, and (2) that favorable effects on the LV function can be obtained by a small dose of digoxin administered to the patients who had artificial pacemakers but no congestive heart failure.
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PMID:Favorable effects of oral digoxin therapy on the left ventricular performance in patients with artificial pacemakers. 743 29

Oropharyngeal dysphagia due to iatrogenic neurological dysfunction may relate to either medication side effects or surgical complications. There are several general mechanisms by which neurological side effects of medications can cause or aggravate oropharyngeal dysphagia. These include decreased level of arousal, direct suppression of brainstem swallowing regulation, movement disorders (dyskinesias, dystonias, and parkinsonism), neuromuscular junction blockade, myopathy, oropharyngeal sensory impairment, and disturbance of salivation. Postsurgical oropharyngeal dysphagia due to neurological dysfunction has been described in association with carotid endarterectomy, esophageal cancer surgery, anterior cervical fusion, and ventral rhizotomy for spasmodic torticollis. A potential explanation for oropharyngeal dysphagia following these surgical procedures is intraoperative mechanical disruption of the innervation of the pharyngeal constrictor muscles by the pharyngeal plexus. Posterior fossa and skull base surgery can lead to dysphagia as a result of intraoperative damage to brainstem centers and/or cranial nerves involved in swallowing. Perioperative stroke is the most likely explanation for oropharyngeal dysphagia appearing acutely following surgery, especially if the type of surgery predisposes to embolism or hypoperfusion.
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PMID:Oropharyngeal dysphagia due to iatrogenic neurological dysfunction. 749 5

Posterior choroidal artery (PChA) territory infarcts remain the least well-known type of thalamic infarcts. Our study of 10 personal cases, selected from 2,925 stroke patients admitted consecutively to a community-based primary care center, and 10 published cases of unilateral PChA territory infarct suggests that they can often be differentiated clinically from other thalamic infarcts. Patients with PChA territory infarct associated with superficial posterior cerebral artery territory infarct or with another infarct were excluded. Damage was characteristically limited to the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyros, without involvement of the upper midbrain and the anterior nucleus of thalamus. In lateral PChA territory infarct, the most common clinical manifestations included homonymous quadrantanopsia, with or without hemisensory loss and neuropsychological dysfunction (transcortical aphasia, memory disturbances). A homonymous horizontal sectoranopsia is exceptional but particularly suggestive of the involvement of the lateral geniculate body in this territory. Media] PChA territory infarct was less frequent. Its neurologic picture was dominated by eye movement disorders not particularly suggestive of thalamic involvement. Late disability was usually absent or slight, being related to pain and delayed abnormal movements. The most common stroke etiology was presumed small-vessel occlusive disease.
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PMID:The syndrome of posterior choroidal artery territory infarction. 865 50

Bow hunter's stroke results from vertebrobasilar insufficiency caused by mechanical occlusion or stenosis of the vertebral artery (VA) at the C1-2 level on head rotation. Surgical treatment of this condition may be chosen to avoid life-threatening accidents or because patients complain that conservative treatments such as verbal warnings or use of a neck brace to limit head and neck rotation are ineffective and thus restrict their lifestyle. Posterior fusion involving C1-2 has long been used to limit atlantoaxial rotational movements. However, it has the serious disadvantage that the range of head motion is severely reduced. Recently, decompression of the atlantoaxial portions of the affected VA has been used because it does not limit physiological neck movements. However, no long-term follow-up review of patients who have undergone this procedure has been conducted, and it is unclear whether this procedure always provides relief of symptoms. To answer this question, the results of C1-2 posterior fusion were compared with decompression of the VA for the treatment of bow hunter's stroke.
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PMID:Comparison of C1-2 posterior fusion and decompression of the vertebral artery in the treatment of bow hunter's stroke. 912 Jun 24

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and longterm outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemimedullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extracranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.
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PMID:Proximal intracranial territory posterior circulation infarcts in the New England Medical Center Posterior Circulation Registry. 913 26


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