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

Despite adequate diagnostic evaluation and prolonged follow-up, the causes of epilepsy in the elderly patient frequently remain unknown. Some of these may be of occult, degenerative or vascular central nervous system disease origin--entities which are often difficult to incriminate specifically. Unquestionably, in a few cases, seizures occur at the time of the initial cerebrovascular accident, although in some patients seizures may follow such an episode after a latent interval, particularly when cortical motor areas have been damaged by the initial vascular insult. It is important to differentiate this group from those with recurrent vascular episodes, in whom diagnostic studies and treatment may differ. Brain tumour is as prominent a cause of seizures in the seventh decade as it is in younger adults, but probably is of lower incidence thereafter. Focal, clinical and electroencephalographic findings and a progressive clinical course are particularly common in this group. A heterogeneous group of causes, a few of which are liable to affect the ageing patient, are responsible for some of the seizures in old age and should be searched for when the etiology is obscure. Diagnostic studies will vary with the individual problem and, whenever possible, should be restricted to non-invasive studies such as electroencephalography and computer-assisted tomography, after initial baseline clinical assessment and laboratory studies have been performed. Contrast procedures such as angiography are sometimes hazardous to patients with atherosclerosis and should be reserved for selected patients. Treatment follows conventional guidelines with some modifications due to the vulnerability of the ageing patient to degenerative disease and complications of immobilization.
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PMID:Seizures after the age of sixty. 99 28

For years the conventional approach to treatment of atrial fibrillation has centered around use of digoxin for rate control and type IA agents for conversion to normal sinus rhythm and has avoided use of anticoagulation therapy for most patients. Current data suggest that new conventions are needed. beta-Blockers or calcium channel blockers should be considered equal to, if not better than, digoxin for rate control. Type IA agents are still the drugs of choice for conversion to and maintenance of normal sinus rhythm, but the newer agents propafenone and flecainide, and perhaps even amiodarone, may be more efficacious if preliminary data are truly indicative of their effect. The use of antiarrhythmic agents requires caution and careful attention to factors that may predispose patients to their inherent proarrhythmic effects. Finally, anticoagulation therapy is no longer reserved for a few patients but should be used in low doses in most patients (when not contraindicated) to lower risk of stroke. This new approach must be challenged as well to minimize the morbidity and mortality of this common clinical problem.
Heart Dis Stroke
PMID:Atrial fibrillation: conventional wisdom reappraised. 134 90

The authors present a series of six patients with large symptomatic benign pineal cysts and review the 27 patients previously reported in the literature. Patients with symptomatic pineal cysts most often present with one of three syndromes: 1) paroxysmal headache with gaze paresis; 2) chronic headache, gaze paresis, papilledema, and hydrocephalus; or 3) pineal apoplexy with acute hydrocephalus. Surgical intervention with radical cyst removal is the treatment of choice for all symptomatic pineal cysts. Complete cyst removal is desirable; however, radical subtotal resection is appropriate if the cyst cannot be easily separated from the quadrigeminal plate. Ventricular shunting should be reserved for patients with persistent hydrocephalus after cyst resection.
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PMID:Surgical management of symptomatic pineal cysts. 143 32

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of ticlopidine are reviewed. Ticlopidine appears to inhibit platelet aggregation induced by adenosine diphosphate. Ticlopidine hydrochloride is rapidly absorbed after oral administration, and maximum antiplatelet effects occur one to three hours after the dose. In multicenter, randomized, double-blind trials, ticlopidine was more effective than aspirin or placebo in preventing stroke, myocardial infarction, or death caused by vascular events. Ticlopidine was more effective than aspirin in preventing recurrent transient ischemic attacks after six months of therapy. Ticlopidine has also been used to prevent occlusion and improve patency of aortocoronary bypass grafts, to prevent ischemic ulcers in patients with chronic arterial occlusive disease, and to slow the progression of diabetic microangiopathy. The most serious adverse effect, neutropenia, occurred in about 1% of patients. The most frequently reported adverse effects are diarrhea, nausea, vomiting, and abdominal cramps. Ticlopidine is indicated for reducing the risk of thrombotic stroke in patients who have experienced a minor stroke, transient ischemic attack, or completed thrombotic stroke. The recommended dosage is 500 mg/day in two divided doses taken with food. Ticlopidine is an alternative agent for the primary and secondary prevention of stroke. Because of the risk of neutropenia and agranulocytosis and the high cost of therapy, ticlopidine should be reserved for patients who are intolerant of or lack benefit from aspirin.
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PMID:Ticlopidine: a new platelet aggregation inhibitor. 161 11

Two groups of rats were tested on a variety of motor and cognitive tasks after either 10 minutes of two-vessel occlusion forebrain ischemia (n = 8) or sham operative procedures (n = 6). Histological injury was absent in the sham-operated group. In the ischemic group, hippocampal injury was restricted to field CA1, while damage in the neocortex and caudoputamen was sparse. Motor tests performed on postoperative days 18 and 28 revealed no significant differences between the ischemic and sham-operated groups. Retention performance of a radial maze discrimination task was impaired, with a significant but transient increase in both working and reference memory errors. Passive avoidance acquisition and retention were not significantly affected, although conclusions concerning the utility of this task must be reserved because of variability in the behavior of the sham-operated rats. Morris maze spatial navigation (place learning) and open-field activity were insensitive to treatment group. These functional results are consistent with the observed histological injury and what is known about hippocampal injury and behavior, and they provide further guidance for the development of neurological assays appropriate for discriminating outcome from forebrain ischemia in rats.
Stroke 1991 Aug
PMID:Forebrain ischemia induces selective behavioral impairments associated with hippocampal injury in rats. 186 51

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to nonhypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk of cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must...do no harm."
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PMID:50% dextrose: antidote or toxin? 212 May 1

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to non-hypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk for cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must ... do no harm."
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PMID:50% dextrose: antidote or toxin? 218 38

Migraine headaches that occur in the 15- to 30-year-old age group are well documented. In patients in the stroke age bracket, however, who present with a history of neurologic deficit, transient ischemic attacks can be confused with migraine accompaniments. The typical patient is 50 years old, is without a past history of migraines, and complains of scintillating visual disturbances (20 percent), marching paresthesis (22 percent), or a myriad of neurologic deficits. In one series of 70 neurology patients aged over 55 years, 16 percent reported that they experience the new onset of scintillations. Once fully evaluated, the cause of unexplained marching paresthesias, dysphagia, or hemiplegia, once reserved for thrombotic or embolic phenomena, may be attributed to migraine accompaniments. In the face of a normal evaluation, neurologic deficit in the stroke age bracket may be attributed to migraine accompaniments. A case of a 47-year-old woman with sudden onset of left-sided paresthesia, dysarthria, and confusion is presented. The discussion includes a description of migraine pathophysiology and a review of concepts regarding accompaniments.
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PMID:Late-life migraine accompaniments: a case presentation and literature review. 358 61

During a 7-year period, 4047 patients underwent a battery of noninvasive carotid tests before cardiac surgery. Two thirds of the patients with abnormal studies underwent carotid angiography. One hundred fifty-three patients (3.8%) had significant carotid disease, narrowing the luminal diameter by greater than 50%. The incidence of transient ischemic attack or cerebrovascular accident following cardiac surgery was 1.9% in those patients with no carotid disease and 9.2% in those patients with carotid lesions. The incidence of transient ischemic attack or cerebrovascular accident in 32 patients with inoperable (occluded) carotid vessels was 15.6% and in 121 patients with operable (stenotic) lesions was 7.4%. In the group of patients with stenosis, 57 patients underwent carotid operation with an 8.8% incidence of neurologic deficit. During the last 1 1/2 years, no patient with asymptomatic carotid stenosis underwent simultaneous carotid and coronary surgery. Four of 64 patients with combined lesions but no carotid surgery (6.3%) had a neurologic deficit, one of which was severe and permanent. The highest incidence of neurologic dysfunction occurred in patients with unilateral occlusions and contralateral stenosis. Four of 12 patients in this group had a deficit (three of seven patients underwent operation; one of five did not), one of which was permanent. The operative mortality rate after cardiac surgery was three times higher in patients with carotid disease than in those patients with normal carotid arteries. Combined carotid and coronary surgery is currently reserved for patients with neurologic symptoms and severe cardiac disease.
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PMID:The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study. 382 Apr 1

Duplex carotid sonography was performed on 254 asymptomatic patients over the age of 55, yielding 500 adequate vessel examinations. Overall, 19.8 per cent of vessels were normal, 27 per cent had mild disease (less than 30 per cent diameter stenosis), 23 per cent had 30-49 per cent stenosis, 18.8 per cent had 50-69 per cent stenosis, 8.6 per cent had severe stenosis of 70-99 per cent, and 2.8 per cent of vessels were occluded. Many of the patients eventually underwent major surgical procedures and there were no cases of operative or perioperative morbidity or mortality. Only one of 254 patients has had a stroke in the two-year study period. Arteriosclerotic disease is common in patients over 55 years of age, but, in this series, does not seem to be of clinical significance. This supports the view that invasive tests and carotid endarterectomy should be reserved for symptomatic patients. Duplex sonography is an excellent noninvasive method of evaluation and follow-up of asymptomatic patients, and long-term studies with this modality should help to determine the natural history and clinical significance of extracranial carotid arteriosclerotic disease.
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PMID:Duplex ultrasound screening for carotid arteriosclerotic disease in asymptomatic patients. 389 63


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