Neurotoxicity due to imipenem/cilastatin in patients on continuous ambulatory peritoneal dialysis.
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Biomedical subjects
Publications and source records attributed to M Crespo.
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BACKGROUND: Focal spasticity can be a major drawback in the rehabilitation of stroke patients. Previous studies suggest a beneficial effect for botulinum toxin A (BTX-A) for relief of spasticity. OBJECTIVE: To evaluate the safety and efficacy of BTX-A in the treatment of spasticity in a homogeneous group of stroke patients. METHODS: In this phase III open label trial 19 stroke patients stable for at least six months were enrolled (mean age 53.1 (SD 3.27) years; range 26-72). There were 16 males and 4 females. ASSESSMENTS: Clinical (Ashworth spasticity rating scale, scores for joint mobility, pain and frequency of spasms, Frenchay arm test (FAT)) and subjective (semi-quantitative rating scale filled out by the patient). Only hand and finger flexors were injected. The maximum dosage was 150 U BOTOX (25 U/muscle), the mean dosage was 92.1 +/- 31.6 U BOTOX. RESULTS: Ashworth rating scale and joint mobility scores improved from a median value of 2 at baseline to a median value of 1 one month after treatment, FAT scores also improved from a median value of 0 at baseline to a median value of 1 one month after treatment (Kruskall-Wallis test p < 0.01). Two-thirds of the patients rated their functional improvement as none or mild. CONCLUSIONS: Our study confirmed that BTX-A has an anti-spastic effect but its functional impact needs further evaluation.
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INTRODUCTION: The syndrome, or disease, or Sturge Weber (SSW) is a neuro-ectodermic disorder of unknown incidence, sporadic presentation and specific sex incidence. It is characterized by the presence of a flat, facial angioma which affects at least the first branch of the trigeminal nerve, association with ipsilateral leptomeningeal vascular anomalies, one or more symptoms (epilepsy, hemiparesia, hemiplegia or mental retardation) and ipsilateral vascular lesions of the choroid which lead to glaucoma. As a consequence of lepto-meningeal involvement, homolateral cerebral hemi-atrophy develops together with cortico-subcortical calcifications with a characteristic "railway line" appearance. CLINICAL CASE: We present the case of a six month old girl with a flat port wine angioma on the left half of her face, including three branches of the trigeminal nerve and the left half of her body. She had partial motor crises of the right leg. On the cranial CT there were left periventricular calcifications and calcifications of the choroid plexus. Gadolinium-MR showed signs of left cerebral hemi-atrophy, which was confirmed on the cerebral SPECT (left temporal hypoperfusion). CONCLUSION: This case is interesting on account of the presence of atypical calcifications, both with regard to the sites and age of presentation. We emphasize the need for cranial CT to rule out the presence of calcifications, (as in this case) not seen on Xray of the skull or on MR. We favour the use of cerebral SPECT as a complementary diagnostic technique.
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A group treatment for hypochondriasis was administered to 14 subjects. It was based on Barsky, Geringer and Wool (1988) [General Hospital Psychiatry, 10, 322-327] cognitive-behavioral formulation and presented as an educational course to explain the origins of an enhanced perception of somatic symptoms. Initially, one experimental group (N = 9) and a waiting list control (N = 8) were formed. Experimental subjects showed significant reductions in illness fears and attitudes, reported somatic symptoms and dysfunctional beliefs. Waiting-list controls also changed some illness attitudes, but showed no change in somatic symptoms and increased the number of visits to doctors. Experimental and control subjects differed on several change measures. Afterwards, part of the waiting list subjects (N = 5) received treatment. Overall, treatment was effective for the target measures and produced long-term positive effects on other fears, dysphoric mood and well-being. After treatment, subjects were significantly more extroverted, open and warm. The clinical impression was that treatment was not limited to less severe cases.
BACKGROUND AND PURPOSE: Interobserver reliability of the diagnosis of transient ischemic attack (TIA) is low, and diagnosis of TIA made by nonneurologists is often erroneous. We sought to validate the diagnosis of TIA made by general practitioners (GPs) and by hospital emergency service physicians (emergency MDs). METHODS: A list of 20 neurological symptoms was distributed to 20 GPs and 22 neurologists who graded the compatibility of each symptom with the TIA diagnosis. At least two neurologists validated TIA diagnoses made by GPs for patients under their care or by emergency MDs. RESULTS: Compared with neurologists, GPs considered "confusion" and "unexplained fall" more often compatible with TIA and "lower facial palsy" and "monocular blindness" less often compatible with TIA. Validation of diagnosis by GP was confirmed in 10 patients (19%); 26 patients had strokes, and 16 (31%) had a noncerebrovascular disorder. Validation of diagnosis by emergency MD was confirmed in 4 patients (13%); 10 patients had strokes, and 17 (55%) had noncerebrovascular disorders. The most frequent conditions misdiagnosed as TIAs were transient disturbances of consciousness, mental status, and balance. CONCLUSIONS: The TIA concept is understood differently by neurologists and nonneurologists. GPs and emergency MDs often label minor strokes and several nonvascular transient neurological disturbances as TIAs. Until this misconception of TIA is changed, the term TIA should probably be avoided in the communication between referring physicians and neurologists. If not referred to a neurologist, one third to one half of patients labeled with a diagnosis of TIA will be inappropriately managed.
The present study was designed in an attempt to better define the pattern of growth in five-sixths-nephrectomized rats. Male Sprague-Dawley rats underwent two-stage (days 0 and 7) five-sixths nephrectomy (NX, n = 16) or sham surgery (SHAM, n = 9). At the time of sacrifice (day 21), renal failure (CRF) of NX rats was confirmed by elevated (p < or = 0.0001) serum concentrations (X +/- SEM) of urea nitrogen (SUN) (56 +/- 5 vs. 20 +/- 1 mg/dl) and creatinine (0.7 +/- 0.04 vs. 0.4 +/- 0.02 mg/dl) and reduced SUN (0.13 +/- 0.02 vs. 0.44 +/- 0.05 ml/min/100 g) and creatinine clearances (0.23 +/- 0.02 vs. 0.58 +/- 0.05 ml/min/100 g). As shown by lower cumulative gains of weight (41 +/- 6 vs. 74 +/- 4 g) and length (5.0 +/- 0.4 vs. 6.8 +/- 0.3 cm), NX rats grew subnormally. Detailed analysis of growth data revealed: (1) In spite of being identically matched in weight and length on day 0, at day 7, NX rats already weighed less than SHAM animals (147.1 +/- 2.3 vs. 153.4 +/- 1.9 g, p = 0.03). (2) From day 7 on, daily gain of weight was lower in the NX group only on days 8 (-6.08 +/- 0.52 vs. -1.60 +/- 0.69 g/100 g body weight) and 9 (-0.41 +/- 1.73 vs. 5.18 +/- 0.63 g/100 g body weight). (3) Following the early post-second-nephrectomy period, two subgroups of NX rats were clearly differentiated according to whether or not their daily growth rate was lower than that of SHAM animals. Maintained subnormal growth rate was observed in rats with severe CRF (SUN 73 +/- 5 mg/dl, range 54-90) but not in rats having milder uremia (42 +/- 3 mg/dl, range 31-51). Thus, growth in five-sixths-nephrectomized rats should be reported based on daily weight increments (g/100 g body weight). Subnormal growth can be attributed to CRF provided SUN is at least 3 times as high as normal while growth impairment of rats with less marked reduction of renal function is likely related to transient acute renal failure and postsurgical catabolic state.
PURPOSE AND SETTING: To describe the prevalence and risk factors for carotid stenosis in TIA/stroke patients with non valvular atrial fibrillation (AF) and to compare clinical and CT characteristics of TIA/stroke in AF patients with and without carotid stenosis. SUBJECTS: 50 TIA/stroke patients with AF who had ultrasound investigation of the extracranial vessels, included in a prospective hospitalar registry. RESULTS: Twenty-two patients had some degree of carotid stenosis, but only 5 had more than 50% stenosis, including one with occlusion. Stenosis was neither more frequent nor more severe on the symptomatic side. Smokers were significantly more frequent in AF patients with > 50% stenosis. Clinical and CT features were quite similar in patients with and without carotid stenosis. CONCLUSION: The association in a TIA/Stroke patient of AF and severe carotid stenosis on the symptomatic side is exceptional. TIA/strokes related to carotid stenosis cannot be identified by their clinical/CT characteristics. Management of these patients must be decided by stratification of risk of recurrence for AF and from carotid stenosis and balance of these risks with that of endarterectomy.
Thirty-four percent of 182 ischemic stroke patients registered during 1 year in a prospective hospital stroke data base complained of headache within a 72-hour interval of stroke onset. Headache was more common in patients under 70 years of age, in nonsmokers, in those with a past history of migraine, and in subjects presenting transient loss of consciousness, nausea/vomiting, or visual field defects. Headache was more frequent in vertebrobasilar (57%) than in carotid (20%) territory strokes, more so in posterior cerebral artery (90%) and cerebellar infarcts (80%), and was infrequent in subcortical infarcts (7%) and lacunes due to single perforator disease (9%). In multiple regression analysis, vertebrobasilar stroke (odds ratio 6.9), lacuanr stroke (odds ratio 0.06), and past history of migraine (odds ratio 6.7) were significant independent predictors of headache, suggesting that ischemic stroke location is the major determinant of stroke-associated headache, most probably related to activation of the trigeminovascular system, whose threshold may be modified by individual susceptibility.
Sixty (29%) of 205 consecutive patients with transient ischemic attacks registered in a hospital stroke data base had headache within 72 hours of onset. Headache was significantly more common in nonsmokers (odds ratio = 2.8; 95% confidence interval = 6.7 to 1.2). Headache was infrequent in patients with amaurosis fugax, and was not significantly associated with any other particular clinical presentation of transient ischemic attack. Headache was more common in vertebrobasilar (33%) than in carotid distribution (24%) episodes, and was not rare in transient ischemic attacks presenting as lacunar syndromes (29%). Headache was less frequent in patients whose computerized tomograms showed an infarct appropriate to the symptoms (odds ratio = 0.2; 95% confidence interval = 0.02 to 1.4). A diffuse headache was more common in patients with lacunar events than in patients with cortical attacks (odds ratio = 3.0; 95% confidence interval = 13 to 0.07). No other association was found between headache location and the presumed involved vascular territory. Headache in patients with transient ischemic attacks is poorly related/explained by the clinical characteristics of the ischemic event.
BACKGROUND: The role of the kidney in the development of essential hypertension is subject of debate. METHODS: We compared the renin, kallikrein and prostaglandin renal systems in two groups of normotensive boys, aged 7-16 years, with different degrees of risk for future hypertension: 27 had parents with essential hypertension and 12 had normotensive parents. Supine, standing and post-exercise plasma renin activity as well as levels of urinary kallikrein and prostaglandin E2 before and after exercise were measured. RESULTS: The ratio of post-exercise plasma renin activity (ng/ml/h) to 24 h urinary sodium excretion (mEq/kg/day) was lower in children with hypertensive parents (mean +/- SEM 1.86 +/- 0.24 compared with 3.62 +/- 0.94, P = 0.02). The boys with hypertensive parents had a lower ratio of urinary kallikrein to creatinine before (0.70 +/- 0.13 compared with 1.54 +/- 0.36, P = 0.01) and after exercise (0.80 +/- 0.13 compared with 1.35 +/- 0.23, P = 0.03). The ratio of urinary prostaglandin E2 to creatinine levels did not differ between the groups before or after exercise. CONCLUSION: The plasma renin activity response to exercise and urinary kallikrein excretion were decreased in boys at increased risk of future essential hypertension. These early abnormalities in the renin and kallikrein renal systems may be associated with the development of essential hypertension.