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Biomedical subjects

M Alday

Publications and source records attributed to M Alday.

9 recordsLinked to original sources
PubMed1997

Periventricular white matter lucencies in patients with lacunar stroke. A marker of too high or too low blood pressure?

BACKGROUND: Periventricular white matter lucencies (PWML) have been described in stroke patients with arterial hypertension, hypotensive episodes, or increased nocturnal fall of blood pressure (BP). As a result of these mixed factors, the relationship between PWML and BP remains unsettled and the appropriate management of arterial BP in stroke patients with PWML is unknown. OBJECTIVE: To clarify the relationship between PWML, arterial BP, and cerebral hemodynamics. DESIGN: Cohort study followed up 6 months after index stroke. SETTING: Referral center. PATIENTS: In 41 consecutive patients with first-ever lacunar infarction, the extent of PWML detected on brain magnetic resonance images was measured. Six months after stroke, BP values were monitored during a 24-hour period and transcranial Doppler examinations were performed at rest and following the administration of acetazolamide. MAIN OUTCOME MEASURES: Correlation of cerebral hemodynamics and BP values with the extent of PWML. RESULTS: The severity of PWML varied substantially among patients, suggesting that PWML and lacunar infarctions could be due to several different mechanisms. Older age, elevated awake systolic BP, increased cerebrovascular tone, and the interaction between history of heart disease and the lowest heart rate were the strongest independent predictors of the severity of PWML. Diastolic BP and the vasodilatory capacity of the resistance vessels did not predict the severity of PWML. CONCLUSIONS: Overall, PWML are markers of systolic damage in older lacunar stroke patients with stiffer arteries. In addition, hemodynamic failure may be relevant in patients with concomitant heart disease.

Aged↗
PubMed1997

Blink reflex in patients with Wallenberg's syndrome.

Knowledge of the neural circuits involved in Wallenberg's syndrome (WS) is incomplete. Study of the blink reflex (BR) in patients with WS can help in reaching a better understanding of the physiopathology underlying clinical symptoms and may help in the prediction of clinical outcome. We evaluated the BR in response to supraorbital nerve electrical stimuli in 20 patients with WS. All patients were studied within the 1st week after onset of symptoms, and 10 of them were also studied repeatedly during a follow-up period of 3-12 months. At the first examination the long latency bilateral responses (R2 and R2c) to stimulation of the supraorbital nerve of the affected side were absent in 11, delayed in 4, and normal in 5 patients. At follow-up, there was a normalization of the BR in all patients who had absent or delayed responses at the first examination except for one patient whose responses remained absent at the 9th month. Late responses elicited on the side of the lesion by stimulation of the non-affected supraorbital nerve were normal in all but one patient. This patient died from cardiorespiratory arrest within the 1st month of the illness. One patient with normal BR responses also died in the acute phase. The BR is abnormal in most patients with acute WS and tends to normalize in a mean period of 7 months. BR pattern is not a predictor of early fatal complications in patients with this syndrome.

Adult↗
PubMed1996

Contribution of arterial blood pressure to the clinical expression of lacunar infarction.

BACKGROUND AND PURPOSE: The relation between symptomatic lacunar infarction, silent stroke, and arterial hypertension is controversial. METHODS: From 500 patients with ischemic or hemorrhagic stroke admitted to the Downtown Barcelona Stroke Registry between July 1992 and December 1994, we evaluated prospectively the prevalence of silent infarction in 249 patients who had a brain MRI. The association of risk factors with silent infarction was investigated with the use of logistic regression analysis. In a selected group of 43 patients with symptomatic lacunes, we performed at stroke follow-up transcranial Doppler sonography and 24-hour continuous blood pressure monitoring to evaluate whether blood pressure, cerebrovascular tone, and cerebral blood flow at rest and after the administration of 1 g acetazolamide correlated with silent infarction. RESULTS: A total of 147 silent infarctions were observed in 83 patients (33%). Most silent infarctions corresponded to small deep lesions in the territory of the lenticulostriate arteries. Patients with silent infarctions had higher systolic and diastolic blood pressure at stroke onset. However, on multivariate analysis, age greater than 60 years was the only risk factor associated with silent infarction. In a subgroup of 43 patients with symptomatic lacunes and patent extracranial vessels, systolic and diastolic pressure at stroke onset and diastolic pressure and vascular resistance at stroke follow-up were higher when silent infarctions co-existed. However, cerebral blood flow at rest and after acetazolamide injection were unrelated to silent infarction. CONCLUSIONS: Silent ischemia in patients with symptomatic lacunar and nonlacunar stroke was only associated with aging. However, a history of arterial hypertension was perhaps unrecognized, since hemodynamic testing and continuous blood pressure monitoring in patients with lacunar stroke suggested that the coexistence of silent lesions indicated a more generalized cerebral arteriolosclerosis.

Acetazolamide↗
PubMed1995

Early anticoagulation after large cerebral embolic infarction: a safety study.

OBJECTIVE: To assess whether hemorrhage after early anticoagulation in nonseptic embolic infarction is related to clinical severity and infarction size. BACKGROUND: Explicit clinical criteria and timing of anticoagulation after large embolic infarctions are unknown. METHODS: Out of 171 patients receiving anticoagulation between July 1992 and December 1993, 83 patients with hemispheric embolisms received heparin within 72 hours from onset (activated partial thromboplastin time [aPTT] 1.5 times control value). Stratified by age and sex, a "high-risk" group (46 patients) was defined as those having stroke symptoms involving three or more CNS domains, Mathew Scale score < or = 74, or hemorrhagic infarction on initial CT, and a "low-risk" group (37 patients) as those having stroke symptoms involving fewer than three cortical domains, or Mathew Scale score > 74, and CT showing no blood. Loss of consciousness, seizures, or history of bleeding were exclusion criteria. Repeated CTs (100%) and MRIs (36%) detailed infarctions according to standard maps and evaluated all unexplained clinical worsening. RESULTS: Prior to therapy, high-risk patients had more severe clinical deficits (p < 0.01), larger infarctions on CT (p < 0.01), and more mass effect (p < 0.01). Hemorrhagic conversion (26% in the high-risk group versus 22% in the low-risk group) and hemorrhagic worsening (4% in the high-risk group versus 13% in the low-risk group) were unrelated to admission clinical severity or infarction size, but they were related to an excessive prolongation of the aPTT (p < 0.01). CONCLUSIONS: Infarction size and clinical severity in alert patients with nonseptic embolic stroke carries no additional bleeding complications after early anticoagulation. If anticoagulants are deemed necessary, treatment delay seems unjustified. However, rigorous monitoring of the aPTT is strongly advised to keep the level at 1.5 to 2 times control values.

Aged↗
PubMed1995

[Limb shaking and loss of consciousness: a carotid-basilar artery syndrome].

We describe the brain MRI and cerebral blood flow characteristics in a patient with hypertension, severe bilateral carotid artery disease and moderate vertebrobasilar atheromatosis. When standing, the patient experienced short repetitive episodes of loss of consciousness and involuntary shaking of the lower extremities. We believe that, in this patient, the combination of bilateral perfusion insufficiency through the carotid artery, the local effects of atheromatosis of the penetrating branches arising from the basilar artery and the systemic effects of orthostatic hypotension may have caused ischemic lesions in the terminal zones of the paramedian branches of the basilar artery.

Carotid Artery Diseases↗
PubMed1994

[Compression of the spinal cord by the amyloid tissue in the thoracic vertebral amyloidoma].

Solitary amyloidoma consists of amyloid tissue deposits in the absence of systemic amyloidosis or plasma cell dyscrasia. Single vertebral amyloidoma is an unusual cause of spinal cord compression. We present the case of a 72-year-old man with medullar compression by amyloidoma affecting the sixth dorsal vertebra and with nuclear magnetic resonance images that were indistinguishable from epidural metastasis. The patient improved notably after resection.

Aged↗
PubMed1983

Percutaneous transhepatic biliary drainage. Complications due to multiple duct obstructions.

The medical histories of fifty-three consecutive patients who were scheduled for percutaneous transhepatic biliary drainage (PTBD) were reviewed for incidents of sepsis. Among the 52 patients who were successfully catheterized, there were 14 incidents of sepsis, three incidents of abscess and sepsis, and two incidents of sepsis following a pulled catheter (a total incidence of 36.5%). In 14 instances, the sepsis was attributed primarily to the presence of enteric bacteria combined with bile stasis caused by multiple duct obstruction from disseminated malignancy. The presence of bacteria in the bile of well-drained patients did not necessarily lead to sepsis. This series highlights the importance of medical alert for signs of sepsis in biliary drainage patients and suggests that external drainage is preferable in patients with incomplete emptying of the biliary system during PTBD.

Abscess↗
PubMed1982

Nephrotoxicity from angiographic contrast material. A prospective study.

Three hundred and seventy-eight hospitalized patients undergoing nonrenal angiography were evaluated for subsequent changes in renal function. Acute renal failure was defined as a rise in the serum creatinine level of 1.0 mg/dl or more. Several factors that appeared to play no significant role in causing acute renal failure included: the volume of contrast material injected, the anatomic site of injection and the presence of a prior history of cardiovascular disease or diabetes mellitus. The single risk factor identified was the presence of preexistent azotemia (blood urea nitrogen of 30 mg/dl and serum creatinine of 1.5 mg/dl). Whereas nonazotemic patients had a 2 percent incidence of definite acute renal failure, patients with chronic azotemia (mean blood urea nitrogen/creatinine = 47/2.3 mg/dl) had a 33 percent incidence. Three patients required short-term dialysis, and two required potassium-exchange resin therapy. No patient required permanent dialysis, and no patient died of acute renal failure. The persistence of a positive nephrogram 24 hours after angiography was a sensitive detector of a rise in the serum creatinine level although more expensive than the creatinine determination. While urine sediment analysis confirmed the diagnosis in many cases, it was relatively insensitive. Monitoring of urine volume proved to be of little value. We recommend a screening serum creatinine determination 24 to 48 hours after infusion of angiographic contrast material in azotemic patients.

Acute Kidney Injury↗