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Biomedical subjects

D P Briley

Publications and source records attributed to D P Briley.

9 recordsLinked to original sources
PubMed2000

Does leukoaraiosis predict morbidity and mortality?

OBJECTIVE: To determine whether leukoaraiosis predicts morbidity and mortality. BACKGROUND: Gait disturbance and leukoaraiosis both are common in the elderly. Gait disturbance predicts mortality. Leukoaraiosis may be a unifying factor to both gait disturbance and mortality. METHODS: We followed 221 patients prospectively evaluated for severity of neurologic deficits by the National Institutes of Health (NIH) stroke scale and for leukoaraiosis in seven brain regions by CT, graded as absent (n = 119, 54%), mild (in at least one of seven brain regions; n = 54, 24%), or severe (present in all seven brain regions; n = 48, 22%). Pneumonia (n = 27, 12%), falls resulting in fracture requiring hospitalization (n = 7, 3%), and death (n = 38, 17%) were end points. RESULTS: Severe leukoaraiosis predicted death (Cox hazard ratio [HR] = 2.91; 95% CI = 1.5 - 5.6), pneumonia (HR = 5.1; 95% CI = 2.4 - 10.9), death from pneumonia (HR = 8.3; 95% CI = 1.5 - 46), and falls (HR = 6.8; 95% CI = 1.5 - 30). Severe leukoaraiosis predicted a combined end point of death, pneumonia, and falls (HR = 3.5; 95% CI = 2 - 6). Other predictors were NIH stroke scale score, age, smoking, diabetes, gait score, and referral diagnosis of either dementia or Parkinsonism. Severe leukoaraiosis remained a predictor after adjustment for these other factors (HR = 2.2; 95% CI = 1.2 - 3.9), but was borderline after adjusting for gait (HR = 1.96; 95% CI = 0.97 - 3.94; p = 0.061). The combination of severe leukoaraiosis and gait disturbance had the highest risk (HR = 4.4; 95% CI = 2.4 - 7.9). CONCLUSION: Severe leukoaraiosis predicts morbidity and mortality independently of preexisting neurologic deficits. The combination of leukoaraiosis and gait disturbance carries a poor prognosis.

Accidental Falls↗
PubMed1998

Persistent inflammatory response in stroke survivors.

OBJECTIVE: Goals were to determine how long acute-phase markers remain elevated after ischemic stroke and how marker levels relate to stroke risk factors, stroke mechanism, and subsequent vascular events. METHODS: Fibrinogen (FIB), C-reactive protein (CRP), leukocytes (WBC), neutrophils (PMN), interleukin-6, and interleukin-1 receptor antagonist were measured at stroke onset and at 6 weeks, 6 months, and 1 year after enrollment, or until a vascular event occurred in 136 acute ischemic stroke patients, 76 patients with comparable risk factors for stroke, and 48 age-balanced healthy subjects. RESULTS: Multivariate logistic analysis showed that prior stroke and FIB level predicted new events in stroke patients (p < 0.04 for both), whereas congestive heart failure (p < 0.02) and creatinine level (p < 0.006) were predictive in at-risk patients. After controlling for infection, FIB, CRP, and PMN levels at baseline were higher in at-risk but not in stroke patients with recurrent events (p < 0.05 for all). At 1 year, FIB levels remained elevated in event-free stroke survivors compared with levels in the risk and control groups (p < 0.001 for both). FIB also remained higher in stroke survivors who had atheroembolism (AE) compared with non-AE stroke survivors (381+/-72 versus 342+/-78 mg/dL, p < 0.02). Peripheral vascular disease was an independent predictor (p < 0.0001) of longitudinal FIB in stroke survivors. Of note, both WBC and PMN levels were chronically elevated in patients with stroke risk factors and in stroke survivors (p < 0.0001 for both) compared with healthy elderly subjects. CONCLUSIONS: Most acute-phase markers decline gradually after stroke, but FIB remains significantly elevated and is associated with increased risk for recurrent vascular events.

Acute-Phase Proteins↗
PubMed1997

Cerebral white matter changes (leukoaraiosis), stroke, and gait disturbance.

OBJECTIVES: Leukoaraiosis, a radiological change of cerebral white matter thought to be caused by ischemia, is associated with gait disturbance. However, because of concomitant stroke and cerebral atrophy, the clinical relevance of leukoaraiosis is uncertain. We, therefore, sought to determine if leukoaraiosis is a predictor of gait disturbance after accounting for cerebral atrophy and stroke in patients with a high prevalence of cerebrovascular disease. DESIGN: Cross-sectional observational study. SETTING: Neurology service (inpatient and outpatient) of a Department of Veterans Affairs Hospital. PARTICIPANTS: Consecutive sample of 130 patients, 127 men and three women. MEASUREMENTS: The findings of a gait scale were correlated to vascular risk factors, neurological examination as quantified by the NIH stroke scale and supplemental motor scale, and to brain CT findings. Brain CT scans were rated for leukoaraiosis, cerebral infarction, and cerebral atrophy. RESULTS: Gait disturbance was more frequent and more severe in subjects with leukoaraiosis, of whom 31% had mild and 49% moderate/severe gait disturbance compared with 27% with mild and 12% with moderate/severe gait disturbance in subjects without leukoaraiosis (P < .001). Leukoaraiosis, cerebral atrophy, a history of multiple strokes, and weakness and ataxia of the legs were independent predictors of gait disturbance. The proportion and severity of leukoaraiosis increased with increasing gait disturbance in subgroups without leg deficit (P < .001) and without multiple strokes (P < .001), but no association with leukoaraiosis was shown in patients with leg deficit or a history of multiple strokes (P = .037 and P = .186, respectively). Gait disturbance was more severe when both leukoaraiosis and cerebral atrophy were present (P = .019). CONCLUSION: In our Veteran population, leukoaraiosis is an independent predictor of gait disturbance after accounting for stroke and cerebral atrophy. Although leukoaraiosis is a form of cerebrovascular disease, it appears to be most closely associated to gait disturbance in the absence of symptomatic stroke or leg deficit.

Adult↗
PubMed1994

Spontaneous echo contrast and hemorheologic abnormalities in cerebrovascular disease.

BACKGROUND AND PURPOSE: Spontaneous echo contrast (SEC) is thought to represent a risk factor for cardioembolic stroke. In vitro studies suggest that SEC results from interaction between red cells and fibrinogen. To better understand the relation between SEC and stroke and to investigate the in vivo genesis of SEC, we examined the relation between SEC, the constituents of the blood, and plasma and serum viscosity in patients with acute stroke or chronic cerebrovascular disease. METHODS: Fifty patients with acute stroke or chronic cerebrovascular disease referred for transesophageal echocardiogram (TEE) were studied by transthoracic echocardiography and TEE. Complete blood count, fibrinogen, albumin, gamma-globulin, and plasma and serum viscosity determinations were made. Left atrial SEC was graded as absent, mild, or marked by means of TEE. RESULTS: SEC was absent in 31 patients, mild in 10 patients, and marked in 9 patients. Higher grade of SEC was associated with a significantly greater percentage of patients with atrial fibrillation and larger left atrial dimension. Atrial fibrillation was present in 23% of the patients in the SEC absent group, 50% of the patients in the mild SEC group, and 78% of the patients in the marked SEC group (P < .01). Left atrial diameter averaged 3.8 +/- 0.6 cm in the SEC absent group, 4.3 +/- 1.1 in the mild SEC group, and 4.9 +/- 0.7 in the marked SEC group (P < .001). Hematocrit, white blood cell count, and platelet count did not differ among the three groups. Fibrinogen, gamma-globulin, plasma viscosity, and serum viscosity values were all significantly higher in the presence of SEC (P < .05). Fibrinogen values were 361 +/- 97 mg/dL in the SEC absent group and 427 +/- 135 mg/dL in the marked SEC group. gamma-Globulin levels were 0.75 +/- 0.23 g/dL in the SEC absent group and 1.06 +/- 0.48 g/dL in the marked SEC group. Both plasma viscosity (1.97 cp) and serum viscosity (1.64 cp) were higher in the marked SEC group than in the SEC absent group (1.77 and 1.50 cp, respectively). CONCLUSIONS: In patients with acute stroke or chronic cerebrovascular disease, the severity of SEC was not related to albumin, hematocrit, white cell count, or platelet count but rather to elevated fibrinogen levels and concomitant increases in both plasma and serum viscosity. Moreover, increasing grade of SEC was associated with significantly increased left atrial diameter and a higher percentage of patients in atrial fibrillation.

Aged↗
PubMed1993

Neutrophil adhesion in central nervous system ischemia in rabbits.

Activated neutrophils appear to be directly involved in potentiating central nervous system ischemic injury. After initial endothelial adherence, neutrophils can potentiate ischemia by causing capillary plugging and infiltrating ischemic tissue to release toxic metabolites. We used an endothelial component adherence assay to characterize neutrophil adhesion following reversible central nervous system ischemia. Rabbit spinal cord ischemia was produced by 40 min of reversible arterial occlusion. Neutrophils were isolated using density gradient centrifugation and adherence to laminin or fibronectin was determined using a myeloperoxidase assay. The baseline (N = 26) percentage of adherent neutrophils was 3.8 +/- 0.3/5.6 +/- 0.6 (laminin/fibronectin), sham-operated controls (2 h post) (N = 6) 3.3 +/- 0.5/3.9 +/- 0.4, 30 min post ischemia (N = 6) 2.5 +/- 1.1/4.1 +/-1.9, 2 h (N = 6) 7.6 +/- 1.4/9.9 +/- 2.6 (p < .05 to baseline and sham), 18 h (N = 8) 4.9 +/- 1.5/7.1 +/- 3.1, and 42 h (N = 6) 3.4 +/- 0.4/6.6 +/- 2.1. Concurrent serum fibrinogen values were baseline 142 +/- 12, sham (18 h) 141 +/- 14, 2 h 166 +/- 21, 18 h 512 +/- 43 (p < .01), and 42 h 580 +/- 86 (p < .01). These results suggest that neutrophil adherence is increased after acute central nervous system ischemia. There appears to be a limited period of increased adherence that occurs earlier than other acute phase reactants.

Acute Disease↗
PubMed1993

Circulating intercellular adhesion molecule-1 levels and neutrophil adhesion in stroke.

To examine whether changes in leukocyte adhesion properties occur during stroke, we measured circulating serum intercellular adhesion molecule 1 (cICAM-1) levels and neutrophil adhesion in acute stroke, patients at high risk of stroke, and in matched controls. Levels of cICAM-1 were significantly lower in the stroke group (186.2 +/- 15.6 ng ml-1) compared to controls (257.7 +/- 24.8) and risks (257.7 +/- 16.5). Neutrophil adhesion was significantly higher in the stroke group (23.6 +/- 4.3%; n = 14) compared to controls (9.7 +/- 2.3%; n = 12) and risks (12.7 +/- 2.5%; n = 13). These data suggest that changes in leukocyte adhesion dynamics are occurring in acute stroke.

Cell Adhesion↗
PubMed1989

Neurological disease associated with antiphospholipid antibodies.

The Hemostasis and Thrombosis Laboratory at the Oregon Health Sciences University identified 80 patients with significantly elevated anticardiolipin antibody (ACLA) levels. We reviewed all of their available medical records and found that 25 of these patients had associated neurological symptoms or disorders. These symptoms and disorders could be grouped into four distinct clinical patterns comprising encephalopathy, multiple cerebral infarctions, migraine-like headaches, and visual abnormalities including amaurosis fugax and ischemic optic neuropathy. Cerebral ischemia best explained these neurological dysfunctions. There was no correlation between the presence or absence of neurological disease and ACLA levels, but ACLA levels were higher in patients with encephalopathy than in others with neurological involvement (p less than 0.05). How neurological dysfunction and the presence of these antiphospholipid antibodies are related remains to be clarified. Nevertheless, in patients with unexplained cerebral ischemia, establishing the presence of ACLA may have prognostic and therapeutic importance. In particular, acute immunosuppressive therapy and plasmapheresis may be useful in patients with acute ischemic encephalopathy.

Adult↗
PubMedDate not supplied

Multiple cerebral infarctions and dementia associated with anticardiolipin antibodies.

Antibodies to negatively charged phospholipids including cardiolipin have been recognized in the sera of patients with systemic lupus erythematosus and other disorders. We report 4 patients who experienced cerebral infarctions and dementia in association with anticardiolipin antibodies. These patients did not have the characteristic lupus anticoagulant or systemic lupus erythematosus. The occurrence of anticardiolipin antibodies in patients with multiple cerebral infarctions who do not have evidence of a systemic vasculitis or inflammatory condition suggests that this association may be more common than previously recognized. It may be useful to test for the presence of anticardiolipin antibodies in patients who have unexplained cerebral infarctions.

Adult↗