Interpreting brain scans of lupus patients taken after seizures or migraines.
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Brain↗
Biomedical subjects
C Millikan
Publications and source records attributed to C Millikan.
Central nervous system disease in patients with systemic lupus erythematosus.
Central nervous system (CNS) dysfunction in patients with systemic lupus erythematosus (SLE) is highly variable, although it is often described under a single heading of "neuropsychiatric" or "CNS" SLE. To clarify these CNS abnormalities, we studied 91 lupus patients, 63 of whom had CNS symptoms or signs, over 599 patient years. By placing patients in relatively homogeneous clinical groups (stroke, seizure, suicide attempt, hallucination, confusion, decreased alertness) we detected significant (but variable among groups) correlations with other manifestations of SLE, suggesting separate mechanisms for each CNS disorder. These correlations were lost if all "CNS-SLE" was considered as a single group. Patients with decreased alertness often had undetected systemic infections and had a high death rate from infection, rather than from CNS-SLE. The understanding of the pathogenesis and potential treatment of CNS disorders in lupus will depend on classifying the patients into homogeneous groups.
Behavior↗
Embolic stroke in aged rats.
BACKGROUND AND PURPOSE: Although stroke is a disorder associated with aging, experimental studies of stroke are conducted in young adult (2-4-month-old) animals (rat life span, 27-29 months). To determine whether histopathologic changes caused by cerebral infarction would be altered in aged animals, we produced embolic cerebral infarction in 17 aged (23-24-month-old) and 16 young (2-4-month-old) rats. METHODS: The right common carotid artery was irradiated with a laser (632 nm, 200 mW/cm2, 15-20 minutes) after the intravenous injection of the photosensitizing dye Photofrin II (12.5 mg/kg). This produces a nonocclusive platelet thrombus that spontaneously embolizes to the brain. Animals were killed 4 days later. RESULTS: Analysis was done on 142 infarcts, 68 in aged rats and 74 in young rats. Hypercellularity, with infiltration of macrophages, was more common within small infarcts (less than 1 mm) in young than in aged rats (p = 0.002), and hypertrophy of astroglial fibers surrounding the infarcts was more prominent in young rats. Larger infarcts (greater than or equal to 1 mm) were often hypocellular, with a trend toward more macrophages in the periphery of the infarcts in young than in old animals (p = 0.170). CONCLUSIONS: The infiltration of macrophages into cerebral infarcts and the hypertrophy of astroglial fibrils surrounding these infarcts are reduced in the aged rat. These age-related differences emphasize the importance of using appropriately aged animals in experimental models of stroke.
Aging↗
Platelet emboli in rat brain cross when the contralateral carotid artery is occluded.
The pathogenesis of embolic events ipsilateral to an occluded carotid artery is uncertain. To examine this question we combined occlusion of the left common carotid artery with embolism from the right common carotid artery in rats. Following ligation of the left carotid artery in 20 experimental rats, we irradiated the right carotid artery with a laser (632 nm, 200 mW/cm2, 12-15 minutes) following the intravenous injection of 12.5 mg/kg of the photosensitizing agent Photofrin II. Controls had left carotid artery occlusion with (n = 13) or without (n = 6) Photofrin II. Fifteen of the 20 experimental rats survived to be perfused at 24 hours; cerebral infarcts were identified in 12 rats, with bilateral infarcts in 10. There were 112 infarcts (101 small [less than 2.5 mm] and 11 large [greater than 2.5 mm] on the right and 103 (93 small and 10 large) on the left. Emboli were seen in association with some infarcts and were evenly distributed in the two hemispheres (37 emboli on the right and 40 on the left, with the midline azygous artery occluded in four animals). Left carotid artery occlusion did not produce infarcts or emboli in the controls. We conclude that cerebral infarcts in the distribution of an occluded common carotid artery may be caused by emboli from the contralateral carotid artery in rats.
Animals↗
The fallacy of the lacune hypothesis.
We review the definition, pathogenesis, natural history, and prognosis and describe the first experimental model of lacunes. Defined pathologically or radiologically, lacunes are small cerebral infarcts which become cystic and are caused by occlusion of small arteries. The clinical definition of lacune is confused. The word "lacune" means a small stroke. While the immediate mortality rate from a small stroke is low, many patients are unable to return to work and the long-term prognosis is guarded. Photochemical damage to the carotid artery of rats produces microemboli to the brain, resulting in cavitary lesions resembling lacunes in humans. The "lacune hypothesis" is a fallacy because small cerebral infarcts are not caused solely by a combination of hypertension and small vessel disease, and the various "lacunar syndromes" are simply small strokes which should be investigated as such.
Arterial Occlusive Diseases↗
Anticoagulant treatment to prevent cerebral infarction.
The indications for anticoagulant treatment to prevent cerebral infarction or progression of cerebral infarction are now clear. The indications are: (1) Prevention of recurrent embolization from a cardiac source (long-term anticoaguland treatment). (2) Transient ischemic attacks (particularly vertebrobasilar system) if a surgically accessible causative lesion, polycythemia, and thrombocytosis are not present (anticoagulants for a few months.) (3) Progressing stroke in either systme assuming that the neurological defect is partial and CT scan shows no evidence of bleeding (anticoagulants for a few months.) (4) Rarely, completed stroke (long-term).
Anticoagulants↗