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C H Millikan

Publications and source records attributed to C H Millikan.

At least 19 recordsLinked to original sources
PubMed2001

Stroke: 1970-1977.

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American Heart Association↗
PubMed1996

Stroke is an emergency.

Stroke is an emergency. Ischemic stroke is similar to myocardial infarction in that the pathogenesis is loss of blood supply to the tissue, which can result in irreversible damage if blood flow is not restored quickly. Public education is needed to emphasize the warning signs of stroke. Patients should seek medical help immediately, using emergency transport systems. Therapy geared toward minimizing the damage from an acute stroke should be started without delay in the emergency room. This includes measures to protect brain tissue, support perfusion pressure, and minimize cerebral edema. Strategies for improving recovery should also begin immediately. All major medical centers need stroke teams and stroke units. Stroke prevention should be given high priority as a public health strategy. Risk factor management should be part of general health care and should begin in childhood, with emphasis on nutrition, exercise, weight control, and avoidance of tobacco. Health screening and early treatment of hypertension and hypercholesterolemia has decreased the incidence of stroke and heart disease, but these efforts need to be expanded to reach all segments of the population. Basic research has opened the door to new therapies aimed at re-establishing blood flow and limiting tissue damage. Clinical trials have already led to changes in stroke prevention, including studies of carotid endarterectomy and ticlopidine and warfarin therapy (for patients with atrial fibrillation). Trials in progress are testing the usefulness of ancrod, neuroprotective agents, antioxidant agents, anti-inflammatory agents, low-molecular-weight heparin, thrombolytic drugs, and angioplasty. Any delay starting therapy after an acute stroke will result in progressive, irreversible loss of brain tissue. Clinicians should remember that for a stroke patient, time is brain tissue.

Anticoagulants↗
PubMed1991

A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride--a review.

Cocaine, especially in its alkaloidal or "crack" form, has been increasingly associated with cerebrovascular disease. Before the crack epidemic, cocaine hydrochloride (HCl) was also implicated as a cause of stroke. However, less is known about the differences in stroke subtypes, age at stroke onset, or presence of underlying structural cerebrovascular disease with different forms of cocaine use. We compared 26 patients (previously reported) from our four institutions plus 16 cases reported in the literature of stroke associated with alkaloidal cocaine to 63 (57 reported in the literature and six not previously reported from our four institutions) cases of stroke associated with cocaine HCl. Ischemic and hemorrhagic strokes are equally likely after alkaloidal cocaine use, whereas cocaine HCl is more likely (approximately 80% of the time) to cause hemorrhagic stroke, with approximately half the intracranial hemorrhages occurring from ruptured cerebral saccular aneurysms or vascular malformations. The presence of an underlying cerebral aneurysm was more common among patients with cocaine HCl-associated strokes than alkaloidal cocaine-associated strokes. Cerebral infarction was significantly more common among the alkaloidal cocaine users than in all the cocaine HCl users, and this was also true when alkaloidal cocaine users were compared with parenteral cocaine HCl (intravenous and intramuscular) users. Only hemorrhagic stroke has been reported with intravenous cocaine HCl use. We conclude that the pathogenesis of cocaine-related stroke is heterogeneous, and depends, in part, on the form of cocaine used.

Administration, Intranasal↗
PubMed1990

Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine.

BACKGROUND AND METHODS: The use of cocaine, especially one of its alkaloidal forms ("crack"), has been increasingly associated with cerebrovascular disease. To clarify the clinical, radiologic, and pathological features of the events associated with cocaine use, we identified 28 patients at four medical centers who had stroke temporally related to the use of alkaloidal cocaine (during or within 72 hours of use). RESULTS: The 28 patients had the following types of cerebrovascular event: cerebral infarction (n = 18 [2 hemorrhagic; 1 fatal]) in the areas supplied by the middle cerebral artery (n = 10), anterior cerebral artery (n = 3), posterior cerebral artery (n = 1), and vertebrobasilar arteries (n = 4); subarachnoid hemorrhage (n = 5); intraparenchymal hemorrhage (n = 4); and primary intraventricular hemorrhage (n = 1). Eighteen patients (64 percent) had acute neurologic symptoms immediately or within one hour of using cocaine. Fifteen patients (45 percent) with either occlusive or hemorrhagic strokes had sever headache as an early symptom. Vasculitis was not suggested by radiography in any patient, nor was it identified on pathological examination in one patient who died. All the patients were young (mean age, 34 years; range, 23 to 49) and had no other apparent, direct cause of stroke. Other risk factors for stroke among the patients included mild mitral-valve prolapse (n = 4), hypertension (n = 4), cigarette smoking (n = 8), and regular alcohol use (n = 6). CONCLUSIONS: There is a strong temporal association of the use of alkaloidal cocaine with both ischemic and hemorrhagic cerebrovascular events. Cocaine-related stroke probably has many causes. A thorough history focusing on the use of cocaine and toxicologic screening of urine and serum should be part of the evaluation of any young patient with a stroke.

Adult↗
PubMed1987

Transient global amnesia: clinical characteristics and prognosis.

We studied the clinical characteristics of transient global amnesia (TGA) in 277 patients with an average follow-up of 80 months. The syndrome occurred most frequently after age 50. There was a history of migraine in 14.1% and cerebrovascular diseases in 11.2% of patients, but these conditions were usually not temporally linked to TGA. Characteristic antecedent events and activity such as exertion existed in 33.4%. The incidence of TGA was 5.2 per 100,000 per year in Rochester, MN. Although 23.8% of the patients had recurrent episodes, they were not at increased risk for subsequent stroke.

Aged↗
PubMed1978

Cerebral circulation.

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Carotid Artery Thrombosis↗
PubMed1976

Progressing stroke. Angiographic aspects.

Progressing strokes were noted in 17 of 256 patients who underwent surgery for atheromatous disease involving the internal carotid artery. This disorder was characterized by an active increase in the neurologic deficit during an 18- to 24-hour period. Although angiographic findings were neither specific for this type of cerebrovascular disease nor uniformly present, the angiography did indicate that not only embolization of the cerebral leptomeningeal conducting vessels but also collaterization through them was a pertinent mechanism.

Aged↗
PubMed1975

Cerebral vasospasm and ruptured intracranial aneurysm.

The literature concerning cerebral vasospasm associated with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysm contains no definitive study of patients to determine whether there is (1) any clinical picture consistently present coincident with known cerebral vasospasm, (2) any relationship between mortality and known vasospasm, and (3) any relationship between serious brain damage (morbidity) and known vasospasm. To answer these important questions, experience with 198 consecutive acute SAH patients (every patient had a cerebral angiogram demonstrating one or more intracranial aneurysms) was studied. The experience with these 198 consecutive patients led to the conclusions that (1) there is no clinical picture consistently present coincident with known cerebral vasospasm; (2) cerebral vasospasm has no effect on the mortality from SAH due to ruptured aneurysm; and (3) there is no relationship between the frequency and severity of the complications from surgical or conservative treatment and the presence or absence of vasospasm.

Adolescent↗
PubMedDate not supplied

Treatment of progressing stroke.

Adequate management of a patient with progressing stroke should include the following. (1) Understanding of the pathophysiologic mechanisms causing cerebral infarction. (2) prompt diagnosis. When the possibility of progressing stroke is considered by the physician, it automatically becomes the priority diagnosis. (3) Prompt clinical and laboratory evaluation should be initiated. (4) Prompt institution of anticoagulant treatment unless contraindicated is appropriate. Heparin followed by coumadin is used most commonly. (5) If there is not prompt cessation of progression over the next 1--3 hr (following adequate anticoagulation), the patient should have a repeat CAT scan, and in many instances, a carotid angiogram to investigate the possibility of misdiagnosis or that an ulcerated atherosclerotic plaque is present releasing emboli not affected by anticoagulation. (6) If any progression occurs, the question of antiedema treatment should be raised.

Acute Disease↗