Refer to: Garner JT, Jacques S: Positional vertigo and bruit-A surgical emergency. West J Med 127: 414-416, Nov 1977
Positional Vertigo and Bruit -A Surgical Emergency JOHN T. GARNER, MD SKIP JACQUES, MD Pasadena '!I. .7 ..I
ATHEROMATOUS DISEASE of the extracranial arteries as a major cause of stroke has been amply documented.'-1' Furthermore, it is now apparent that transient isehemic attacks (TIA) can be a prelude to stroke and signify serious underlying vascular disease.1 Retrospective analysis indicates that many cases of cerebral infarction are heralded by single or multiple episodes of transient cerebral ischemia.2 We present three cases in which vertigo produced by positional change of the head was superimposed on a TIA symptom complex. Each of these patients had a high-grade stenosis of the internal carotid artery without evidence of pathology in the vertebral circulation. The symptoms were eliminated by carotid endarterectomy.
Reports of Cases CASE 1. A 61-year-old white man was seen because of intermittent symptoms of visual disturbance and one episode of transient aphasia From the Departments of Neurological Surgery and Radiology. Huntington Memorial Hospital and the Huntington Institute of Applied Medical Research, Pasadena. Dr. Jacques is now a postdoctoral Fellow in Biology, California Institute of Technology.
Pasadena. Submitted December 10, 1976. Reprint requests to: John T. Garner, MD, 744 FairmouLnt Avenue, Pasadena, CA 91105.
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Figure 1.-Pronounced narrowing at carotid bifurcation is shown (case 1).
over several weeks. A bruit was auscultated over the left carotid bifurcation in the neck. Arrangements were made for admission to hospital and angiography. Two days before admission, the patient reported vertigo when he turned his head. These spells could be brought on at will by looking to the right. The patient was admitted to hospital and four-vessel angiography was carried out which showed a 90 percent stenosis of the left internal carotid artery (Figure 1). The remainder of the examination gave essentially negative findings. Plans were made for carotid endarterectomy the following day. During the night a massive cerebrovascular accident occurred, leaving the patient with a persistent hemiparesis and nominal
Figure 2.-String-like segment of internal carotid is evident (case 2).
aphasia. Subsequent angiography showed an occluded internal carotid artery. CASE 2. A 55-year-old white man was seen because of intermittent attacks of left-sided weakness and numbness of six months' duration. Three days before admission he noted the onset of vertigo on turning his head. Examination showed a loud bruit over the right carotid bifurcation. On the morning of consultation the patient stated that the episodes of vertigo on head turning had increased in intensity. Based on the experience in case 1, immediate four-vessel angiography was carried out which showed a 90 percent stenosis of the right internal carotid artery by a large arteriosclerotic plaque (Figure 2). The vertebrobasilar circulation was normal. The patient was taken immediately to surgery from radiology and a successful endarterectomy was done with complete resolution of symptoms.
CASE 3. A 57-year-old white man, a physician, was seen with a history of fleeting attacks of aphasia and lapses of attention. He had not planned to seek medical attention until after the Christmas holidays but became concerned at the onset of vertiginous attacks of mounting severity on head turning or extension. A loud bruit was auscultated over the left carotid bifurcation. Immediate four-vessel angiography showed a 90 percent stenosis of the internal carotid artery on the left (Figure 3), a 40 percent stenosis on the right and a normal vertebrobasilar circulation. Prompt endarterectomy was followed by complete amelioration of symptoms. Findings on vertebral angiograms in all three cases were normal.
Figure 3. Pronounced narrowing of internal carotid artery is shown, with imprint of large plaque and superimposed clot projecting into lumen from anterior portion of vessel wall (case 3).
Discussion Transient ischemic attacks are episodes of reversible focal neurological dysfunction caused by an interruption of blood supply to an area of the brain. The interruption is usually vascular in origin but may also have a cardiac-related cause or a combination of both. Embolization of fragments of vessel wall or atheroma and hemodynamic changes are the usual mechanisms invoked to explain TIA'S.3A-; The importance of TIA"S as harbingers of impending stroke is becoming increasingly more apparent.12'7 It therefore appears that surgical correction of atheromatous lesions, especially of the carotid bifurcation in selected patients, is a major therapeutic approach to prevent catastrophic neurological dysfunction.6'9 Classically, the manifestations of TIA's are classified according to the site of focal cerebral ischemia with vertigo being ascribed to the vertebrobasilar system.. '10 The cases presented here would suggest that vertigo, accentuated by a change in head position, can be a sequela of highgrade stenosis of the internal carotid artery in the neck. The three patients shared a common symptom complex of occasional TIA'S, sudden onset of positional vertigo, bruit over the carotid bifurcation and a 90 percent stenosis of the affected carotid artery. In no case was there a pathologic condition evident in the vertebrobasilar circulation. The pathogenesis of the positional THE WESTERN JOURNAL OF MEDICINE
vertigo is probably due to kinking and occlusion of the stenotic portion of the internal carotid artery when the head is turned. The frightening nature of the symptom immediately caused each patient to resume a neutral head position. In the first patient, total occlusion probably occurred because of absence of response to the symptoms during sleep. In each of the operated cases there was complete immediate resolution of symptoms. It is of interest that a recently published selfevaluation of stroke gave remarkably similar symptoms to those in our cases, as well as similar angiographic findings." The "dizziness" in this instance was ascribed to a lesion of the posterior internal capsule based on recent neurophysiological data.'2,"3 The authors conclude that the symptom complex described here may constitute an acute surgical emergency and should be treated as such.
Summary Three cases of atheromatous disease of the carotid artery heralded by vertigo on head turning are described. In all cases auscultation showed a bruit and angiographic findings were consistent with pronounced carotid stenosis and plaque formation without involvement of the vertebral circulation. The authors stress the need for immediate evaluation in patients with this symptom complex. REFERENCES
1. Whisnant JP: Epidemiology of stroke: Emphasis on transient
cerebral ischemic attacks and hypertension. Stroke 5:68-70, 1974 2. Heyman A, Leviton A, Millikan CH, et al: Report of the Joint Committee for Stroke Facilities-XI. Transient focal cerebral ischemia: Epidemiological and clinical aspects. Stroke 5:275-287, 1974 3. Blaisdell FW, Glickman H, Trunkey DD: Ulcerated atheroma of the carotid artery. Arch Surg 108:491-496, 1974 4. Atik M, Dein 10, Wolfson NJ: Significance of ulcerated lesions of the carotid arteries. Am Surg 39:681-687, Dec 1973 5. Houser OW, Sundt TM, Holman CB, et al: Atheromatous disease of the carotid artery: Correlation of angiographic, clinical, and surgical findings. J Neurosurg 41:321-331, 1974 6. Fields WS: Selection of stroke patients for arterial reconstructive surgery. Am J Surg 125:527-529, 1973 7. Toole JF, Janeway R, Choi K, et al: Transient ischemic attacks due to atherosclerosis: A prospective study of 160 patients. Arch Neurol 32:5-12, 1975 8. Millikan CH: Summary of the Ninth Princeton Conference on cerebral vascular diseases, January 9-11, 1974. Stroke 5:429-438, 1974 9. DeWeese JA, Rob CG, Satran R, et al: Results of carotid endarterectomies for transient ischemic attacks-five years later. Ann Surg 178:258-264, 1973 10. Toole JF, Tuscott BL, Anderson WW, et al: Report of Joint Committee for Stroke Facilities-VII. Medical and surgical management of stroke. Stroke 4:269-320, 1973 11. Brodal A: Self-observations and neuroanatomical considerations after a stroke. Brain 96:675-694, 1973 12. Boisacq-Schepens N, Hanus M: Motor cortex vestibular responses in the chloralosed cat. Expl Brain Res 14:539-549, 1972 13. Gildenberg PL, Hassler R: Influence of stimulation of the cerebral cortex on vestibular nuclei units in the cat. Expl Brain Res 14:77-94, 1971
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Refer to: Liebman WM, Rosental E: Benign lymphoid hyperplasia of the colon. West J Med 127:416-418, Nov 1977
Benign Lymphoid Hyperplasia of the Colon WILLIAM M. LIEBMAN, MD ELDAD ROSENTAL, MD San Francisco
BENIGN LYMPHOID HYPERPLASIA of the colon in children has been frequently confused with multiple polyposis of the colon, resulting in unnecessary surgical procedures.' Yet, this disease has distinctive roentgenographic features suggestive of its diagnosis, although a biopsy is necessary for confirmation of the nature of the nodular lesions.2'3 This paper describes the case of an infant with benign hyperplasia of the colon and reviews the current state of knowledge about this disease.
Report of a Case A 10-month-old girl was admitted to the University of California Medical Center with a history of recurrent blood, predominantly occult, in the bowel movements since 6 months of age. Macrocytic megaloblastic anemia was diagnosed after extensive study including urine and plasma amino acid screen (normal), serum folate and vitamin B,2 levels (low) and bone marrow examination. Treatment was begun with folate and vitamin B12. There was no response to this regimen, and a 1-unit transfusion of whole blood was administered by the private physician, which raised the hemoglobin level from 7.5 grams per 100 ml to 9.0 grams per 100 ml and the hematocrit reading from 23 to 27 percent. The patient weighed 4.2 kg (9.3 pounds) at birth. The pregnancy had lasted 40 weeks. She fed well initially but subsequently had isolated episodes of vomiting or atypical, segmental rashes while receiving several types of formula and baby From the Division of Gastroenterology, Department of Pediatrics, University of California, San Francisco. Submitted, revised, January 25, 1977. Reprint requests to: William M. Liebman, MD, Department of Pediatrics, University of California, San Francisco, San Francisco, CA 94143.