Ocular Manifestations of Insufficiency or Thrombosis of the Internal Carotid Artery*

Hollenhorst, Robert W.

doi:10.1016/s0002-9394(14)76496-7

Cited by 71 publications

(25 citation statements)

References 36 publications

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“…3 It was evident that, as reported in other studies, 4 " 7 the neurovascular signs utilized were helpful in making an inference about the presence of disease in the ipsilateral vessel, but we were unable to predict in any given situation whether the responsible vessel was normal, stenotic, or occluded, since each possibility was noted to be present for any given set of parameters. One patient with unilateral transient ischemic attacks of the carotid system had a carotid bifurcation bruit, cholesterol emboli in the ipsilateral retina, and a decreased ipsilateral retinal artery pressure, yet had bilaterally normal carotid and intracranial vessels.…”

Section: Discussionmentioning

confidence: 74%

Clinical Indicators of Extracranial Carotid Artery Disease in Patients With Transient Symptoms

Ramírez-Lassepas

Sandok

Burton

1973

Stroke

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Clinical Indicators of Extracranial Carotid Artery Disease in Patients With Transient Symptoms• The clinical findings in 64 patients with transient symptoms of unilateral carotid system ischemic disease (amaurosis fugax or transient focal cerebral ischemic attacks or both) were reviewed in an effort to determine the value of the neurovascular examination in predicting the presence and extent of roentgenographically demonstrated ipsilateral extracranial internal carotid artery disease. Amaurosis fugax seems to be a highly specific indicator of disease, being associated with 4% of normal vessels as compared to 27% for patients with transient focal cerebral ischemic attacks alone. In patients with transient symptoms, the incidence of a normal, ipsilateral carotid artery was 36% in the absence of any positive neurovascular findings, 15% in the presence of an ipsilateral carotid bruit, 6% in the presence of ipsilateral retinal embolic events, 5% in the presence of ipsilateral reduction in superficial temporal or carotid (or both) pulse, 4% in the presence of an ipsilateral reduction in retinal artery pressure, and 3% when more than one of these findings were noted. The neurovascular examination appears to be a useful adjunct in detecting the presence or absence of ipsilateral carotid disease. However, no combination of symptoms or signs would, in all cases, allow one to accurately determine whether a vessel was abnormal, stenotic, or occluded.

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Section: Discussionmentioning

confidence: 74%

Clinical Indicators of Extracranial Carotid Artery Disease in Patients With Transient Symptoms

Ramírez-Lassepas

Sandok

Burton

1973

Stroke

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“…Intra-arterial source. Although this source of cerebral emboli was postulated 66 and evidence of an intracarotid source of retinal cholesterol emboli was presented 67 more than 30 years ago, workers in the neurovascular area have been reluctant to infer that similar emboli are carried to the brain. As with emboli from a cardiac source, 60 it is seldom possible to prove that an embolus from an intra-arterial source has occluded a cerebral vessel.…”

Section: Pathogenesis (Cause) Of Lacune(s) Hypertensionmentioning

confidence: 99%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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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. (Stroke 1990;21:1251-1257) T he "lacune hypothesis" states that lacunes are caused by a combination of hypertension and characteristic vascular lesions involving single perforating brain arteries.

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“…These lesions, however, can also occur in persons with conditions other than diabetes, 1 such as hypertension, [2][3][4][5][6] carotid atherosclerotic disease, 7 blood dyscrasias, 8 systemic infections, [9][10][11] and those who have previously undergone radiotherapy. 12 Recent population-based studies in older persons without diabetes have indicated a link between the presence of these retinopathy lesions and an increased risk of subsequent stroke.…”

Section: Introductionmentioning

confidence: 99%

Five-year incidence and progression of vascular retinopathy in persons without diabetes: the Blue Mountains Eye Study

Cugati

Luisa

Wang

et al. 2005

Eye

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Purpose To assess the 5-year incidence of vascular retinopathy and its associations in an older nondiabetic population. Methods The Blue Mountains Eye Study examined 3654 residents aged 49 þ years (82.4% response rate) during 1992-1994, and re-examined 2335 (75.1% of survivors) during 1997-1999. Retinopathy lesions (microaneurysms, haemorrhages, hard or soft exudates) were assessed from 6-field retinal photographs in persons without diabetes. Incident retinopathy was assessed in those at risk. Hypertensive status was defined following the WHO/International Society of Hypertension guidelines. Results Of the 2335 re-examined, 195 had retinopathy lesions at baseline and 1725 were at risk of retinopathy after excluding subjects with diabetes (n ¼ 261), retinal vein occlusion (n ¼ 52) or missing/un-gradable photographs (n ¼ 102). The cumulative 5-year incidence was 9.7% (95% confidence intervals (CI) 8.3-11.1%). Age was the only factor significantly associated with incident retinopathy (P for trend ¼ 0.012). Neither fasting blood glucose (age-sex-adjusted P ¼ 0.147) nor hypertension (adjusted P for trend ¼ 0.43) was associated with incident retinopathy. Of the 195 with retinopathy lesions at baseline, 3.5% developed diabetes, 13.3% progressed, and 72.3% regressed/disappeared over 5 years. Progression was positively associated with elevated blood pressure (BP) (adjusted odds ratio (OR) 1.3, 95% CI 1.1-1.6 per 10 mmHg systolic BP) and inversely associated with fasting glucose level (OR 0.36, CI 0.14-0.92 per mmol/l increase). Aspirin use was weakly associated with regression (OR 2.4, CI 1.0-6.0). Conclusions Over 5 years, retinopathy developed in 10% of older people without diabetes, while 72% of baseline lesions regressed. Age was significantly associated with the development of these lesions.

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Ocular Manifestations of Insufficiency or Thrombosis of the Internal Carotid Artery*

Cited by 71 publications

References 36 publications

Clinical Indicators of Extracranial Carotid Artery Disease in Patients With Transient Symptoms

Clinical Indicators of Extracranial Carotid Artery Disease in Patients With Transient Symptoms

The fallacy of the lacune hypothesis.

Five-year incidence and progression of vascular retinopathy in persons without diabetes: the Blue Mountains Eye Study

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