Elsevier

Journal of the Neurological Sciences

Volume 9, Issue 2, September–October 1969, Pages 285-320
Journal of the Neurological Sciences

Ischaemic cerebrovascular diseases in an autopsy series Part 2. Prevalence, location, pathogenesis, and clinical course of cerebral infarcts

https://doi.org/10.1016/0022-510X(69)90078-1Get rights and content

Abstract

Among 994 consecutive autopsies, 320 cases of ischaemic cerebrovascular disease were found. In 196 of the cases the disease had given clinical symptoms; they constitute 76.3% of all patients with stroke. The median age for men with ischaemic cerebrovascular disease was 73.2 years, for women 75.6. The ratio of men to women was 1:1.04.

Altogether there were 400 infarcts with a diameter over 0.5 cm. In addition, 155 cases had one or more deep-seated infarcts less than 0.5 cm in diameter (lacunar state). Thrombi or emboli in relevant arteries were found by gross examination in 89.0% of all large recent infarcts. Cases where no gross occlusion could be found were grouped as non-embolic or embolic. Whenever there was doubt as to the genesis of the lesion, the case was assigned to a group of unclassified lesions.

The thrombotic and other non-embolic infarcts were evenly distributed in the brain. The infarcts due to embolism were preferentially located in the territory of the middle cerebral artery.

Many of the infarcts without verified gross occlusion were probably due to thrombi or emboli which had been overlooked or had resolved. Alternatively, they could have been due to a combination of localized arterial stenosis and systemic factors. Overt hypotension was present only in a few cases.

In patients with occlusion distal to the circle of Willis the extent of the infarct depended upon the efficiency of the circulation in the neighbouring arterial territory, and probably also upon the level of the systemic blood pressure. In the group of infarcts without gross occlusion, the embolic lesions were generally larger than the non-embolic ones.

Platelet aggregates were frequently found in small leptomeningeal and intracerebral arteries. They were more prevalent in cases with verified thrombi and non-embolic infarcts than in cases of embolism.

In 58 of 138 recent infarcts the brain lesions were haemorrhagic. The bleeding appeared to depend upon a renewed blood flow into the ischaemic area. Most haemorrhagic infarcts were due to embolism. Anticoagulant therapy did not appear to be the primary factor initiating haemorrhage but it had possibly aggravated the bleeding.

In 211 instances the occlusions and infarcts had given rise to clinical symptoms. In addition, 7 patients had suffered a clinical stroke syndrome, but no relevant thrombo-embolic occlusion or infarct could be found. Patients with embolism had a shorter length of survival after the onset of the symptoms than patients with ischaemic lesions of other types.

Sudden onset, followed by a steady course, was observed in 81.3% of the cases with known clinical course. The remaining cases, most of which had thrombi or non-embolic infarcts without gross occlusion, presented an intermittent, recurring, stepwise, or gradual course. In some of the cases with thrombi, repeated attacks of symptoms could be ascribed to periods of active extension of the thrombus. Platelet aggregates in small arteries were particularly frequent in cases with intermittent or recurring symptoms, but they occurred also in cases with all other types of course. Multiple, deep-seated infarcts or a lacunar state could at times give a clinical history similar to the cases with intermittent, recurring, or stepwise course. These cases should be separated from those in which the stuttering or progressive course was caused by one localized vascular lesion.

References (104)

  • J.H.A. Van der Drift

    Ischemic cerebral lesions

    Angiology

    (1961)
  • J.H. Adams et al.

    The effects of systemic hypotension upon the human brain

    Clinical and neuropathological observations in 11 cases

    Brain

    (1966)
  • R.D. Adams et al.

    Vascular diseases of the brain

    Bull. New Engl. med. Cent.

    (1947)
    R.D. Adams et al.

    Vascular diseases of the brain

    Bull. New Engl. med. Cent.

    (1947)
    R.D. Adams et al.

    Vascular diseases of the brain

    Bull. New Engl. med. Cent.

    (1947)
  • R.D. Adams et al.

    Pathology of cerebral arterial occlusion

  • R.D. Adams et al.

    Progressing stroke: Pathogenesis

  • R.D. Adams et al.

    Vascular diseases of the brain

    Ann. Rev. Med.

    (1953)
  • W.C. Alvarez

    Little Strokes

  • S.K. Battacharji et al.

    Stenosis and occlusion of vessels in cerebral infarction

    Brit. med. J.

    (1967)
  • R. Bauer et al.

    Arteriographic study of cerebrovascular disease, Part 2 (Cerebral symptoms due to kinking, tortuosity, and compression of carotid and vertebral arteries in the neck)

    Arch. Neurol. (Chic.)

    (1961)
  • J. Bøe et al.

    The blood pressure in a population

    Blood pressure readings and height and weight in the adult population of the city of Bergen

    Acta med. scand.

    (1957)
  • J. Cammermeyer

    The agonal nature of cerebral red softenings: Re-evaluation of the morphological findings

    Acta psychiat. neurol. scand.

    (1953)
  • A.B. Carter

    Ingravescent cerebral infarction

    Quart. J. Med.

    (1960)
  • S. Cobb et al.

    Cerebral hemorrhage from venous and capillary stasis

    Amer. J. med. Sci.

    (1929)
  • M.M. Cohen

    Cerebrovascular accidents

    A study of two hundred and one cases

    Arch. Path.

    (1955)
  • F.M. Cole et al.

    Comparative incidence of cerebrovascular lesions in normotensive and hypertensive patients

    Neurology (Minneap.)

    (1968)
  • E. Corday et al.

    The clinical aspects of cerebral vascular insufficiency

    Ann. intern. Med.

    (1957)
  • C.B. Courvillle

    Pathology of the Central Nervous System

  • P.M. Dalal et al.

    Cerebral embolism

    Angiographic observations on spontaneous clot lysis

    Lancet

    (1965)
  • T. Dalsgaard-Nielsen

    Survey of 1000 cases of apoplexia cerebri

    Acta psychiat. neurol. scand.

    (1955)
  • N.J. David et al.

    Fatal atheromatous cerebral embolism associated with bright plaques in the retinal arterioles

    Report of a case

    Neurology (Minneap.)

    (1963)
  • D. Denny-Brown

    Recurrent cerebrovascular episodes

    Arch. Neurol. (Chic.)

    (1960)
  • D. Denny-Brown et al.

    The cerebral collateral circulation, Part 2 (Production of cerebral infarction by ischemic anoxia and its reversibility in early stages)

    Neurology (Minneap.)

    (1957)
  • J.R. Derrick et al.

    Carotid kinking as a cause of cerebral insufficiency

    Circulation

    (1962)
  • W.K. Ehrenfeld et al.

    Embolization and transient blindness from carotid atheroma

    Surgical considerations

    Arch. Surg.

    (1966)
  • L. Emblem

    Apoplexy

    Pathogenesis

    Acta psychiat. neurol. scand.

    (1961)
  • J.P. Evans et al.

    Histologic studies of the brain following head trauma, Part 3 (Post-traumatic infarction of cerebral arteries, with consideration of the associated clinical picture)

    Arch. Neurol. Psychiat. (Chic.)

    (1943)
  • A.A. Faris et al.

    Pathogenesis of hemorrhagic infarction of the brain. Part 1 (Experimental investigations of role of hypertension and of collateral circulation)

    Arch. Neurol. (Chic.)

    (1963)
  • A.A. Faris et al.

    Radiologic visualization of neck vessels in healthy men

    Neurology (Minneap.)

    (1963)
  • C. Fazio et al.

    Experimentally produced red softening of the brain

    J. Neuropath. exp. Neurol.

    (1954)
  • M. Fisher

    Occlusion of the carotid arteries

    Further experiences

    Arch. Neurol. Psychiat. (Chic.)

    (1954)
  • C.M. Fisher

    Observations of the fundus oculi in transient monocular blindness

    Neurology (Minneap.)

    (1959)
  • C.M. Fisher

    Clinical syndromes in cerebral arterial occlusion

  • C.M. Fisher

    Lacunes: Small, deep cerebral infarcts

    Neurology (Minneap.)

    (1965)
  • C.M. Fisher et al.

    Observations on brain embolism with special reference to the mechanism of hemorrhagic infarction

    J. Neuropath. exp. Neurol.

    (1951)
  • C.M. Fisher et al.

    Atherosclerosis of the carotid and vertebral arteries — extracranial and intracranial

    J. Neuropath. exp. Neurol.

    (1965)
  • C.M. Fisher et al.

    The nonsudden onset of cerebral embolism

    Neurology (Minneap.)

    (1967)
  • H. Florey

    Microscopical observations on the circulation of the blood in the cerebral cortex

    Brain

    (1925)
  • C. Foix et al.

    Contribution à l'étude du ramollissement cérébral envisagé au point de vue de sa fréquence, de son siège et de l'état anatomique des artères du territoire nécrosé

    J. Neurol. (Brux.)

    (1927)
  • N.R. Gershon

    Les infarcissements hémorragiques de l'écorce cérébrale

    Étude anatomoclinique et statistique

    Acta neuroveg. (Wien)

    (1957)
  • H. Grendahl

    Spontane cerebellumblødninger og emollisjoner

    Nord. Med.

    (1958)
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