Über den Bau und die Altersveränderungen der Gehirnarterien

Hackel, Werner

doi:10.1007/bf02227867

Cited by 28 publications

(8 citation statements)

References 5 publications

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“…The absence of a discrete and thick external elastic layer was reported by Triepel (I896), Hackel (1928), Glynn (1940), Duff (195^) and Baker and lannone (1959a).…”

Section: ?mentioning

confidence: 77%

“…The subsequent changes represented the thickenings at these sites projecting into the lumen and causing reduction in the lumen size. These cushions were ob served to be present in the fetuses and young ones by Tuthill (1931), Hackel (1928) and Benke (1931) also. Hackel (1928) and Robertson (1960a,b) observed that these cushions remained unchanged in their morphology until twenty years of age.…”

Section: ?mentioning

confidence: 89%

“…The physiological nature of the intimai cushions has been recognized by various authorsi Hackel (1928), Glynn (19^0), Rotter, et (1955), Hassler (I96I, 1962a) Stehbens (i960, 1963, Legait (19^7,19^9). Robertson (1960a,b), Serban and Ovuia (I961), Elias and Pauly (I966), and Jaffe, et al (1968).…”

Section: ?mentioning

confidence: 94%

“…Ranke (I915), Hackel (1928), and Benninghoff (1930) studied the cerebral arteries and found that internal elastic lamina became laminated early in life. They observed that the elastic tissue did not increase but was replaced by con nective tissue which appeared in the spaces left by the de generated elastic tissue.…”

Section: Cerebral Arteries Of Manmentioning

confidence: 99%

“…He described the adventitia as a delicate layer of connective tissue which was not at tached to the muscle layer, Binswanger and Schaxel (1917) studied the normal histology of the cerebral arteries and inferred that the small cerebral arteries differed from the larger ones by having less elastic tissue in their media. Hackel (1928) observed that there was no external elas tic lamina, the adventitia was small but the internal elas tic lamina was thicker than the other systemic arteries, Benninghoff (1930) described the internal elastic lamina as the fenestrated membrane. Ranke (1915) believed that the internal elastic lamina was not a layer but a mesenchymal network which was continuous from the subendothelium to the adventitia.…”

Section: (1934)mentioning

confidence: 99%

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Extrinsic and intrinsic blood supply and histomorphological changes associated with age in the cerebral arteries and brain nuclei in dog (Canis familiaris) and pig (Sus scrofa domestica)

Nanda

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“…The absence of a discrete and thick external elastic layer was reported by Triepel (I896), Hackel (1928), Glynn (1940), Duff (195^) and Baker and lannone (1959a).…”

Section: ?mentioning

confidence: 77%

Section: ?mentioning

confidence: 89%

Section: ?mentioning

confidence: 94%

Section: Cerebral Arteries Of Manmentioning

confidence: 99%

Section: (1934)mentioning

confidence: 99%

See 3 more Smart Citations

Extrinsic and intrinsic blood supply and histomorphological changes associated with age in the cerebral arteries and brain nuclei in dog (Canis familiaris) and pig (Sus scrofa domestica)

Nanda

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Postoperative, Focal, Nonseptic Necrosis of Vertebral and Cerebellar Arteries

Kernohan¹

1943

JAMA

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Subarachnoid hemorrhage caused by focal, nonseptic necrosis of the vertebral artery or of its branch, the posterior inferior cerebellar artery, is an unusual occurrence.We here record our observations made on 4 elderly, generally slightly hypertensive patients who showed no evidence of endocarditis or of a general or local infectious process, who died of this condition within a few days of uncomplicated abdominal operations. Only the apparently relevant features of the histories and examinations are given.There is a voluminous literature on the subject of subarachnoid hemorrhage ; however, much of this is in reference to ruptured congenital aneurysms. Sands,1 in a recent study of subarachnoid hemorrhage, reported 120 cases and pointed out that it "is caused by (1) trauma, (2) arteriosclerotic degeneration of vessel walls, (3) septic or infectious emboli, (4) ruptured intracranial aneurysms, (5) massive cerebral hemorrhage invading the subarachnoid space, (6) intraventricular hemorrhage, (7) blood dyscrasias and (8) ruptured vascular neoplasm." In addition to the foregoing there is a relatively large group which Sands listed as of "unknown or undetermined cause."Necrosis of the arteries of the brain is a well known phenomenon in large infarcts and we have also seen extensive necrosis of meningeal blood vessels in many cases of tuberculous meningitis or septic meningitis as well as in cases of "periarteritis nodosa," septic endo¬ carditis and other conditions, but we have not seen any of these that had vessels ruptured and produced exten¬ sive subarachnoid hemorrhage. As a rule in such cases the entire wall of a small artery becomes necrotic and not a small segment of the circumference, leaving the remaining portion of the wall normal. Winternitz and LeCompte 2 produced varying degrees of inflammation and proliferation of the walls of arteries by injecting organisms of different degrees of virulence into the walls of arteries but did not produce areas of focal necrosis.We have been unable to find any record in the available literature of a case of subarachnoid hemorrhage due to rupture of a noninflammatory necrotic focus in the wall of a cerebral artery. REPORT OF CASESCase 1.-An educator aged 62 was registered at the Mayo Clinic on Feb. 2, 1942 for a general examination and considera¬ tion of a right inguinal hernia. Examination disclosed a systolic blood pressure of 160 mm. of mercury and a diastolic pressure of 100 mm. There were slight hypertensive sclerosis of the retinal arterioles and slight sclerosis of the choroidal vessels.An apparently old retinal detachment was noted in the lower temporal sector on the right. Bilateral direct inguinal hernias were present. Numerous leukocytes were noted in the prostatic secretion. An occasional erythrocyte was found in the urine. Cystoscopic examination gave negative results.On February 24, with the patient under spinal anesthesia, both inguinal hernias were repaired. On February 28 he com¬ plained of an occipital headache, vomited, became confused, had a convulsion and...

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Hyperplastic Arteriosclerosis Versus Atherosclerosis

Moschcowitz¹

1950

JAMA

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This paper was stimulated by the serious need of a precise definition of the term "arteriosclerosis" as judged by the diversity of opinions expressed in recent years. Thus, a recent laborious review of many hundreds of articles on arteriosclerosis leaves one bewildered for the reason that under that eponym such different lesions as hyperplastic arteriosclerosis, atherosclerosis, infectious arteritis and M\l=o"\nckeberg's sclerosis are included, with little or no attempt at differentiation.In another instance, a review of "arteriosclerosis" represents an excellent presentation of atherosclerosis. The necessity for a precise definition of arteriosclerosis is not merely an academic matter. Aside from the obvious advantage of inducing precision of thought, it will help to clarify many current clinical problems associated with vascular disease. In order to arrive at a correct definition of the term, it is essential to survey the problem as a whole, not only from the point of view of morphology and morphogenesis but from the etiologic, the physiologic and especially the dynamic aspects. Regrettably, this has been done in only a desultory manner, and only too often a part of the total summation of processes that are represented within the rubric of arteriosclerosis have been emphasized to the exclusion of the whole.The main issue lies in the alleged identity of arterio¬ sclerosis with atherosclerosis, since these terms are so often used interchangeably. There is no doubt that the impetus created by Anitschkow'sx experiments is largely responsible for this misconception. He was one of the first to produce a lesion that simulated that observed in the human arterial tree. There is no question that both grossly and histologically these experiments reproduce some of the characters of human arteriosclerosis, especially in respect to distribution of the lipid deposits. However, there are many points of difference. 1. The ascending aorta is always and intensely involved, an unusual occurrence in the human aorta. 2. The deposits of lipid are not limited to the arteries of the greater circulation but involve the pul¬ monary artery, the veins, the reticuloendothelial system, the adrenal glands, the sciera, the cornea, the ciliary body of the eye, the tympanic membrane and even the tendons. As I have tried to show,2 the incidence of gross arteriosclerosis in the pulmonary artery is hide-pendent of that in the aorta, and phlebosclerosis never occurs unless a venous segment is subjected to increased intravascular pressure. 3. The renal arteries are sel¬ dom affected while in man arteriosclerotic lesions are practically omnipresent in senescence. 4. The lipid infiltration of the media occurs early in experimental arteriosclerosis but is a' late phenomenon in the human variety. 5. Ulcération of the atheromatous deposits rarely results. 6. Hyperplasia of the elástica and the deposition of collagen, when it occurs, are entirely dif¬ ferent in localization from that occurring in human arteriosclerosis. 7. The lesions are produced under un...

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Über den Bau und die Altersveränderungen der Gehirnarterien

Cited by 28 publications

References 5 publications

Extrinsic and intrinsic blood supply and histomorphological changes associated with age in the cerebral arteries and brain nuclei in dog (Canis familiaris) and pig (Sus scrofa domestica)

Extrinsic and intrinsic blood supply and histomorphological changes associated with age in the cerebral arteries and brain nuclei in dog (Canis familiaris) and pig (Sus scrofa domestica)

Postoperative, Focal, Nonseptic Necrosis of Vertebral and Cerebellar Arteries

Hyperplastic Arteriosclerosis Versus Atherosclerosis

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