The Psychiatric Aspects of Temporal Arteritis

1952 ◽  
Vol 98 (411) ◽  
pp. 280-286 ◽  
Author(s):  
R. Vereker
Keyword(s):  
Virus Infection ◽  
Giant Cell Arteritis ◽  
Temporal Arteritis ◽  
Giant Cells ◽  
Low Grade ◽  
Internal Elastic Lamina ◽  
Temporal Arteries ◽  
The Media ◽  
Cranial Arteries ◽  
Elastic Lamina

Temporal arteritis, also called giant cell arteritis, or cranial arteritis, was first described in 1932 by Horton and Magath. This syndrome is caused by a reversible inflammation of the cranial arteries, especially the temporal arteries (which are visibly inflamed), causing headache, mental and neurological disturbances as well as general toxic signs, and almost always occurring after the age of fifty-five years.Pathology.—In the arteries involved there is a subacute inflammation of the adventitia and media with focal necrosis of the media, fragmentation and destruction of the internal elastic lamina with gross hypertrophy of the intima, often leading to occlusion of the vessel. In many cases giant cells are found in the media. Besides the cranial arteries other vessels are sometimes involved, e.g., the carotids (Scott and Maxwell 1941; Gilmour 1941), subclavian, coronary and femoral arteries (Cookeet al., 1946), post-auricular (Dick and Freeman 1940).Aetiologyis unknown. There is no evidence of tuberculosis or syphilis. A low-grade bacterial or virus infection of the arteries has been postulated, but repeated bacteriological examinations of the biopsied arteries have failed to isolate any organisms. The predilection which the condition shows for the temporal and cranial arteries is unexplained.

scholarly journals An interesting case of temporal arteritis that manifested as ptosis and diplopia

2020 ◽  
Vol 2020 (11) ◽  
Author(s):  
Anoka Martis ◽  
Romesa Sajjad Hassan ◽  
Ana Goico Alburquerque ◽  
Manasa Kotte ◽  
Anshu Martis ◽  
...  
Keyword(s):  
Temporal Arteritis ◽  
Prognostic Significance ◽  
Giant Cells ◽  
Interesting Case ◽  
Internal Elastic Lamina ◽  
Third Nerve Palsy ◽  
Atypical Symptoms ◽  
Temporal Arteries ◽  
Granulomatous Vasculitis ◽  
Red Flag

ABSTRACT Giant cell arteritis (GCA) or temporal arteritis is a granulomatous vasculitis that affects medium-to-large vessels seen primarily in older Caucasian populations. Here, we describe a 67-year-old male who presented with atypical symptoms of worsening headaches associated with left-sided pupil-sparing, isolated third nerve palsy, blurry vision, diplopia and myalgias in bilateral extremities. He was immediately started on intravenous Methylprednisolone for suspected GCA. Subsequent biopsy of the temporal arteries showed panarteritis without giant cells and disruption of the internal elastic lamina. His symptoms improved in a day following treatment and he was discharged on a Prednisone taper. At the time of writing this case, there are only two cases in the literature of ptosis as a presenting symptom in GCA, thus highlighting the importance of recognizing rare red flag symptoms such as ptosis and diplopia. More study is needed in the prognostic significance of these unusual clinical features.

Histological structural abnormalities of superficial temporal arteries used for extracranial-intracranial anastomosis

1982 ◽  
Vol 57 (3) ◽  
pp. 328-333 ◽  
Author(s):  
Fernando G. Diaz ◽  
Jacob Chason ◽  
Carl Shrontz ◽  
James I. Ausman ◽  
Manuel Dujovny
Keyword(s):  
Medical Condition ◽  
Superficial Temporal Artery ◽  
Temporal Artery ◽  
Histological Evaluation ◽  
Elastic Tissue ◽  
Internal Elastic Lamina ◽  
Content Type ◽  
Temporal Arteries ◽  
The Media ◽  
Elastic Lamina

✓ Histological evaluation of the superficial temporal artery resected at the time of extracranial-intracranial anastomosis was performed in 64 consecutive patients. A neuropathologist who was not aware of the medical condition of these patients studied all specimens under light microscopy with hemotoxylin and eosin, Verhoff, and Mallory strains. Intimal proliferation was observed in 62 samples, intimal fibrosis in 56, fragmentation of the internal elastic lamina in 45, splitting of the internal elastic lamina in 41, fragmentation of the media in 38, and fragmentation of the minimal external elastic tissue in 17. Stenosis of the vessel was observed, and graded from 0% to 50%, with a mean of 20%. The development of intraluminal stenosis was considered to be secondary to the development of intimal fibrosis and hyperplasia. The changes observed were progressive and conformed with those previously described; there was no evidence of correlation with sex, diabetes, or hypertension. The implications for the development of occlusion of the anastomosis or stroke, and for patient survival are discussed.

Functional medial thickening and folding of the internal elastic lamina in coronary spasm

2011 ◽  
Vol 300 (2) ◽  
pp. H423-H430 ◽  
Author(s):  
Yasumi Uchida ◽  
Yasuto Uchida ◽  
Akimasa Matsuyama ◽  
Atsushi Koga ◽  
Yuko Maezawa ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Structural Changes ◽  
Light And Electron Microscopy ◽  
Coronary Spasm ◽  
Cellular Level ◽  
Internal Elastic Lamina ◽  
Circular Smooth Muscle ◽  
The Media ◽  
Medial Thickening ◽  
Elastic Lamina

Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 ± 12% (mean ± SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 μm ( P < 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm.

Blood vessels and the endothelium

2010 ◽  
pp. 2593-2603
Author(s):  
Patrick Vallance ◽  
Keith Channon
Keyword(s):  
Blood Vessels ◽  
Vessel Wall ◽  
Single Layer ◽  
Vasa Vasorum ◽  
Blood Vessel Wall ◽  
Internal Elastic Lamina ◽  
Perivascular Adipose Tissue ◽  
The Media ◽  
Elastic Laminae ◽  
Elastic Lamina

The blood vessel wall consists of the intima, the media, and the adventitia. Not all vessels have each layer, and the layers vary in size and structure between vessels. (1) The intima is made up of a single layer of endothelial cells on a basement membrane, beneath which—depending on vessel size—there may be a layer of fibroelastic connective tissue and an internal elastic lamina that provides both structure and flexibility. Embedded in the intima are pericytes. (2) The media is made up of smooth muscle cells, elastic laminae and extracellular matrix. (3) The adventitia is the outermost part of the vessel, composed mainly of fibroelastic tissue but also containing nerves, small feeding blood vessels (the vasa vasorum), and lymph vessels. The adventitia is directly related to the surrounding perivascular adipose tissue....

scholarly journals An atypical presentation of giant cell arteritis without headache

2020 ◽  
Vol 20 (2) ◽  
pp. 23-25
Author(s):  
Eva Bunting ◽  
◽  
Andrew W Barritt ◽  
Nigel Leigh ◽  
David Wright ◽  
...  
Keyword(s):  
Giant Cell Arteritis ◽  
Giant Cell ◽  
White Matter Lesions ◽  
Giant Cells ◽  
Whole Body ◽  
Oligoclonal Bands ◽  
Temporal Arteries ◽  
Csf Analysis ◽  
Intracranial Involvement ◽  
Transmural Inflammation

We describe an unusual case of giant cell arteritis initially manifesting as insidiously progressive spastic quadriparesis, widespread muscle wasting and fasciculations in the absence of headache, followed by a complete left pupil-involving 3rd nerve palsy 10 months later. MRI and CSF analysis revealed evidence of intracranial involvement with established white matter lesions and intrathecal oligoclonal bands, respectively, whilst whole body FDG-PET demonstrated isolated uptake within the descending aorta. The temporal arteries were clinically and radiologically unremarkable but biopsy showed transmural inflammation and multinucleate giant cells. A rapid, complete and sustained improvement followed steroid therapy.

Exogenous Perioxidase Localization in Irradiated Arteries

1972 ◽  
Vol 30 ◽  
pp. 8-9
Author(s):  
James C. Hampton ◽  
Benjamin Rosario ◽  
Roy R. Adee
Keyword(s):  
Smooth Muscle ◽  
Horseradish Peroxidase ◽  
Mesenteric Artery ◽  
Type Ii ◽  
Internal Elastic Lamina ◽  
Small Branch ◽  
X Irradiation ◽  
The Media ◽  
Intrasplenic Injection ◽  
Elastic Lamina

Mice were exposed to 1500 R X-irradiation and sacrificed on days 1,2,3,3.5 and 4 days postexposure. Two to 3 min before sacrifice each mouse received 5 mg horseradish peroxidase (Sigma type II) in 0.5 ml saline by intrasplenic injection. Tissues were fixed in glutaraldehyde-formaldehyde and incubated according to the method of Karnovsky for histochemical localization of horseradish peroxidase (HRP). Unirradiated tissues and irradiated but unincubated tissues were used as controls.Figure 1 shows only moderate staining of the internal elastic lamina (IEL) in a small branch of the mesenteric artery at 3 days postirradiation. No evidence of deposits of HRP reaction product was observed in either the endothelium or smooth muscle of the media.

scholarly journals Artery tertiary lymphoid organs in giant cell arteritis are not exclusively located in the media of temporal arteries

2017 ◽  
Vol 77 (3) ◽  
pp. e16-e16 ◽  
Author(s):  
Jacoba Carolien Graver ◽  
Maria Sandovici ◽  
Arjan Diepstra ◽  
Annemieke M H Boots ◽  
Elisabeth Brouwer
Keyword(s):  
Giant Cell Arteritis ◽  
Giant Cell ◽  
Lymphoid Organs ◽  
Temporal Arteries ◽  
The Media

Amyloid Deposits of Internal Elastic Lamina in Temporal Arteritis

1975 ◽  
Vol 170 (4) ◽  
pp. 337-344 ◽  
Author(s):  
J. Meretoja ◽  
A. Tarkkanen
Keyword(s):  
Temporal Arteritis ◽  
Internal Elastic Lamina ◽  
Amyloid Deposits ◽  
Elastic Lamina

Finite Element Modeling of Cerebral Angioplasty Using a Multi-Mechanism Structural Damage Model

2009 ◽  
Author(s):  
Dalong Li ◽  
Anne M. Robertson
Keyword(s):  
Structural Damage ◽  
Arterial Wall ◽  
Damage Model ◽  
Transluminal Angioplasty ◽  
Controlled Study ◽  
Internal Elastic Lamina ◽  
The Media ◽  
Observed Damage ◽  
Percutaneous Transluminal ◽  
Elastic Lamina

Percutaneous transluminal angioplasty (PTA) can lead to vascular damage when used to treat atherosclerotic obstructions and vasospasm in cerebral vessels [1–3]. In a controlled study of angioplasty in normal arteries of mongrel dogs, changes to the arterial wall due to over inflation were studied at two dilation levels (24%,50%) [4]. Damage to the wall was progressive — increasing with inflation level. At 25% inflation, localized fractures and stretching of the internal elastic lamina (IEL) were observed. Damage to the media was limited to the inner one-third of the wall. At 50% inflation, further radial damage was seen including extensive damage to the IEL, dissection of the media, distorted SMC and disorganized collagen fibers. At six months, the media exhibited signs of repair such as increased collagen content while the IEL showed no recovery.

Fusiform vertebral artery aneurysms as a cause of dissecting aneurysms

1999 ◽  
Vol 91 (1) ◽  
pp. 139-144 ◽  
Author(s):  
Toshihiro Yasui ◽  
Masaki Komiyama ◽  
Misao Nishikawa ◽  
Hideki Nakajima ◽  
Yasutsugu Kobayashi ◽  
...  
Keyword(s):  
Posterior Inferior Cerebellar Artery ◽  
Internal Elastic Lamina ◽  
Content Type ◽  
Pathological Characteristics ◽  
Vertebral Arteries ◽  
Cerebellar Artery ◽  
The Media ◽  
Dissecting Aneurysms ◽  
Elastic Lamina

✓ Two autopsy cases of angiographically determined fusiform aneurysms of the vertebral arteries (VAs) are reported and the appropriate literature is reviewed to investigate the pathological characteristics of both fusiform and dissecting VA aneurysms and the pathogenesis of dissecting aneurysms. One patient had suffered a subarachnoid hemorrhage (SAH) due to dissection of a previously documented incidental fusiform aneurysm. The other patient had harbored incidental fusiform aneurysms coexistent with a ruptured aneurysm of the posterior inferior cerebellar artery. The location and pathological features of the aneurysms were similar in the two cases. The aneurysms in both cases displayed intimal thickening, disruption of the internal elastic lamina, and degeneration of the media. A mural hemorrhage and patchy calcification were also found in the case that included SAH. Based on their pathological investigation of these two cases and a review of reported cases, the authors propose that incidental fusiform aneurysms in the VAs are characterized by weakness in the internal elastic lamina and, therefore, have the potential to become dissecting aneurysms, resulting in a fatal prognosis. This suggests that long-term control of blood pressure is mandatory in patients with incidental fusiform aneurysms in the VAs.

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