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STROKE

VOL 12, No

5, SEPTEMBER-OCTOBER

1981

FIGURE 1C-D: Left and right carotid arteriogram demonstrating exaggerated tapering of middle cerebral artery branches in their proximal courses.

Although the microscopic appearance of the vessels did not suggest a distinct diagnosis, we consider this less important than the exclusion of vasculitis and atheromatous embolism or stenosis. Although it appears that in TAO the visceral arteries are s o m e w h a t m o r e s u s c e p t i b l e t o a t h e r o s c l e r o t i c o c c l u s i o n s , 1 0 t h e a n g i o g r a p h i c c h a n g e s a n d t h e c l i n i c a l course of our patient suggested TAO more than atherosclerotic disease. In light of her clinical course, angiographic appearances, and microscopic digital vascular changes, we believe that this patient's fea- tures were compatible with a diagnosis of TAO com- p l i c a t e d b y C T A O . T h e h i s t o r y o f e x p o s u r e t o t o b a c c o supports this diagnosis. 1 1

As this patient illustrates, the antemorten diagnosis of CTAO may depend heavily on the exclusion of other diseases that lead to digital gangrene and cerebral ischemic events. The incidence of CTAO in patients with TAO ranges between 0.5% and 18%.12- " Zulch14 found only 2 cases of CTAO among thousands of autopsies. In spite of the rarity of CTAO interest remains, as shown by publications emphasizing the selective aspects of CTAO'-6' ls-17 and TAO.18-2" McLoughlin et al.27 reported a greater prevalence of HLA-A9 and HLA-B5 antigens in patients with TAO when compared to patients with arteriosclerosis

obliterans munological

and normal subjects. Recent im- studies2" implicate a hypersensitivity

reaction of TAO.

directed against arterial antigens as a cause However, the basic question of whether TAO

and CTAO are distinct clinico-pathological can not be answered until the pathogenesis diseases is clarified and specific pathological

entities of these changes

agreed

upon.

Strong

clinical

evidence

and

supportive

References

1.

2

Winiwartcr F. von: Ober eine eigentdmliche Form von End- arteritis und Endophlebitis mit GangrSn des Fusses. Arch Klin Chir 23: 202, 1879 Buergcr L: Thrombo-angiitis obliterans: A study of the vascular lesions leading to presenile spontaneous gangrene. Am J M Sc

136: 567-580, 1908

3.

Spatz H: Ober Buergerschen

die Beteiligung des Gehirns bei v.

Krankheit

(Thrombocndangiitis

Winiwarter- obliterans)

4

Dtsch Z Nervenheilk 136: 86-132,

Lindenberg

R,

Spatz

H:

Ober

1935 die

Thromboendartcntis

obliterans dcr Buergerschen

Hirngefdsse. Cerebrale Form der v. Winiwarter- Krankheit. Virchows Arch path Anat 305: 531,

5.

1939 Fisher critical

CM: Cerebral thromboangiitis obliterans (including a review of the literature). Medicine 36: 169-209, 1957

6.

Wessler S, evaluation

Ming SC, Gurevich V, Frciman DG. A

of

thromboangiitis

obliterans

The

case

critical against

7.

Buerger's disease. New Engl J Med 262: 1 Wessler S: Thromboangiitis obliterans. fact

149-1160, 1960 or fancy. Circula-

8.

9.

tion 23: 165-167, 1961 McKusick VA, Harris Shelley WM, Bloodwell clinical and pathological Foix C, Chavany JA,

WS, Ottesen OE, Goodman RM,

RD: Buerger's disease: a distinct entity. JAMA 181: I: 5-12, 1962

Marie J: Diplegie facio-linguo-

10.

masticatrice d'ongine cortico sous-corticale membres. Rev Neurol 45: 214-219, 1926 Juergens JL: Thromboangiitis Obliterans. Hines, Peripheral Vascular Diseases (Fifth

sans paralysie des

In Allen-Barker- ed) Philadelphia,

WB

Saunders Company,

London, Toronto, 1980, pp

469-491

11.

Hill

GL: A rational basis

for management of patients

with the

12.

Buerger syndrome. Br J Surg 61: 476-481, Lippman HL: Cerebrovascular thrombosis

1974 in patients

with

13.

14.

Buerger's disease. Circulation 5: 680-692, 1952 Dzialek E: Cerebral manifestations of Buerger's disease. Med J 9, 5: 1212-1218, 1970 ZQlch KJ: The cerebral form of Von Winiwarter-Buerger's ease: Does it exist? Angiology 20: 61-69, 1969

Pol

dis-

15.

Jaeger E: obliterans

Zflr patologischen Anatomic der bei juvenilcr Extremititengangran.

Thromboangitis Virchows Arch

pathologic

data,

as

in

the

present

patient,

tinue to form the basis for considering diagnosis of TAO and CTAO.

the

should

con-

antemortem

16.

path Anat 284: 584-622, 1932 Eicke WJ: Die endangitis obliterans dcr d. spez. pathol Anat.v.Histol, XII1/IB,

Springer, 1957, 1536-1562

Hirngefasse. In Handb. Scholtz W (ed), Berlin,

17.

Parker

JC,

Schwartzman

RJ:

Cerebral

thromboangiitis

Acknowledgment

The authors are grateful to Mrs. Carol Purdy for manuscript preparation.

obliterans In Handbook of Clinical Neurology, Vol 39. Vinken PJ, Bruyn GW, Klawans, HL (eds), Elsevier/North Holland Biomedical Press 1980, pp. 201-211 18. Silbert S. Etiology of thromboangiitis obliterans. JAMA 129;

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