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Ischemic Chiasma Syndrome

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Ischemic Chiasma Syndrome 777 . '. ". - " . '.l_. • Ischemic Chiasma Syndrome K . Franc is Lee 1 Thirty patients with chiasma syndrome attributed to ischemic (4) poly tome encephalography (contin uous insufflation technique processes of various origins are described. The initial diagnosis with 50-80 ml of nitrous oxide). In recent years, poly tome gas was made after an investigation based on polytome pneumoen­ encephalography has been replaced almost completely by high­ cephalography and angiography. This diagnosis was confirmed resoluti on CT. later with the use of high-resolution computed tomography (CT) We now use a GE 8800 CT scanner with a high-dose contrast and refined angiographic techniques. The ischemic chiasma mediu m enhancement. Excellent opacification of the circle of Willis, syndrome may be classified into five pathogenetic categories: cavernous sinus, and the pituitary gland is obtained with a rapid (1) mechanical compression of the chiasm secondary to ectatic bolus injection and drip infusion (up to 82 g of iodine). Axial CT tortuous arteries; (2) vascular occlusion secondary to athero­ secti ons of the sell a turcica and suprasellar region inc luding the matous plaque formation; (3) arachnoiditis with fibrosis; (4) ar­ orbits are obtained wi th 1.5 mm contiguous sections (25-30 slices). teritis of various origins; and (5) postpartum necrosis. Sophisti­ Coronal and sagittal reformatted images are then obtain ed. When cated neurologic procedures including magnification angiogra­ the sell a turcica is not grossly enlarged, we perform direct coronal phy and high-resolution CT are essential in ruling out a mass CT scanning by the 1.5 mm contiguous imaging method. The 5 mm lesion and correlating the clinical and radiologic findings of this with 3 mm increments technique is suitable for the evaluati on of syndrome. patients with enlarged sella in axial and coronal planes. With these methods, the hypothalamic part of the third ventricle including the optic and infundibular recesses is clearly delineated , Chiasma syndrome is most commonly caused by a neoplastic as are the ch iasm, optic nerves, pituitary gland, infundibulum, and lesion near the sell a turcica that affects the optic chiasm. However, adjacent vessels. We stil l occasionall y perform poly tome gas en­ identical chiasmati c visual defects may li kewise be produced by a cephalography with N2 0 for evaluation of optochiasmatic arach­ vari ety of nonneoplastic processes involving the chi asm. Arterio­ noiditis when CT findings are equivocal. sclerosis is accepted as one of these [1 , 2]. We have also reported the chiasma syndrome attributable to several ischemic processes [3]. Results More recentl y, we evaluated ischemi c chiasma syndrome (ICS) using high-resolution computed tomog raphy (CT) with high-dose Thirty patients in fi ve eti ologic categories of ICS were identified contrast medium enhancement and magnification angiography. In on the basis of clinical and neu roradiologic evaluations (table 1). ord er to correlate clinical and radiologic features of ICS, it is Type 1 consisted of ICS caused by mechanical compression of essential to demonstrate the precise anatomic relations among the the optic nerve and c hiasm due to red undant ectatic an teri or cere­ optic nerve, chi asm, pituitary gland, and adjacent vascul ature. The bral and / or carotid arteries. Ei ght patients (four men and four anatomi c relation of the neurovascular structu res in and around the worn en) made up this group. Low-lying ectatic anterior cerebral sell a turcica has been studied by many investigators [4-7]. We have arteri es were readily demonstrated to compress the chiasm or optic also studied the vasculature of the optic nerve, chi asm, hypothala­ nerve against th e sell a as seen on poly tome gas encephalogram [3] mu s, pituitary gland, and diaphragma sellae in cadavers, showing or on CT (fig. 1). Seven of the eight cases showed an empty sell a. multiple common blood supplies in the area [8]. Type 2 consisted of ICS caused by atheromatous narrowing or occlusion of the carotid arteries and their branches. Five patients (three men and two women) were in th is category. Angiograms with Materials and Methods subtraction technique demonstrated atheromatous narrowing or occlusion of the carotid arteries, with the carotid siphon and / or the Over a 16 year peri od, more than 300 patients with chiasmatic origin of the internal carotid artery ollen being involved bil aterally visual fi eld defects were evaluated at Thomas Jefferson University (fig. 2). Empty sell a was noted in four of the five cases. One patient Hospital, Willis Eye Hospital, and the University of Texas Health showed a focal infarct in the right parietal region. Science Center at Houston. Extensive neuroophthalmologic, neu­ Type 3 ICS was caused by vascular encasement and occlusion roradiologic, and endocrinologic investigations were carried out in secondary to diffuse arachnoidal adhesion and thic kening. This th ese patients to determine the cause of chiasma syndrome. In most group consisted of nine patients (si x women and three men). Dis­ cases, the syndrome was caused by prim ary or secondary neo­ tortion and / or obliteration of the suprasellar cistern and recesses plasms. of the third ventricle could be demonstrated clearly on poly tome Before the advent of CT, our protocol for neuroradiologic evalu­ gas encephalography and CT (figs. 3 and 4). Seven of the nine ati on of chiasma syndrome compri sed: (1) plain skull fil ms, (2) optic patients showed an empty sella. foramen views, (3) magnificati on angiography with subtraction, and Type 4 ICS was caused by arteritis of various ori gins. There were 1 Department of Radiotogy, University of Texas Health Science Center at Houston. 6431 Fannin St., Houston, TX 77030. AJNR 4:777-780, May/ June 1983 0195-6108/ 83/ 0403-0777 $00.00 © American Roentgen Ray Society 778 MISCELLANEOUS AJNR:4 , May/ June 1983 TABLE 1: Summary of Findings in Ischemic Chiasma Syndrome No. Cases Type of fCS (Age Range) Visual Im pairment Pi tuitary Function Total With Empty Sella 1: Low-lying ectatic anterior cer- ebral and carotid, pericall osal, or carotid arteries (60-80) 8 7 Slowly progressive Low normal 2: Atherosclerotic plaque forma- Gradual or acute tion (50-70) 5 4 onset Usually low 3: Optochiasmatic arachnoiditis Gradual and and fibrosis (20-60) 9 7 progressive Usually low 4 : Arteritis with stenosis and dil- atation of vessels (50-70) 3 2 Acute onset Low 5: Postpartum pituitary necrosis Acute onset, slow and ischemia (20-30) 5 5 recovery Depressed 30 25 A c Fig . .- 79-year-old woman with progressive bitemporal hemianopia due ing optic chiasm. Piluitary stalk run s diagonally in front of dolichoectatic 10 low-lyi ng arleriosclerolic anlerior cerebral arteri es (ICS type 1). A, High­ basilar artery (8). Note partly empty sella. C, Coronal reformatted image with resolution CT scan demonstrates excellent opacification of circle of Willis. high window level shows ectatic cavernous carotid (C) and anterior cerebral Figures include carotid arlery (C), basilar artery (8), infundibulum of pituitary arteries (arrows) with scleroti c margin due to calcified vascular wall s. Anterior (I), and low-lyin g anlerior cerebral arteries (arrow). B, Reformatted sag ittal cerebral arteries are situated so low th at optic chiasm is compressed and image of axial CT shows low-lying anterior cerebral artery (arrow) compress- fl attened beneath low-lying vessels. Part of pituitary stalk is seen in center. three patients (two women and one man) who showed angiographic Ischemic chiasma syndrome is believed to be secondary to evidence of arteritis, associated with pituitary insufficiency and various ischemic processes without evidence of mass lesion. There­ bitemporal hemianopia. Two of the three patients demonstrated an fore, a mass lesion should be categorically excluded by neuroradi­ empty sell a. Angiography with subtrac tion showed evidence of ologic prqcedure before the diagnosis of ICS is considered [2, 3, arteritis with vascular stenosis (fig. 5). 10]. Type 5 consisted of postpartum chiasma syndrome associated Tubular or fusiform dil atation of arteries may compress the ad­ with pituitary necrosis. The five women in this group had an empty jacent structures, producing neurologic symptoms [9, 10]. Similarly, sell a on poly tome gas encephalogram [3, 9] or CT scan (fig. 6). ICS may develop secondary to mechanical compression of the optic Only one patient showed a slightly enlarged sella turcica. chiasm, optic nerve junction, or both by a tortuous ectatic anterior cerebral artery [2, 3, 10]. In the case of a pituitary tumor growing Discussion upward , the anterior cerebral artery may act as a restrictive cord on the dorsal surface of the prechiasmatic optic nerve, with the The chiasma syndrome is usually produced by compression of resultant notching or grooving accounting for chiasmatic visual field the chiasm. A variety of parasellar mass lesions, including neo­ defect [1 , 4]. Infarction of the chiasm may develop as a result of plasms, granulomas, aneurysms, foreign bodies, and hematomas, focal ischemia produced by an intrinsic or extrinsic tumor [1 , 11]. may be responsible [1]. Nontumorous lesions such as demyelinating In order to establish the diagnosis of type 1 ICS, the anatomic disease and trauma are rarer but definite causes. relation of the anterior and/ or carotid arteries to the' chiasm and AJNR:4, May/ June 1983 MISCELLANEOUS 779 A B Fig. 4.-25-year-old woman with progressive bitemporal hemianopia due to optochiasmati c arachnoiditis (ICS type 3). A, Axial CT with 1.5 mm section shows part ial obliterati on of suprasell ar cistern. B, Optic chiasm appears prominent with indistinct margin (arrows). C, Sagittal reformatted image shows partial eHacement of recesses of third ventricle with matt ed chiasm and opti c nerve complex (arrow). Sella is partly empty. A B tuous anterior cerebral artery against th e chi asmati c sulcus or Fig, 2.
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