Clinical Anatomy 27:1149–1158 (2014)

REVIEW

The Optic Chiasm DESMOND KIDD1,2* 1

Department of Neuro-Ophthalmology, Royal Free Hospital, Pond Street, London NW3 2QG, United Kingdom 2 University College Hospital Medical School, United Kingdom

The optic chiasm is formed when the optic nerves come together in order to allow for the crossing of fibers from the nasal retina to the optic tract on the other side. This enables vision from one side of both the eyes to be appreciated by the occipital cortex of the opposite side. This review makes note of the embryology, anatomy and vascular supply of the optic chiasm, then discusses the clinical syndromes associated with chiasmal disease, and the diseases which commonly influence its function. Clin. Anat. 27:1149–1158, 2014. VC 2014 Wiley Periodicals, Inc. Key words: optic chiasm; visual disorders; neuroanatomy

EMBRYOLOGY The anlage of the structure of optic chiasm is seen initially within the floor of the third ventricle at around three weeks of gestation, rostral to the hypophysial duct and between the optic stalks, at the junction of telencephalon and diencephalon. Nerve fibers develop and it dissociates itself forwards from the ventricle. Fibers from the optic nerves reach the chiasm between the 4th and 6th weeks (Barber et al., 1954) and crossed and uncrossed fibers can be seen by the 11th week; hemidecussation of fibers is completed by the 13th week. It assumes its characteristic shape by the 15th week, when the eyes have moved from a lateral to a more anterior position. In the Rhesus monkey uncrossed axons reach the chiasm, and indeed have already grown into the ipsilateral tract, before the crossed axons arrive (Meissirel and Chalupa, 1994), suggesting that the retinotopic organization of fibers is preordained at the earliest possible time.

ANATOMY The chiasm lies above the sphenoid bone, over the diaphragma sellae (Fig. 1); anatomical variations are common and can influence the presenting visual symptoms and signs in chiasmal disorders. In the majority of cases, the chiasm is situated overl’ying the diaphragma sellae (Schaeffer, 1924), pre-fixed when lying above the tuberculum sellae or within the sulcus chiasmatis (17% of cases), and post-fixed when it lies above or even behind the dorsum sellae (4%) (Bergland et al., 1968). The intracranial optic nerves rise from the canal to the chiasm at an angle of 15–45 . The pia mater is

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contiguous with that of the nerves and that of the anterior tracts. The chiasm lies postero-superiorly within the wall of the third ventricle and anteriorly with the CSF within the chiasmatic cistern (Fig. 1). Above lies the hypothalamus, bounded by the lamina terminalis which itself forms the anterior wall of the third ventricle. The chiasm invaginates the ventricle, so separating the optic recess above and the infundibular recess below. Below the chiasm lie the sella turcica, the pituitary gland, and the diaphragma sellae. It is separated from these structures by the basal cistern. Here too there are variations which may influence the visual disorders arising from disease within these structures; the width of the cistern, the shape of the pituitary gland, and the size of the diaphragma sellae all influence what size a lesion must attain before compression of the chiasm occurs. The infundibulum of the pituitary lies immediately posteriorly and the mamillary bodies behind this, medial to the two optic tracts. The internal carotid arteries as they emerge from the cavernous sinuses lie to either side, and the anterior communicating artery lies directly above; aneurysms of the anterior communicating artery or first segment of anterior cerebral artery may therefore compress the chiasm.

*Correspondence to: Desmond Kidd. E-mail: [email protected] Received 8 December 2013; Revised 22 January 2014; Accepted 1 February 2014 Published online 14 May 2014 in Wiley Online (wileyonlinelibrary.com). DOI: 10.1002/ca.22385

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1150 Kidd information on the nature and in particular the site of the causative lesion. Traditionally, field defects have been divided anatomically into the anterior angle, the body, the posterior angle, and the lateral aspect of the chiasm (Fig. 2).

The Anterior Angle

Fig. 1. T1 weighted axial MRI showing the position and immediate relationship of the chiasm to adjacent anatomical structures.

Over two million nerve fibers pass through the optic chiasm from the eyes; fibers from the nasal retina cross; the ratio of crossed to uncrossed fibers within the chiasm is 53:47 (Kupfer et al., 1967). This crossing is of necessity very precise; only fibers from the temporal retina pass to the ipsilateral lateral geniculate nucleus, and only those from the nasal retina pass contralaterally. Those which cross do so as soon as they enter the chiasm and maintain their rostral to caudal position within. Those which are uncrossed continue in the lateral chiasm into the ipsilateral tract. Fibers from the macula on each side which account for the majority of fibers within the chiasm (Hoyt and Luis, 1963) are found more centrally and caudally than other fibers. Rarely the chiasm may fail to develop (achiasmia). Patients studied have associated midline developmental disorders but intact fields; the visual evoked potential characteristically is monocular (Sami et al., 2005).

BLOOD SUPPLY The blood supply is variable, but in general comes from feeder vessels arising from branches of the anterior communicating artery, anterior cerebral, posterior communicating, posterior cerebral, and basilar arteries (Wollschlaeger et al., 1971). The dorsal parts are supplied by branches of the ICA and the more ventral parts from the posterior circulation. There is considerable collateral supply; hence infarction of the chiasm is very rare indeed.

Lesions which involve the anterior angle of the chiasm, the point at which the optic nerve passes into and forms the chiasm, may show a junctional scotoma (Traquair, 1949) since there is at this point separation of the crossing and uncrossed fibers. If the lesion is not large this will result in an ipsilateral monocular central field defect (from the optic nerve) and a small contralateral upper temporal homonymous field defect from involvement of the crossing fibers anteriorly (Fig. 2a). If the nerve itself is not affected as well, then the defect will be monocular and temporal, since only the crossing fibers are affected; if only the macular fibers are involved then the defect is a midlineobeying temporal scotoma (Fig. 2b). This defect may be very small and can be missed with kinetic perimetry; it is usually picked up using static perimetry, however. Wilbrand’s knee is said to be an extension of the crossing fibers from retinal ganglion cells located nasal and inferior to the fovea into the ipsilateral distal optic nerve; the contralateral field defect arising with involvement of these. Horton (1977), however, has stated that Wilbrand identified an artifactual state in examination of enucleated eyes. Nonetheless, the identification of a small asymptomatic contralateral defect in the presence of a symptomatic monocular defect should encourage the examining physician to proceed with haste to imaging studies rather than diagnosing an inflammatory optic neuropathy incorrectly.

The Body of the Chiasm Lesions which affect the body of the chiasm produce the typical bitemporal hemianopia (Figs. 2c and 3). This may affect the whole hemifield, upper or lower quadrants and peripheral or central areas. The macula is usually but not always split. In general, central visual acuity is unaffected. Clearly, it is possible that the field defects are not the same in each eye, since the causative lesion may exert a greater effect on one side than the other. Complete defects tend only to occur in the case of trauma. When the peripheral fields are affected, the defect progresses in a clockwise direction in the right and anti-clockwise in the left (Cushing and Walker, 1915). Lesions compressing from above cause the lower field to be affected first (Fig. 2e) and the defects are less congruous; those from below affect the upper fields first (Fig. 2d) and tend to be more congruous in appearance.

VISUAL FIELD DEFECTS IN CHIASMAL DISORDERS

The Posterior Angle of the Chiasm

A careful study of the bilateral visual field defect acquired in chiasmal lesions can provide important

Lesions within the posterior aspect of the body of the chiasm produce bitemporal hemianopic scotomas

The Optic Chiasm 1151 (Larmonde and Larmonde, 1977) (Fig. 2f). These may be confused with centrocaecal scotomas (Fig. 4), but the former will not be associated with significant reduction in visual acuity whereas the latter will. More posteriorly placed lesions will also involve the optic tract, with the results that the field defected will be predominately one of a homonymous hemifield defect.

The Lateral Aspect of the Chiasm Involvement of this region by compression leads to a homonymous hemifield defect on the contralateral side (Fig. 2g).

VISUAL SYMPTOMS When lesions damage chiasmal fibers, there is a progressive loss of central visual acuity and a noticeable dimming of the temporal visual fields. Patients may also notice a disturbance of depth perception at fixation which is due to crossing of the two blind hemifields after the point of fixation in convergence (Fig. 5). Hence an object seen at a distance to be behind another will disappear when the eyes focus on the one in front. “Hemifield slide” causes difficulty in reading in which the patient notices a doubling, loss or vertical deviation of words on a horizontal line. Normally there is an overlap between the temporal field on one side and the nasal field on the other to allow fusion, which helps to stabilize ocular alignment, with the result that the image is clear. Patients with minor phoric deviations of the eyes will lose this overlap and therefore develop tropia (strabismus), with the result that minor horizontal or vertical misalignment occurs, leading to distortion or even doubling. Those whose lesions involve not only the chiasm but also the cavernous sinus or orbital apex may also have IV–VI neuropathies leading to diplopia and trigeminal sensory loss or pain. Some patients with chiasmal syndromes may rarely complain of photophobia; the mechanism by which this comes about is not clear.

NEURO-OPHTHALMIC SIGNS When a chiasmal lesion leads to optic nerve fiber atrophy “band” or “bowtie” atrophy is seen, in which atrophy is more evident in the nasal and temporal Fig. 2. Visual field defects seen in chiasmal disorders: (a) ipsilateral central field defect and contralateral junctional scotoma in a lesion involving the anterior angle of the chiasm; (b) also at the anterior angle, when only the crossing macular fibers are affected; (c) bitemporal hemianopia when the body of the chiasm is affected; (d) and (e) bitemporal upper and lower quadrantinopia when the lesion compresses the chiasm from below and above, respectively; (f) bitemporal hemianopic scotomas when a lesion involves the posterior angle of the chiasm; (g) a non-congruous hemianopia occurs when the tract is affected. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

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Fig. 3. Goldman field showing bitemporal hemianopia caused by a lesion involving the body of the chiasm. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

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Fig. 4. Goldman field showing a field defect associated with a lesion involving the posterior angle of the chiasm. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

arising nasal to the fovea (associated therefore with the bitemporal hemianopia) being affected and passing into the nerve from these sections of the disc. Seesaw nystagmus; when vestibular fibers associated with the interstitial nucleus of Cajal are involved in tumors of the diencephalon and parasellar region a rhythmic synchronous alternating rotation of the eyes, in which one elevates and intorts whilst the other simultaneously depresses and extorts may arise. It is exceedingly rare (Leigh and Zee, 1991).

DISEASES WHICH MAY AFFECT THE CHIASM Inflammatory Diseases

Fig. 5. Cartoon illustrating the mechanism of postfixational blindness in bitemporal hemianopia. , Area of area of monocular vision; , area of binocular vision; blindness.

sides of the disc and relatively spared from the superior and inferior sectors (Unsold and Hoyt, 1980) (Fig. 6). This is due to involvement of only those fibers

Granulomatous infiltration. Sarcoidosis. Sarcoidosis is an autoinflammatory disorder of uncertain aetiology in which granulomatous inflammation develops leading to tissue destruction and fibrosis. It is thought that some 10% of cases arise within or also involve the central nervous system. The neurological disorder is a meningeal based inflammatory infiltration (Kidd and Beynon, 2003). The anterior visual pathway may be involved at any region (Frohman et al., 2003; Koszman et al., 2008), or an optic perineuritis may arise. Involvement of the chiasm comes about by the development of an inflammatory mass within the pituitary gland (Guoth et al., 1998) (Fig. 7). Patients present with symptoms of hypopituitarism and with visual field defects in keeping with a chiasmal problem. ANCA positive vasculitis. ANCA positive vasculitis is a granulomatous inflammatory disorder with features of arteriolar and venular perivasculitis which affects the lungs, skin, eyes, and kidneys. Neurological involvement arises as a hypertrophic pachymeningitis, as an isolated inflammatory mass or as a central or peripheral manifestation of inflammatory perivasculitis (Seror

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Fig. 6. Photographs of the optic fundus showing bowtie atrophy of both discs in a patient with a large chromophobe adenoma of the pituitary gland. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Fig. 7. T1 weighted sagittal MRI showing enhancement of the hypothalamus and pituitary stalk in Sarcoidosis.

et al., 2006). Most cases with pituitary involvement present with diabetes insipidus and not with a mass lesion (Yung et al., 2008), although the pituitary stalk may be thickened. Visual impairment is uncommon. Lymphocytic infiltration. It is well known that the chiasm may be involved in multiple sclerosis (Beck et al., 1983; Newman et al., 1991); in which chiasmal type field defects are seen in a subacute unilateral or bilateral visual loss typical of an optic neuritis. MRI shows swelling and oftentimes enhancement of the chiasm. Idiopathic optic chiasmitis may be diagnosed when other infective and inflammatory causes have been out ruled. One series (Kawasaki and Purvin, 2009) described 20 patients, 60% of whom were female, 40% presented with monocular visual loss but with

evidence for chiasmal field defects, the remainder showing bitemporal hemianopia. MRI scans revealed chiasmal swelling with or without enhancement in 12/ 15 cases, and white matter lesions were seen elsewhere in 6/15 cases. Over time around half develop multiple sclerosis. An optic chiasmitis has also occasionally been seen in other systemic inflammatory diseases, for example, systemic lupus erythematosis (Frohman et al., 2001) and sarcoidosis. Lymphocytic Hypophysitis. This uncommon condition is more common in women (by a factor of 5:1) and often occurs in the late stages of pregnancy or the early post-partum period (Kidd et al., 2003). Patients present with headache then signs of an expanding sellar lesion with visual impairment and endocrine hypofunction. Many have other organspecific autoimmune diseases. Hypopituitarism arises as a consequence of immune mediated attack on the pituitary cells, rather than simply a compressive effect. MRI shows a symmetrical intensely enhancing tissue mass within the pituitary and there may be a dural tail (Sato et al., 1998). The pathology of the lesion is one of intense infiltration by lymphocytes and plasma cells, often with lymphoid follicles, associated with evidence for necrosis of adjacent pituitary tissue. Antipituitary antibodies may be detected (Bensing et al., 2007) although the assays appear not yet to have clinical utility (De Bellis et al., 2008). Histiocytic Infiltration. These conditions are rare; Xanthomatous hypophysitis is thought to be an incomplete form of the systemic disorder ErdheimChester disease and Rosai Dorfman syndrome presents with large often multiple inflammatory masses resembling meningiomas on MRI (Kidd et al., 2006).

Infections Tuberculosis. Pituitary hypofunction and visual field defects may arise as a result of the development of tuberculoma within the pituitary, giving rise to a

The Optic Chiasm 1155

Fig. 8. T1 weighted sagittal MRI showing enlargement and enhancement of the pituitary gland and stalk in tuberculosis.

mass lesion with chiasmal compression (Domingues et al., 2002) (Fig. 8) or to optochiasmal arachnoiditis, in which a basal tuberculous meningitis encroaches upon that region and induces visual loss, frequently in

Fig. 9. Pituitary adenoma: T1 weighted coronal MRI showing a large chromophobe adenoma with cystic change causing chiasmal compression.

Fig. 10. Craniopharyngioma: T1 weighted sagittal MRI showing a cystic suprasellar lesion arising above and behind the chiasm.

association with diabetes insipidus (Akhadder et al., 2001). Pituitary tuberculomas are indistinguishable from other mass lesions on MRI, although some say that thickening of the pituitary stalk is more common in TB. In optochiasmatic arachnoiditis imaging, there is perichiasmal enhancement (Silverman et al., 1995). Pituitary abscess. One recent series noted that patients with abscesses present not with signs of fever or meningitis but with headache and visual loss mimicking a pituitary mass; most cases were only diagnosed at surgery when a pus filled mass was opened (Vates et al., 2001). Of 25 cases reported within the past 5 years around half grew no organisms, whilst the majority of the remainder were pyogenic organisms, fungi, or parasites (Dalan and Leow, 2008). Cryptococcus. Optic neuropathy is common in cryptococcal meningitis; a pathological study showed that the nerves and chiasm were damaged as a result of direct infiltration by the organism from the adjacent meninges (Cohen and Glasgow, 1993). The prognosis for visual recovery even with prompt treatment is very poor. Cysticercosis. Cases in which there was compression from the third ventricle onto the chiasm or intrasellar cysts causing compression from below have been reported (Chang and Keane, 2001). Viruses. Isolated chiasmitis related to viral infections seems rare, but has been reported with VZV and EBV (Purvin et al., 1988; Greven et al., 2001). It is more common to occur alongside a severe syndrome in which the uveal tract, retina and optic nerve, and chiasm may all simultaneously be affected (Brazis and Miller, 2005).

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Tumors and Cysts Pituitary adenoma. These constitute 10% of all intracranial tumors; the prevalence increases with age. Adenomas arise from tissues within the anterior pituitary; functioning or secreting adenomas secrete prolactin, somatotrophin, ACTH, and TSH. Most are microadenomas (measuring less than 10 mm in diameter and the majority will therefore present with the effects of hormone hypersecretion or as incidental findings. Non-secreting adenomas account for only 10% of cases but are more likely to be large, and present with visual loss and headache (Wilson, 1992) (Fig. 9). Prolactinomas account for 40% of pituitary tumors and present with galactorrhea and amenorrhoea; the majority (90%) are microadenomas (Schlechte, 2003). Corticothroph and somatotroph secreting tumors produce Cushing’s disease and acromegaly/giantism, respectively. TSH secreting tumors are rarer. Craniopharyngioma. These are benign lesions which nonetheless can cause prominent and irreversible pituitary and hypothalamic dysfunction. They arise from squamous epithelium at the junction of the infundibular stem and the anterior pituitary and are thought to be remnants of Rathke’s pouch. There is a bimodal incidence, in childhood and again in middle to late life, with clinical features of a sellar or hypothalamic lesion. They may be situated above or below the chiasm, and rarely within it (Brodsky et al., 1988). The lesions are cystic (Fig. 10) and often contain viscid, oily (“engine oil”) fluid. Cholesterol clefts, calcium and keratin may also be present. In children, these lesions present with hypothalamic dysfunction and hydrocephalus; in adults, with features of chiasmal dysfunction, optic nerve or tract signs, and ophthalmoparesis. Rathke’s cleft cyst. These benign cysts form in embryogenesis if the lumen of Rathke’s pouch does not close, giving rise to a cyst situated between the anterior and intermediate lobes of the pituitary. Most are asymptomatic and do not enlarge. Patients with symptoms are predominately female and present in middle life with visual loss due to chiasmal compression, headache, and hypopituitarism (Voelker et al., 1991). It is difficult to diagnose with certainty on MR; there are features of craniopharyngioma or pituitary adenoma, and the diagnosis is usually made at surgery. Epidermoid cysts in this region present with visual loss and hypothalamic dysfunction (Mtanda et al., 1986). They are lined by stratified squamous epithelium; enlargement occurs due to progressive exfoliation from the epithelium of keratinous material which is laid down in a lamellar pattern. The rate of growth of these lesions is exceedingly slow. Choristomas in the sellar region. Dermoid cysts are also rare and similar to epidermoids except that the cyst is lined by pilosebaceous structures leading to the formation of hair. Whilst epidermoids are often laterally placed, dermoids tend to arise in midline structures. Rupture of these cysts is associated with a chemical meningitis and seizures; those in the suprasellar region may therefore present with an apoplectic disorder similar to pituitary adenomas.

Fig. 11. Meningioma: T1 weighted coronal MRI showing a medial sphenoid ridge meningioma extending onto the lateral body of the chiasm.

Occasionally cystic lesions also arise in the optic nerve, chiasm, or tract. The lesions are found to be composed of muscle and adipose tissue (Zimmerman et al., 1983) Suprasellar arachnoid cysts. These arise relatively frequently and present with signs of compression of the underlying structures, but occasionally upwards leading to hypothalamic dysfunction and hydrocephalus. It is difficult with imaging to differentiate these from other cystic lesions such as Rathke’s cleft cyst (Rao et al., 2008), and the diagnosis is often only made at surgery; treatment is with incision and fenestration of the cyst with a low risk of recurrence. Chordoma. During development of the axial skeleton the notochord is compressed and sequestration occurs but notochordal remnants may persist into life. Most are found in the sacrococcygeal region but some 25% arise in the base of the skull (Stippler et al., 2009). Here they arise most commonly from the clivus, where they present with diplopia due to sixth nerve paresis, but extension upwards may lead to optic tract or chiasmal involvement and hypothalamic dysfunction. The prognosis depends on the histological appearances, but in general these are slow growing lesions. Germinoma. These uncommon tumors of early adult life arise most commonly in the pineal region but may also be seen in the suprasellar region, where they may arise from the floor of the third ventricle or from the chiasm itself (Tageuchi et al., 1978). Those in the sellar region present with visual failure and hypothalamic dysfunction, particularly diabetes insipidus. Germinomas are locally invasive and may metastasise. Other germ cell tumors such as teratoma and yolk sac tumors are rare and response to treatment is usually very poor.

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Vascular Disorders Cavernoma. The majority present acutely with visual loss due to bleeding. A total of 87% of one series who underwent surgery showed an improvement in visual acuity post-operatively (Crocker et al., 2008). Arteriovenous malformations may rarely arise within the chiasm and provoke a variety of syndromes, including transient bilateral visual obscurations, and field defects due to bleeding (Sibony et al., 1982). Ischaemia. The extensive blood supply to the chiasm has been noted above and for this reason ischaemic infarction of the chiasm is exceedingly rare.

Compression from Hydrocephalus

Fig. 12. Chiasmal compression from downwards displacement of the third ventricle in hydrocephalus due to obstruction by a lesion of the tegmentum.

A host of visual field defects has been seen in hydrocephalus, due to compression of the optic nerve, chiasm, and tract (Osher et al., 1978; Humphrey et al., 1982). When the third ventricle presses downwards directly and symmetrically onto the chiasm, a bitemporal hemianopia or upper quadrantinopia would be expected (Fig. 12).

Traumatic Chiasmal Syndrome Glioma. Gliomas may involve the chiasm either by arising within the chiasm itself or by infiltration from the hypothalamus. They show similar histological features to those of unilateral optic nerve gliomas, and may also arise in neurofibromatosis-1. They may present at any age but are more common in children. The onset of visual loss is usually insidious, and may even be discovered at a routine check up. The discs are usually pale at presentation, and the field defects bitemporal (Dutton, 1994). Headache may also be a feature. Imaging shows enlargement of the chiasm, sometimes with cysts and rarely with calcification (Hoyt et al., 1987). Treatment is more often hazardous than helpful; the long-term visual prognosis is overall fair (Cappelli et al., 1998). Malignant optic nerve glioma may also affect the chiasm. This presents with a much more rapidly evolving clinical syndrome and responds poorly to treatment (Rudd et al., 1985). Metastasis to other parts of the nervous system may arise (Murphy et al., 2003). The pathology of the lesion is very different to that of the benign chiasmal glioma, and is more similar to that of glioblastoma multiforme (Hamilton et al., 1973). Meningioma. These tumors are twice as common in women as men and arise more frequently in the second half of life. They tend to be benign and slow growing but some may infiltrate the underlying tissues. The chiasm may be affected by those which arise from the sphenoid wing, the clivus, and the olfactory groove (Cockerham et al., 2005), and primary optic nerve sheath meningiomas may grow backwards to involve the chiasm (Dutton, 1992; Miller, 2008). Tuberculum sellae or parasellar meningiomas are uncommon (Fig. 11), accounting for some 3% of intracranial meningiomas. Metastatic tumors. Metastasis to the sellar region has been reported with most carcinomas and lymphoreticular cancers.

These usually develop in victims of motor accidents and are associated with skull and facial fractures. The field defect is a complete bitemporal hemianopia. In one series, the prevalence of associated diabetes insipidus was 37% (Hassan et al., 2002).

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