lingual visual processing: altitudinal · visuo-spatial gnosias were normal: ghent" 35/36,...

Journal of Neurology, Neurosurgery, and Psychiatry 1987;50:607-614

Lingual and fusiform gyri in visual processing: a

clinico-pathologic study of superior altitudinalhemianopia

JULIEN BOGOUSSLAVSKY, JUDIT MIKLOSSY, JEAN-PIERRE DERUAZ,GIL ASSAL, FRANCO REGLI

From the Department ofNeurology, Division ofNeuropathology and Centre ofNeuropsychology, Centre

Hospitalier Universitaire Vaudois, Lausanne, Switzerland

SUMMARY A macular-sparing superior altitudinal hemianopia with no visuo-psychic disturbance,except impaired visual learning, was associated with bilateral ischaemic necrosis of the lingual gyrus

and only partial involvement of the fusiform gyrus on the left side. It is suggested that bilateraldestruction of the lingual gyrus alone is not sufficient to affect complex visual processing. Thefusiform gyrus probably has a critical role in colour integration, visuo-spatial processing, facialrecognition and corresponding visual imagery. Involvement of the occipitotemporal projectionsystem deep to the lingual gyri probably explained visual memory dysfunction, by a visuo-limbicdisconnection. Impaired verbal memory may have been due to posterior involvement of theparahippocampal gyrus and underlying white matter, which may have disconnected the intactspeech areas from the left medial temporal structures.

Altitudinal hemianopia due to occipital lobe damageis rare. Pathological verification has been reportedonly in three cases, which all showed inferior alti-tudinal hemianopia.-̀ In fact, both vascular cases2 3also showed a partial quadrantanopia in the superiorhemifield and cannot be considered as pure cases ofaltitudinal hemianopia. No case of superior alti-tudinal hemianopia with pathological study could befound in the literature, but complete defects of thesuperior hemifield have been sometimes reported inbilateral occipital stroke diagnosed clinically.4- lBilateral involvement of the infero-medial part of theoccipital lobe (lingual and fusiform gyri) has beendemonstrated by CT in four patients. 12 - 15 In a seriesof 39 patients with visual field defects due to occipitalinfarction shown by CT, only one had a superior alti-tudinal hemianopia.'2We present the first case of superior altitudinal

hemianopia from occipital lobe damage with apathological study. Apart from confirming previous

Address for reprint requests: Dr J Bogousslavsky, Department ofNeurology, CHUV, 101 I Lausanne, Switzerland.

Received 25 February 1986 and in revised form 9 May 1986.Accepted 15 May 1986

deductions concerning the cortical representation ofthe superior visual field in man, our case providesfurther insight in the understanding of the role ofthe lingual and fusiform gyri in complex visualprocessing.

Case report

A 73 year old man with chronic arterial hypertension, atrialfibrillation and insulin-independent diabetes was admittedafter he had an episode of bilateral leg weakness associatedwith rotatory vertigo and nausea which lasted 30 minutes.Three days before, he had experienced throbbing bilateraltemporal headaches associated with lightning phenomena inthe left visual hemifield, followed by intermittent blindnessin the upper visual field on both sides.On admission, he was well-oriented and collaborated well

with the examiner. Blood pressure was 160/100 mm Hg, withan irregular pulse suggesting atrial fibrillation (60/min).There were no carotid or subclavian bruits and no heartmurmur. The ophthalmological and visual findings aredescribed below. The remainder of the cranial nerves did notshow any abnormality. The tendon reflexes were normallybrisk and symmetrical. The abdominal reflexes were absentbilaterally. The plantar reflexes were downgoing. In thelimbs, no abnormality of tone, strength and coordinationwas found. Tactile, pain, temperature, posture and vibrationsenses were normal. The gait was unremarkable.

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Bogousslavsky, Miklossy, Deruaz, Assal, Regli

Fig 1 Goldmann perimetry: test target 1-59 mm at 100 apostilbs intensity. Macular-sparing congruent superior altitudinalhemianopia with complete sparing of the inferiorfield.

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Lingual andfusiform gyri in visual processingOphthalmological and visual examination Visual acuity was1 25 on both sides. The pupils reacted symmetrically to lightand accommodation, optic fundi were normal. The retinalartery pressure was 70/30 mm Hg on both sides. No visualperception was present in the upper hemifield for light ormotion. On Goldmann perimetry (fig 1), a congruentmacular-sparing superior altitudinal hemianopia wasshown. Vision in the inferior field was normal, includingrecognition of objects, faces and colours. There was no inat-tention to double simultaneous visual stimulation. On theIshihara plates,'6 no error was made and the patient had nodifficulty sorting the Holmgren coloured wools. Hue dis-crimination (ordering of 12 variations of the four primarycolours) was normal. Mental colour imagery was preservedand the patient could state the colours of 10 different fruits.The flight of colours was present and normal in both eyes.The patient had no difficulty describing and interpretingcomplex pictures like the Cookie Theft picture. 7Identification of the faces of famous people on photographswas normal and the patient had excellent results on Benton'sfacial recognition test (51/54). 8 When asked, the patientcould readily imagine faces of members of his family andanimals, with an accurate description. Visuo-spatial gnosiaswere normal: Ghent" 35/36, Poppelreuter20 4/4, and pre-served orientation on a geographic map of Switzerland.

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609Visually-guided reaching with each upper limb into eachhemifield was normal. Mental imagery and verbal descrip-tion of famous streets in town were unimpaired. Ocularmovements were full in all directions, without nystagmus.They were recorded on AC ENG (time constant: 5 s). Pur-suit eye movements were normal when tested as the patientfollowed a spot of light projected on a circular screen placedI m infront of him (50 and 10°/s). Optokinetic nystagmuswas induced by projecting alternating black and whitestripes on the screen (20° and 40°/s) and showed a normal(gain = 09) and symmetrical response, with a normaloptokinetic after-nystagmus.

Reading of a printed text was normal, spelling and reversespelling of words and non-words did not show any abnor-mality. Spontaneous speech, naming, repetition (words,non-words, sentences up to 15 words) and comprehension ofsimple and complex (Pierre Marie's three papers) orderswere normal. Writing on dictation was unimpaired. Sponta-neous drawing of a cube was normal. There was no bucco-linguo-facial apraxia and limb praxias did not show any dis-turbance (4/4 on symbolic gestures, 5/5 on imitationgestures). There was no apparent difficulty on evocation ofrecent and ancient events but there were significantdifficulties in verbal and visual learning: Rey Auditorylearning2' (26/75, recognition: 8/15, delayed evocation:

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6100/15), Hebb's recurring digits22 (maximal span of 7, failureof span + 1 learning), Learning of 15 signs23 (21/75, recog-nition 13/15, delayed evocation 4/15), Corsi's block-tapping24 (maximal span of 6, failure of span + 1 learning).The CT (fig 2) showed bilateral areas of infarction

involving the inferior occipito-temporal region. An archangiography and bilateral carotid angiography showed astenosis of the right internal carotid artery reducing thelumen by 50% of the diameter. The left internal carotidartery showed a subtotal stenosis at the sinus and was com-pletely occluded at the siphon. The left subclavian artery wasstenosed by more than 50% of the lumen diameter justbefore the origin of the vertebral artery, which also showeda 75% stenosis. The right vertebral artery was occluded at itsorigin. The left middle cerebral artery territory was suppliedby the right internal carotid artery. The posterior commu-nicating arteries were not opacified. The ECG showed anatrial fibrillation with a ventricular rhythm of 65 per minute.On 24 hour-Holter monitoring, there were episodes ofbradyarrhythmia as slow as 28/min. On chest radiographs,the size of the heart was normal. The haematocrit was 0 5(haemoglobin 16 7 g/dl), fasting blood glucose was 7-4mmol/l, fasting blood cholesterol was 7 5 mmol/l. The otherstandard blood tests were normal.Evolution The altitudinal hemianopia remained un-changed on sequential testing until the patient's death. Hewas readmitted 6 months after his stroke for chest pains. CTat the thoracic level showed a dissecting aneurysm of theaorta. The patient developed severe renal failure and diedtwo weeks later.

General findings at necropsyThe patient had generalised atherosclerosis with a largeulcerated and thrombosed aneurysm in the suprenal segmentof the abdominal aorta. Atheromatous emboli were found inthe kidney and acute bilateral pyelonephritis was present.

Neuropathological findings (figs 3-5)The brain weighed 1360 g. The middle cerebral arteries andthe intracranial portions of the internal carotid arteriesexhibited a mild degree of atherosclerosis. The anterior andposterior cerebral arteries as well as the vertebro-basilarsystem showed no atherosclerotic changes. The occipito-temporal branches of both posterior arteries were occludedby a yellow-grey material, but the calcarine arteries were notinvolved. Coronal sections of the brain showed well-delineated infarcts in both inferior temporo-occipitalregions. The lesions were asymmetric, the one on the left sideextending farther anteriorly and laterally than the one on theright side. Both lingual gyri were completely destroyed,whereas the middle third of the fusiform (occipito-temporal)gyrus and the posterior third of the parahippocampal gyruswere affected only on the left side.

There was no involvement of the cunei or the precunei.The optic chiasm, the optic tracts and the lateral geniculatebodies showed no alteration. No other infarct was present.Microscopic examination from the occipital lobes sectionsshowed that the occipito-temporal branches of both pos-terior cerebral arteries were occluded by an organised andpartly recanalised thrombo-embolus. The infarcts involvedboth the cortex and the subcortical white matter, leaving

Bogousslavsky, Miklossy, Deruaz, Assal, Reglicystic spaces, crossed by a few small vessels. Groups ofmacrophages staining strongly with Prussian blue werepresent. Sections stained for myelin showed a well-definedmargin of the infarct bordered by few protoplasmic as wellas many fibrillary astrocytes. In summary, the histologicalfindings corresponded with those of an infarct severalmonths old.

Discussion

Our patient showed a purely superior congruenthemianopia with macular sparing associated with ver-bal and visual memory dysfunction, but without thevisuo-psychic disturbances classically produced byoccipito-temporal infarcts, as he had no achro-matopsia, no prosopagnosia, no impairment of visualimagery and no alexia.

This superior altitudinal hemianopia correspondedto selective involvement of the inferior lip of the cal-carine area with sparing of the superior lip. Theoccipital pole was not involved and this sparingexplained the absence of macular blindness.

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Lingual andfusiform gyri in visual processingFissuro calcarina

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Fig 5 (A) Diagram showing representation of the visualfield in the calcarine cortex, after Holmes.5I (B) Schematicrepresentation of the actual lesion on the mesial surface ofthe occipital lobe. (C) Corresponding visualfield defect: Black: leftoccipital lesion and corresponding visualfield defect; Hatched: right occipital lesion and corresponding visualfield defect.



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Colour visionAchromatopsia, colour anomia, colour imagery andflight of colours dysfunction were not present. Upperfield defects are common in a central achro-matopsia.6- 10 12-14 This can be explained by the factthat the lesion responsible for achromatopsia in one

hemifield has been localised in the inferior and medialpart of the contralateral occipital lobe.26 The cal-carine cortex and the optic radiations must be rela-tively spared in order to have some vision preserved.Achromatopsia was present in three of the four cases

with superior altitudinal hemianopia studied byCT'2-' (table), but a detailed anatomical analysiswas provided only in one,'3 who had an infarctinvolving the infero-medial part of the occipital lobeand the parahippocampal and inferior temporal gyribilaterally. The fourth patient'5 had no achro-matopsia and CT suggested involvement of the lin-gual gyri, the medial aspect of the fusiform gyri andparts of the parahippocampal gyri. This patient was

very similar to ours because he did not show proso-

pagnosia and because he had only partialinvolvement of the fusiform gyrus contrasting withapparently bilateral destruction of the lingual gyrus.In our patient, the lingual gyrus was destroyed on

both sides, but the fusiform gyrus was involved onlyin its middle third on the left. As he had no

impairment of colour recognition, naming, matchingand imagery, we suggest that the fusiform gyrus matbe the critical structure for cortical colour integration,and that bilateral destruction of the lingual gyrus isnot able to cause achromatopsia.

Recognition offaces and objectsOur patient had no difficulty recognising, describingand mentally imaging human and animal faces as wellas objects. Damasio et a!27 reviewed eight necropsy


cases of prosopagnosia and concluded that bilateralmedial occipito-temporal lesions were responsible.This view has been corroborated in one more nec-

ropsy case28 and recent CT studies.293' Because

these lesions are inferior to the calcarine sulcus,prosopagnosia is frequently associated with upperfield defects46-9 13 1432 and with achro-matopsia.6-9 13 14 26 31 As in our patient, two of thefour reported cases'12-'5 with superior altitudinalhemianopia studied by CT (table) had no proso-pagnosia. One of them'5 showed bilateralinvolvement of the lingual and fusiform gyri, butcomplete destruction cannot be ascertained in theabsence of pathologic study. In the other, 12 a detailedtopographic analysis of the lesion on CT was not pro-vided. Our case supports previous views33 that inbilateral occipito-temporal lesions, destruction of thefusiform gyrus at least on one side is critical in theproduction of prosopagnosia; partial unilateralinvolvement does not appear to be sufficient, even

when both lingual gyri are destroyed.

Visuo-verbal processingAlexia without agraphia is generally associated withright hemianopia and is usually related toinvolvement of the paraventricular part of the leftoccipital lobe and of the splenium of the corpus cal-losum, with subsequent disconnection between thevisual areas and the posterior parietal region.34Involvement of the lingual and/or the fusiform gyriand underlying white matter on the left side has beenreported in necropsy and surgical cases,34 usuallywith involvement of the corpus callosum. The corpuscallosum was spared in five patients who had lesionslimited to the ventral aspect of the occipitallobe,35 -39 as in our non alexic patient. In one, whohad a right hemianopia, the left lingual, fusiform and

Table Cases ofsuperior altitudinal hemianopia with anatomical correlation

Congruent visual MacularAuthors Sex Age Achromatopsia Prosopagnosia field defect sparing Localisation

McAule et al, &T 55 + - - CT: occipital lobes (no19791 detail)

Young, et al, & 70 + + - - CT: lingual, fusiform,19801 3 parahippocampal,

inferior temporal gyriBrazis et at, & 68 + + ? ? CT: "inferior occipito-

198114 temporal whitematter"

Newman et al, s 57 - - + + CT: lingual gyri, medial19841 aspect fusiform gyri,

parahippocampalgyri more left thanright

Present case s 73 - - + + autopsy: lingual gyri,middle third of leftfusiform gyrus,posterior third of leftparahippocampalgyrus

+ present; - absent; ? not reported.



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Lingual andfusiform gyri in visual processing

parahippocampal gyri were infarcted36 and inanother,39 who had normal visual fields, a cerebralhaemorrhage involved the left fusiform and inferiortemporal gyri on CT, with sparing of the other struc-tures. In the three remaining cases,35 38 39 the extentof the occipito-temporal lesion cannot be establishedwith precision from the reports. Our case suggeststhat in the absence of corpus callosum involvement,destruction of the lingual gyrus and partial destruc-tion of the fusiform gyrus, parahippocampal gyrusand underlying white matter on the left side is notsufficient for the production of alexia. These lesionsdo not seem to interrupt the inputs travelling from thecortical visual areas towards the speech areas. Exten-sive involvement of the fusiform gyrus with destruc-tion of the underlying white matter is probably criti-cal for producing alexia when the corpus callosum isspared, a view which is supported by the CT findingsin the patient of Henderson et al.39 In that case, it wassuggested that the lesion interrupted the fibres carry-ing the visual impulse towards the angular gyrus, withsubsequent visuo-verbal disconnection.

Visual and verbal memoryImpairment of visual memory was the sole abnormal-ity of visuo-psychic processing in our patient. Amne-sia due to occipital lobe damage was first mentionedin 1902 by Dide and Botcazo.40 However, in the caseswith non selective anterograde amnesia, associatedbilateral lesions of the medial temporal lobe havealways been found. 141 42 Selective amnesia forvisual items have been reported in lesions limited tothe occipital lobe29 30 41 43 and is probably related toa disconnection between the visual areas and themedial temporal structures.304344 Involvement ofthe short fibres which form the occipito-temporalprojection system (formerly called inferior longi-tudinal fasciculus)45 may explain the impairment ofvisual memory seen in our patient, with a visuo-limbicdisconnection. The disturbances of verbal memoryobserved in our patient may have been due toinvolvement of the posterior third of the left hippo-campal gyrus and underlying white matter, possiblyby disconnecting the intact speech areas from themedial temporal region. No other cortical, whitematter or thalamic lesion could explain this dis-turbance of verbal learning.

Visuo-spatial processing and ocular trackingThe absence of visual disorientation, optic ataxia andspatial imagery in our patient confirms recent work31suggesting that dysfunction of visuo-spatial pro-cessing is not due to bilateral lesions ventral to thecalcarine sulcus. The lesions incriminated in visualdisorientation are more dorsal, at the level of the infe-rior and superior parietal lobules, dorsal part of the

613

occipital lobe and underlying white matter.3'4647Unilateral lesions in this area also impair smooth pur-suit movements of the eyes, ipsilaterally more thancontralaterally.4849 These movements were normalin our patient on bedside examination and on ENGrecording, with physiological optokinetic responses.In a necropsy case with a lesion involving the internalsagittal stratum, no abnormality of smooth pursuitmovements was observed.50 The findings in ourpatient show that the pathways carrying the corticalimpulses implicated in visual tracking do not travel inthe white matter deep to the lingual and fusiform gyri.The negative findings in our patient suggest that

extensive bilateral involvement of the lingual gyrusdoes not compromise complex visuo-psychic pro-cessing. The fusiform gyrus and underlying whitematter seem to be the principal structure involved incolour integration, facial recognition, visuo-verbalprocessing and corresponding mental imagery.

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