28ournal ofNeurology, Neurosurgery, and Psychiatry 1995;59:238-242

Clinical and topographical range of callosalinfarction: a clinical and radiological correlationstudy

Maurice Giroud, Raymond Dumas

AbstractA prospective clinical and radiologicalcorrelation study was performed todetermine the frequency, and the clinicaland radiological features of callosalinfarction. From 1 January 1993 to theend of December 1993 282 cases of cere-bral infarction seen in the Neurology ser-vice of the University Hospital of Dijonwere studied prospectively. Eight caseswith callosal ischaemic lesions were iden-tified by CT and MRI. A callosal discon-nection syndrome occurred in only five ofeight patients, related to a single, largeinfarct or several infarctions in the ante-rior part of the corpus callosum. Clinicalfeatures were characterised by left ideo-motor apraxia, construction apraxia, andleft agraphia in all five cases. Alien handwas noted in only two cases. There weregait disorders in three cases with MRIfeatures of multiple lacunes in a largepart of the corpus callosum, and also thesubcortical areas of both hemispheres. Itis emphasised that callosal infarctionsare not rare and that they contribute tothe clinical features of strokes. As well asthe classic incomplete callosal disconnec-tion syndrome, these callosal ischaemiclesions may induce non-specific gait dis-orders.

(7 Neurol Neurosurg Psychiatry 1995;59:238-242)

Keywords: infarction; corpus callosum; disconnection;gait disorders

The NeurologyService, GeneralHospital, University ofBurgondy, Dijon,FranceM GiroudR DumasCorrespondence to:Dr M Giroud, H6pitalGeneral, 3 Rue duFaubourg Raines, 21000Dijon, France.

Received 13 December 1994and in final revised form2 May 1995Accepted 11 May 1995

Cerebrovascular disease has played a majorpart in the understanding of callosal dys-connection syndromes and enabled Liepmannand Maas to show the role of the callosallesion in the genesis of unilateral apraxia.'The anatomical and clinical correlations are

not easy to demonstrate in many cases

because infarction is not usually limited to thecorpus callosum, and multiple infarctionsoften coexist. Early studies2 on callosal symp-toms preceded MRI and CT but more recentstudies have used these techniques.3 Lesionsof the corpus callosum producing distur-bances of higher brain function are oftenrecognised as disconnection syndromes ofwhich unilateral left hand apraxia, agraphia,and tactile anomia are the most common.' 2 4-6Because of the absence of systematic studieson the range of clinical and imaging features

of callosal infarction, we performed this popu-lation based MRI study to determine theprevalence of the involvement of the corpuscallosum in ischaemic strokes and to establishthe clinical features.

Patients and methodsFrom 1 January 1993 to the end of December1993, we examined prospectively all thepatients with ischaemic stroke admitted to theneurological service of the University Hospitalof Dijon (France).' Our aims were firstly, todetect a clinical callosal syndrome in anypatient with the usual features of an ischaemicstroke, and secondly, to detect callosal infarc-tion by CT and MRI. An ischaemic strokewas defined as an acute neurological deficit,lasting more than 24 hours, with spontaneousimprovement.

Clinical symptoms related to a callosal syn-drome were systematically collected by thefive senior neurologists of the service accord-ing to established criteria. 1-68 These were lefthand ideomotor apraxia, left hand agraphia,left hand tactile anomia, left alien hand syn-drome (as described by Brion and Jedynak9with three characteristics: inability to recog-nise the arm as one's own when held by theother arm with the eyes closed; a feeling ofloss of control of left arm movements; andpersonification of the left arm), left visualanomia, left auditory extinction, and alexiawithout agraphia.

Proximal and distal motor examination ofthe limbs, locomotor ability, sensory stretchreflex examination, visual examination, testsfor language (fluency, repetition, writing,reading), buccolinguofacial apraxia, gnosias offamous faces, colours, right-left and fingertest, visuospacial and visuoconstructive tasks(drawing a cube, orientation on a map ofFrance), memory functions, frontal functions,and neglect (line bisection test, simultaneousapplication of sensory, visual, or auditorystimuli), were studied. An ischaemic strokewas defined by a hypodense abnormality onCT and by a hyposignal on Ti weightedimage and a hypersignal on T2 weightedimage with gadolinium uptake after day 7 onMRI. Ti weighted images were acquired on a1-5 Tesla Siemens MRI machine, with a shortTR (480 ms) and a short TE (15 ms), and T2weighted images with a TR of 250 ms and aTE of 20 ms. We determined the presenceand the topographic localisation of callosal

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239Clinical and topographical range of callosal infarction: a clinical and radiological correlation study

Figure 1 Areas suppliedby the branches of theACA: (1) orbitofrontalartery, (2) frontopolarartery, (3) anteriorinternalfrontal artery,(4) middle internalfrontalartery, (5) posteriorinternalfrontal artery,(6) paracentral artery,(7) precumeal artery,(8) internal parieto-occipital artery,(9) callosomarginalartery, (10) pericallosalartery.

ischaemic stroke on CT with the templatesdefined by Matsui and Mirano'" and on MRIfrom the atlas of Duvernoy."' Figure 1 showsthe classification of the territory of the ante-rior cerebral artery (ACA) used. 12 Dopplerultrasound examination of the cervical arter-ies, electrocardiography, and two dimensionaltransthoracic echocardiography were per-

formed on all patients. Angiography was per-

formed on 32. Serological and bloodexaminations excluded syphilis, hypercoagu-lability, hyperfibrinogenaemia, and homo-cystinaemia in all the patients. Weprospectively collected data on age (years),sex, hypertension (systolic blood pressure

greater than 160 mm Hg/90 mm Hg), dia-betes mellitus (serum glucose greater than1-40 g/l), dyslipidaemia (fasting cholesterolserum higher than 2-5 g/l or fasting serum

triglycerides greater than 1-5 g/l), cigarettesmoking (> 20 packs per year), previousstroke or transient ischaemic attack (focalcerebral dysfunction presumably ischaemic inorigin lasting less than 24 hours without any

sequelae), previous myocardial infarction withECG sequelae, atrial fibrillation, presence ofechocardiographic abnormalities such as leftventricular hypertrophy or akinesia, mitralvalve prolapse, patent foramen ovale, or

aneurysm of the interatrial septum, and signif-icant atheroma of the internal carotid arteries(narrowing of 50% or more of the lumen as

documented by Doppler ultrasonography).The presumed causes of stroke were definedaccording to the criteria used by Adams et al.13Large vessel disease was considered as thecause of the infarcts when there was a stenosisof 50% or more in one carotid artery on

Doppler ultrasonography or on angiography.Microangiopathy due to hypertension was

diagnosed when infarction was in the territoryof a deep perforating artery in the absence ofanother aetiology. Potential cardiac sources ofembolism were considered if cardiac arrhyth-mia, valvulopathy, or cardiac failure withdilatation of ventricular cavities were present.

ResultsOf 282 patients with ischaemic strokes col-lected during the 12 months, eight patients(2-7%; three women, five men (mean age 68,range 61 to 82 years)) had a radiologicallyidentifiable callosal infarction. Four patientshad a right sided associated cerebral infarct,one a left sided associated infarct, and threean infarction only in the corpus callosum.Table 1 summarises the clinical features andthe radiological findings.

TWO MAIN PATrERNS OF CALLOSAL SYNDROMEClassic callosal disconnection syndromeLeft hand apraxia was noted in six patients(3-8). It was easy to see in the patient (No 7)with right hemiplegia, but more difficult in theother five cases. All these six patients couldnot perform actions with their left hand on

verbal commands after motor recovery. Fourpatients (5-8) also had impaired imitationand object use with the left hand on com-

mand. In these six patients, the body of thecallosum was involved. The left hand apraxiawas associated with a constructive apraxia.Alien hand syndrome occurred in only two

patients, those with an extended callosalinfarction (7 and 8).

Left hand agraphia was apraxic in four

Table 1 Clinical and MRIfeatures of callosal infarction

Left Left Left Left Frontaltactile ideomotor Left visual Left Constructive tactile gait

Patients anomia apraxia agraphia anomia hemideafness apraxia alexia Alien hand disorders MRIfeatures

I 0 0 0 0 0 0 0 0 +

2 0 0 0 0 0 0 0 0 +

3 0 + 0 0 0 + 0 0 +

4 0 + 0 0 0 + 0 0 0

5 0 + + 0 + + 0 0 0

6 0 + + 0 0 + 0 0 0

7 + + + 0 0 + + + 0

8 0 + + 0 0 + 0 + 0

|: associated intemal frontal infarction.

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240Giroud, Dumas

patients (5-8) because they had the ability ofleft hand writing with anagram letters. Theright hand was neither agraphic nor apraxic inall of these cases. Left tactile anomia occurredin one case (No 7) with ischaemic lesionsoccurring within the four fifths of the corpuscallosum and associated with internal fronto-parietal ischaemia. Left visual anomia was notfound. Left hemideafness as studied by thedichotic test, occurred in only one patient (No5). Left tactile alexia was present in onepatient (No 7).

Gait disorders offrontal typeOf eight patients with callosal infarctionestablished by radiology, three had no specificclinical symptoms (Nos 1-3). The syndromewas characterised by gait disorders with loco-motor difficulties of frontal type. The patientsused a wide base with feet rooted to theground. Gait consisted of shuffling with shortsteps (marche a petit pas) and freezing, withno arm swing, and slight extension of thetrunk. In patient 1, there were lacunes in thegenu of the corpus callosum, in patient 2,there were lacunes in the middle part of thecorpus callosum. Patient 3 had a small infarc-tion in the middle of the corpus callosum. Allthree patients had lacunes in the white matterof the centrum ovale.

MOTOR DYSFUNCTIONPatient 4 had crural monoplegia and hemi-plegia was predominantly in the legs inpatients 5-8.

OTHER DEFICITSHemihypoaesthesia ipsilateral to the hemi-plegia was seen in patients 7 and 8 both onupper and lower limbs. Hemineglect waspresent and forced grasping occurred in thesame two patients.

STROKE TOPOGRAPHYTwo types of ischaemic lesions were identifiedby CT and MRI: lacunes < 10 mm diameterin the corpus callosum associated with bilat-eral subcortical lacunes, in white matter intwo patients (1 and 2; fig 2) and large infarc-tions in six patients (3 to 8), associated withleukoaraiosis in patient 3 (fig 3) and with asmall infarction in the ipsilateral centrumovale in patient 7 (fig 4). Patient 4 had twoseparated infarctions within the corpus callo-sum (fig 5). Patients 6 and 8 showed an ante-rior right corpus callosum infarction (fig 6)

also involving the ipsilateral internal frontalarea on MRI, corresponding to the ACA terri-tory. Patient 5 had a large infarction in themiddle part of the corpus callosum associatedwith a right internal frontal infarction onMRI, corresponding to the ACA territory. Wefound in total 13 cases of ACA territoryinfarctions out of 282 cerebral infarctions.

RISK FACTORS (TABLE 2)Hypertension was the most frequent risk fac-tor. It occurred alone in patients 1 and 2 andwas associated with diabetes mellitus inpatients 4 and 7, with dyslipidaemia in

Figure 2 (patient 1) Several lacunes <10 mm diameterall along the corpus callosum but also within the ovalecentrum on sagittal Tl weighted MRI.

Figure 3 (patient 3) Large infarct in the middle of thecorpus callosum, on sagittal Ti weighted MRI.

Table 2 Deficits, risk factors and causes of stroke in the patients with callosal infarction

PresumedcausePatients Sex Age (years) Hemiplegia Hemihypoaesthesia Other deficits Risk factors of stroke

1 F 63 0 0 0 HT SVD2 M 68 0 0 0 HT SVD3 M 61 0 0 0 0 SVD4 F 69 Left L 0 0 HT + DM SVD5 M 82 Left U + L 0 0 HT + DL + CA LVD6 M 72 Left U + L 0 0 HT + DL + CA LVD7 F 62 Right U + L Right U + L FG + HN HT + DM + DL + CA LVD8 M 69 LeftU + L RightU + L FG + HN A + HT CEU = upper limb; L = lower limb; FG = forced grasping; HN = hemineglect; A = arythmia; DL = dyslipidaemia; DM = diabetes melitus; HT = hypertension;CA = carotid atheroma; SVD = small vessel disease; LVD = large vessel disease; CE = cardioembolism.

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241Clinical and topographical range of callosal infarction: a clinical and radiological correlation study

Figure 4 (patient 7)Infarction involving the leftposterior part of the corpuscallosum and the ovalecentrum, on horizontal T2weighted MRI.

Figure S (patient 4) Twosmall infarctions in themiddle of the corpuscallosum on sagittal Tiweighted MRI.

Figure 6 (patient 6)Infarction of the rightACA territory involvingthe right anterior part ofthe corpus callosum on

horizontal CT.

patients 5, 6, and 7, with stenosis of the inter-nal carotid artery in patients 5 and 6, and withatrial fibrillation in patient 8. Patient 3 had noapparent risk factors.

PRESUMED CAUSES OF STROKE (TABLE 2)Small vessel occlusion was presumed to be thecause of the callosal infarction in four patients(1-4), large vessel occlusion in three patients(5-7), and cardioembolism in one patient (8).

DiscussionPrevious studies based on CT and on selectedpostmortem studies have underestimated thefrequency of infarction of the corpus callosum.By using MRI in a well defined cohort study, itis possible to know exactly the extent of cal-losal involvement in comparison with otheranatomical structures implicated in ischaemicstroke. We found 13 patients with ACA terri-tory infarctions out of 282 ischaemic strokes(4 6%). These data are similar to the 4%found by Bogousslavsky et al14 in another hos-pital based study. Among these 13 patients werecorded eight (61%) cases of callosal infarc-tion by CT and MRI, a percentage similar tothat found by Bogousslavsky and Regli,3 butgreater than the 36% reported by Hung andRyu8 before MRI was available.The earliest descriptions of the supply areas

of the ACA were by Duret in 1874,'5 by Foixand Hillemand in 1925,'2 and Critchley in1930.2 The ACA irrigates the medial surfaceof the frontal and parietal lobes, the anteriorlimb of the internal capsule, the head of thecaudate, and the corpus callosum (fig 1).Infarction of the entire vascular territory ofthe ACA is rare (4%).8 In most instances, theinfarction is subtotal, involving individualbranches, singly or in combination.

Despite advances in diagnostic technology,involvement of the corpus callosum in ACAsyndromes has not been well recognised onepidemiological, clinical, or radiologicalgrounds.' 68 There are many reasons for this:spontaneous onset of callosal infarction israre,'9 manifestations depend largely on the siteand size of the infarct, which is related to thesite of occlusion, and motor dysfunction mayhide the neuropsychological effects of a lesionin the corpus callosum. In 1907, Liepmannand Maas' described a 70 year old carpenterwho had transcortical motor aphasia, apraxia,and agraphia of the left arm, and right hemiple-gia. The left apraxic hand did not improve withimitation or actual object usage, and the lefthand agraphia did not improve with the use ofanagram letters. A postmortem examinationshowed a left ACA infarction with damageextending from the first frontal convolutionthrough the white matter to the paracentrallobule with involvement of the anterior twothirds of the corpus callosum. A callosal lesionwould disconnect the left hemisphere from theright premotor cortex and cause apraxia iso-lated to the left hand.2122 We found ideationalapraxia and construction apraxia exclusivelylimited to the left extremities.

Only two patients (7 and 8) showed alien

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hand signs.923 These had been thought to besecondary to callosal dysfunction but recentlywere attributed to damage of the medialfrontal cortex, including the supplementarymotor area and cingulate gyrus controlateralto the alien hand.23 This correlation was clearin patients 7 and 8. Grasp reflex and motor orverbal perseveration were found in these twopatients. Therefore, infarction localised to theanterior one third of the corpus callosum wasassociated with an ideomotor apraxia and aconstruction apraxia as shown by patients3-8. When infarction encompassed morethan the anterior two thirds of the callosal cor-pus, we found an associated tactile anomia(patient 7). There was no visual anomia,because no case showed a posterior callosallesion.As well as the well known classic callosal

disconnection syndrome, we have identified apure gait disorder syndrome related to lacunesin the anterior part of the corpus callosum.The gait disorder with locomotor difficultydescribed in this paper seems to be a frontaltype,24 with small step height or "marche 'apetits pas", with a wide base, a reduced num-ber of steps per minute, with the feet rooted tothe ground, shuffling with short steps andfreezing, with imbalance, loss of arm swing,and slight extension of the trunk. The patientshave considerable difficulties initiating the legmovements required to walk (yet can performthe movements of pedalling a bicycle wellwhen lying on the bed), and turn. Thisimpairment of gait may be related to aninvolvement of efferents from the leg area ofthe motor cortex.2429 We think that thelacunes in the anterior part of the corpuscallosum may compromise the afferent path-ways from the minor forceps to the frontalcortex, but lacunes outside the corpus callo-sum could explain this gait disorder in threepatients. The last question focuses on thefact that lacunes may be present within thecorpus callosum due to involvement of per-forating branches of the ACA and this local-isation is underestimated in the medicalliterature.26 27

In summary, MRI shows that there hasbeen an underestimated frequency of callosalinfarction in ACA territory infarction.Secondly, the callosal infarction may con-tribute to the neurological deficit. Thirdly, aswell as the classic anterior callosal disconnec-tion syndrome, we found gait disorders inpatients with lacunes affecting the anteriorpart of the corpus callosum.

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