Journal of Neurology, Neurosurgery, and Psychiatry 1987;50:709-713 Deep left parietal lobe syndrome: conduction aphasia and other neurobehavioural disorders due to a small subcortical lesion M PONCET, M HABIB, A ROBILLARD From the Department of Neuropsychology, Neurological Clinic, University Hospital, Marseilles, France A patient with sudden onset of conduction aphasia in the context of an ischaemic stroke is reported. Other neurological and neuropsychological findings included bilateral ideomotor apraxia, right hemisensory defect and paradoxical left ear extinction on a dichotic listening test. Lesion location, as inferred from magnetic resonance imaging, involved a restricted subcortical area in the left parietal lobe, near the lateral wall of the cerebral ventricle. The anatomical correlate for each of the clinical findings is discussed in the light of classical anatomo-clinical correlations. It is concluded that this tetrad constitutes a specific syndrome which may be easily recognised and ascribed to a single lesion in the deep white matter of the left parietal lobe. SUMMARY In neurological practice, clinical attempts at predicting lesion localisation are usually derived from analysing neurobehavioural changes in correlation with their classical anatomical substrate. When several signs and symptoms are observed, an estimate about the lesion site may be obtained by combining their respective anatomical correlates. The purpose of this paper is to emphasise the localising value of the combination of four neurological and neuropsychological symptoms: conduction aphasia, bilateral ideomotor apraxia, hemisensory defect and paradoxical left ear extinction, a combination which specifically points to a restricted subcortical area of the left parietal lobe. Case report A 70 year old right-handed man, habitual smoker and neglected hypertensive, presented with a sudden onset of language difficulties and tingling in the right limbs. There were no headache, nausea or vomiting, nor was consciousness impaired at any moment. The patient was examined on admission as well as on numerous other occasions thereafter. He remained fully oriented and perfectly understood all spoken or written commands, but answered in a fluent paraphasic speech, mainly made up of phonemic paraphasias. Naming tasks brought evidence of considAddress for reprint requests: Dr M Poncet, DIpartement de Neuropsychologie, CHU Timone, F- 13385 Marseille Cedex 5, France. Received 2 May 1986. Accepted 26 June 1986 erable word-finding difficulties, and a tendency to approximate phonetically the designated image or object ("conduites d'approche"'). Repetition was marred by numerous phonemic paraphasias and neologisms (fig 1). Comprehension of written language was normal but reading aloud gave rise to numerous phonemic transformations and writing was made nearly impossible by the right hand sensory defect. This pattern of speech disturbance was consistent with the diagnosis ofconduction aphasia.1 Visual fields were full, and cranial nerves appeared normal. Reflexes were slightly brisker on the right, but there was no weakness. Plantar responses were flexor bilaterally. There was a right, proportional sensory deficit, more evident in the upper limb where pin sensation was inconsistently perceived, and always poorly localised; recognition of finger and toe movement was faulty, as were perception of vibration, graphesthesia, and stereognosia. On praxis testing, the patient would, both on command and imitation, produce bilaterally only poorly organised gestures, or perseverations. Frequently, body-part was assimilated to object. This pattern, notwithstanding the right sensory defect, was typical of bilateral ideomotor apraxia. However, gesture comprehension, as assessed by asking the patient to discriminate between apraxic and non-apraxic gestures, was found normal. The dichotic listening task was administered both in repetition and designation (multiple-choice) conditions: the patient showed a complete left ear extinction, none of the words sent to his left ear being repeated or designated. The EEG was normal, and the CT scan, obtained on the 6th hospital day, only showed a questionable deep parietal hypodensity (fig 2). Magnetic resonance imaging (MRI) obtained 2 months after stroke, showed a well-circumscribed abnormal area in the depth of the parietal white matter, near 709 Poncet, Habib, Robillard 710 2 3 5 4 Limited to short phrases and stereotyped expressions 6a 7I Runs through entire sentence MELODIC LINE Intonational contour 1 Absent PHRASE LENGTH Longest occasional (1/10) uninterrupted word runs 1 word 4 words 7 words ARTICULATORY AGILITY Facility at phonemic and syllable level Always impaired or impossible Normal only in familiar words and phrases Never impaired GRAMMATICAL FORM Variety of grammatical None available Limited to simple declaratives and stereotypes . Once per minute of conversation Normal range Information Speech exclusively construction (even if incomplete) PARAPHASIA IN RUNNING SPEECH WORD FINDING Informational content in relation to fluency AUDITORY COMPREHENSION Converted from objective z-score mean _00r Present in every utterance I I Absent I. Fluent without information proportional to fluency content words .I , Absent (z= -2) (z= -1-5) (z= -1) (z= -0'5) (z= 0) (z= +0'5) Fig 1 Boston Diagnostic Aphasia Examination rating scale profile of the patient's speech characteristics. Fig 2 CTscan showing a small deep parietal white mau-er infarction (arrows). Normal (z= +1) 71 Deep lgft parietal lobe syndrome e~~~~~: F i",~~~~E e7 p- Z4i V ~ ~ ~ ~ ~ ~ Z ~ ~ ~ ~ ~ ~ ~ ~ ~ ~~~4 Kl8o fr-~~~(b ii 7N 0-17 I , $ ->W\ |r L 47 NJ.'~ _ e~ | .t \fS Fig 3 Magnetic resonance imaging obtained 2 months after stroke. (a) Saggital section, and schematic reconstruction showing the arcuatefasciculus (stippled area), probably damaged by the ischaemic infarct (hatched). (b) Coronal section at the level of the 3rd ventricle, and reconstruction illustrating the projected thalarno-corticalfibres and lesion site (hatched). (c) Coronal section at the level of the splenium showing the posterior extension of the infarct (hatched). the insula, posterior and superior to the lenticular nucleus (fig 3), consistent with a small subcortical ischaemic infarct. Discussion The present observation deals with the coincident occurrence of conduction aphasia, bilateral ideomotor apraxia, right hemisensory defect, and paradoxical left ear extinction. In contrast with these dramatic neurological and neuropsychological changes, absence of any clouding of consciousness and nearly normal CT scan were suggestive of a very small lesion, which was confirmed by MRI. We will try to reconcile these apparently discrepant findings. tradictions,7 it is generally admitted that a disconnection theory is able to account, at least schematically, for most cases of conduction aphasia,'0 whether of the first or the second type. Our case probably belongs to the first type, as it clearly appears from MRI and accompanying anatomical reconstructions (fig 3a) that the small, subcortical lesion involves the arcuate fasciculus during its course under the parietal cortex, where it arches forward in the direction of the frontal premotor cortex." (2) Ideomotor apraxia Classically, bilateral apraxia may result from lesions involving either the lower parietal region (the angular and supramarginal gyri) or more anterior regions of (1) Conduction aphasia Historically, from the earliest monograph of Wer- the left hemisphere. As for language processing, the nicke,2 up to the modem disconnection theories of arcuate fasciculus is thought, here again, to play a Geschwind,3 conduction aphasia has been mainly central role in motor behaviour.2 -14 Benson et a14 related to disruption of subcortical and/or cortical came to isolate within conduction aphasics a group of connecting systems between Wernicke's and Broca's patients showing bilateral apraxia. These patients areas, especially the arcuate fasciculus. It has been always had supra-sylvian lesions. To explain this shown that conduction aphasia may be associated association, these authors proposed that the arcuate with two distinct anatomical patterns:4 (1) lesions fasciculus received, on its way towards the frontal involving the region of the left supra-marginal gyrus, cortex, input from the parietal lobe and especially deep enough to compromise the arcuate fasciculus. In from the supramarginal cortex. Thus, bilateral ideothis case, a strictly subcortical lesion seems to be motor apraxia may result from lesions involving (1) sufficient to produce the syndrome (Benson et al:' the parietal cortex; (2) white matter subjacent to it; or (3) the arcuate fasciculus. According to Heilman et case 3). (2) damage to the insular and auditory cortial,"S among apraxic patients, those with good gesture ces and underlying white matter, probably compromising another connecting pathway running through comprehension will prove on CT to have lesions sparing the parietal cortex. This was the case of our or underneath the insular cortex.6 Despite some con- 712 patient whose strictly subcortical infarct was so situated as to cause bilateral ideomotor apraxia by producing a disconnection between the parietal cortex and the arcuate fasciculus, and/or by compromising the arcuate fasciculus itself (fig 3a). (3) Hemisensory defect Along with the two above disorders, a dense unilateral right sensory deficit, equally involving superficial, deep and combined sensations, was observed. According to classical anatomy of the sensory systems,16 sensory fibres from the posterior nuclear group of the thalamus are organised in a somatotopic fashion and directed toward the parietal cortex. As they leave the thalamus, they run in the posterior limb of the internal capsule, forming the superior thalamic peduncle. It is quite readily admitted, since works by Fisher17 -19 and Mohr et al20 that small, but strategically located lesions may be responsible for proportional sensory deficits. The location of the lesion depicted on fig 3b, lying just above the posterior nuclear group of the thalamus, and probably damaging the thalamo-parietal fibres provides a satisfactory explanation for the sensory symptoms. Poncet, Habib, Robillard from the present case report. First, it provides an example of a striking discrepancy between a discrete lesion, without clinical evidence of any mass effect and hardly detectable on CT scan, and massive neurobehavioural disorders. Such a discrepancy represents, per se, a good argument for predicting a subcortical lesion. It also identifies a neurological entity which could be acknowledged as a new syndrome: in the context of conduction aphasia, discovering the other three elements of the tetrad should strongly suggest the lesion site illustrated in our case. Moreover, it helps distinguish between the two forms of conduction apha- sia: the "temporo-insular form" without sensory defect and with "typical" right-ear dichotic extinction26 and the "parietal form", exemplified by our patient. The association of conduction aphasia with a right "pseudo-thalamic" sensory syndrome has been reported by Bogousslavsky et al.27 The authors discussed the relation of their case to Luria's28 afferent motor aphasia and the participation of a deafferentation mechanism. It is in fact conceivable that, in some conduction aphasics, both mechanisms (deafferentation and temporo-frontal disconnection) may jointly contribute to the speech disturbance pattern. As already mentioned, the association of conduc(4) Paradoxical left ear extinction In dichotic conditions, some hemispheric lesions are tion aphasia with ideomotor apraxia has been pointed known possibly to cause a phenomenon of extinction out by Benson et al4 as suggestive of a parietal lesion. of either ear. In such cases, according to classical Yet one cannot be sure clinically that the parietal cordemonstrations,21 22 the extinction usually concerns tex is spared, since a similar pattern may result from the contralaterally received message. In a number of lesions involving the supramarginal gyrus. Such right-handed patients with left hemisphere lesions, lesions, however, would not produce the other two the reverse pattern is realised (that is, a "paradoxical" elements of the syndrome unless they extend deep left ear extinction): in such cases, it is assumed that enough to damage the relevant subcortical pathways: the lesion has compromised callosal fibres conveying one may contend that, in such cases, the deepest part verbal information from the right hemisphere to the of the lesion is sufficient to cause the full syndrome. Finally, one may speculate about the aetiology of intact left auditory cortex. The exact location of this callosal pathway, connecting the right and left audi- the infarct responsible for this syndrome in our tory areas is still not defined. In the Rhesus mon- patient. Rather than a true lacune according to key,23 such inter-temporal connections have been Fisher's'9 definition or occlusion of a single vessel,27 demonstrated to course at the junction between the it seems to us that the location is more compatible body and the splenium of the callosum, just rostral to with a watershed infarction occurring in a zone of the visual inter-occipital fibres. The human pattern of high susceptibility to decreased blood flow, supplied callosal connections is probably very similar.24 Dam- by the terminal perforating branches of the distal asio and Damasio25 proposed, through correlations middle cerebral artery. If this is actually the case, then based on CT of several patients with paradoxical the syndrome described in this paper should, when extinction, that this inter-temporal connecting tract is systematically searched for, be diagnosed much more situated deep in the parietal or parieto-occipital white often. matter, near the lateral wall of the lateral ventricle, References outside the optic radiations. Coronal views of MRI (fig 3c) in our patient show H, Kaplan E. The Assessment ofAphasia and that the situation of the lesion is quite consistent with 1 Goodglass Related Disorders. Philadelphia: Lea & Febiger, -1972. this explanation. 2 Wernicke C. Der Aphasische Symptomenkomplex. Breslau: Cohn & Weigert, 1874. In our view, several points of interest may be drawn 3 Geschwind N. Disconnexion syndromes in animal and Deep left parietal lobe syndrome man. Brain 1965;88:237-94; 585-644. 4 Benson DF, Sheremata WA, Bouchard R, Segarra JM, Proce D, Geschwind N. 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