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Mutism Following Left Hemisphere Infarction J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.12.1342 on 1 December 1984. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1984;47:1342-1344 Short report Mutism following left hemisphere infarction AS DAVID,* I BONE From the Department ofNeurology, Institute ofNeurological Sciences, Southern General Hospital, Glasgow, UK SUMMARY A case of mutism due to left hemisphere infarction is described. Recovery revealed mild motor dysphasia. Review of the literature showed that the case resembles aphemia but is unique by virtue of its duration, and the absence of associated apraxia and paresis. Mutism is a rare clinical entity. It may occur trans- any limb. Reflexes were symmetrical and the plantar iently in lesions of Broca's area,' or the inferior responses flexor. Indirect laryngoscopy showed normal rolandic region.2 We describe a case of total mutism larynx and vocal chord movement. following left common carotid artery occlusion in CT scanning without contrast showed a very small area guest. Protected by copyright. the absence of hemiparesis and oro-bucco-lingual of reduced density in relation to the left sylvian fissure. A to a highly repeat scan with contrast revealed a large area of apraxia which we believe to be due the left to specific apraxia of speech. enhancement in fronto-parietal region extending Case report A 51-year-old, right-handed housewife, with a history of controlled hypertension, was on holiday abroad when she awoke, unable to speak. A relative noticed right sided facial weakness. On her return, the patient was admitted to her local hospital and on the 12th day after the onset of her illness was transferred to this Institute for further investiga- _ tion. On admission she was alert and undistressed. Blood pressure was 140/90 mm Hg. Slight upper motor neuron facial weakness was detected on the right. She was unable l to speak or indeed utter any sound though she could cough to command. The patient could not whisper, hum or mouth words either spontaneously or in imitation. Her com- prehension appeared to be good in that she could follow simple written and verbal instructions. Questions were http://jnnp.bmj.com/ answered by nodding "yes" or "no". Writing was printed initially with some paraphasic errors but was adequate for day-to-day communication. The patient could perform a range of buccal, lingual, and facial movements on request. Such manoeuvres as licking lips and rolling the tongue were carried out with ease, as were chewing and swallow- ing. General neurological examination was entirely nor- mal, in particular there was no weakness or dyspraxia of on September 30, 2021 by *Present address and address for reprint requests: Dr AS David, Department of Psychiatry, The Bethlem Royal and Maudsley Hos- pitals, Monks Orchard Road, Beckenham, Kent BR3 3BX, UK. Received 2 December 1983 and in revised form 1 June 1984. Fig CT scan with contrast enhancement showing large Accepted 11 June 1984 lesion in left fronto-parietal region. 1342 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.12.1342 on 1 December 1984. Downloaded from Mutism following left hemisphere infarction 1343 the brain surface (fig). An isotope brain scan showed an mutism and the absence of obvious motor or dys- irregular area of increased uptake in the left inferior fron- praxic signs. LeCours2 described a case of mutism tal region. Angiography was performed and though techni- without apraxia who recovered without dysphasia cally difficult showed absent filling of the left common and due to a lesion in the inferior rolandic region, spar- internal carotid arteries. There was no evidence of ing Broca's area. Mutism is seen in lesions of the arterio-venous malformation. supplementary motor area,'9 but dysgraphia and The diagnosis was made of cerebral infarction secondary the hemiparesis are outstanding. Subcortical lesions give to common carotid artery occulsion. Assessment on and motor deficits20-22 Boston Diagnostic Aphasia Examination one day after rise to a variety of language admission showed some auditory comprehension failure on but not mutism. complex sequential commands and abstract reasoning Critchley23 stated that even severe aphasics can material. Reading comprehension and narrative writing say something and that "total speechlessness" usu- also showed slight impairment. Verbal expression was of ally lies outwith "organic neurology". An appeal- course absent. Follow-up assessment 12 days later showed ingly eclectic alternative explanation to our patient's substantial improvement to virtually normal in reading, mute state was that it was a hysterical reaction to writing, and comprehension. The patient could write long- aphasia. The ability to cough despite appar- errors. Screening parietal genuine hand with only a few paraphasic ent aphonia is a classic sign of hysteria though such tests showed no abnormalities. Nevertheless, she was still weeks, until speech patients usually whisper.8 mute and remained so for a further 5 as returned abruptly. Examination at that time revealed The varieties of emotional response are non-fluent, laboured speech with dysprosody, articulation numerous as there are patients, yet common reac- errors and some phoneme substitutions ("I have tions are either frustration, the so-called catas- difficult... in finding right words"). Transient word block- trophic reaction,24 or withdrawal. However, in the ing was evident, though repetition reduced errors. Verbal latter, the patient is too embarrassed or depressed to expression was however functional and easily understood. so withdraws, but in more total speak abnormally guest. Protected by copyright. way than just keeping silent, from interpersonnal Discussion communication.6 We postulate that this case of mutism was due to Mutism is a rare clinical entity. It may occur in an apraxia, so localised that it only affected those patients with gross dementia, bilateral basal ganglia movements directly subserving the execution of lesions,3 pseudo-bulbar palsy,4 or in the syndrome of speech and voice production. The centre of the akinetic mutism.5 In these instances, the underlying causative lesion probably lies in the inferior part of cause is usually self-evident. Other causes include the pre-central gyrus,2 overlapping Broca's area yet psychotic illness,6 elective mutism, relatively com- not impinging upon the motor area. We wish to mon in children,7 and hysteria.8 The above case is draw attention to this syndrome firstly because it remarkable in that for 7 weeks the patient remained demonstrates the discreteness of certain language totally mute in the absence of significant receptive functions in the brain each of which may be put out dysphasia, dysgraphia, dyspraxia or hemiparesis. of action by localised infarctions, and secondly Recovery was sudden with only residual language because it may be mistaken for hysteria. impairment. The inability to speak with retained capacity to read, write and understand has been called pure motor aphasia9 where recovery uncovers References A second pattern of agrammatism and paraphasia. 'Mohr JP, Pessin MS, Finkelstein S, Funkenstein HH, recovery exists whereby speech, when it returns, Duncan GW, Davis KR. Broca aphasia: pathologic as though laboured is not aphasic.23 Terms such and clinical. Neurology (Minneap) 1978;28: 311-24. http://jnnp.bmj.com/ aphemia,'"01 cortical dysarthria,'2 and pure word 2 LeCours AR, Lhermitte F. The "pure form" of the dumbness,'3 have been used to describe this. Many phonetic disintegration syndrome (pure anarthria); modern authors regard it as an apraxia of anatomo-clinical report of a historical case. Brain Lang 1976;3:88-113. speech.'4-'6 In: Recent clinico-pathological studies of lesions in 3 Geschwind N. Non-aphasic disorders of speech. Papers on Language and the Brain. Boston: D Broca's area (3rd inferior frontal convolution),''7 Selected at the Reidel Publishing Co, 1974:74-85. showed that many patients were nearly mute 4 Houlihan JP, Crosenfeld LF. Most Cummings JL, Benson DF, onset of their illness but made good recoveries. Mutism: Loss of neocortical and limbic vocalization. J on September 30, 2021 by could utter some sounds or words or were mute for a Nerv Ment Dis 1983;171:255-9. few days only. They all had some degree of right 5 Plum F, Posner JB. The Diagnosis ofStupor and Coma. sided motor weakness with one exception,'8 and Philadelpia: Davis, 1980. prominent oro-bucco-lingual dyspraxia. Our patient 6 Benson DF. Psychiatric aspects of aphasia. Br J differed in the sustained and absolute nature of her Psychiatry 1973; 123:555-66. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.12.1342 on 1 December 1984. Downloaded from 1344 David, Bone Reed GF. Elective mutism in children: a reappraisal. J 17Ruff RL, Arbit E. Aphemia resulting from a left frontal Child Psychol Psychiatry 1963; 4:99-107. haematoma. Neurology (NY) 1981;31: 353-6. Charcot J-M. A case of hysterical mutism in a man. In: 18 Masdeu JC, 0'Hara RJ. Motor aphasia unaccompanied Clinical Lectures on Diseases of the Nervous System. by faciobrachial weakness. Neurology (NY) 1983; London: The New Sydenham Society, 1889:360-73. 33:519-21. Brown JW. Aphasia, Apraxia and Agnosia. Illinois: 9 Masdeu JC, Schoene WC, Funkenstein H. Aphasia fol- Charles C Thomas, 1972:117-26. lowing infarction of the supplementary motor area. 10 Bastian HC. On different kinds of aphasia, with special Neurology (Minneap) 1978;28: 1220-3. reference to their classification and ultimate pathol- 20 Damasio AR, Damasio H, Rizzo M, Varney N, Gersh F. ogy. Br Med J 1887;2:985-90. Aphasia with nonhemorrhagic lesions in the basal Schiff HB, Alexander MP, Naeser MA, Galaburda AM. ganglia and internal capsule. Arch Neurol Aphemia. Clinical-anatomic correlations. Arch 1982;39: 15:20. Neurol 1983;40:720-7. 21 Damasio H. Cerebral localisation of the aphasias. In: 12 Bay E.
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