alexia and agraphia in wernicke's aphasia andagraphia in wernicke's aphasia...

Journal of Neurology, Neurosurgery, and Psychiatry 1982;45:719-724

Alexia and agraphia in Wernicke's aphasiaHOWARD S KIRSHNER, WANDA G WEBB

From the Departments ofNeurology and Hearing and Speech Science, Vanderbilt University School ofMedicine, Nashville, Tennessee, USA

SUMMARY Three patients. with otherwise typical Wernicke' s aphasia showed consistently greaterimpairment of reading than auditory comprehension. While this syndrome resembles alexia withagraphia, the paraphasia of speech, repetition, and naming underline the aphasic nature of thedisorder. Together with previous reports of isolated word deafness in Wernicke's aphasia, thesecases suggest a relative independence of auditory and visual language processing.

Wernicke's aphasia is traditionally characterised' 2as a disorder of central language processes, affectingthe different modalities of language input and out-put more or less equally. Thus reading is impairedalong with auditory comprehension, and writing,like spontaneous speech, is marred by paraphasicsubstitutions. Anomia and paraphasic substitutionsin naming and repetition complete the picture. Theequivalence of deficits in reading and auditory com-prehension is often explained by the concept thatreading is learned by transcoding of visual languagestimuli to previously acquired auditory word associ-ations, stored in Wemicke's area.3 Disruption of theauditory association area would thus interfere notonly with auditory comprehension, but also withreading.

In a previous communication,4 we discussed casesof Wemicke's aphasia with spared reading abilityand compared this auditory-predominant sub-typeof Wernicke' s aphasia to the traditional syndrome ofpure word deafness. The present report concernsthree cases of Wernicke's aphasia, all secondary toischaemic stroke, in which reading was moreimpaired than auditory comprehension, both acutelyand after partial recovery. Whereas the auditory-predominant cases of Wernicke's aphasia resemblepure word deafness, this second, visual-predominantsub-type resembles the classical syndrome of purealexia with agraphia, an acquired illiteracy in whichreading and writing are impaired in the absence ofother language deficits. The paraphasic productionsof our patients in spontaneous speech, naming,

Address for reprint requests: Howard S Kirshner, MD, Depart-ment of Neurology, Vanderbilt University School of Medicine,Nashville, Tennessee 37232, USA.

Received 21 November 1981 and in revised form 6 March 1982.Accepted 18 March 1982

repetition, ano oral reading, however, distinguishtheir deficit from pure alexia without agraphia andlink them more closely to Wernicke's aphasia. Thesecases add to previous evidence that the auditory andvisual modalities of language may be affected to dif-ferent degrees in Wemicke's aphasia and suggest atleast a partial independence of auditory and visuallanguage processing.

Methods and report of cases

Three aphasic patients, all victims of acute left hemispherestrokes, were studied within five days after onset and againfour to six weeks later. All had at least a partial high schooleducation and good premorbid reading skills. The testsemployed are the same as those described previously.4Case I This 67-year-old right-handed male, in goodhealth except for hypertension and prior myocardial infarc-tion, entered the hospital after an episode of blurred vis-ion, lightheadedness, nausea, and left-sided weakness. Ini-tial examination disclosed only a left homonymoushemianopsia and left hemisensory deficit, both of whichresolved over the next few hours. A computed tomo-graphic (CT) scan was normal. Three days later, duringcerebral arteriography, the patient became restless and"confused". The arteriogram showed nonstenosing plaqueformation at the right carotid bifurcation; the left carotidbifurcation and intracranial vessels were unremarkable.On examination the patient repetitively uttered phrasessuch as "let me out, . . . let me get over". He followed no

commands, called his daughter "Mama", and made manyparaphasic errors. He had a dense right homonymoushemianopsia but no apparent motor or sensory deficits. Bythe next morning he followed some simple commands butnot multistep directions. He manifested almost totalanomia for objects and colours.The patient improved steadily over the next few days.

Five days after onset he named eight of ten pictures, five ofsix colours, and eight of ten small letters. He correctlyfollowed seven of eight commands of increasing complex-ity, either spoken or presented in printed form. On a

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matching-to-sample test battery modified from Sidman etal,5 he performed with greater than 90% accuracy inmatching single, dictated or printed small letters to printedcapital letter choices and in matching single words pre-sented in printed, dictated, or dictated, spelled form toprinted word choices. He read aloud 10/10 3-letter words.On the Boston Diagnostic Aphasia Examination(BDAE),6 performed four days after onset, the patient'soral expression was fluent but marked by both literal andverbal paraphasias and word-finding difficulty. Confronta-tion naming showed prolonged latencies and some errorson pictures, body parts, and colours. Auditory comprehen-sion subtests showed normal responses to multistep com-mands and complex ideational material. Repetition wasmarked by paraphasic substitutions, especially on lowprobability phrases. On reading tests he was unable tocomprehend passages of more than two sentences, and oralreading was slow, effortful, and contaminated by paralexicerrors. He could write short sentences to dictation butmade spelling errors on longer words. Re-examinationwith the BDAE four weeks after onset showed improve-ment in all areas, but with continued paraphasic errors inspontaneous speech, repetition, and oral reading. His mostsignificant disability remained that of alexia, with inabilityto comprehend paragraph-length material.The Token Test7 was performed four weeks after onset,

both in the standard, auditory form and with the instruc-tions presented in printed form. He correctly performed94% of the auditory and 82% of the visual instructions (byweighted scores).A repeat CT scan (fig 1), performed 6 days after onset,

showed an area of low density involving predominantly theleft angular gyrus, with extension into the supramarginalgyrus, posterior-most superior temporal gyrus, and

inferior-most superior parietal lobule, along with subjacentwhite matter.8 The patient continued to improve in speechand language, with mild paraphasia of spontaneous speechand continued reading difficulty when last seen threemonths after onset.Case 2 This 69-year-old hypertensive, diabetic right-handed lady presented with several episodes of left mono-cular blurred vision and one of transient left hemiparesisassociated with "slurred" speech. Examination revealedright carotid and left supraclavicular bruits. No fixedneurologic deficits were found. CT scan of the head wasnormal. Cerebral arteriography revealed tight stenosis ofthe right internal carotid artery, severe plaque formationand 50-60% stenosis of the left internal carotid artery, andstenosis of the proximal left vertebral and subclavianarteries. Following the arteriogram the patient was notedto be "confused"; on examination, her speech was rambl-ing, with numerous spontaneous paraphasic errors andneologisms. She did not respond to commands or yes/noquestions. She showed no apparent appreciation of visualstimuli and failed to count fingers or blink to visual threat.Spontaneous movements and withdrawal to pinprick werestrong and symmetric in all extremities. Reflexes weresymmetic, with flexor plantar responses. On the followingday she remained confused but reached out to graspobjects with either hand, more consistently in the left fieldof vision. She continued to speak paraphasically but ex-pressed some appropriate phrases, including a complaint ofheadache. She failed to identify objects or colours. By thefourth day she looked about the room, recognised familymembers, and spoke in full sentences, though with manyword substitutions. Over the next few days she regainedthe ability to name some objects but not uncommonobjects or parts of objects. Her auditory comprehension

Fig 1 Computed tomographic(CTscan), Case 1, showing an areaofreduced attenuation, consistentwith infarction in the region of theleft angular gyrus.

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and following of commands recovered substantially, exceptfor left-right errors. In contrast, she remained almostentirely unable to read or write. She could not read more

than single words aloud, follow the simplest printed com-

mands, or sign her name. She was unable to perform even

simple calculations, such as "7 + 5", to copy or constructgeometrical figures, or to identify left and right. She was

able to point to specific fingers on her own and theexaminer's hand.Speech and language evaluations were carried out 2-3

weeks after onset. She named 16/20 capital letters, 17/20pictures, and read aloud 19/20 picture names. In contrast,she could not write the names of any of ten pictures. Onthe matching-to-sample battery, she correctly matched19/20 dictated and 8/10 printed small letters to the correctcapital letters. She also matched 20/20 printed, 20/20 dic-tated, and 19/20 dictated, spelled words to pictures. Givena series of word lists differing in length and frequency ofoccurrence, she read aloud the frequent words accurately,whether short or long, but she made frequent errors on theunfamiliar words and was totally unable to pronounce non-

sense trigrams. At the time of retesting six weeks afteronset, the patient named 20/20 pictures orally and 10/20 inwriting. On the BDAE, spontaneous speech was fluent,with frequent literal paraphasic errors. The patient exhi-bited moderate dysnomia for objects, actions, colours,numbers, and body parts. Auditory comprehension was

impaired only for multistep commands and complex idea-tional material. Single word and sentence repetitionshowed literal paraphasic errors. Oral reading was severelyimpaired, with marked hesitancy and both literal and ver-

bal paraphasic errors. She failed to read sentences or para-graphs for meaning and made occasional errors even insingle word recognition. Writing ability was limited to thecopying of single letters and numbers; she failed to write

Fig 2 CT scan, Case 2, showing-; _ infarction in the vicinity of the lefti F4 angular gyrus. The small area of

increased density representshaemorrhagic infarction.

letters, numbers, or words to dictation. Retesting six weeksafter onset revealed almost normal auditory comprehen-sion and mild, persistent dysnomia and paraphasic speech.Reading and writing, though improving, remained severelydeficient. The Token Test, performed three weeks afteronset, showed 90% correct for auditory and 39% correctfor visual instructions.A second Cf scan, 18 days after onset, revealed a low

density area involving the left angular gyrus and subjacentwhite matter, with slight extension into the supramarginalgyrus and superior parietal lobule. The entire temporallobe appeared spared." The patient's subsequent coursewas one of gradual improvement, with mild paraphasicspeech and word-finding difficulty, but persistent and frus-trating impairments in reading and writing.Case 3 This 60-year-old right-handed male was previ-ously in good health except for hypertension, amputationof the right leg, and a progressive left ear hearing loss.Audiometry disclosed a moderate conductive hearing losson the left, with only high frequency loss on the right.While hospitalised for evaluation of the hearing loss hesuddenly developed a right hemiparesis and aphasia, withinitial descriptions of his speech as "slurred" and "nonsen-sical". By day 5 he manifested a clearcut fluent aphasia,while the hemiparesis had improved to mild weakness ofthe right face and arm. Visual fields were intact. Bedsideaphasia testing six days after onset revealed fluent speechwith word-searching pauses, circumlocutions, and frequentliteral and verbal paraphasic errors. He named 8/8 objects,3/3 parts of objects, and 10/10 pictures. He repeated sim-ple and complex phrases with few errors. Despite the hear-ing loss he followed 8/8 spoken commands of increasingcomplexity and answered appropriately to yes/no and non-sense questions. In contrast, he was able to carry out orread aloud only 5/8 printed commands. Writing was

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limited to his signature and single, dictated words; he couldnot write even short sentences to dictation. Matching wasnearly errorless for the single letter, word, and pictureitems.On the BDAE, performed on days 5-7, spontaneous

speech was characterised by fluent phraseology with manycliches, few meaningful nouns, paraphasic errors, and someneologistic jargon. Naming was mildly impaired, and repe-tition was accurate but contaminated by paraphasic errors.Auditory comprehension was impaired only on four andfive part commands and complex ideational material. Incontrast, reading comprehension was severely impaired formore than single word items. He correctly answered only20% of questions on sentences and paragraphs. Oral read-ing of sentences contained many paraphasic errors. Writingwas poor even for dictated single words and copying ofwords and sentences. Retesting five weeks after onsetshowed improvement in spontaneous speech and auditorycomprehension, with persistent paraphasic errors andword-finding difficulty. Reading of sentences, both aloudand for comprehension, remained impaired. The TokenTest was performed 16 days after onset, by which timecomprehension had improved in both modalities. Thepatient correctly carried out 93% of the auditory and 88%of the visual instructions.A cT scan, performed within five hours of onset, was

normal. A repeat study was not obtained. The clinicalcourse was one of substantial improvement in all aspects oflanguage. Only mildly paraphasic speech and readingdifficulty remained as clinically evident deficits.

Discussion

Since its original description in 1874,9 Wernicke'saphasia has been considered a disorder of centrallanguage processes, independent of specific lan-guage modalities. Disruption of the auditory wordassociation area in the superior temporal gyrus(Wernicke's area) interferes with auditory proces-sing. Reading, by the traditional formulation,39 islearned by the transcoding of visual language stimulito previously learned auditory word associations;alexia would thus also be expected with lesions inthis region.

In a previous communication,4 we discussed casesof Wernicke's aphasia with poor auditory com-prehension but relatively spared reading. This dis-order resembles the syndrome of pure word deaf-ness, except for the paraphasic speech, repetition,and naming. The preserved reading ability in thesecases appears to reside in the left parietal and occipi-tal lobes,4 10 or possibly even in the right hemis-phere."IThe three cases discussed here suggest a second

modality-specific deficit pattern in Wernicke'saphasia, that of greater impairment of reading thanauditory comprehension. All three patients hadcompleted at least ten years of school and read

fluently prior to their strokes. The greater involve-ment of reading than of auditory comprehensionpersisted over time and was apparent in bedside test-ing, on the BDAE, and on the auditory and visualforms of the Token Test. Cases 2 and 3 showedsignificant agraphia as well as alexia, suggesting aprimary diagnosis of pure alexia with agraphia. AlRthree cases, however, had persistent paraphasicspeech, repetition, naming, and oral reading, linkingthem more closely to Wernicke's aphasia.The anatomic substrate of this syndrome, as

judged by the CT scans of Cases 1 and 2, involvedthe left inferior parietal region, especially the angu-lar gyrus and subjacent white matter. In Case 1 theposterior-most part of the superior temporal gyrusalso appeared involved. In Case 2 the aphasiaremained as a persistent focal deficit after the reso-lution of a more diffuse postarteriography syndromeof confusion and cortical blindness. Cortical blind-ness is a recognised complication of cerebralarteriography and may represent a direct effect ofthe contrast material.'2 The focal lesion seen on CTscan, however, suggests embolisation to posteriorbranches of the left middle cerebral artery, as doesthe sudden onset of the language disorder in allthree cases.While Wernicke himself assigned the auditory

word association area to the posterior part of thesuperior temporal gyrus,9 subsequent aphasiologistshave differed in its localisation. The inferior parietallobule, or supramarginal and angular gyri, has beenincluded by some authors.'3 Paraphasic speech andimpaired auditory comprehension are thus notunexpected with lesions in this vicinity. The greaterinvolvement of reading than of auditory comprehen-sion, however, cannot be explained by involvementof the auditory association area alone, but rathermust reflect the importance of the angular gyrus reg-ion to reading.

Dejerine,'4 in 1892, described the syndrome ofpure alexia with agraphia in a patient with an infarctof the left angular gyrus. He believed the angulargyrus to be a centre for visual word images, analog-ous to the superior temporal gyrus as a centre forauditory word images. Wernicke,9 and morerecently Geschwind,'5 emphasised the role of theangular gyrus in cross-modal sensory associations.Instead of removing a cortical word-image centre, alesion of the angular gyrus would disrupt reading bydisconnecting visual to auditory transcoding. Byeither explanation, an angular gyrus lesion wouldproduce alexia without affecting either auditorycomprehension or speech production. Dejerinel4stated that alexia and agraphia could either accom-pany a Wernicke's aphasia or exist in pure form.Some recent authors2 16 17 have attempted to distin-

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guish alexia with agraphia from "aphasic alexia", orthe alexia associated with Wernicke's aphasia. Onthe other hand, both Kertesz ' and Brain'8 notedthat alexia with agraphia can remain as a residualdeficit after recovery from Wernicke's aphasia. Ben-son'9 stated that only in rare instances does alexiawith agraphia occur without any signs of aphasia.Modem classifications of alexia have emphasised

three principal groups: alexia with agraphia, alexiawithout agraphia, and alexia associated withaphasia.3 Alexia with agraphia has already been dis-cussed. Alexia without agraphia is an easily separ-able syndrome seen with lesions of the left occipitallobe, often including the splenium of the corpus cal-losum. Dejerinel4 explained this syndrome by a dis-connection of visual information perceived by theintact right occipital lobe from the left angular gyrus.Aphasic alexia has included different groups ofaphasic cases. Benson'9 has called attention to alexiain Broca's aphasia, under the term "third alexia".The nonfluent speech of these patients, of course,should distinguish them readily from the other alexicgroups. Finally, the alexia of Wemicke's aphasiamay be considered as a separate, fourth group, or itmay be combined with the first syndrome, alexiawith agraphia. Benson'9 has suggested the terms"central alexia" for the alexia with agraphia cases,"posterior alexia" for alexia without agraphia, and"anterior alexia" for the reading disorder seen withBroca's aphasia.An alternative explanation for the findings of

fluent aphasia and alexia in our patients would be acombination of conduction aphasia and alexia withagraphia. Conduction aphasia, a syndrome in whichparaphasic speech and impaired repetition occur inthe presence of intact auditory comprehension, isassociated with lesions of either the left supramargi-nal gyrus or the left superior temporal gyrus.20 Fac-tors against the diagnosis of conduction aphasia inour patients include the presence at least initially ofauditory comprehension deficit, the absence of asevere repetition disturbance out of proportion toother language deficits, and the absence of dispro-portionate literal as compared to verbal paraphasicerrors. For these reasons we prefer the diagnosis ofWemicke's aphasia with alexia. The most importantpoint, however, is the linkage of alexia with agraphiato the fluent aphasias.Numerous studies have attempted to distinguish

alexic syndromes by their relative impairments ofword versus letter reading. In alexia withoutagraphia, preservation of individual letter readinghas been amply documented.2'-24 The alexia ofBroca's aphasia, on the other hand, produces amajor deficit in the naming and reading of singleletters, even when some words can be read in a

global manner.'92526 In Wernicke's aphasia, singleletters may be processed well, as seen in our cases,and difficulty increases with increasing complexity ofwords and phrases.'6 In alexia with agraphia, someauthors2 27 have found letter greater than wordalexia, much like that seen in Broca's aphasia. Otherauthors,'6 however, have not found letter alexia inalexia with agraphia, and indeed occasional cases ofalexia with agraphia have been reported with intactoral spelling and comprehension of dictated, spelledwords.2830 Performance in letter versus word read-ing would thus not appear to be a reliable factor indistinguishing alexia with agraphia from alexiarelated to Wemicke's aphasia, though certainly itdoes distinguish alexia without agraphia, or "post-erior alexia", from the alexia associated with frontallesions. Inability to perceive a word as a whole is themost consistent deficit in "posterior" alexia, whilesingle letter reading and phonetic processing ofgraphemes may be intact. In both the "anterior" and"central" alexias, on the other hand, whole wordperception may be the only preserved function,while letter reading and phonetic processing areimpaired.'9 25 26

Cases of Wemicke's aphasia with alexia out ofproportion to auditory comprehension deficit havenot been generally recognised, though as discussedabove some cases of alexia with agraphia maybelong to this category. H6caen'6 described a subsetof Wemicke's aphasics with auditory predominantdeficits, but he related this to a deficit in the percep-tion of phonemes. His second subgroup, withdeficient semantic comprehension, was said to haveequal impairment of auditory comprehension andreading. Mohr, Hier, and Kirshner,'0 in a retrospec-tive review of CT scan lesions, found two cases ofWemicke's aphasia with greater impairment of read-ing than of auditory comprehension. Both hadparieto-occipital lesions. This compared to six casesof auditory-predominant deficit and 23 in which nodisproportion could be judged. The present threecases are part of an ongoing investigation of selec-tive involvement of specific language modalities inaphasia secondary to ischaemic stroke. Of 18 casesof Wernicke's aphasia studied, two showed theauditory and three the visual-predominant syn-drome. Selective impairment of either auditorycomprehension or reading thus appears to be notuncommon in Wernicke's aphasia.The independence of deficits in reading and

auditory comprehension in Wernicke's aphasia sug-gests at least partial independence of the brainmechanisms for auditory and visual language pro-cessing. This independence belies the simple con-cept that reading can proceed only via transcodingof visual to phonetic information. The evidence

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from Wernicke' s aphasia thus confirms evidencefrom other sources31 32 that reading can occur frompurely visual to semantic processing, without accessto auditory or phonetic information.

This research was supported by NINCDS TeacherInvestigator Development Award No.5K07NS00429-03 to Dr Kirshner and also by theVeterans Administration. The authors thank MrsAnne Morgan for technical assistance and Mrs JaneS Smith for assistance with preparation of themanuscript.

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