aphasia: clinical and anatomic issues

Chapter 14APHASIA I: CLINICAL ANDANATOMIC ISSUESMichael P. Alexander

The clinical study of aphasia began in 1861 withthe observations of Paul Broca.1 Within 40 or 50years, all of the basic clinical phenomena re-viewed here had been described and many of themajor flashpoints of clinical and theoretical dis-agreement had been identified. In the past 20years, fresh interest has come to clinical aphasiaresearch from two directions: modern neuroimag-ing and cognitive neurosciences. Together, theyhave additionally provided tools to carry outaphasia-related language experiments in normals.Furthermore, old questions such as cerebral later-ality, the influence of handedness, the effects ofgender and bilingualism on aphasia, and themechanisms of recovery have been reexplored.Much of this chapterwhich reviews the basicclinical features of aphasiacould have beenwritten 20, 50, or even 100 years ago. In 1995, itis possible to consider this material with greaterappreciation of the variability found in the basicsyndromes, of their anatomic complexities, of thenatural history of recovery, and (although hereonly briefly) of the cognitive and linguistic deficitsthat fundamentally underlie the classic syn-dromes. The chapters on neuroimaging and oncognitive analysis of aphasia should be read alongwith this chapter.

CLINICAL SYNDROMES

The description of syndromes of aphasia arose outof much the same motivation as the identificationof other clinical neurologic syndromes: the need

to identify clinically useful associations betweenspecific clusters of signs and the likely anatomyof the lesion producing them. The most clinicallytransparent signs of aphasia have generally beentaken to be independent signs of brain damage.Thus, syndromes have been constructed out of re-duced language output as well as impaired com-prehension, repetition, and naming. Disorders ofwritten language have been divided into addi-tional syndromes only as reading and writing havebeen impaired beyond spoken language impair-ments. Using three independent signs will gener-ate eight syndromes, assuming naming to be im-paired in all aphasics.

Although these syndromes have reasonableclinical validity, there are numerous limitations tothis type of syndrome construction. First, the syn-dromes depend on a sign being normal or not,much as a hemiparesis is present or absent; butthe complexity of impairments in comprehensionand language production are less amenable tosimple dichotomous judgments. Thus, distinctionscome to depend on the statistical properties andstructural assumptions of the test. Second, there isno certainty that signs all have the same patho-physiologic mechanism in all patients. For compre-hension at the sentence level, in particular, theremay be several independent pathways to impair-ment.2 Third, the syndromes are not stable evenwhen the anatomy is. A patient with a temporopa-rietal stroke may have an initial Wernicke's apha-sia, but, over weeks, language improves to reachthe clinical diagnosis of conduction aphasia.3 Does

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one conclude thai the behavioral-anatomic corre-lations are with Wernicke's or conduction apha-sia? Can one be certain that there are two distinctsyndromes if they blur into each other? Shouldone conclude tha t only the early-phase correla-tions hold, t ha t all correlations have built in corol-laries about recovery, or that both are true?Fourth, most syndromes are polytypicthat is,they are defined by several criteria.' What do weconclude if only some of (he criteria are met?Would this be a less severe syndrome? A subsyn-drome? A different syndrome altogether?

Despite these limitations, the classic syn-dromes do have util i ty. They serve as a type ofshorthand for clinical communications. If told thata patient has transcortical motor aphasia 2 weeksalter a stroke, one would know approximatelywhat to expect of language examinations, whatthe range of possible brain lesions would be, whatthe prognosis should be, and what some reason-able treatments might be. If inclined, one wouldeven know what interesting cognitive neurosci-ence issues the patient might i l l umina t e .

Broca's AphasiaIn Broca's aphasia, language output is nonflu-en tthat is, it is reduced in phrase length andgrammatical complexity. This reduction can rangefrom no recogni/.ahle output or repeated mean-ingless utterances to short, truncated phrases us-ing only the most meaning-laden words (substan-tives). There is usually considerable hesitationand delay in production. Speech qual i ty is im-paired. Articulation is poor (dysarlhria). Melodicline is disrupted (dysprosody). partly due to dysar-thria but often more than just secondary to it. Vol-ume is usually reduced at first (hypophonia). Withtime, speech takes on hyperkinetic (dyslonie and

spastic) qualities. Language comprehension isadequate although rarely normal. Response toword-recognition tasks, simple commands, androutine conversation is generally good. Responseto multistep commands and complex syntacticalrequests is generally poor. Repetition is poor, al-though often better than speech. Relational words(functorsarticles, conjunctions, modifiers, etc.)

may be produced in repetition, but they are ex-ceedingly uncommon in spontaneous speech.Written language parallels spoken, although somepatients, while never regaining useful speech, de-velop writing that is telegraphic. Oral reading isusually agrammatic; so-called deep dyslexia (seeChap. IS) may emerge with this.5 Naming is usu-ally poor, but it may be surprisingly good inchronic patients. All types of errors can occur, al-though semantic errors are most typical for sub-stantive words/' Objects are frequently namedbetter than are actions.7

Broca's aphasia is commonly accompaniedby right hemiparesis, buccofacial apraxia, andideomotor apraxia of the left arm (or both armsin the nonparetic case). Right-sided sensory lossand right visual field impairments (extinctionand/or lower-quadrant deficit) are less frequent.Depression, frequently major, develops in ap-proximately 40 percent of patients with Broca'saphasia."

Many patients have fractional syndromes ofBroca's aphasia. Because all of these fractionaldisorders are still taxonomically closer to Broca'saphasia than to any of the other seven classic diag-noses, many aphasia systems will classify them allas Broca's aphasia." In analy/ing reports of Bro-ca's aphasia, it is crucial to understand the taxo-nomic rules of the report's assessment tool. If allfractional cases are considered Broca's aphasia,the ciinicoanatomic correlations will seem impre-cise. This is an example of the difficulty inherentin building syndromes with polytypic qualities.Analysis of the ciinicoanatomic relationshipswi th in these fractional cases may be much moreinformative than lumping them all together on thebasis of some overlap with the full syndrome.

Chronic Broca's AphasiaThis syndrome, as described above, often emergesout of global aphasia.'" Damage can vary in ex-tent; there does not seem to be a necessary andsufficient lesion profile. The most common pat-tern is extensive dorsolateral frontal, opercular,rolandic, and anterolateral parietal cortical dam-age plus lateral striatal and extensive paraventric-

CHAPTER 14/APHASIA I: CLINICAL AND ANATOMIC ISSUES 167

Figure 14-1Typical lesion associated with severe chronic Broca'saphasia.

ular white matter damage (Fig. 14-1)." Particu-larly critical to chronic Broca's aphasia is thesubcortical extension of the lesion.'2 Long-lastingmutism can be seen after anterior deep lesions,undercutting supplementary motor area and cin-gulate-caudate projections.'3 Deep anterior peri-ventricular white matter lesions disrupt dorsolat-eral frontal-caudate systems involved in readyaccess to complex output procedures.'4 They mayalso disrupt ascending anterior thalamic-frontalprojections. Anterior supraventricular deep whitematter lesions disrupt callosal frontal projections.Large periventricular and subcortical white mat-ter lesions can disrupt all of the long parietotemp-oral to frontal projection pathways. All the distantcorticocorlical systems will be disrupted. A com-bination of these systems' disruptions seems to bethe structural basis of persistent Broca's aphasiaeven with subcortical lesions only.

Acute Broca's AphasiaInfarctions or trauma that produce acute Broca'saphasia often involve the frontal operculum,lower motor cortex, lateral striatum, and subcorti-cal white matter (Fig. 14-2).'" These patients re-cover over weeks to months, with variable mix-tures of initiation delay, syntactic simplification,paraphasias, speech impairment, and usually withimpaired repetition.

lower motorcortex

Figure 14-2Lesion distributions of incomplete forms of Broca'saphasia. The entire lesion would produce "acute"Broca's aphasia. The anterior component involvedalone (stippled area) would typically evolve towardtranscortical motor aphasia. The posterior componentinvolved alone would typically evolve toward aphemia.In either case, the residual aphasia would be mild.

"Broca's Area" LesionDamage to the frontal operculum (areas 44 and46) produces an acute aphasic disorder roughlycompatible with Broca's aphasia (Fig. 14-2), butthere is quite rapid improvement usually to trans-cortical motor aphasia or even just mild anomicaphasia."5 Damage to the dorsolateral frontalcortex (areas 44, 46, 6, and 9) produces classictranscortical motor aphasia13 (discussed in detailbelow). Damage to the subcortical frontal whitematter or even to the dorsolateral caudate nucleimay produce the same deficit.H These observa-tions suggest the existence of a "frontal-caudate"regional network required for construction ofcomplex output procedures of languagesyn-tax and narrative discourse at a minimum. Dam-age to this system is part of classic Broca'saphasia.

Lower Motor Cortex LesionDamage to the lower 50 percent of the prerolan-dic gyrus can acutely produce a deficit patternroughly compatible with mild Broca's aphasia, butthere is rapid recovery to a much more limited

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disorder of speechpredominantly of art icula-tion and prosodysometimes called aphemia(Fig. 14-2).'" Damage to the suhcorlical outflow oflower motor cortex can produce the same speechdeficit, suggesting the existence of a local (rolan-dic) network for ar t iculat ion and some aspects ofprosody tha t project to the brainstcm. This, too, ispart of classic Hroca's aphasia.

A rare var iant of this restricted damage tomotor systems of speech production is the foreign-accent syndrome." A small number of cases havebeen described, usually emerging out of mild Bro-ca's aphasia. In these patients, the predominantdefici t is in speech prosody, but the quali ty of theprosodic delicit sounds to the listener like a for-eign accent, not pathologic prosody. The reportedlesions have all been in some component of themotor system for speech, either lower motor cor-tex"' or pulamen or deep connections betweenlower motor cortex and basal ganglia.'"'1 The pre-cise speech impairment has not been consistent,and the foreign accent syndrome probably repre-sents a heterogeneous group with partial damageto the motor speech apparatus.

For all of these variants and fractional syn-dromes of Broca's aphasia, some improvementcan be expected. The severe cases that oftenemerge from global aphasia typically have belterrecovery of comprehension than of speech; thisrecovery that may continue over a very longtime.12" Minimal recovery of spoken or writtenoutput from essentially none to classic telegraphicoutput is usually accompanied by lesion extentthroughout the deep frontal white mailer from themiddle perivenlricular region to the region ante-rior and superior to the frontal horn.1- The out-come of the milder cases is partly determined bylesion size," but for these smaller lesions, preciselesion site seems to best account for evolution intothe various fraclional systems.""51" In both severeand milder cases, some patients may recover byreorganizing cerebral functions lo allow someright-brain control of speech. Evidence for thiscomes from patients with serial frontal lesions'1and from temporary inactivalion of the right brain(Wada test) after left-brain slroke has producedsevere nonfluent aphasia."

Wernicke's Aphasia

In this disorder, language output is f luentthat is,normal in mean phrase length, generally sentence-length, and using all grammatical elements avail-able in the language. Content may be extremelyparaphasic" or empty. Paraphasic speech con-forms to the general rules of the language but con-tains substitutions at the phonemic level (phone-mic paraphasias such as "smoon" for spoon), theword level (semantic paraphasia.s such as "cup"for spoon), or entirely novel but phonologicallylegal words (neologisms such as "snopel"). Emptyspeech may consist of either vague circumlocu-tions or single words (thing, one, un i t , it , going,etc.). Lengthy, complex, phonologically rich out-put with varied neologisms is jargonaphasia. Al-though statements may be of sentence length,grammar may become quite imprecise, usually he-cause of semantic ambiguity; this is paragramma-tism.2-1 Speech is normal. Language comprehen-sion is poor at the levels of word recognition,simple commands, and simple conversation. Rep-etition is very poor. Wri t ten language is compa-rable lo spoken. Naming is very poor. Errors areparaphasias, circumlocutions, and nonresponses.

Apraxia to command is common, but whenthe patient is given a model to imi ta te , perfor-mance can be extremely variable, from persis-tently severe apraxia to normal performance.'4Deficits in the right visual field are common. Inthe acute phase, patients may be anosognosic; butwith awareness of deficits, agitation and suspi-ciousness may emerge.

Fractional syndromes of Wernicke's aphasiaare less common but can occur. Some patients haverelatively belter auditory comprehension (andusually repetition); others have relatively betterreading comprehension. Severe limb apraxia(both ideomotor. even with imitation of gestures,and ideational) is sometimes seen.

The minimal lesion producing Wernicke'saphasia is damage to the superior temporal gyrusback to the end of the sylvian fissure (Fig. 14-3).11If damage includes additional adjacent structures,either the deep temporal while matter or the su-pramarginal gyrus or both, problems will be more

CHAPTER 147 APHASIA I: CLINICAL AND ANATOMIC ISSUES 169

superior temporalgyrus

Figure 14-3Typical lesion producing Wernicke's aphasia. Persis-tence and severity would depend on lesion extent(see text).

persistent.25 -' If damage includes middle and inte-rior temporal gyri, ini t ial deficits will be more se-vere, anomia will he more persistent, and readingcomprehension will he poor even if auditory com-prehension improves. Patients with lesions re-stricted to the superior temporal gyrus may havepredominantly auditory comprehension difficul-ties with relatively l i t t le anomia and much lessreading impairment. The differential effects of le-sion placement in the posterior temporal lobe cer-t a in ly reflect variable damage to converging re-gional networks lor several language processingsystems. The auditory language system may bemore specifically temporal, thus the relativelygreater impairment of auditory comprehension.Visual language processing surely emerges out ofthe more posterior lemporooixipitoparietal asso-ciation cortex.:* Cross-modal lexical and semanticknowledge emerges out of a broad range of re-gions in the posterior association cortex, hut avail-able evidence highlights the inferior temporal andmiddle temporal/angular gyrus transition as theparticularly key regions for word retrieval.''

Severe and persistent Wernicke's aphasiaseems to require damage to all of these regions orlo their deep functional connections. The mecha-nisms of recovery are not completely known. Asnoted above, the brain regions involved in lexical-semantic (unction are broadly distributed in pos-terior association cortex. Size of lesion in these re-

gions, extent of involvement of the superior tem-poral gyrus,:u7 and extent of coincident damageto supramarginal and angular gyri:" have all beenimplicated as factors in recovery of comprehen-sion. Studies with positron emission tomography(PET) have demonstrated a variety of effects re-lated to recovery. Heiss and colleagues, studyingsubacute recovery in a mixed group of aphasicsyndromes, demonstrated that recovery of com-prehension was proportional to recovery of rest-ing blood flow in the surviving (eft hemisphere,particularly the lemporoparietal junction.1"Weiller and coworkers demonstrated that recov-ery in Wernicke's aphasia is closely related to ashift in PET activation to semantic tasks from lefttemporal in normals to right temporal in Wer-nicke's aphasics who recover." The precise mean-ing of these related studies is not known, but theyall converge on the importance of posterior asso-ciation cortex, either left or, if it is too damaged,right for recovery of comprehension.

Pure word deafness is sometimes considereda separate syndrome reflecting exclusive impair-ment to the auditory language processing system."Most patients are only relatively "pure," emergingout of Wernicke's aphasia with relatively betterrecovery of reading comprehension for anatomi-cally specific reasons proposed above. Some pa-tients have had only small left temporal lesions;1-others have had bilateral temporal lesions." De-pending upon the relative size and location of thebilateral lesions, these patients may be effectivelydeaf" (cortical deafness: bilateral Heschl gyruslesions) or have agnosia for the meaning of allsounds (machinery, animals, musical instruments,etc.) even though they hear them (auditory envi-ronmental agnosia: large right lesion, whatever theleft lesion14). Also, depending on specific lesionsites, language output can be variably abnormal,although to he "pure," it should be normal. In thiscase, the implication is that underlying knowledgeof word phonology is preserved because sponta-neous production is normal. Depending on lesionsite, "relatively pure" cases may have consider-able phonemic paraphasia or anomia.

The mechanism of pure word deafness ispresumably damage to a system that converts the

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acoustic signal into a phonoiogically meaningfulstimulus." This is necessary hut not sufficient forcomprehension; for example, normals can repeatsentences in languages phonoiogically similar totheir native one without understanding anything.There must still be merger of the processed acous-tic signal with a semantic system. In some patientswith Wernicke's aphasia, the phonological processseems very impaired; in others, the mapping to se-mantics and in yet others both are impaired.

Conduction AphasiaIn conduction aphasia, language output is fluent.Content is paraphasic, usually predominantlyphonemic.6 There may be frequent hesitations andattempts to correct ongoing phonemic errors (so-called conduit d'approche). Speech is normal.Language comprehension is good except for audi-tory span. Repetition is poor, not always worsethan spontaneous output but dominated by pho-nemic paraphasias on substantive words, particu-larly phonoiogically complex target words("happy hippopotamus") or words embedded inphonoiogically complex sentences ("Dogs chasebut rarely catch clever cats"). Written language isextremely variable in this syndrome. Writing israrely better than speech, but it can be much moreimpaired. Oral reading is usually comparable tospeech but can be better or worse. Reading com-prehension is usually comparable to auditory butcan be worse. Patients with the agraphia withalexia syndrome usually have conduction aphasia.Naming is also extremely variable, from ex-tremely poor to nearly normal. Errors are pa-raphasias (phonemic especially).

Limb ideomotor apraxia is common initiallybut clears in most patients.24 Right-sided sensory

loss or visual field impairment (extinction and/orlower quadrant deficit) are common.

Most patients with conduction aphasia haveprominently reduced auditory verbal short-termmemory (STM), tested as digit-span, word-span,or sentence-length effect in repetition. There is,however, little specificity of the STM problem, asmany patients with perisylvian aphasias have asimilar problem. The STM deficit also has little

relevance to the language production problem, assimilar output occurs in spontaneous output, oralreading and naming, as well as repetition. Thereis converging evidence that the inferior parietallobule, particularly the supramarginal gyrus, iscritical for all aspects of phonologic processing.Thus, lesions there have been blamed for pureSTM deficits,35 phonologic agraphia,3'37 and pho-nologic alexia, all of which commonly emergefrom conduction aphasia.

The necessary and sufficient lesion to pro-duce conduction aphasia is damage to supramar-ginal gyrus38 (Fig. 14-4). The classic correlationwas with the arcuate fasciculus, putatively con-necting temporal lobe to frontal lobe.39 Lesions insubcortical parietal white matter disrupt this fas-ciculus and may represent the classic correlation.4"Lesions in white matter deep to sensory cortex orin the subinsular extreme capsule as well as supra-marginal cortex lesions may also produce conduc-tion aphasia.41 These observations suggest thattemporoparictal short association pathways (i.e.,a regional network) may support the phonologicoutput structure of speech. This network is re-quired for phonologic accuracy in spontaneousoutput, repetition, oral reading, and naming. Ifdisturbed phonologic structure of output is thehallmark of conduction aphasia, this would be thecriterion structural basis.

Some patients have very extensive parietal

Figure 14-4Typical lesion producing conduction aphasia. Smallerlesions within this region may also produce similaraphasia (see text).

supramarginalgyrus

CHAPTER 14/APHASIAI: CLINICAL AND ANATOMIC ISSUES 171

lesions with more severe anomia, agraphia, andlimb ideomotor apraxia. Partial involvement ofthe superior temporal gyrus can produce initialWernicke's aphasia that evolves into conductionaphasia With very paraphasic output and severeanomia. Again, the overlap of syndromes shouldbe evident. Patients whose perisylvian arterial ar-chitecture just happens to catch the superior tem-poral lobe in a predominantly parietal stroke willhave elements of pure word deafness (decreasedauditory comprehension) with conduction aphasia(phonemic paraphasias, anomia, and agraphia).That combination would be indistinguishablefrom Wernicke's aphasia; in fact, it probably isWernicke's aphasia except that recovery of com-prehension would be "surprisingly" good.

Most patients with acute conduction aphasiahave good recovery over a few weeks, althoughresidual writing impairments, mild anomia, andoccasional phonemic errors can he observed.' Forthe more severe cases with marked anomia andvery paraphasic output, recovery is less complete.The combination of significant phonologic and se-mantic deficits despite good comprehension canbe very long-lasting. Over time, patients becomeless neologistic and more empty and circumlocu-tory, even if the basic deficits do not improve.42

Global AphasiaIn many ways global aphasia is the easiest syn-drome to define. By definition, patients have sig-nificant impairments in all aspects of language.Language output is severely limitedthere is nomore than "yes," "no," and a recurring slereotypicutterance ("da, da," "no way, no way." etc.). Insome global aphasics (and Broca aphasics) the re-curring utterance may be repeated rapidly in arichly inflected manner that suggests fluent outputif only it could he comprehended." This is not jar-gonaphasia; it has none of the phonological rich-ness or preservation of grammatical infrastructureof jargonaphasia. The mechanism of this richly in-flected stereotype is unknown, and it has noknown prognostic significance.

Comprehension is very impaired. The Bos-ton Diagnostic Aphasia Examination (BDAE)

definition allows comprehension up to the 30thpercentile for an aphasic population.44 This iscompatible with considerable single-word com-prehension. The language comprehension tasksmost likely to be preserved in global aphasia arepointing to a named location on a map,45 pointingto personally highly familiar names from multiplechoice or acknowledging them when they are pre-sented auditorily, and a small subset of commands("take off your glasses," "close your eyes," "standup").24 Some global aphasics can do those tasksbut little else. There is no repetition, naming, orwriting.

Buccofacial and limb apraxia, to commandand imitation, are nearly universal.24 Right hemi-plegia, hemisensory loss, and visual field impair-ments are all common but not invariable.

The most typical lesion involves or substan-tially undercuts the entire perisylvian region." Atleast, this would require a combination of the Bro-ca's and Wernicke's aphasia lesions, but muchclinical variability is seen. Some patients with Bro-ca's aphasia lesions present as global aphasicswithout evident temporal lesions.4"47 Conversely,some patients with very extensive posterior lesionsthat extend into subrolandic white matter presentwith global aphasia without any definite frontal oreven anterior periventricular lesion.'' The mecha-nism of severe comprehension loss without a tem-poral lesion in a substantial fraction of global apha-sics, is not known. The same effect is not seenwithout coincident frontal lesionsthat is, evenenormous cortical and subcortical parietal lesionsalone do not cause such deficits in comprehension.The coincident frontal lesion may produce addi-tional cognitive problemssuch as inattention,underactivation, unconcern, poor problem solving(particularly relevant when the Token Test is thedefining tool of comprehension), or persevera-t ionthat interact with more modest phonologic/semantic deficits to produce more profound func-tional comprehension deficits. Alexander and as-sociates have suggested that a sufficiently great le-sion of the deep temporal white matter mightundercut connections to the temporal lobe.48Naeser and colleagues found these deep temporallesions to be associated with poor comprehension


in many global aphasics.21 There was good recov-ery of comprehension in cases with deep temporallesions but intact temporal cortex. Heisse and co-workers have demonstrated a very high correla-tion between reduced leniporoparictal blood flowin resting I'ET and poor comprehension, whateverthe anatomic limits of the infarction.1" Vignoloand associates46 and DC Kcn/i and colleagues,"who have provided the most meticulous descrip-tion of global aphasia without temporal lesions,have not found tha t temporal while matter lesionseasily account for the deficits in comprehension.

Some patients with global aphasia have nohemiparesis. As a group, they are likely to haveonly a large frontal lesion or separate frontal andtemporal lesions.4'' The purely frontal lesions areagain presumably causing a quasicomprehensiondeficit due to inattention, activation, persevera-tion, and so on. These patients are also likely tohave a better prognosis, but absence of hemipare-sis is not a guarantee of a good outcome, as theabsence of hemiparesis only means that a smallportion of paraventricular white matter has beenspared.5"

When caused by infarction, global aphasiahas a poor prognosis. Smaller lesions (some with-out hemiparesis) will improve quickly. After in-farction, patients still meeting taxonomic criteriafor global aphasia at I month postonset have avery low probability of improving substantially.3Large hemorrhages may be associated with morelate recovery, but by 2 months without improve-ment, the prognosis remains grim. Many patientsshow gradually improving comprehension overweeks and months and eventually reach taxo-nomic criteria for severe Broca's aphasia.

Transcortical Motor AphasiaIn this syndrome, language output is commonlyviewed as nonfluent because there is substantialinitiation block, reduction in average phraselength, and simplification of grammatical form."Many patients with transcortical motor aphasia(TCMA) are initially mule and may remain muleor nearly so for days or weeks. Nole lhat, if theyare mule, repetition is obviously absent and, by

strict taxonomic criteria, such paticnls would ini-lially be called Broca's aphasics. Frank agramma-lism is uncommon; responses are simply lerse anddelayed. Echolalia in various forms is frequentlyobserved. Completely uninhibi ted echolalia is un-usual, but fragmentary echoing, particularly ofcommands, may be observed. Incorporation echo-lalia is more common. The patient incorporates aportion of a question into the initial portion of hisresponse. Speech qual i ty is normal in the classiccase. Repetition is, by definition, normal or at leastvastly superior to spontaneous output. Recitationof even very complex overlearned material (e.g.,Ihe Lord's Prayer) may be flawless. Language com-prehension is supposed to be normal, but, as ob-served above, the large frontal lesions most oftenassociated with TCMA may produce substantialimpairment of comprehension. Writing is usuallysimilar to spoken output, but patients rarely writeto dictation as well as they repeat. Reading com-prehension parallels auditory. Oral reading maybe quite normal if ini t ial prompts are provided.Naming is quite variable; errors are nonresponses,semantic paraphasias, or perseverations.*

Transcortical motor aphasia may have anyrange of associaled motor deficits, depending uponlesion site. The classic case has no motor deficit.Hemiparesis accompanies many cases of subcorti-cal TCMA.14 Inverted hemiparesis (leg worse thanarm) and a contralateral grasp reflex accompanymedial frontal TCMA." Sensory loss and visualfield deficits are nol usually seen except in suncor-lical cases. Buccofacial apraxia may be seen, hutlimb idcomotor apraxia is less common."

The classic patient has a large dorsolaleralfrontal lesion, typically extending into the deepfrontal white matter (Fig. 14-5)." Identical caseshave been reported wi th just a white matter lesionabutting the frontal horn of the lateral ventricle.4*Very similar cases involve the capsulostrialal re-gion, parlicularly the dorsolateral caudate and ad-jacent paraventricular white matter (Fig. 14-6)."The similari ty of the aphasia associaled with thesedisparate lesions is paralleled by the nearly identi-cal reduction in blood flow seen on resting PETor single proton emission computed tomography(SPECT) in dorsolateral frontal cortex, whatever


Figure 14-5Typical lesions producing transcortical motor aphasia.Note overlap with Broca's area lesions (Fig. 14-2).

(he lesion site.5'5;57 The more posteriorly thelesion extends along the paraventricular whitematter, the likelier the presenee of dysarthria (seediscussion of aphemia, above) and hemiparesis.Damage to the medial frontal lobe, particularlythe supplementary motor area, produces TCMA-like disturbance." Mutism may be more pro-longed. When patients begin to speak, they rarelyshow any frankly aphasic qualities. They simplydo not speak much.

Analysis of cortical and subcortical cases

Figure 14-6Large lenticulostriate lesion, which is often associatedwith transcortical motor aphasia, frequently accompa-nied by speech disturbance and hemiparesis. Smallerlesion (cross-hatched area) may produce mild trans-cortical motor aphasia without motor deficits.

with TCMA suggests that one fundamental deficitis in generative language tasks.14-54 The patientsseem to have very limited capacity to generatecomplex syntax. They may reuse the syntax in aquestion they are asked (incorporation echolalia).They may produce short responses, even shortsentences, quite well. When asked an open-endedquestion, however, they do not have timely accessto the range of syntax needed to answer.54" Bed-side generative tasksword-list generation, story-telling, or producing sentences using providedmain verbswill be impaired out of proportionto other language tasks. Patients with large dorso-lateral frontal lesions may have little or no aphasiaon standard tests but still be unable to tell a storyor recite a narrative in normal fashion.

A second fundamental deficit in TCMA isreduction in activation to speak (or to write).Analysis of lesion site effects, particularly the pro-found mutism that occurs with medial frontaldamage, suggests that reduced activation is due toloss of ascending dopaminergic pathways. Themedial frontal regions are primary targets of thenonnigral dopaminergic system.5* Bilateral dam-age to this system anywhere from the upper mid-brain to the frontal cortex results in akinetic mut-ism,57 evolving into less flagrant forms often calledabulia.58 Transcortical motor aphasia may repre-sent a subsyndrome of akinetic mutism with morerapid clearing of mutism and less global akinesiabecause the lesion is only unilateral. The improve-ment in fluency and speech rate after administra-tion of direct dopamine agonists supports thisproposition.w6" Improvement with bromocriptineis almost uniquely seen in TCMA.

Transcortical Sensory AphasiaIn transcortical sensory aphasia (TCSA), lan-guage output is fluent. Content is very empty, withsemantic paraphasia predominating. All patientsmake abundant use of one-word circumlocutionsand nonspecific filler words, such as one, things,docs, etc. Phonemic paraphasias and neologisticjargon arc less common, so that output is moreaccurately described as extended English jar-gon. Content is also often perseverative. Speech


qual i ty is normal. Repetition is, by definition, nor-mal. Language comprehension is impaired. In par-ticular, single-word comprehension may he quitepoor. When accompanied by accurate repetitionof the test words and even their incorporation insentences, ("A watch? I should know that. Is oneof these a watch?"), the behavior has been calledalienation of word meaning." There may be cate-gory-specific comprehension impairments withparticularly good performance at following com-manded actions and very poor performance atpointing to named targets. Many patients will ac-cept incorrect names or quibble over accuracy.("You could call it a watch, but I don't think it isone.") Naming is poor, and again some category-specificity may be observed. Some patients areworse at naming animals, insects, and other ani-mate objects than tools and other inanimate ob-jects.62 There is no important discrepancy betweennaming performance to different sensory modal-ities. Many patients respond quickly to phonemiccues but will then reject or be uncertain about thecorrect response. This behavior has been called atwo-way naming impairment.'1' Written outputmay be similar to spoken, but patients usually donot write extensively and are very perseverative.Reading aloud and reading comprehension areboth abnormal. In many patients reading com-prehension is even worse than auditory compre-hension.

Transcortical sensory aphasia has been de-scribed after lesions in middle and inferior tempo-ral gyri (Fig. I4-7).6' The temporal lesion may pro-duce a right visual field defect if white matterextent reaches the geniculocalcarine pathways.Many cases of TCSA have unexpected lesion sitesinvolving the entire perisylvian cortex, a lesionmuch likelier to produce global aphasia." Themechanism for this is unknown, although somevariant on bilateral language representation isusually recruited. Some cases with temporal le-sions may also involve the inferior temporooccipi-tal regionfor instance, after posterior cerebralartery infarction. These patients will certainlyhave very impaired reading.2* Many have associa-tive agnosia.65 Not only can they not name an ob-ject or point to a named object but they cannot

Inferior angulareyruj

Poilerior inferiortemporal evrus

Figure 14-7Typical lesion producing transcortical sensory aphasia.Lesions more medial and inferior, usually posterior ce-rebral artery infarctions, may produce similar aphasia(see text).

indicate its use or sort it into a correct functionalcategory (i.e., put a pencil with chalk rather thanwith a knife). Thus, the deficit is not restricted tolexical semantic knowledge but involves actual se-mantic knowledge. This may be modality-specific,with visually presented tasks more impaired,''5 orit may affect all modalities equally."

Transcortical sensory aphasia is almostmonotypic in that it is fundamentally a disorder ofsemantic processing. Nevertheless, different as-pects of semantic knowledge and access to seman-tic knowledge may be impaired in different cases.The inabil i ty of patients with TCSA to associatea name with an object is the result of a semanticdisorder at the interface between language andsemantic memory. When semantic memory ismore globally affected, patients are unable to dem-onstrate recognition of objects by nonverbalmeans as well (see Chap. 23). This is most com-monly seen in degenerative diseases with a pre-dilection for temporal cortex, such as AlzheimerDisease, Pick Disease, and so-called SemanticDementia.2"-"2''7 ""

Anomic AphasiaAnomic aphasia is a much less homogeneousgrouping than any of the other classic syndromes.By definition, language is fluent, comprehensiongood, and repetition good. The only deficit in spo-


ken language is in word retrieval. Paraphasias areinfrequent. Word-finding problems usually pro-duce filler words' or circumlocutions. Other im-pairments vary with lesion site.

Ahomic aphasia is the residual state of manyaphasic disorders after time for improvement.2'As a primary diagnosis, anomic aphasia usuallyaccompanies lesions in the same regions asTCMA or TCSA.'0"

As noted, most patients with TCMA are orat least become basically fluent but with terse, un-elaborated utterances. When it is accompanied byword-finding deficits, this condition would qualifyas anomic aphasia. Anomic aphasia is also themildest form of TCSA, representing a deficit onlyin lexical retrieval from semantic stores. Thus,when anomic aphasia is caused by a dorsolateralfrontal lesion, there are no accompanying neuro-logic signs. When it is caused by a deep frontal-striatal lesion, there may be dysarthria, hemipare-sis, and buccofacial apraxia, depending uponlesion extent. When it is caused by a posterior as-sociation cortex lesion, there may be a visual fielddeficit and alexia, depending upon lesion extent.When anomic aphasia is the residual of partlyrecovered conduction or Broca's aphasia, theaccompanying signs are as expected for thosedisorders.

Mixed Transcortical AphasiaIn mixed transcortical aphasia (MTA), languageoutput is nonftuent. Comprehension is impaired.Naming is poor. Repetition is preserved. Echolaliaand fragmentary sentence starters ("I don't . . . ,""Not with the ...") are common. Speech qualityis normal. Writing and reading are similarly re-duced.

In the patient whose case report defined thissyndrome, MTA was due to bilateral hypoxic neu-ronal loss in the arterial border zones, but isch-emic damage in the left border zones could pre-sumably cause the same disorder. The implicationis that MTA requires a combination of the lesionsof TCMA and TCSA, with perisylvian structuresallowing repetition preserved. Most cases are ac-tually due to large frontal lesions in the region of

TCMA lesions. The comprehension defect isprobably due to a mixture of frontal impairments,exactly as described for restricted frontal lesionsand global aphasia. Comprehension improves,and patients evolve toward TCMA. Associated le-sions are as described for TCMA.

Large anterior thalamic lesions also produceMTA.71~73 Most cases have involved the anterior,ventrolateral, and dorsomedian nuclei at a mini-mum."72 Damage to those three nuclei effectivelydeprives the frontal lobe of thalamic input andmodulation. Patients are often mute initially.When they speak, the reduction in narrative andterseness of structure are similar to those ofTCMA. The impairment in comprehension maybe due to the speculative "frontal" mechanisms.The associated signs depend upon lesion extentout of the thalamus. Recovery of language is usu-ally good.

CROSSED APHASIA AND APHASIAIN LEFT-HANDERS

The foregoing review is valid for most right-handers with lesions of the left hemisphere. Forthe 10 percent of the population that is left-handed and for the approximately 2 to 5 percentof the right-handed population that becomesaphasic after a right-brain lesion (crossed apha-sia), some modifications of the clinical rules arerequired. For left-handers, the phenomenology ofaphasia is complicated by the very issue of left-handedness. More than right-handers, all left-handers are not created equal; they vary greatlyin degree and nature of hemispheric specializationfor language. For both populations the phenome-nology is further complicated by irregularities inlateral dominance for other typically lateralizedfunctions, such as praxis and some aspects ofvisuospatial function. Only a brief summary ofthese issues is possible here.

Crossed AphasiaThe incidence of crossed aphasia has been re-ported as anywhere from 1 to 13 percent.74'76 The


stroke population" is least contaminated by pos-sible bilateral lesions, but in all populations meth-odological l imitations (defining handedness andaphasia testing strategies) leave the actual inci-dence uncertain. A reasonable estimate is 2 to 5percent.

Patients with crossed aphasia fal l into twobroad categories. About 70 percent have a stan-dard aphasia syndrome associated with, at leastapproximately, the lesion site expected in theleft hemisphere." All types of aphasia profilescan occur with the expected lesions (albeit inthe right hemisphere). The other 30 percenthave striking anomalies in the aphasia-lesion re-lationship." In this group, unexpectedly mildaphasia syndromes occur despite large lesionsthat would typically cause a more severe apha-sia. Conduction aphasia or phonologic agraphiahave been seen despite large perisylvian le-sions.7'7* In other patients with large perisylvianlesions, transcorlical sensory aphasia or anomicaphasia has been described."*1 Alexander andAnnett have suggested that these anomalouscases point to possible discrepant latcralizationsof phonologic and semantic functions.7'' Patientswith crossed aphasia may have a better capacityfor recovery.

Laterali/.ation of praxis and visuospatialfunctions in crossed aphasia has not been as defi-nitely addressed as the language functions. Castro-Caldos and coworkers claim that these functionsshow anomalous lateralizalion less frequently thanlanguage, asserting that praxis remains in the lefthemisphere contralateral to the preferred righthand and that visuospalial functions remain in theright hemisphere.74 Others have disputed this, ar-guing from case reports that all functions show ahigh rate of anomalous lateralization.*" Alexan-der and coworkers have reviewed the case re-ports of anomalous visuospatial lateralization tothe left hemisphere in right-handers." They haveproposed that there is a subset of right-handerswho have chance lateralization of all functions.These authors, among others, have even pro-posed that a genetic basis for the inheritance ofhandedness and laterality of cognitive functionssuch as the right shift theory of Annett777 ' ' can

account for the rates of all anomalies. The bio-logical basis of crossed aphasia, however, re-mains unknown.

Aphasia in Left-HandersLeft-handers make up 10 percent of the popula-tion, but they are a much more heterogeneousgroup than right-handers. If a strict criterion forleft-handedness is used, most of the left-handedpopulation becomes relabeled as being mixed-handed.76 Thus, some authorities simply refer tonon-right-handers. The rate of cerebral lalerali-zation of left-handers depends to some extenton the criteria used to define the group. Largestudies of left-handed aphasics have been rea-sonably consistent, however, in finding thatabout 70 percent have left-brain lesions and 30percent have right-brain lesions." Hecaen hascomputed that approximately 15 percent prob-ably would be aphasic a f t e r a lesion of eitherhemisphere; that is, they have bilateral languagerepresentation. Whether aphasic after left orright brain lesions, the proportion of cases withanomalous aphasia-lesion relationships is higherthan in right-handers.*' It has been claimed thatleft-handers have better recovery than right-handers,112 but, as with crossed aphasia, this ques-tion is muddied by the higher proportion of mildaphasics.*' It is also unclear if better recoverymeans bilateral language capacity so all func-tions have higher potential for recovery or diver-gent lateralization of functions so that some areleft uninvolved by any lateralized lesion."7'""Both factors are probably operative, but in dif-ferent patients.

Lateralization of praxis and visuospatialfunction shows anomalies at a rate similar to thoseof crossed aphasia. Every possible arrangementof impaired and preserved functions has beenreported after left or right lesions.'" Since thebiological basis of neither handedness nor thelateralization of cognitive functions has been es-tablished, it remains an open question how theseanomalies occur in left-handers as well as right-handers.


EFFECT OF ETIOLOGY

InfarctionsAlmost all of the foregoing is based on the litera-ture accumulated from strokes. Infarcts have nu-merous advantages for clinicoanatomic correla-tions. They are sudden in onset, and there istherefore no accommodation and compensationprior to clinical presentation. Boundaries betweendamaged and nondamaged brain are fairly pre-cise, so correlations are clearer. Nevertheless, thevascular system cannot provide every topographicvariation of brain injury; therefore much of whathas come to us as classic syndromes could easilybe par t ia l ly artifactual correlations produced bythe limited independence of lesions sites frominfarctions.

There arc some aphasic syndromes that arecommonly believed to be caused by emboli be-cause the distribution of infarction seems mostplausibly to be in the territory of a branch of themiddle cerebral artery. The fractional Broca'saphasias, conduction aphasia, and Wernicke'saphasia all seem likely to have an embolic basiswhen due to infarction. Global aphasia and Bro-ca's aphasia require more extensive damage in theterritory of the middle cerebral artery. There is,however, no basis for presuming an infarctionmechanism simply on the basis of these aphasiatypes.

HemorrhagesAll of the rules established for infarctions applyfor hemorrhages if the hemorrhage happens to bein the same brain topography as an infarction pat-tern. Patients with hemorrhages may be muchmore impaired ini t ial ly because of physiologicdelicits not primarily related to aphasiamass ef-fects, intraventr icular blood, and so on. Hemor-rhages are not constrained by vascular patterns,so entirely novel arrangements of lesions can beseen. This may be exemplified most clearly withlesions of the lenticulostriate region. Infarctionstend to be partially or completely limited to themiddle cerebral artery perforators, but hemor-rhages can dissect out of tha t l imited region. Much

of the variability reported after lenticulostriate le-sions*5 may be due to idiosyncratic extensions ofhemorrhages.*6

TraumaFocal contusions can occur anywhere, dependingupon the direction of the blow, skull fragments,and so forth. When the contusion is in a perisyl-vian region, the resulting aphasia will usually fol-low the rules established by infarctions. Conduc-tion and Wernicke's aphasias may be seen withpredominantly superficial lesions and so may bequite typical. Cortical contusions rarely cause in-jury deep enough to damage all of the requireddeep structures (see above) and thus to producenonflucnt aphasia. There is a strong tendency fortraumatic contusions to arise from hasal structuresdue to inertial effects. Focal contusions of the in-ferior temporal lobe will cause anomic aphasia. Ifthe lesions are large and extend into lateral tem-poral lobe or hemorrhage dissects up into thedeep temporal white matter, patients may presentwith Wernicke's aphasia or TCSA, Trauma canalso cause large epidural or subdural hematomasthat do not directly affect language zones. Theycause cerebral herniation with entrapment of theposterior cerebral artery, causing occipitotemp-oral infarctions with alexia and anomia. This her-nialion-caused infarction can be superimposed ondirect temporal contusion, resulting in a very se-vere fluent aphasia.

TumorsThe lesson for aphasia is no different than that forany cognitive function. In general, large tumorsproduce relatively much less cognitive impairmentthan an infarction of the same size would produce,but tumors produce symptoms qualitatively ap-propriate for the region involved. Tumors tend toinf i l t ra te and gradually disrupt function, allow-ing substantial compensation as the disorderprogresses. The conformity with patterns estab-lished by infarctions will be correlated largelywith the malignancy and speed of growth of thetumor.

178 PART MI/LANGUAGE

Herpes Simplex EncephalitisAlthough rare, herpes simplex encephalitis (HSE)has a predilection for the medial temporal lobes,basal-medial frontal lobes, and insular cortices.Survivors of HSE frequently have severe amne-sia.'12"7 Patients wi th extensive left-sided HSE le-sions, including the inferolemporal lobe, com-monly show category-specific semantic deficits.62-"7

DementiaThe most common dementing illnessesDATand multi-infarct dementia (MID)both causelanguage impairments. Dementia of the Alzhei-mer type typically presents with memory and lan-guage disturbances.'" The language problem be-gins as anomia and is often misidentified byfamilies as memory impairment. With time, thelanguage disorder evolves toward TCSA, and thepatients' semantic memory erodes."" The structureof this erosion is fair ly predictable. Highly typicalsemantic associations survive longer than the se-mantic associations and attributes of low typi-cality.*" For instance, the patients may still recog-nize the words and concepts behind "cat," but notthe words and then even the concepts of "leop-ard," "fang," or "litter." It has been proposed thatthis slow erosion of semantic knowledgefirstwords and (hen conceptsis the fundamentalcognitive deficit of DAT.*'1 Its presumed patho-logic basis is the loss of neurons in posterior asso-ciation cortex.

If one of the infarcts is in (he language /one,MID may cause aphasia directly. The more typicalpathology of MID is, however, numerous small in-farcts in subcortical regions. These lesions mayproduce a variety of motor speech impairmentssuch as articulatory problems, hypophonia, dys-prosody, and rale disturbances. A recognizableaphasic syndrome does not occur, but patientsmay show cognitive deficits similar to those seenwith frontal lobe lesions, including disturbances inall aspects of generative language: reduced word-list generation, terse or unelaborate utterances,and poor narrative ability. It has been suggested

that a single small infarct in the genu of the leftinternal capsule is sufficient to disconnect frontal-thalamic circuitry and produce these deficits.1"'

A rarer form of degenerative dementia, pri-mary progressive aphasia, is virtually restricted tolanguage deficits.'" The most common form is pro-gressive loss of semantics and has therefore alsobeen called semantic dementia1" (see Chap. 23).The presentation is usually similar to the languageimpairments of DATanomia initially prog-ressing to TCSA and finally to loss of semanticconcepts and knowledge. Unlike DAT, other cog-nitive functions remain intact in these cases. Pa-thology is restricted to the anterior inferior tem-poral lobes, and the histopathology is usually Pickdisease.""293 Nonfluent forms of primary progres-sive aphasia have also been described;'4 however,the pathology has not always been established.

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