Which part of the brain would a lesion most likely result in a disruption of language comprehension and expression?

Migraine aura

Migraine auras occur in about one-third of migraine patients (Cutrer and Huerter, 2007). Most patients who have migraine attacks with aura also have attacks without aura, with only one-fifth of migraine-with-aura patients having aura with every migraine attack. Typical aura symptoms develop and progress gradually over several minutes and then resolve within 60 minutes. The resolution of aura symptoms often coincides with the onset of headache. Much less commonly, aura symptoms can occur during the headache phase of the migraine attack, after the headache phase, or in the absence of headache altogether (“acephalgic migraine” or “aura without headache”). Individual aura symptoms may occur in isolation during an individual migraine attack or more than one aura symptom may occur sequentially.

Visual phenomena are the most common aura symptom, reported by over 80% of patients with migraine aura (Eriksen et al., 2004;Russell and Olesen, 1996). Like all migraine aura symptoms, visual symptoms progress slowly, moving across the visual field. Visual auras consist of positive symptoms such as seeing flashing lights and wavy lines (“scintillating scotoma”), often followed by negative scotomas within the same distribution of the preceding positive visual phenomena.

Sensory aura, the second most common aura type, is, like the visual aura, characterized by positive symptoms (paresthesias) followed by negative symptoms (numbness), which slowly spread or migrate (Eriksen et al., 2004;Russell and Olesen, 1996). Sensory aura is usually unilateral and has a predilection for the hand, arm, shoulder, and face.This may be due to the large representation of these structures in the sensory cortex or thalamus. Commonly, sensory symptoms begin in the hand and then slowly spread up the ipsilateral arm to the shoulder and face with perioral and tongue involvement. The rate of spread of a sensory aura is important to help distinguish it from a sensory seizure and the sensory disturbance of a TIA. Just as a visual aura spreads across the visual field slowly, taking as long as 20 minutes to reach maximum, the paresthesias may take 10–20 minutes to spread from the point at which they are first felt to their maximal distribution. This is slower than the spread of a sensory seizure and much slower than the spread of sensory symptoms associated with TIA. A migrainous sensory aura generally resolves over the course of 20–60 minutes, most often within 30 minutes.

After sensory aura, the next most common type is a language aura (Eriksen et al., 2004;Russell and Oleson, 1996). Expressive dysphasias, including paraphasic errors, are the most common language symptoms of migraine aura, with receptive dysphasias being less common. Language symptoms of migraine aura are typically of mild severity.

When unilateral motor weakness is present with migraine aura, the diagnosis is “hemiplegic migraine.” Hemiplegic migraine can be “familial” or “sporadic.” Motor weakness of hemiplegic migraine most often involves the hand and arm. Although the term “-plegia” suggests paralysis, the motor symptom of hemiplegic migraine is usually weakness as opposed to true paralysis. In addition to the hemiparesis, there must be at least one other aura symptom, including a visual, sensory, or language/speech symptom. Like with all migraine auras, the aura symptoms of hemiplegic migraine have a slow spreading onset over several minutes, with each symptom resolving within 60 minutes. However, the motor weakness of hemiplegic migraine can endure for several days. The genetics of familial hemiplegic migraine are discussed further under Migraine Genetics.

II.L Broca's Aphasia

Broca's aphasia is one of the most commonly known syndromes of frontal language disorder. The core features of this syndrome include nonfluent, effortful speech production, semantic and phonemic paraphasias, articulatory errors, agrammatism, and relatively preserved comprehension. Widely accepted definitions of Broca's aphasia also include poor repetition, reading, and writing ability.

The lesion in classical Broca's aphasia involves the left posterior, inferior frontal gyrus. With the advent of sophisticated neuroimaging techniques, researchers have discovered that circumscribed damage to Broca's area does not necessarily result in the complete syndrome of Broca's aphasia. Moreover, some individuals with Broca's aphasia do not have lesions in Broca's area. Therefore, it seems that the underlying pathology in Broca's aphasia can be relatively extensive and varied. Regions including the inferior central Rolandic area, the insula, subcortical regions, and the anterior parietal regions have also been implicated in this language syndrome.

Migraine With Aura

Up to one-third of patients with migraine have symptoms of a migraine aura, which was previously termed “classic migraine.” These are transient, completely reversible neurologic symptoms with gradual onset and spread over at least 5 minutes that are followed by headache, but they can occur at any point during a headache or without headache. Headache associated with aura may not fulfill criteria for the migraine previously mentioned, but it is still considered migraine because of the association. Each symptom of an aura may last up to an hour and may occur in succession. Aura symptoms are more likely to consist of positive (flashing) or positive and negative (scintillating scotoma) symptoms than purely negative symptoms. The symptoms correspond to a cortical spreading depression wave of activation followed by the suppression of neurons of eloquent areas.

Typical (“classical”) aura symptoms:

Visual: Most common of all aura symptoms. Described as sparkling objects forming a growing spot, or a zigzag figure enlarging and spreading to the periphery. Patients have a hard time describing these symptoms and find it helpful to see images they can relate to, such asFig. 15.2. Description of monocular, rather than homonymous, visual disturbance is a common mistake: patients should be asked to describe how they visualize a face or a clock and asked to test eyes individually with future episodes.

Sensory: Pins and needles followed by numbness spreading over one side of face or body. Numbness may be the only symptom, but gradual spread is an important feature.

Aphasic: May range from mild to dense, and expressive aphasia is more common than receptive or complete.

The following rare forms of aura should be identified and closely worked up for secondary etiologies including stroke, ophthalmic pathology, and, if brief, seizures. Triptan and ergot therapy is contraindicated in patients with these auras.

Hemiplegic aura:

Fully reversible weakness, typically unilateral, that may last up to 72 hours, in rare cases up to weeks, along with at least one typical aura symptom above. Mutations in genes responsible for facilitating cortical spreading depression, including CACNA1A, ATP1A2, SCN1A, may be causative. In patients with mutations, attacks can be triggered by mild head trauma. In 50% of families, progressive cerebellar ataxia may occur independent of migraine attacks.

Broca's Aphasia

Broca's aphasia has also been called verbal aphasia, expressive aphasia, efferent motor aphasia, and motor aphasia. The primary modality of language that is affected is speech production, but writing is often affected, too. Comprehension of spoken language and reading are usually much better preserved. According to the older scheme of dividing the aphasias into fluent and non-fluent, Broca's aphasia is the common variant of non-fluent aphasia. Speech output tends to exhibit poorly articulated words with missing, added, or transposed sounds, and there is usually difficulty in initiating speech. The range of vocabulary is often reduced from premorbid levels, and speech output tends to rely a great deal on basic, highly familiar, and thus overlearned speech patterns. Speech is likely to be in short phrases with fewer words than expected, punctuated with frequent pauses. Commonly seen in Broca's aphasia is agrammatism, speech and writing in which the small elements of grammatical structure, typically the so-called function words such as articles, auxiliary verbs, and some prepositions, are omitted or unrecognized. Anomia is also fairly common, causing patients to struggle with finding the appropriate word, both in conversational speech and in confrontational naming. Although comprehension is noticeably better than production, some patients with Broca's aphasia have difficulty comprehending less frequent syntactic structures, although most demonstrate the ability to comprehend single nouns, verbs, or adjectives. Errors may occur in word order, which is called paragrammatism, but this is more common to Wernicke's aphasia (discussed next). Nouns tend to be preserved better than verbs and adjectives in Broca's aphasia, but grammatical function words are the most impaired. A concomitant of the shorter phrases and frequent pauses seen in Broca's aphasia is an impairment in prosody, alterations such as impaired inflection, pitch, and rhythm; this is commonly referred to as dysprosody. Repetition often shows the same impairments as in conversational speech. Writing in Broca's aphasia tends to be impaired analogously to speech output, but reading ability may be only mildly impaired; writing will exhibit misspellings, letter omissions, poor formation of letters, and agrammatism. Patients with Broca's aphasia are generally more aware that their speech and language is impaired than those with Wernicke's aphasia and thus may struggle to produce more correct responses.

The lesions typically leading to Broca's aphasia most often affect both the inferior frontal lobe and the anterior inferior portion of the parietal lobe; this is generally more extensive than the part of the third (inferior) frontal gyrus and surrounds that have been identified as Broca's area.

Clinical Manifestations

A patient with a brain tumor can present with one or both of two types of symptoms and signs.Generalized symptoms typically reflect the increased intracranial pressure (ICP) that often accompanies cerebral tumors, including headache, lethargy, personality change, nausea, and vomiting.Lateralizing symptoms reflect the specific location of the tumor, including hemiparesis, hemisensory deficits, aphasia, visual field impairment, and seizures (Table 180-2).

Most patients have symptoms that progress during a week to a few months. A sudden intensification of symptoms may precipitate the patient’s initial visit to the physician; however, a careful history usually reveals symptoms that predated the acute deterioration and slowly worsened over time. Two exceptions are the new appearance of a seizure in a previously asymptomatic individual (Chapter 375) and sudden hemorrhage into a tumor.

Symptoms of brain tumors can be produced by tumor invading brain parenchyma, tumor and edema compressing brain tissue, cerebrospinal fluid (CSF) obstruction caused directly by the tumor or by a shift of brain tissue, and herniation. Invasion and compression typically produce focal symptoms, many of which can be relieved if the compression is reduced. Obstruction of CSF flow and herniation are frequently a consequence of elevated ICP and typically produce generalized symptoms of headache, nausea, and vomiting, but they can also cause false localizing signs, such as an abducens nerve palsy as a result of diffuse increased ICP.

Headache (Chapter 370) is a presenting symptom of approximately 35% of brain tumors. It is more common in younger than in older patients and more common in patients who have rapidly growing tumors than in those whose tumors have evolved slowly (Fig. 180-1). Mental and cognitive abnormalities may be a reflection of local tumor (e.g., aphasia, alexia, agnosia) or of general impairment (e.g., lethargy, confusion, word finding difficulty, apathy). Seizures affect approximately one third of patients with brain tumors, and they are especially common as the presenting and only symptom of a low-grade tumor. The seizures, which are focal because they originate at the site of the tumor, may remain restricted (e.g., focal motor seizures), or they may generalize secondarily, producing loss of consciousness, sometimes so quickly that the focal signature is missed by the patient or even an observant witness.

Broca's Aphasia

Broca's aphasia, also referred to in some syndrome classifications as verbal aphasia, expressive aphasia, efferent motor aphasia, or motor aphasia, typically results from a lesion to the left posterior and lower frontal lobe and the subjacent white matter, often extending back through the lower precentral and postcentral gyri, and possibly including the inferior anterior parietal lobe, a rather wider geographical region than the region known as Broca's area, generally Areas 44 and 45 of the left hemisphere. Paraphrasing from Goodglass (1993: 210), a continuing Broca's aphasia would typically involve a lesion encompassing Broca's area (pars opercularis and pars triangularis) in the left frontal lobe cortex, usually extending posteriorly to include the lower portion of the motor strip. A lesion causing Broca's aphasia typically extends downward to the periventricular white matter, because a purely cortical or shallow lesion produces only a transient disorder.

Broca's aphasia is a common variant of the category nonfluent aphasia. Patients with Broca's aphasia tend to produce poorly articulated words and commonly transpose phonemes, and there is usually difficulty in initiating speech. Vocabulary is often limited and grammatical output tends to be confined to basic and overlearned speech elements. The production of speech tends to be in short phrases with a fewer number of words than expected, with many pauses. Overall linguistic ability seems to rely on the familiarity of the message that is spoken (Goodglass, 1993). It is common to observe agrammatism in patients with Broca's aphasia; agrammatism is a term used to describe speech output in which elements of grammatical structure are omitted, typically the so-called function words or grammatical functors (Benson and Ardila, 1996). Anomia is also fairly common; anomia causes patients to struggle with finding the appropriate word, both in conversational speech and in confrontational naming (e.g., what is this?). Many patients with Broca's aphasia have difficulty comprehending both relational words and varying syntactic structures (Benson and Ardila, 1996), although most demonstrate the ability to comprehend single nouns, verbs, or adjectives (Goodglass, 1993). Errors may occur in the ordering of words, although strictly speaking, word order errors would be called paragrammatism. Nouns appear to be preserved best in Broca's aphasia, whereas grammatical functors are the most impaired (Benson and Ardila, 1996). Usually there are also prosodic changes, including changes in inflection, pitch, and rhythm, that may distort speech output; this is commonly referred to as dysprosody (Benson and Ardila, 1996). Repetition often shows the same impairments as in conversational speech.

The writing ability of patients with Broca's aphasia tends to be affected in a manner analogous to speech output, but reading ability may be only mildly impaired (Benson and Ardila, 1996; Goodglass and Kaplan, 1983). Certain lesions giving rise to Broca's aphasia can also affect ‘nonspeech oral movements’ (Goodglass and Kaplan, 1983). A large majority of parients will show weakness of right-sided motor movements (Benson and Ardila, 1996). Writing ability tends to be affected with misspellings, letter omissions, and poor formation of letters occurring (Benson and Ardila, 1996).

People affected with Broca's aphasia are generally aware of their language impairment and will often struggle to produce the correct response. Once such patients begin to recover, they are often able to name objects at a functional level, whereas the syntactic structure of speech production is still limited. Current research shows that the lesions typically leading to Broca's aphasia most often affect both the inferior frontal lobe and the anterior inferior portion of the parietal lobe; thus, research suggests that both these areas are the probable sites for the production of language output and thus are an essential component of the so-called language core.

Broca's Aphasia

Broca's aphasia, which many people refer to as “expressive” aphasia, is regularly associated with a middle cerebral artery stroke affecting the third frontal convolution of the frontal lobe (classical Broca's area, Brodmann's areas 44 and 47)1,18,19,32 and extending into the white matter (the internal capsule). This lesion is anterior to the inferior portion of the precentral gyrus, a location that explains the co-occurrence of this syndrome with weakness in the right upper extremity.34,50,51,66 In the acute stage, the patient may be mute.34 Speech production may evolve over the next few weeks to a few automatic expressions and perhaps a spoken “Yes.”34 These patients are typically alert, aware of their surroundings, and frustrated by the absence of speech.10,50 Their preserved affect can mislead the untrained observer to overestimate the language competency of the patient.83 The five main features of the evolving pattern are awkward labored articulation, difficulty initiating speech, reduced utterance length, telegraphic speech, and reduction in melodic contours.10,34 The following is an example of a patient with Broca's aphasia describing the “Cookie Theft Picture”34 (see Fig. 29-1). “Boy … Cuh … Cuh … Cookie … girl … mama … kay … water … sinking … ice … ay … ch … ch … no … water … sinking … ee … why?” Given the limited flow of speech, one would think that little is being communicated. However, the words are substantive and appropriate, so that giving the patient with Broca's aphasia time and using context to anticipate content allow the individual to be successful in communicating content.28,33,50,79 In addition, using visual stimuli, key words, or simple pictures to supplement context and accepting gestures and drawing make it possible for the patient with severe Broca's aphasia to communicate not only thoughts and feelings but also specific information.14,58,82,84

The comprehension of spoken language in Broca's (nonfluent) aphasia is better than the production of speech, but it is far from perfect.34,50 In addition, understanding spoken language tends to improve faster in Broca's aphasia than in other types of aphasias.50,51 At least in the early stages of the condition, the tendency when working with patients with Broca's aphasia is to overestimate the patient's adequacy of comprehending spoken language.41 Some of the signs of overestimation are the complaints that “the patient fails to carry out the activities that I have told him, and he understands everything I say” or “the patient comes at the wrong time … too early or too late.…”

Common breakdowns in comprehension for the person with Broca's aphasia occur with complex grammar and syntax (tense, number, negation, comparison, words relating to space, subordinate clauses).23 One needs to provide extra processing time for comprehension of more complex language structures.41,50,84 This strategy can be accomplished by inserting pauses between phrases or thought groups. Communication can be further enhanced by using simple, clear, and direct adult sentences.41 It is a good idea to verify that the patient with Broca's aphasia comprehends communication, no matter how intact the social behavior appears. Another common symptom is that many patients with Broca's aphasia make errors processing spoken numerical information involved in stating time and dates. Providing a written appointment slip, for example, helps to compensate for this problem and ensure that the patient with aphasia understands a scheduled appointment time.

Breakdowns of reading comprehension also occur in patients with Broca's aphasia.50 They may read the content words (nouns and verbs) and then guess at the overall meaning of the sentences.34 Their ability to read improves over time, but there are almost always persisting limitations of adult level reading material. Dysgraphia (writing) is usually severe due to the combination of the language component and the necessity of using the nondominant hand.50 The combination of word retrieval, spelling, and letter formation impairments makes writing extremely difficult. The use of computer-assisted programs may be helpful. Some patients improve sufficiently to use computer-based typing, text messaging, and e-mailing to communicate with friends.60

Recovery with Broca's aphasia has a longer course than with other types of aphasias.6 Persons with Broca's aphasia can continue to improve their communication skills long after the acute stage. This improvement corresponds with an amelioration of the motor component associated with Broca's aphasia (i.e., apraxia of speech) and a gradual improvement in speech comprehension.77 If in the early stages the aphasia is mild, it may improve to an anomic aphasia or resolve almost completely.51,79

Whenever possible, collaboration with the speech-language pathologist may be helpful when planning compensatory and supportive techniques to facilitate language-based activities. Occupational therapists may address functional language-based daily tasks, for example, following written instructions for medication management, reading written instructions for exercises, or following written recipes in the kitchen. Any activity involving numbers (e.g., check writing and reconciliation of a bank account) may be a challenge for the person with Broca's aphasia. It is important to set realistic therapy goals with respect to these tasks.

A Core Syndromes

Broca's aphasia refers to a complex of language disorders that fall under the rubric of language output or production problems. Other terms used in the past for a very similar symptom–complex have been (efferent) motor aphasia, expressive aphasia, or verbal aphasia (Goodglass & Kaplan, 1983). The several lesions frequently associated with Broca's aphasia are in the left posterior inferior frontal lobe (Broca's area), the inferior anterior parietal lobe above the Sylvian fissure, the insula and the white matter deep to those three cortical regions. Lesions producing Broca's aphasia are typically fairly large. The impairments in language functions that identify an aphasic syndrome differ somewhat according to the test battery being employed; thus the Western Aphasia Battery (Kertesz, 1982), does not always agree with the Boston Diagnostic Aphasia Examination (BDAE) (Goodglass & Kaplan, 1983), nor do these two with others. Nonetheless, one usually recognizes a selection of the following language impairments as part and parcel of the syndrome of Broca's aphasia: effortful (nonfluent) speech production, short phrases with pauses in between, sound segment errors of repetition or ordering or omission or addition, errors of syntax (grammar) as in the omission of function words, written language similar to spoken language, relatively better preserved comprehension and reading ability, difficulty with word-finding or naming (anomia), and a self-awareness of the aphasic impairment. The typical interpretation is that large, more anterior lesions will compromise language production more than comprehension systems, an interpretation which in gross measure corresponds to interpreting left hemisphere posterior inferior frontal and anterior inferior parietal brain as the most probable cortical language output sites.

Wernicke's aphasia is in some respects opposite to Broca's aphasia, in that it is a complex of language impairments related mostly to input or the reception of language. Previously used terms for similar impairments are syntactic aphasia, receptive aphasia, sensory aphasia, or acoustic aphasia. The characteristic left-hemisphere sites in which fairly large lesions give rise to Wernicke's aphasia extend from the superior and middle temporal lobe back to the occipital lobe and inferior parietal-temporal lobe in the vicinity of the supramarginal and angular gyri. A selection of the following language impairments would likely lead to a diagnosis of Wernicke's aphasia: fluent speech output with relatively long phrases, the substitution of one word for another or one sound for another (paraphasias), the appearance of neologisms or jargon aphasia, impaired auditory comprehension of speech, and, frequently, impaired reading as well, impaired word-finding or naming, grammatical or syntactic errors often resulting from improper use of or addition of extraneous function words, and, in distinct contrast to the expressive aphasias, an unawareness of aphasic deficit.

Conduction aphasia is, conceptually, a simpler form of aphasia; its primary distinguishing characteristic is an impairment in repetition out of proportion to the relatively preserved comprehension of language and relatively preserved fluency of output. There may be various other language impairments accompanying the repetition impairment, such as errors in the sound segments, agrammatism, or anomia. Although many authors use the term conduction aphasia, the syndrome has also been referred to as central aphasia and as afferent motor aphasia. In keeping with the classical model's notion that information flow moves from the temporal lobe to the frontal through the arcuate fasciculus, which is a fiber tract that connects the two lobes, lesions to the arcuate fasciculus were thought to be responsible for conduction aphasia.

In the classical literature the core aphasic syndromes, Broca's, Wernicke's, and conduction aphasia reflected the then-prevailing view point that the essential language cortex was peri-Sylvian. The fourth core syndrome, anomia, known also as nominal aphasia, semantic aphasia, or amnesic aphasia, differs in one very significant way from all other classical syndromes: no specific localization was proposed. On the contrary, anomia was thought to arise from any changes to any language cortex, whether from a small lesion or a distortion caused by a space-occupying lesion elsewhere or from some other alteration in structure or physiology. Anomia is characterized by the prominence of word-finding difficulties, out of all proportion to other language deficits; reading and writing may be variably preserved but auditory comprehension is usually good and the anomic aphasic patient is usually quite fluent. A fifth classical core syndrome, alexia with agraphia, follows from a lesion in the angular gyrus, which is located just posterior to the supramarginal gyrus. The angular gyrus bridges temporal, occipital, and parietal language cortices, an anatomic convergence that was thought to be the substrate for the multivalent nature of reading and writing (i.e., visual, tactile, and acoustic input coupled to both articulatory and gestural output) (Geschwind, 1965). Although an isolated problem with reading and writing with relatively well-preserved speech and hearing was rare, it had been described following lesions to the angular gyrus. More typical for posterior cortical lesions, speech and hearing are affected, usually in the form of a mild to moderate anomia (Goodglass & Kaplan, 1983).

Functional neuroanatomy of Broca's aphasia

Broca's aphasia is typically produced by fairly large lesions in the territory of the superior division of the left middle cerebral artery. Right hemiparesis, particularly involving the face and arm, is typically present as a neighborhood sign. Broca's area, the anterior insula, and the basal ganglia are often all damaged, and the lesion usually also includes the middle frontal gyrus and the anterior parietal lobe. Involvement of Broca's area alone is not a sufficient condition for the emergence of the syndrome of Broca's aphasia. Neuroimaging findings have suggested that damage to Broca's area impairs the production of all forms of speech (propositional and nonpropositional; see Blank et al, 2002). Propositional speech refers to newly formulated language output that conveys an idea, as opposed to nonpropositional speech, which is more automatic in nature and conveys nonideational content such as feeling states. At a clinical level, it is well accepted that propositional speech is most severely affected and that automatic nonpropositional aspects of speech are often preserved. Grammatical output depends on the interaction between Broca's area and other cortical regions. Functional neuroimaging in normal subjects demonstrates that the middle frontal gyrus is commonly activated by language tasks that activate Broca's area, which suggests that this region should also be included in a language production network (see Blank et al., 2002). Tractography of the arcuate fasciculus suggest that this pathway terminates in the middle frontal and inferior precentral gyri (Fig. 3-1), as well as in classically defined Broca's area (see Catani et al., 2005).

Nonfluent Aphasias

Broca's aphasia is one of the first described and most well-known aphasia syndromes. Patients are nonfluent and characteristically speak in a halting, telegraphic manner with a paucity of grammatical elements. Sentences contain mostly content words. For example, a patient asked about recent pain in his legs might respond with, “doctor, legs…no good.” Comprehension is relatively preserved; however, patients often struggle to understand complex syntactic constructions (e.g., passive sentences such as “The girl was kissed by the boy.”). Broca's aphasia is typically associated with frontal lesions in the left (or dominant) hemisphere. Motor speech deficits often cooccur in individuals with anterior perisylvian lesions. Thus, all aspects of verbal output may be compromised (e.g., naming, syntax, and repetition).

The most severe form of nonfluent aphasia is termed global aphasia, in which both language comprehension and production are profoundly impaired and functional communication extremely limited. Speech output is limited to single words, which may be stereotyped utterances or neologisms (nonwords). Comprehension is impaired, even at the single-word level. Patients often present with global aphasia subsequent to large lesions in the left hemisphere, which typically involve anterior and posterior perisylvian regions as well as underlying white matter. Physiological restitution and rehabilitation often result in evolution to a less severe form of aphasia.

The two remaining nonfluent aphasias, transcortical motor and mixed transcortical aphasia, are relatively rare. These aphasia types are similar in that repetition is preserved relative to spontaneous speech output, which is very limited. Transcortical motor aphasia, however, has relatively spared comprehension, whereas mixed transcortical aphasia has severely impaired comprehension (even at the single-word level). Transcortical motor aphasia results from left frontal, extrasylvian lesions (e.g., supplementary motor area and underlying subcortical white matter pathways) and mixed transcortical aphasia results from diffuse or multifocal extrasylvian lesions, usually in the watershed region of the left middle cerebral artery.