Language

Lichtheim’s Model of Language Localization

Key to Symbols in the Diagram

A The area containing “sensory memory images for the sounds of words” Wernicke proposed these images were stored in the posterior portion of the first (superior) temporal gyrus in the left hemisphere. Damage in this area results in “sensory aphasia” or “Wernicke’s aphasia.” Auditory comprehension is impaired – patients hear the words, but the meaning of the words is lost

a Central projection pathway for auditory information (i.e. pathways between acoustic nerves and “A”). Damage results in “subcortical sensory aphasia” or “pure word deafness” (patients report can no longer hear the words….sounds like a foreign language)

M Area containing “motor memory images for the control of speech articulation”, i.e. Broca’s area – posterior portion of the third (inferior) frontal gyrus. Damage leads to “motor aphasia” or “Broca’s aphasia.”

m The central motor output pathway for speech articulatory muscles. Damage results in “subcortical motor aphasia”, with impaired speech expression but not written expression

B A diffuse set of associations between memory images (in A and M, as well as other areas) involving the memory images and the interconnecting fiber pathways. Therefore “B” involves a large part of both sides of the brain.

O The optic area containing visual memory images

E The area containing motor memory images for control of the hand musculature

ABILITIES

(any disruption of the indicated pathway impairs the ability) Auditory Comprehension a – A – B

Voluntary Speech b – M – m

Repetition a – A – M – m

Voluntary Writing B – M – A – E

Reading Comprehension O – A – B

Reading Aloud O – A – M – m

Copying Writing O – E

APHASIAS (area or pathway lesioned)

Broca’s M

Wernicke’s A

Conduction M – A

Transcortical Motor B – M

Subcortical Motor M – m

Subcortical Sensory a – A

GLOBAL M & A

Anomia Lichtheim said this results from any disturbance in B, M, A, B Circuit, and may be first symptom

Localization of Language

Little tidbits of knowledge you may not already know….

• The speech zones (i.e., Broca’s area, Wernicke’s area, sensory/motor areas of face and supplementary speech areas) are located in both hemispheres
• Penfield & Roberts – stimulation of speech zones results in positive effects (e.g., vocalizations, but not speech… “oooo”) and negative effects (inability to vocalize or use words appropriately)
  • However, their data (and others) do not support strict localization model – stimulation outside of speech zones can disrupt speech while stimulation of speech zones affects more than just speech
  • Damage to Broca’s area does not lead to as severe aphasia as does damage to posterior speech zones

Subcortical components of Language

• Thalamus (pulvinar and lateral posterior, lateral central complex) plays a large role in language; stimulation of this zones leads to speech arrests, naming problems, perseveration and protracted speech

Right Hemisphere Contribution to Language

Has a major role in prosody, attitudinal, emotional and gestural aspects of language and behavior

• Little or no speech but good auditory comprehension
• Good reading/not writing; good semantic/poor syntactic
• RH lesions or removal result in:
  • changes in vocabulary selection, responses to complex statements
  • poor understanding of metaphors
  • right orbital removal leads to decreased fluency
  • reduction in understanding and use of prosody
• prosody – the melody, pauses, intonation, stresses, and accents applied to the articulatory line.
• Gestural activity – lesions of the right frontal operculum can cause a complete loss of spontaneous gesture without a disturbance of praxis (aphasic patients, in contrast, generally have preserved gestural activity)

Aphasia

definition

The loss or impairment of language caused by brain damage; an acquired disorder, not a developmental retardation; can include multiple types of language including:

• Not primary sensory, thought, or memory disorder
• gestural, prosodic, semantic, syntactic and pragmatics
• most discussions of aphasia center on semantics and syntactics
• aphasics have normal turn-taking, head movements, eye movements – psychotic patients do not
• lesions in L temporal regions and outside of Broca and Wernicke’s areas produce word retrieval/naming problems for nouns, but may leave verbs intact
• general rule – in aphasia, the disturbance of language function is manifested by either incorrect grammar or incorrect choice of words
• mutism – most frequently misdiagnosed disorder as aphasia
• crossed aphasia – the occurrence of aphasia in a right-handed patient following right-hemispheric damage.
  • Relatively rare
  • High percentage of cases based on tumor or trauma, suggesting that many cases may actually represent bilateral damage

General info re: Aphasia

• Children with acquired aphasia, even those with posterior lesions, almost invariably produce a nonfluent verbal output
• Certain features, particularly dysarthria, phrase length, and agrammatism will only be present in those with anterior lesions
• In acute stage, patients with posterior lesions may have nonfluent output for several days
• Aphasia resulting from anterior lesions without hemiparesis or with transient paralysis have an excellent prognosis for recovery
• Some degree of naming disturbance is present in almost every aphasic patient
• Apraxia is often associated with aphasia as well

Recovery

• Spontaneous recovery is generally better for comprehension defects than for output problems
• Aphasic syndromes caused by smaller lesions (e.g., conduction aphasia) characteristically show a better overall improvement
• While early treatment is recommended, evidence suggests that treatment begun late can also be successful

Language Deficits can occur in basic skill areas

(Goodglass Kaplan)

1. Auditory Comprehension
2. Visual Comprehension – e.g., alexia; a disturbance of reading is commonly associated with impaired comprehension of auditory material, they can occur independently too
3. Articulation – may be due to 3 different causes:
   1. dysarthria – defect in mechanisms of speech (larynx, pharynx and tongue)
   2. deficit in motor system w/c prevents desired sound from being pronounced properly
   3. defect in choosing the desired sound
4. Paraphasia- the production of unintended syllables, words or phrases during the effort to speak. Differs from difficulties in articulation, b/c the sounds are correctly pronounced by they are the wrong sounds and either distort the intended words (e.g., pike instead of pipe) or produce completely unintended words (e.g., my mother instead of my wife)
5. Loss of grammar and syntax
6. Repetition – may result from deficits in comprehension or articulation or from a selective dissociation b/t the two centers involved in this task (in this latter type, repetition may be the only deficit seen)
7. Verbal Fluency – ability to produce words in uninterrupted strings. Low verbal fluency may be due to word-finding difficulties or frontal lesions
8. Writing – may be disturbed by:
   1. deficits in movement in limb to produce letters (but not considered a language impairment)
   2. an inability to recall the form of letters – agraphia
9. many of the deficits observed in language may also occur in written language (e.g., paragraphia – writing the incorrect word)
10. Prosody – tone or accent of language

• fluent aphasias – fluent speech but difficulties either in auditory verbal comprehension and/or the repetition of words, phrases or sentences spoken by others

• nonfluent aphasias – difficulties in articulating but relatively good auditory verbal comp.

• “pure aphasias” – selective impairments of reading (alexia w/o agraphia), writing (agraphia) or recognition of words (word deafness).

Assessments of Aphasia

• look at the way patient relates to you
• auditory and verbal comprehension
• cadence, inflections, prosody
• oral and written expression
• tests of repetition, reading, naming and fluency
• conversational speech
• word string length

Differential Diagnosis

• Aphemia – (coined by Broca) disturbance of motor verbal output alone; occurs when pathology affects the left medial frontal cortex, the supplementary motor area, and/or the cingulate gyrus
  • Mutism or severely sparse verbal output with normal language characteristics is noted originally, usually accompanied by akinesia or paresis of the contralateral lower extremity and proximal upper extremity
• lesions of the subcortical structures) or subcortical white matter in the dominant hemisphere can produce aphasia that can be mistaken for a cortical lesion

Rehabilitation of Aphasia

• Limited evidence to support efficacy of aphasia therapy, though some patients clearly benefit
• considerable spontaneous recovery usually occurs during 1st month post onset and continuing for several months
• recovery of fxn is rarely complete

Broca’s Aphasia

damage to the 3rd frontal convolution/frontal operculum of left frontal lobe (Brodman’s areas 44 & 45) often involves subcortical involvement (e.g., white matter, basal ganglia), can also affect areas 6 and 47 fxn of Broca’s area – specialized for producing motor programs for speech (the “motor image of the word.”

Frequent etiology – CVA of dominant (left) MCA (superior division)

Fluency

• nonfluent output; loss of melody
• person speaks in a very slow, deliberate manner w/very simple grammatical structure and limited prosody
• limited use of verbs, adjectives, adverbs, and articles – only key words are used

syntax

• agramaticism, content but limited function words

repetition

• poor, but can be superior to spontaneous speech

naming/word finding

• can have poor naming (aided by cueing, either contextual or phonetic)

comprehension

• intact, except for syntactically dependent structures

reading comprehension

• generally intact, although trouble comprehending function words

reading aloud/writing

• slow, effortful, agrammatic quality simlar to deficits in spoken language

associated symptoms

• may have right hemiplegia (which can affect written output) and/or ideomotor apraxia affecting the “good” side; dysarthria

psychological presentation

• frustrated and aware of deficits

Big vs. Little

• “Big Broca’s” is caused by large lesions (usually left MCA superior division infarct) and starts with global aphasia improving to Broca’s aphasia • “Little Broca’s” is caused by smaller, more localized lesions and starts with Broca’s aphasia and improves to naming difficulties and mildly decreased fluency

Wernicke’s Aphasia

damage to the 1st temporal gyrus (Heschel’s gyrus); the auditory association cortex (area 40) (can also involve areas 22, 37, and 21)

fxn of Wernicke’s area – center of language comprehension most common etiology – infarct in left MCA (inferior division)

fluency

• fluent verbal output, normal rate, articulation, melody and inflection; but contaminated w/paraphasias and neologisms (new words, whose meaning may only be known to the patient; word salad)
• paraphasias can be both semantic e.g., “ink” for “pen”, and phonemic e.g., “pish” for “fish”

syntax – normal syntax but empty speech

repetition

• disturbed; anomia is common and prompting is rarely helpful

naming

• poor

comprehension

• inability to comprehend words or to arrange sounds into coherent speech

writing

• impairment in writing b/c they cannot categorize the sounds so cannot transcribe sounds into correct graphemes

reading

• poor like speech, but reading may not be equal to spoken language

associated symptoms

• some patients have a contralateral, superior quadrantanopsia; apraxia (difficult to elicit due to impaired comprehension) may also have anosognosia.

psychological presentation

• may be anxious because of changes in communication, agitated or may demonstrate a total lack of concern
• Luria proposed there are 3 characteristics of this disorder:

1. the inability to isolate the significant phonemic characteristics and to classify sounds into known phonemic systems
2. defect in speech due to confusion of phonetic characteristics; word salad
3. impairment in writing b/c cannot discern phonemic characteristics, and therefore graphemes (letter representation of phonemes) to form the word

Transcortical Motor Aphasia

can repeat and understand words and name objects, but cannot speak spontaneously or unable to comprehend words although they can still repeat them

general characteristics

• like Broca’s aphasia (i.e., impaired fluency with normal comprehension) but repetition is spared

location of lesion

• believed to be due to loss of the secondary sensory cortex (association cortex) – border zone of parietal lobe

most common etiology

• watershed infarct of MCA-ACA branch that destroys the frontal lobe areas connected to Broca’s areas without afecting connections b/t Broca’s and Wernicke’s areas

Mixed Transcortica

• analogous except able to repeat
• Doesn’t speak unless spoken to
• Echos
• No conversational speech

Transcortical Sensory Aphasia

Location

• border zones, temporal/parietal lobes

• Like Wernicke’s (i.e., impaired comprehension but normal fluency) but repetition is spared

Fluency

intact, but paraphasias sometimes present

Syntax

• good, but empty content

Repetition

• good (unlike Wernicke’s)

Naming

• impaired

Comprehension

• good

Reading

• poor comprehension

Writign

• poor

Associated symptoms

• echolalic, sometimes agitated

Most common etiology

• watershed infarct of MCA-PCA that destroys parietal and/or temporal connections to Wernicke’s w/o afecting conections between Broca’s and Wernicke’s areas

Mixed Transcortical Aphasia

isolation of the speech area Like global aphasia (i.e., impaired fluency AND comprehension) but repetition is spared

– most common cause is combined watershed infarcts of MCA-ACA and MCA-PCA branches but also can be due to subcortical lesion

Fluency

• does not speak unless spoken to; echolalic

word finding

• poor

repetition

• Relatively preserved

comprehension

• poor

reading/writing

• poor

location

• Anterior & posterior border zones, generally due to hypoxia, head trauma or acute carotid occlusion

most common etiology

• watershed infarcts of MCA-ACA an MCA-PCA branches, but also can be due to subcortical lesions

Conduction Aphasia

best characterized by paraphasias

Fluency

• intact, but paraphasic output (literal paraphasias)

repetition

• impaired

Naming

• somewhat impaired due to phonemic paraphasias

comprehension

• intact

reading

• aloud impaired, but reading for comprehension intact

writing

• impaired, but less than speech

associated symptoms

• bilateral apraxia to command or imitation; sometimes hemiparesis or sensory loss
• different from Wernicke’s b/c comprehension is clearly better; different from Broca’s b/c of fluent speech
• location of lesion – the arcuate fasciculus (white matter) w/c connects Broca’s area and Wernicke’s area **but there has never been any proof that cutting these connections actually cause this symptom and there is debate as to whether this symptom really occurs in isolation

• often confused with Wernicke’s aphasia but comprehension is intact

Anomic Aphasia

can comprehend speech, produce meaningful speech and can repeat speech but have difficulty finding the names of objects

fluency

• intact

repetition

• intact

comprehension

• intact

reading/writing

• usually good (except for word-finding problems in writing)
• often find this upon recovery from other aphasias

lesion

• most likely the angular gyrus but nearly all aphasics have naming difficulties

Global Aphasia

Fluency/Repetition/Comprehension

• all aspects of language are involved
• severe, non-fluent output, severe disruption in comprehension, little or no ability to repeat

reading/writing

• also disturbed

Lesion

• degree of impairment and localization may vary considerably, usually w/damage to the middle cerebral artery
• a very large lesion affecting left frontal/parietal/temporal areas

associated symptoms

• Right hemiparesis, hemisensory loss; hemianopsia

most common etiology

• large left MCA infarcts affecting both superior and inferior divisions and with large subcortical lesions (can also be seen in initial stages of large left MCA superior infarcts that eventually improve to Broca’s aphasia)

Subcortical Aphasia

frequently a transient condition considerable variation in the clinical picture – depends on structures involved

• acute onset – usually mutism or hypophonic voicing and hemiparesis and/or hemisensory loss
• improves to paraphasic output, nonaphasic state or residual aphasia

fluency

• mutism, hypophonic, poor articulation

repetition

• better than speech due to fewer paraphasias and no dysarthria

comprehension

• variable, but often relatively good

location of lesion

• associated w/damage to basal ganglia (caudate and putamen) and thalamus as well as in the SMA

associated symptoms

• some patients show spastic dysarthria (high pitched, slow and effortful speech) – others produce hyper or hypokinetic speech (i.e., rapid or slowed speech with slurred articulation)

Subcortical Type I

Anterior superior extension

fluency

• short phrases, impaired articulation

repetition

• poor for low frequency phrases

comprehension

• intact for semantic comprehension, but poor for syntactic comprehension

writing

• poor

associated symptoms

• right hemiplegia

Subcortical Type II

Posterior extension

fluency

• intact, but with paraphasias

repetition

• poor

comprehension

• poor, but better than Wernicke’s

naming/word finding

• impaired letters, but better than objects

Reading/writing

• poor

associated symptoms

• right hemiplegia

Subcortical Type III

Posterior and anterior extension

• global aphasia

Pure Word Deafness

apperceptive auditory agnosia does not understand language and can’t repeat

fluency

• intact

repetition

• Impaired

comprehension

• impaired
• may complain that speech is muffled or foreign
• slowing of presentation may sometimes improve comprehension
• good hearing and identification of non-verbal sounds

reading , writing and speaking

• usually intact

paralinguistic features

• may be preserved (e.g., able to tell who is speaking, identification of certain languages by their accent or language features, emotional expression of speech)

location of lesion

• bilateral (some unilateral) symmetrical cortical-subcortical lesions of superior temporal gyri (with some sparing of Heschel’s gyrus on the left); bilateral discnxn of Wernicke’s area from auditory input