Aphaxia
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Aphasia
Aphasia is an acquired disorder of language - not a disorder of speech articulation or thought - caused by damage to language-dominant (almost always left) cerebral hemisphere areas. It affects the ability to speak, understand, read, and/or write.
Bedside Language Examination
A structured bedside assessment tests:
- Spontaneous speech - fluent vs. nonfluent?
- Naming - ask the patient to name objects
- Auditory comprehension - yes/no questions, pointing commands
- Repetition - repeat phrases of increasing complexity
- Reading - both aloud and for comprehension
- Writing - spontaneous writing and dictation
The results of these, combined with associated neurological signs (e.g., hemiparesis, hemianopia), localize the lesion and classify the aphasia subtype.
Classification of Aphasic Syndromes
(Bradley & Daroff's Neurology in Clinical Practice)
1. Broca Aphasia (Non-fluent)
Named after Paul Broca (1861), who described patients with loss of expressive speech.
| Feature | Finding |
|---|---|
| Spontaneous speech | Nonfluent, mute, telegraphic (agrammatism) - e.g., "wife come hospital" |
| Naming | Impaired (tip-of-tongue phenomenon; literal paraphasias) |
| Comprehension | Relatively intact (mild difficulty with complex syntax) |
| Repetition | Impaired |
| Reading | Often impaired ("third alexia") |
| Writing | Impaired - dysmorphic, dysgrammatical |
| Associated signs | Right hemiparesis, hemisensory loss, ± apraxia of left limbs |
Lesion: Inferior left frontal lobe (Broca area, BA 44/45) and surrounding structures.
2. Wernicke Aphasia (Fluent)
| Feature | Finding |
|---|---|
| Spontaneous speech | Fluent (sometimes logorrheic), paraphasias, neologisms, jargon |
| Naming | Impaired (bizarre paraphasic misnaming) |
| Comprehension | Impaired - even simple commands |
| Repetition | Impaired |
| Reading | Impaired comprehension and reading aloud |
| Writing | Preserved motor writing, but paragraphic errors |
| Associated signs | ± Right homonymous hemianopia; usually NO hemiparesis |
Lesion: Posterior left superior temporal gyrus (Wernicke area, BA 22).
Psychiatric note: Wernicke aphasics often have poor insight (anosognosia), unlike Broca aphasics who are typically aware of their deficit and often depressed.
3. Global Aphasia
Essentially Broca + Wernicke combined.
| Feature | Finding |
|---|---|
| Speech | Mute or nonfluent |
| Naming | Impaired |
| Comprehension | Impaired |
| Repetition | Impaired |
| Reading/Writing | Both impaired |
| Associated signs | Dense right hemiparesis, hemisensory loss, hemianopia |
Lesion: Large left MCA territory infarct involving both frontal and temporal-parietal regions. Recovery may be prolonged - global aphasics can continue improving beyond 6 months.
4. Conduction Aphasia
The hallmark is disproportionately impaired repetition.
| Feature | Finding |
|---|---|
| Speech | Fluent, hesitant, literal paraphasic errors |
| Naming | Moderately impaired |
| Comprehension | Intact |
| Repetition | Severely impaired - out of proportion to spontaneous speech |
| Reading | Aloud impaired; comprehension largely intact |
| Associated signs | ± Apraxia, mild right sensory/motor signs |
Lesion: Arcuate fasciculus (disconnects Wernicke and Broca areas) or supramarginal gyrus.
5. Anomic Aphasia
- Naming is the principal deficit; all other functions largely intact
- Circumlocutions and word-finding pauses in otherwise fluent speech
- Least localizing of all aphasia types; also seen in Alzheimer disease and as a recovery stage of other aphasias
- Severe isolated anomia can point to left temporal lobe (nouns) or frontal lobe (verbs) lesions
6. Transcortical Aphasias
Key feature: Repetition is preserved (the perisylvian circuit is intact; lesions interrupt connections from other cortical areas into it).
| Type | Speech | Comprehension | Repetition | Lesion site |
|---|---|---|---|---|
| Transcortical Motor | Nonfluent | Intact | Preserved | Anterior to Broca (ACA-MCA watershed) |
| Transcortical Sensory | Fluent, echolalic | Impaired | Preserved | Posterior to Wernicke (MCA-PCA watershed) |
| Mixed Transcortical (Isolation) | Echolalic, no propositional speech | Impaired | Preserved | Large watershed infarct or advanced dementia |
Special Subtypes
- Optic aphasia: Cannot name objects presented visually, but can name by touch or when described - lesion disconnects visual input from language
- Tactile aphasia: Cannot name objects by touch, but can describe use
- Congenital aphasia: Failure of normal language development (vs. acquired)
- Primary Progressive Aphasia (PPA): Neurodegenerative aphasia - insidious onset without acute stroke; subtypes include nonfluent/agrammatic (tau pathology), semantic variant (TDP-43), and logopenic variant (Alzheimer pathology)
Epidemiology and Recovery
- In a prospective Danish stroke study, 38% of stroke patients had aphasia on admission; by rehabilitation discharge, only 18% remained aphasic
- Patients with mild aphasia reached peak recovery at 2 weeks; moderate at 6 weeks; severe at 10 weeks
- Only 8% of severe aphasics fully recovered by 6 months
- Best predictor of recovery: less severe initial aphasia
Treatment and Rehabilitation
Speech-language therapy is the mainstay, using:
- Stimulation-facilitation techniques: picture matching, sentence completion, repetition, positive reinforcement
- Phoneme-based treatment: targets phonological production to reduce anomia
- Constraint-induced language therapy: intensive massed practice with phonemic cues - increases use of trained words
- Neurolinguistic assessment: identifies specific impaired units (phoneme, syntax, semantics) to guide targeted therapy
Behavioral approaches address withdrawal and isolation; establishing reliable yes/no responses early is a priority. Activity-dependent plasticity is exploited by linking language tasks to physical activities and daily relevance (Hebbian-type learning).
Sources: Bradley and Daroff's Neurology in Clinical Practice, Chapters 13 & 55; Kaplan & Sadock's Comprehensive Textbook of Psychiatry
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