Aphaxia

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Aphasia is a language disorder caused by brain damage - typically a stroke, head injury, or tumor - affecting the ability to speak, understand speech, read, or write. It results from damage to language areas in the dominant (usually left) hemisphere, particularly Broca's area (frontal lobe) or Wernicke's area (temporal lobe).
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aphasia classification treatment

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I now have comprehensive content from Bradley & Daroff's Neurology. Here is the full answer:

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:
  1. Spontaneous speech - fluent vs. nonfluent?
  2. Naming - ask the patient to name objects
  3. Auditory comprehension - yes/no questions, pointing commands
  4. Repetition - repeat phrases of increasing complexity
  5. Reading - both aloud and for comprehension
  6. 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.
FeatureFinding
Spontaneous speechNonfluent, mute, telegraphic (agrammatism) - e.g., "wife come hospital"
NamingImpaired (tip-of-tongue phenomenon; literal paraphasias)
ComprehensionRelatively intact (mild difficulty with complex syntax)
RepetitionImpaired
ReadingOften impaired ("third alexia")
WritingImpaired - dysmorphic, dysgrammatical
Associated signsRight hemiparesis, hemisensory loss, ± apraxia of left limbs
Lesion: Inferior left frontal lobe (Broca area, BA 44/45) and surrounding structures.

2. Wernicke Aphasia (Fluent)

FeatureFinding
Spontaneous speechFluent (sometimes logorrheic), paraphasias, neologisms, jargon
NamingImpaired (bizarre paraphasic misnaming)
ComprehensionImpaired - even simple commands
RepetitionImpaired
ReadingImpaired comprehension and reading aloud
WritingPreserved 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.
FeatureFinding
SpeechMute or nonfluent
NamingImpaired
ComprehensionImpaired
RepetitionImpaired
Reading/WritingBoth impaired
Associated signsDense 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.
FeatureFinding
SpeechFluent, hesitant, literal paraphasic errors
NamingModerately impaired
ComprehensionIntact
RepetitionSeverely impaired - out of proportion to spontaneous speech
ReadingAloud 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).
TypeSpeechComprehensionRepetitionLesion site
Transcortical MotorNonfluentIntactPreservedAnterior to Broca (ACA-MCA watershed)
Transcortical SensoryFluent, echolalicImpairedPreservedPosterior to Wernicke (MCA-PCA watershed)
Mixed Transcortical (Isolation)Echolalic, no propositional speechImpairedPreservedLarge 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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