Language is a uniquely human cognitive function that involves the use of symbols for communication. It can be expressed through various modalities, such as speaking, writing, or signing. Language processing is highly complex and involves a network of interconnected brain regions, primarily localized in the left hemisphere for the majority of individuals. While classic models of language processing have focused on specific areas like Broca's area (expressive language planning) and Wernicke's area (comprehension), recent functional imaging studies suggest that language function is mediated by larger, distributed global networks across the brain.

What is aphasia and what are some classic aphasia syndromes?

Aphasia is a disorder characterized by dysfunction in the brain's language network. It results in impairments in the ability to understand or produce language. Classic aphasia syndromes, based on older connectionist models, include Broca's aphasia (difficulty with speech production), Wernicke's aphasia (difficulty with comprehension), Global aphasia (impairment in all language processing), Conduction aphasia (difficulty with repetition), and Anomic aphasia (difficulty with word finding). Each syndrome is typically associated with damage to specific brain regions, although newer research indicates language processing is more broadly distributed.

Language function is divided into expressive and receptive domains. Each domain encompasses several components:

These domains work in tandem and are differentially impaired in various types of aphasia.

What is the neuroanatomical basis of language function?

Language is supported by a widely distributed left-dominant perisylvian network. Key regions include:

Damage to these areas, or to the white matter tracts that connect them, results in characteristic language syndromes.

How does damage to subcortical structures affect language?

While language function is predominantly associated with cortical areas, injury to subcortical structures can also lead to aphasia. Thalamic aphasia, resulting from damage to the left thalamus, can present as a fluent aphasia with relatively preserved comprehension and repetition, sometimes resembling transcortical sensory aphasia. Striatal-capsular aphasia, caused by lesions in the left caudate nucleus, putamen, and surrounding white matter, often presents as a nonfluent aphasia and can be associated with motor deficits due to involvement of the internal capsule. Thalamic aphasias are generally fluent, while striatal-capsular aphasias are typically nonfluent, although this distinction is not universal.

What are aprosodias and alexias?

Aprosodias are disorders affecting prosody, the rhythm and intonation of speech which conveys emotional information and clarifies meaning. Injury to the right hemisphere, analogous to the left hemisphere's role in language, can impair the production, comprehension, and repetition of prosody. Alexias are reading impairments. There are three types: Alexia with agraphia (inability to read and write, often associated with left inferior parietal lobule lesions), Alexia without agraphia (inability to read with intact writing, typically linked to lesions in the left medial occipitotemporal junction), and Alexia associated with aphasia (alexia occurring as part of a broader aphasia syndrome).

What disorders commonly affect language?

Beyond focal brain lesions like stroke, traumatic brain injury, and brain tumors, many neurodegenerative disorders progressively impact language function. Alzheimer disease often initially presents with memory impairment and anomia (difficulty naming), although some individuals have a primary language presentation. Primary progressive aphasias (PPAs) are a group of neurodegenerative syndromes where language disturbance is a defining feature early in the disease. These include the agrammatic variant (impaired grammar and nonfluent speech), semantic variant (anomia and impaired single word comprehension), and logopenic variant (nonfluent speech with word-finding pauses and repetition difficulties). PPAs can have underlying Alzheimer disease or frontotemporal lobar degeneration pathology.

Language dysfunction may arise from a wide variety of structural, degenerative, or systemic causes. These include:

• Primary progressive aphasia (PPA):
  • Nonfluent/agrammatic variant (nfvPPA) – effortful speech, grammar errors
  • Semantic variant (svPPA) – fluent but empty speech, loss of word meaning
  • Logopenic variant (lvPPA) – word-finding pauses, impaired repetition
• Stroke (left MCA territory):
  • Broca's, Wernicke's, conduction, transcortical, global aphasia
• Alzheimer's disease:
  • Logopenic features, anomia, circumlocution
• Frontotemporal dementia (FTD):
  • Often overlaps with semantic and agrammatic profiles
• Other causes:
  • Tumor, traumatic brain injury, encephalitis, epilepsy, developmental disorders

What are the characteristics of psychogenic or functional language disorders?

Functional or psychogenic language disorders occur without a clear underlying medical condition that accounts for the symptoms. They can manifest as atypical halting or stuttering speech. Clues suggesting a psychogenic origin include the absence of a medical cause, late-onset or progressively worsening symptoms, inconsistent speech patterns, and significant distress about the condition. Factors like psychological trauma, histrionic personality traits, and potential secondary gains can be associated with these disorders. Diagnosis involves a thorough medical and neurological workup to exclude organic causes, and treatment often involves psychotherapy.

How is language function assessed in a clinical setting?

Language function can be assessed through both bedside testing and formal neuropsychological evaluation. Bedside testing involves observing spontaneous speech, testing comprehension (verbal and written), repetition, naming, and writing. Observing for paraphasic errors (unintended word or sound substitutions) and testing for apraxia of speech (a motor speech disorder) are also part of this. Neuropsychological testing offers a more comprehensive and objective assessment using standardized tests with normative data. It provides detailed evaluation of expressive and receptive language, repetition, naming, verbal fluency, and sometimes prosody, accounting for demographic factors and premorbid cognitive status.

Diagnosis begins with a detailed clinical interview, often triggered by word-finding complaints or conversational breakdowns. Assessment should evaluate all domains of language:

• Fluency (rate, phrase length, pauses)
• Grammar and syntax (agrammatism, sentence construction)
• Naming (confrontation, generative)
• Repetition (simple to complex)
• Comprehension (words and sentences)
• Semantic knowledge (category-based reasoning, associations)

Standardized screening tools (e.g., MoCA, BDAE short form) can identify gross deficits. Comprehensive evaluation includes formal neuropsychological or speech-language pathology testing.

Neuroimaging (MRI, FDG-PET, amyloid/tau PET) and speech-language evaluation contextualize deficits within disease processes.

How does recovery from language impairment occur and what factors influence it?

Recovery from language impairment depends on the cause and severity of the injury. Neuroplasticity, the brain's ability to reorganize itself, is a mechanism for recovery, with the brain recruiting different areas for language tasks after injury. While the most significant spontaneous recovery often happens in the initial months, speech, physical, and occupational therapies can facilitate improvements. Factors influencing recovery include the size and location of the lesion, the individual's premorbid cognitive status and reserve, emotional state, family support, and access to rehabilitation services. Pharmacological interventions like donepezil have shown some promise in treating poststroke aphasia, and their use in PPA variants is being explored.

Summary Pearls

1. Language function spans expressive and receptive domains; both must be assessed.
2. Aphasia is not a unitary condition but reflects a specific pattern of breakdown.
3. The three PPA variants serve as key models for understanding degenerative language disorders.
4. The left perisylvian network, including Broca's and Wernicke's areas, supports core language functions.
5. Many etiologies are reversible or modifiable; early identification is essential.
6. Neuropsychological and speech-language assessments provide the most detailed insights into language breakdown.