Language impairment (aphasia)

Page most recently updated 7 September 2026

This page focuses on presentations with language-predominant cognitive impairment of insidious onset and progressive course suggestive of a neurodegenerative process. Key differential diagnoses to consider include:

  • Logopenic variant primary progressive aphasia (lvPPA)

  • Nonfluent/agrammatic variant primary progressive aphasia (nfvPPA)

  • Semantic variant primary progressive aphasia (svPPA)

  • Corticobasal syndrome (CBS)

  • Progressive supranuclear palsy (PSP)

The approach below begins with relevant features on history and neurocognitive testing, followed by the relevant differential diagnoses, with further distinctive history and examination findings provided for each diagnosis.

● History (direct and collateral)

  • Symptoms reported or elicited typically include difficulty with:

◦ Language expression difficulties (in speaking or writing), such as:

Word-finding difficulties (e.g., forgetting names of people or common objects, needing to ‘talk around a word’ by paraphrasing it)

Paraphasic errors, including phonemic and/or semantic

Difficulty understanding the meaning of words

Speech that is difficult to understand or lacks clear meaning

Reduced speech output (e.g., speaking only in short utterances or a few words at a time)

◦ Language comprehension difficulties (e.g., in following complex or simple instructions, via listening or reading)

  • Along with the above features, screening can also be performed for prosopagnosia. Although not technically a form of language impairment, prosopagnosia can be a feature of svPPA. In addition to difficulty recognizing familiar people, patients may also have difficulty recognizing familiar objects or familiar places, such as their own home.

● Neurocognitive testing

For patients with language-predominant cognitive impairment, neurocognitive testing should assess language and related cognitive functions across the major relevant domains. The purpose is not to administer a comprehensive battery of language-related tasks, but to assess the specific language functions that help characterize the clinical phenotype and distinguish the major differential diagnoses. Examples of initial screening tasks are typically incorporated into commonly used neurocognitive screening instruments, such as the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA).

1. Naming

a. Initial screening tests

• Asking the patient to name objects that vary in familiarity and specificity, progressing from common whole objects to less familiar objects or individual components of familiar objects.

b. Supplementary tests

• Multilingual Naming Test
• Boston Naming Test
• ACE-III naming task

Impaired naming may occur across the major language-predominant neurodegenerative syndromes. The pattern and context of the naming impairment are therefore important, with prominent anomia accompanied by impaired semantic knowledge supporting svPPA, while anomia with impaired repetition, particularly sentence or phrase repetition, may occur in lvPPA.

2. Semantic knowledge

a. Initial screening tests

• Asking the patient to describe the meaning of familiar objects.

b. Supplementary tests

• Semantic knowledge tests

Impaired semantic knowledge is particularly suggestive of svPPA, in which loss of knowledge about the meaning of words, objects, and concepts is a defining feature.

3. Repetition

a. Initial screening tests

• Asking the patient to repeat individual words and increasingly complex phrases or sentences.

b. Supplementary tests

• Sentence repetition tests

Impaired repetition, particularly for longer phrases or sentences, accompanied by word-finding difficulty or phonological errors, may support lvPPA.

4. Comprehension

a. Initial screening tests

• Asking the patient to follow verbal instructions of increasing length and complexity, including instructions requiring the patient to perform actions in a specified sequence (such as a three-stage command).

b. Supplementary tests

• Sentence comprehension tasks assessing grammatical comprehension

Impaired grammatical or complex sentence comprehension may support nfvPPA, particularly when accompanied by agrammatism or effortful speech.

5. Reading and writing

a. Initial screening tests

• Asking the patient to read a short passage and produce a written sentence.

b. Supplementary tests

• Written and oral description of the Cookie Theft picture

Abnormalities of reading or writing may occur in several language-predominant neurodegenerative syndromes and should be interpreted in the context of the broader language profile. They may also provide additional information when distinguishing a primary language disorder from a more focal cortical syndrome such as CBS.

Along with the above language domains, screening can also be performed for impaired recognition of familiar faces, which may support svPPA, particularly when accompanied by impaired semantic knowledge. This can be assessed by asking the patient to identify familiar people from photographs, particularly well-known public figures or people personally familiar to the patient. Formal assessment of facial recognition may be considered where indicated.

● Interpretation in the differential diagnosis

The pattern of language impairment should be interpreted together with the history and neurological examination. A language-predominant presentation with prominent semantic impairment supports svPPA; impaired repetition, particularly for longer or phonologically complex material, supports lvPPA; and grammatical or sentence-comprehension abnormalities accompanied by effortful or agrammatic speech support nfvPPA.

Language impairment accompanied by asymmetric motor or cortical findings raises consideration of CBS, while language impairment accompanied by characteristic oculomotor, axial, postural, or gait abnormalities raises consideration of PSP. These neurological findings are therefore particularly important when distinguishing CBS or PSP from a primary progressive aphasia.

● Differential diagnoses, including distinctive history and examination findings

▪ Semantic variant primary progressive aphasia

Patients typically initially present with progressive anomia accompanied by loss of knowledge about the meaning of words, objects, or concepts. Prosopagnosia may also occur, particularly as the disorder progresses. Neurocognitive testing typically demonstrates impaired naming and semantic knowledge, with impaired single-word comprehension and other semantic deficits. svPPA is most commonly associated with frontotemporal lobar degeneration, particularly TDP-43 pathology, although other underlying pathologies may occur. The neurological examination is often initially unremarkable, although some patients may subsequently develop parkinsonism or motor neuron disease, with upper and/or lower motor neuron signs.

▪ Logopenic variant primary progressive aphasia

Patients typically initially present with word-finding difficulty and anomia, often with circumlocution and difficulty repeating phrases or sentences. Neurocognitive testing typically demonstrates impaired naming and verbal working memory, with impaired sentence repetition and possible phonological errors. lvPPA is most commonly associated with Alzheimer disease pathology, although other underlying pathologies may occur. General physical and neurological examination, including cranial nerves, motor examination, and gait, is typically unremarkable in the early stages.

▪ Nonfluent/agrammatic variant primary progressive aphasia

Patients typically initially present with effortful, halting speech, often accompanied by agrammatism, impaired sentence construction, or apraxia of speech. Anomia may also occur, with circumlocution and other word-finding difficulties. Neurocognitive testing typically demonstrates language impairment with prominent deficits in grammatical processing and/or speech production, with other cognitive domains variably affected. On neurological examination, findings may initially be normal, although some patients develop parkinsonism or motor neuron disease, with upper and/or lower motor neuron signs such as hyperreflexia, pathological reflexes, weakness, or muscle wasting.

▪ Corticobasal syndrome

Patients may initially present with language dysfunction, executive dysfunction, apraxia, visuospatial impairment, and/or slowed cognition, which may be accompanied by asymmetric motor or cortical features. Neurocognitive testing typically supports the predominant cognitive deficit and may reveal additional executive, language, visuospatial, or other cognitive dysfunction. On neurological examination, there is typically markedly asymmetric rigidity and parkinsonism, often accompanied by limb apraxia, cortical sensory abnormalities, alien-limb phenomena, dystonia, or myoclonus. Hyperreflexia or other upper motor neuron features may also occur, and gait may show a combination of parkinsonian and hemiparetic features. CBS may result from corticobasal degeneration or other underlying neurodegenerative pathologies, including Alzheimer disease and progressive supranuclear palsy.

▪ Progressive supranuclear palsy

Patients may initially present with slowed cognition, executive dysfunction, or language dysfunction, often accompanied by early falls or postural instability. PSP can present with several clinical phenotypes, including a frontal-predominant phenotype (PSP-F) with prominent executive and behavioural dysfunction, a speech/language-predominant phenotype (PSP-SL), and phenotypes characterised predominantly by parkinsonism, gait freezing, or postural instability. Neurocognitive testing typically demonstrates executive dysfunction and slowed processing, with other cognitive domains variably affected. On cranial nerve examination, there may be slowing of vertical saccades or a supranuclear limitation of vertical gaze (limited range of voluntary gaze with relative preservation of range on the vestibulo-ocular reflex [doll’s-eye manoeuvre]), particularly affecting downgaze. There is typically axial-predominant rigidity, and gait may be stiff and shuffling, with reduced stride length, freezing, early postural instability, retropulsion, and falls.

Selected references and further reading — Cognitive lens

Tang-Wai DF, Freedman M. Bedside approach to the mental status assessment. Continuum (Minneap Minn). 2018 Jun;24:672-703.

Hodges JR. Cognitive assessment for clinicians. 3rd ed. Oxford: Oxford University Press; 2017.

Dickerson BC, Atri A, editors. Dementia: comprehensive principles and practices. Oxford: Oxford University Press; 2014.

Jankovic J, Mazziotta JC, Pomeroy SL, Newman NJ, editors. Bradley and Daroff's neurology in clinical practice. 8th ed. Philadelphia: Elsevier; 2022.

Dening T, Thomas A, editors. Oxford textbook of old age psychiatry. 3rd ed. Oxford: Oxford University Press; 2021.

Blazer DG, Steffens DC, Busse EW, editors. The American Psychiatric Publishing textbook of geriatric psychiatry. 5th ed. Washington (DC): American Psychiatric Publishing; 2015.

Arciniegas DB, Yudofsky SC, Hales RE, editors. The American Psychiatric Association Publishing textbook of neuropsychiatry and clinical neurosciences. 6th ed. Washington (DC): American Psychiatric Association Publishing; 2018.

Agrawal N, Faruqui R, Bodani M, editors. Oxford textbook of neuropsychiatry. Oxford: Oxford University Press; 2020.

Boland R, Verduin M, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 11th ed. Philadelphia: Wolters Kluwer; 2024.