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ULY CLINIC

ULY CLINIC

17 Mei 2025, 12:04:06

Aphasia

Aphasia
Aphasia
Aphasia

Aphasia, also known as dysphasia, is a neurological disorder characterized by impairment in the expression or comprehension of spoken and written language. It reflects damage to the brain's language centers, typically located in the dominant (usually left) hemisphere. Aphasia can range from mild communication difficulties to complete inability to use or understand language, profoundly impacting patient quality of life. Understanding the types, causes, clinical presentation, and management is essential for health professionals to optimize patient outcomes.


Pathophysiology and types of Aphasia

Aphasia results from damage to key brain areas involved in language processing, predominantly:

  • Broca’s area: Adjacent to the motor cortex, responsible for speech production.

  • Wernicke’s area: Center for language comprehension, situated near the auditory cortex.

  • Arcuate fasciculus: A nerve bundle connecting Broca’s and Wernicke’s areas, enabling speech repetition.


 Types of aphasia – Summary table 1

Type

Location of Lesion

Signs and Symptoms

Anomic Aphasia

Temporal-parietal area; may extend to angular gyrus; often poorly localized

- Fluent speech lacking meaningful content - Word-finding difficulty, circumlocution - Understanding of language relatively intact - Rare paraphasias

Broca's Aphasia (Expressive)

Broca’s area (3rd frontal convolution, usually in left hemisphere)

- Nonfluent, effortful speech - Limited vocabulary, simple sentence construction - Cannot repeat words/phrases - Relatively good comprehension - Often hemiparetic - Recognizes own errors (if Wernicke’s intact)

Global Aphasia

Broca’s and Wernicke’s areas

- Severe impairment in both understanding and producing speech - Cannot repeat or follow directions - Occasional jargon or paraphasias

Wernicke's Aphasia (Receptive)

Wernicke’s area (posterior/superior temporal lobe)

- Fluent, often rapid and rambling speech - Poor comprehension of spoken and written language - Cannot repeat words/phrases - Paraphasias and anomia - Unaware of errors

Based on the lesion location and severity, aphasia is classified as:

  • Broca’s aphasia: Non-fluent speech with relatively preserved comprehension.

  • Wernicke’s aphasia: Fluent but often nonsensical speech with poor comprehension.

  • Anomic aphasia: Difficulty naming objects; often improves over time.

  • Global aphasia: Severe impairment of both expression and comprehension; usually irreversible.


Etiology

Aphasia commonly arises due to te following medical condition as described in table 2

Medical causes of aphasia – Summary table 2

Condition

Type of Aphasia

Onset

Associated Signs & Symptoms

Alzheimer’s Disease

Anomic → Global (progressive)

Insidious

Memory loss, poor judgment, behavioral changes, myoclonus, rigidity, late incontinence

Brain Abscess

Any type

Insidious

Hemiparesis, ataxia, facial weakness, increased intracranial pressure (ICP)

Brain Tumor

Any type (progressive)

Progressive

Behavioral/memory changes, weakness, seizures, hallucinations, visual deficits, ↑ICP

Creutzfeldt-Jakob Disease

Aphasia with dementia

Rapid onset

Myoclonus, ataxia, paralysis, visual disturbances, rapid decline in cognition

Encephalitis

Usually transient

Sudden

Fever, headache, vomiting, seizures, stupor/coma, nystagmus, ocular palsies, facial weakness

Head Trauma

Any type

Sudden

Blurred vision, headache, CSF leak, paresis, behavior changes, ↑ICP

Seizures

Transient (postictal)

Sudden

Confusion, brief language dysfunction if language areas involved

Stroke

Wernicke’s, Broca’s, Global

Sudden

Hemiparesis, ↓LOC, hemianopsia, paresthesia, sensory loss

Transient Ischemic Attack (TIA)

Any type (resolves < 24 hrs)

Sudden/temporary

Hemiparesis, hemianopsia, paresthesia, dizziness, confusion

Clinical presentation

Patients with aphasia present with:

  • Impaired speech fluency or comprehension depending on aphasia type.

  • Associated neurological deficits such as hemiparesis, ataxia, or cranial nerve abnormalities.

  • Signs of increased intracranial pressure (ICP) in cases of tumors or abscesses: vomiting, altered consciousness, pupillary changes.

  • Confusion, disorientation, or frustration due to communication difficulties.

It is important to differentiate aphasia from dysarthria and speech apraxia, which affect speech production without language impairment.


Diagnostic evaluation

  • History and Physical Examination: Obtain history from family if needed; assess language function, neurological status, and vital signs.

  • Neuroimaging:

    • CT or MRI to detect stroke, tumors, or hemorrhage.

    • Angiography in vascular pathology.

  • Functional Assessments:

    • Speech and language evaluation by a speech pathologist.

    • Electroencephalogram (EEG) if seizures suspected.

  • Laboratory Tests:

    • Infection markers in encephalitis or abscess.

    • Blood tests for metabolic or systemic causes.

  • Endoscopic or other specialized assessments if indicated.


Emergency interventions

  • Monitor and manage signs of increased ICP using mannitol and supportive care.

  • Prepare for emergency neurosurgical interventions if indicated.

  • Stabilize airway, breathing, and circulation.

  • Address underlying cause promptly (e.g., thrombolysis for stroke if within therapeutic window).


Management

  • Acute phase: Treat underlying cause (e.g., stroke, infection, tumor).

  • Supportive care: Ensure patient safety, nutrition, hydration, and prevention of complications.

  • Speech and language therapy: Early referral to speech pathologists to improve communication.

  • Psychological support: Address depression and frustration; educate family and caregivers.

  • Communication aids: Use nonverbal tools like communication cards, gestures, and simple language.

  • Risk factor modification: Manage hypertension, diabetes, smoking cessation to prevent recurrent stroke.


Special considerations

  • Patients may show confusion or disorientation; reorient frequently.

  • Expect emotional outbursts linked to frustration; respond gently and supportively.

  • Avoid speaking loudly or slowly with a condescending tone; aphasia is a language disorder, not a hearing or intellectual problem.

  • Ensure visual and dental aids are used to facilitate communication.


Patient and family counseling

  • Educate on the nature of aphasia and prognosis.

  • Train families on alternative communication strategies and patience.

  • Stress importance of rehabilitation adherence and risk factor control.


Conclusion

Aphasia is a complex disorder necessitating multidisciplinary care. Prompt recognition, thorough evaluation, targeted treatment of underlying causes, and supportive rehabilitation can significantly improve functional outcomes. Health professionals play a vital role in diagnosis, emergency management, ongoing therapy coordination, and patient-centered communication to enhance quality of life.


References
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  2. Koedam EL, Lauffer V, van der Vlies AE, van der Flier WM, Scheltens P, Pijnenburg YA. Early-versus late-onset Alzheimer’s disease: More than age alone. J Alzheimers Dis. 2010;19(4):1401–8.Damasio AR. Aphasia. N Engl J Med. 1992;326(8):531-9.

  3. Kertesz A. Clinical Neuropsychology and Aphasia. 2nd ed. San Diego: Academic Press; 1994.

  4. Goodglass H, Kaplan E, Barresi B. The Assessment of Aphasia and Related Disorders. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001.

  5. Caplan D. Neurolinguistics and Linguistic Aphasiology. Cambridge: Cambridge University Press; 1987.

  6. Hillis AE. Aphasia: Progress in the last quarter of a century. Neurology. 2007;69(2):200-13.

  7. Broca P. Remarques sur le siège de la faculté du langage articulé. Bull Soc Anat (Paris). 1861;6:330-57.

  8. Wernicke C. Der aphasische Symptomenkomplex. Breslau: Cohn & Weigert; 1874.

  9. Mesulam MM. Primary progressive aphasia. Ann Neurol. 2001;49(4):425-32.

  10. World Health Organization. Neurological Disorders: Public Health Challenges. Geneva: WHO; 2006.

  11. Adams RD, Victor M, Ropper AH. Principles of Neurology. 6th ed. New York: McGraw-Hill; 1997.

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