Agnosia

ByJuebin Huang, MD, PhD, Department of Neurology, University of Mississippi Medical Center
Reviewed/Revised Aug 2023
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Agnosia is inability to identify an object using one or more of the senses. Diagnosis is clinical, often including neuropsychologic testing, with brain imaging (eg, CT, MRI) to identify the cause. Prognosis depends on the nature and extent of damage and patient age. There is no specific treatment, but speech and occupational therapy may help patients compensate.

Agnosias are uncommon.

Etiology of Agnosia

Agnosia results from damage to (eg, by infarct, tumor, abscess, or trauma) or degeneration of areas of the brain that integrate perception, memory, and identification (eg, Alzheimer disease, Parkinson disease dementia). The area affected is usually the unimodal association cortex for the affected sense.

Types of Agnosia

Discrete brain lesions can cause different forms of agnosia, which may involve any sense. Typically, only one sense is affected:

  • Hearing (auditory agnosia—the inability to identify objects through sound such as a ringing telephone)

  • Taste (gustatory agnosia)

  • Smell (olfactory agnosia)

  • Touch (somatosensory agnosia)

  • Sight (visual agnosia)

For example, patients with somatosensory agnosia have difficulty identifying a familiar object (eg, key, safety pin) that is placed in their hand on the side of the body opposite the damage. However, when they look at the object, they immediately recognize and can identify it.

Other forms of agnosia involve very specific and complex processes within one sense.

Prosopagnosia is inability to identify well-known faces, including those of close friends, or to otherwise distinguish individual objects among a class of objects, despite the ability to identify generic facial features and objects. Prosopagnosia often accompanies damage to the inferotemporal lobe—often bilateral small lesions, especially in the fusiform gyrus.

Anosognosia is lack of awareness that a deficit exists or lack of insight into an existing deficit. It often accompanies damage to the right, nondominant parietal lobe (which is usually due to an acute stroke or traumatic brain injury). Patients with multiple impairments can be unaware of one impairment but fully aware of others. Patients with anosognosia may deny their motor deficit, insisting that nothing is wrong even when one side of their body is completely paralyzed. When shown the paralyzed body part, patients may deny that it is theirs.

In an often related phenomenon, patients ignore the paralyzed or desensitized body parts (hemi-inattention) or the space around them (hemineglect). Hemineglect most often involves the left side of the body.

Simultanagnosia is inability to see more than one object or component of an object at a time; patients cannot perceive a whole scene. For example, when shown a picture of a kitchen table with food and various utensils on it, they report seeing only one item, such as a spoon. Simultanagnosia usually results from damage to the bilateral parieto-occipital junction.

Balint syndrome is the triad of simultanagnosia, optic ataxia (misreaching for visual targets), and ocular apraxia (inability to control voluntary eye movements, although the eyes can move spontaneously in all directions). Balint syndrome appears to be perceptual-motor dysfunction that affects the heteromodal cortex of bilateral dorsal occipitoparietal areas.

Occipitotemporal lesions may cause agnosia associated with abnormalities in visual perception including

  • An inability to recognize familiar places (environmental agnosia)

  • Visual disturbances (visual agnosia)

  • Color blindness (achromatopsia)

Right-sided temporal lesions may cause

  • An inability to interpret sounds (auditory agnosia)

  • Impairment of music perception (amusia)

Diagnosis of Agnosia

  • Neurologic examination

  • Neuropsychologic testing

  • Brain imaging

At bedside, patients are asked to identify common objects through sight, touch, or another sense. If hemineglect is suspected, patients are asked to identify the paralyzed parts of their body or objects in their hemivisual fields.

A more detailed neurologic examination is done to detect primary deficits in individual senses or in the ability to communicate that may interfere with testing for agnosias. For example, if light touch is defective, patients may not sense an object even when cortical function is intact. Also, aphasias may interfere with patient’s expression.

Neuropsychologic testing may help identify more subtle agnosias. Neuropsychologic testing is standardized testing that provides information about the brain’s structural and functional integrity. It evaluates intelligence, executive function (eg, planning, abstraction, conceptualization), attention, memory, language, perception, sensorimotor functions, motivation, mood and emotion, quality of life, and personality.

Brain imaging (eg, CT or MRI with or without angiographic protocols) is required to characterize a central lesion (eg, infarct, hemorrhage, mass) and to check for atrophy suggesting a degenerative disorder.

Treatment of Agnosia

  • Treatment of the cause

  • Speech or occupational therapy

When possible, the cause of agnosia is treated (eg, surgery and/or antibiotics for cerebral abscess, surgery and/or radiation for brain tumor).

Rehabilitation with speech or occupational therapists can help patients learn to compensate for their deficits.

Prognosis for Agnosia

Recovery from agnosia may be influenced by the

  • Type, size, and location of lesions

  • Degree of impairment

  • Patient age

  • Effectiveness of therapy

If the cause is self-limited or reversible, most recovery occurs within the first 3 months, but recovery may continue to a variable degree up to a year.

Key Points

  • Agnosias are uncommon but may affect any sense.

  • Diagnose agnosias by asking patients to identify objects or, for subtle agnosias, by doing neuropsychologic tests.

  • Do brain imaging to characterize the causative lesion.

  • Recommend rehabilitation with speech or occupational therapy to help patients compensate for deficits.

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