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Physiology · Systemic Structure of Human Mental Activity

Disorders in parietal cortex lesions

Cortex parietalis

Parietal lobe pathologies lead to specific cognitive and speech disorders caused by a disruption in working memory mechanisms. One of the characteristic manifestations is syndromes in which the patient forgets the names of familiar objects or loses the ability to understand written text while preserving normal hearing and spoken language.

AcalculiaA specific impairment of calculation function in parietal lobe lesions.
Amnestic aphasiaForgetting words (primarily nouns).
Angular gyrusIts isolated damage leads to anomic aphasia.
Pathogenesis of anomiaBlockade of visual information transmission to Wernicke's speech area.
3 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

General lesion symptomatology

Parietal cortex damage is accompanied by a complex of disorders rooted in impairment of the working memory mechanism. Due to this failure, the brain loses the ability to retain and actively use information necessary for current activity.

Key clinical manifestations include:

  • Amnestic aphasia. The patient begins to forget individual words. In the overwhelming majority of cases, nouns are precisely the ones that drop out of the active vocabulary.
  • Substitution symptom. The inability to recall the necessary word is compensated for by verbosity. The patient begins to describe an object through its functions (for example, instead of the word "pen", they say "the thing we usually write with on paper").
  • Acalculia. A pronounced calculation disorder occurs — the patient loses the ability to perform arithmetic operations.

Angular gyrus syndrome (Gyrus angularis)

Of particular interest is isolated damage to the angular gyrus. The main condition for the formation of a specific clinical picture in this pathology is the strict absence of concomitant damage to classical speech centers (Wernicke's area and Broca's area).

With such a local defect, the diagnosis of anomic aphasia is made.

The pathogenesis of this condition lies in the disconnection of brain centers. There is a physical disruption of the transmission of visual information to the sensory speech area of Wernicke. The eyes see an object or text, but the brain cannot correlate the visual image with its verbal equivalent.

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Clinical presentation of anomic aphasia

Because the classical speech centers are not affected, the patient exhibits a clear dissociation between preserved and lost functions.

What is completely preserved:

  • Perception of any auditory information.
  • Understanding of other people's spoken language.
  • Ability to repeat heard phrases.

What is grossly impaired:

  • Understanding of any written language (the patient sees the letters but does not grasp the meaning of what is read).
  • Understanding the meaning of drawn pictures and images.
  • Naming demonstrated objects (anomia).

Thus, when examining such a patient, we will see that they easily perceive speech by ear and can repeat phrases, but fail tests on reading, image analysis, and direct object naming.

Briefly: answers to topical questions

What is the clinical difference between anomic aphasia and Wernicke's sensory aphasia?

In anomic aphasia, the perception of auditory information and spoken language is preserved, whereas in Wernicke's sensory aphasia, they are impaired.

SignAnomic aphasiaWernicke's sensory aphasia
Perception of spoken languagePreservedDisrupted
Spontaneous speechDifficulty in word retrieval, substitution by describing functionsThe ability to pronounce phrases is preserved, but speech is distorted ("word salad")
Localization (typical)Gyrus angularis or lower parts of the temporal lobePosterior pole of the superior temporal cortex (Wernicke's center)

In which other cortical areas, besides the parietal lobe, are working memory mechanisms localized?

Working memory mechanisms are also associated with the medial prefrontal cortex.

How to memorize

To remember the essence of amnestic aphasia, recall the formula: "The noun is gone — a long description remains."

Class and exam questions

What is the main cause of symptoms in parietal cortex lesions?

The development of symptoms is based on impaired functioning of the working memory mechanism.

Is a patient with an angular gyrus lesion able to understand what is being said to them?

Yes, the perception of auditory information and understanding of spoken language in such patients are fully preserved.

Why is reading impaired in anomic aphasia?

Due to impaired neural transmission of visual information (the text seen by the patient) to Wernicke's area, which is responsible for speech recognition.

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What else to study on this topic

  • Mechanisms of working memory functioning
  • Interaction between Wernicke's area and Broca's area
  • Types of aphasias and their differential diagnosis
  • Methods of clinical speech testing (phrase repetition, object naming)

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