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Deficits in Parietal Cortex Lesions

Cortex parietalis

For medical students2 min readUpdated 2026-10-10

Pathologies of the parietal lobe lead to specific cognitive and speech disorders caused by impairments in working memory mechanisms. One of the characteristic manifestations includes syndromes where patients forget the names of familiar objects or lose the ability to understand written text while preserving normal hearing and spoken language.

AcalculiaA specific impairment of calculation functions resulting from parietal lobe damage.
Amnestic AphasiaForgetting of words (predominantly nouns).
Angular GyrusIts isolated damage leads to anomic aphasia.
Pathogenesis of AnomiaBlockage of visual information transfer to Wernicke's speech area.

General Symptomatology of Lesions

Parietal cortex damage is accompanied by a complex of disorders based on impairment of working memory mechanisms. Due to this failure, the brain loses the ability to retain and actively use the information required for current activities.

Key clinical manifestations include:

Angular Gyrus Syndrome (*Gyrus angularis*)

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

With such a localized defect, the diagnosis is anomic aphasia.

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

Clinical Picture of Anomic Aphasia

Because the classic speech centers are unaffected, the patient shows a clear dissociation between preserved and impaired functions.

What is completely preserved:

What is grossly impaired:

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

Mnemonic

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

Frequently asked questions

How does anomic aphasia clinically differ from 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.

FeatureAnomic AphasiaWernicke's Sensory Aphasia
Spoken speech perceptionPreservedImpaired
Spontaneous speechDifficulty retrieving words, replaced by functional descriptionsAbility to produce phrases is preserved, but speech is distorted ("word salad")
Localization (typical)Gyrus angularis or inferior temporal lobePosterior pole of the superior temporal gyrus (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.

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

The development of symptoms is based on the impairment of working memory mechanisms.

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

Yes, the perception of auditory information and understanding of spoken speech in such patients are completely 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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