Superior temporal gyrus (STG)

Page most recently updated 7 September 2026

This page focuses on the neuropsychiatric manifestations associated with lesions of the superior temporal gyrus (STG).

Cognitive, behavioural, and psychiatric effects of lesions may also arise through mechanisms other than network disruption; the potential contribution of these mechanisms can be considered using the Neuropsychiatric Effects of CNS Structural Abnormalities (NECSA) classification.

● Identification using the standardized 15-slice MRI atlas

The superior temporal gyrus is identified by a translucent colour overlay in the relevant slices of the standardized 15-slice MRI atlas. For an explanation of the slices specifically curated for the atlas across the three anatomical planes, together with unmarked MRI images, please see the atlas’s dedicated page ➚.

Superior temporal gyrus - MRI atlas

The superior temporal gyrus is identified by a translucent colour overlay in the relevant T1-weighted slices of the standardized 15-slice MRI atlas, across the coronal, axial and sagittal planes.

Image credit: MRI adapted from the SRI24 Atlas (Rohlfing et al., 2010), CC BY-SA 3.0; anatomical overlays generated using the atlas’s SRI24/LPBA40 label map.

Superior temporal gyrus

Diagram of the cerebrum, with the superior temporal gyrus marked in yellow.

Image credit: Adapted from Gray's Anatomy, via Wikimedia Commons. Public domain.

● Lesion manifestations

▪ Dominant hemisphere:

◦ Wernicke aphasia
◦ Impaired auditory comprehension
◦ Paraphasic speech

▪ Right hemisphere:
◦ Impaired prosody recognition
◦ Difficulty interpreting emotional tone
▪ Bilateral involvement:
◦ Cortical deafness
◦ Auditory agnosia

● Clinical pearls

▪ Posterior STG dysfunction may be mistaken for psychiatric disturbance because patients can produce fluent but meaningless speech.

▪ Right STG involvement can contribute to social communication deficits through impaired prosody processing.

▪ Heschl gyrus (primary auditory cortex, A1) forms part of the STG, lying on its superior surface within the lateral (Sylvian) fissure. It provides the primary cortical processing of sound, while the surrounding superior temporal cortex supports language, auditory recognition, and prosody.

Clinical reminder: consider NECSA mechanisms

(Neuropsychiatric Effects of CNS Structural Abnormalities)

When a structural lesion is identified in a patient presenting with neuropsychiatric symptoms, consider which NECSA mechanisms may explain these symptoms:

● Network disruption

Disruption of functional networks due to the presence of the lesion

● Electrical disturbance

Ictal, preictal, postictal, or interictal effects due to epileptic activity associated with the lesion (particularly if involving or adjacent to cortex)

● Chemical (endocrine) effects

Hormone excess or deficiency caused by the lesion (particularly if involving the pituitary gland or hypothalamus)

● Side effects of treatment

Effects of medications, surgery, radiotherapy, or other interventions

● Alternative explanations

The lesion may be incidental, or symptoms may arise from another cause (e.g., psychological response to illness or a comorbid psychiatric condition)

Selected references and further reading — Lesional lens

Rohlfing T, Zahr NM, Sullivan EV, Pfefferbaum A. The SRI24 multichannel atlas of normal adult human brain structure. Hum Brain Mapp. 2010;31(5):798–819.

Clark DL, Boutros NN, Mendez MF. The brain and behavior: an introduction to behavioral neuroanatomy. 4th ed. Cambridge: Cambridge University Press; 2018.

Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 7th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2016.

Blumenfeld H. Neuroanatomy through clinical cases. 3rd ed. New York: Oxford University Press; 2021.

Hassan I. The neuropsychiatric effects of CNS structural abnormalities (NECSA) classification: an aid to differential diagnosis. Aust N Z J Psychiatry. 2015;49(10):943.

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.