Temporal Lobe Lesions Causes, Symptoms, and Treatment

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Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Temporal Lobe Lesions (Causes, Symptoms, and Treatment) article more useful, or one of our other health articles.

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The temporal lobe is a complex part of the brain, dealing with many 'higher functions'.[1] Therefore, behaviour and intellect may be affected rather than gross motor skills.

Disturbance in function of the temporal lobe may be caused by ischaemic or haemorrhagic damage, as with a cerebrovascular event (CVE). Disturbance of temporal lobe function may also occur with space-occupying lesions and with trauma; it may also be associated with epilepsy.[1]

This article will concentrate on neurological problems caused by temporal lobe deficits. See also separate Temporal Lobe Epilepsy article.

  • The most common cause of temporal lobe lesions is a CVE.
  • Space-occupying lesions may be primary brain tumours - benign (such as meningioma) or malignant. They may also be secondary tumours or metastatic carcinoma, most often from lung cancer or breast cancer.
  • Trauma from head injury may be involved or surgical damage when removing a tumour from that region. Head injury often includes extradural haematoma and contrecoup injuries (brain injury on the opposite side to the point of impact). Surgery for intractable temporal lobe epilepsy is well established and will cause disturbance of temporal lobe function.
  • Progressive deterioration of language functions may be part of frontotemporal dementia.[2] It tends to present earlier than Alzheimer's disease and about 50% have a family history suggesting autosomal dominant inheritance.
  • Encephalitis, especially herpes simplex encephalitis.
  • Other pathologies such as multiple sclerosis can affect the temporal lobes, although this is an unusual manifestation.

A stroke tends to produce a rapid onset of symptoms whilst a space-occupying lesion will produce a more insidious onset. Whilst a hemiparesis is obvious to the patient and family (and will be recognised as such), the manifestations of temporal lobe lesions are more subtle and they may be interpreted as psychosis or dementia.

It is Important to unravel these strange presentations and to suspect the diagnosis. A careful, detailed history is required with examination. Often the patient will be oblivious to symptoms and will be uncomplaining. Some history from a third party can be useful.

There are eight principal symptoms of temporal lobe damage:[1, 3]

  • Disturbance of auditory sensation and perception.
  • Disturbance of selective attention of auditory and visual input.
  • Disorders of visual perception.
  • Impaired organisation and categorisation of verbal material.
  • Disturbance of language comprehension.
  • Impaired long-term memory.
  • Altered personality and affective behaviour.
  • Altered sexual behaviour.
  • Disorders of auditory perception:[4]
    • Lesions of the left superior temporal gyrus produce problems of speech perception with difficulty in discriminating speech and the temporal order of sounds impaired.
    • Lesions of the right superior temporal gyrus produce prosody. Prosody is the study of the metre of verse. Here it means the rhythm of speech.
    • Lesions of the right superior temporal gyrus can produce disorders of perception of music with inability to discriminate melodies.
  • The inferior temporal cortex is responsible for visual perception and lesions produce inability to recognise faces, called prosopagnosia:[5, 6]

    • The area is responsible for the organisation and categorisation of words and pictures. Impairment of this ability to categorise means reduction in both ability and fluency in listing categories.
    • There may be difficulty using contextual information, in extracting information from the environment and using visual and social cues.

  • There may be disturbance of visual and auditory input selection. This presents as impairment of short-term memory (also called working memory) and of judgement about the recency of events.
  • The medial and inferior temporal cortex and hippocampus are responsible for memory.[7, 8] There is complete anterograde amnesia following bilateral removal of medial temporal lobes, including hippocampus and amygdala. There is difficulty recalling information. The left side is responsible for verbal material and the right for non-verbal memory such as faces, tunes and drawings. The difference between retrograde and anterograde amnesia is that retrograde amnesia is loss of memory from before an event. It often happens with head injury with loss of memory leading up to that event, although this is commonly gradually recovered. Anterograde amnesia is loss of memory between the event and the present time.
  • Although somewhat controversial, there is some evidence for a temporal lobe personality, which may display:[9]
    • An emphasis on trivia and the small details of daily life.
    • Egocentricity.
    • Pedantic speech.
    • Perseveration of speech - a continuous but futile attempt to produce a word or perform an action long after others would have given up or tried a different approach.
    • Paranoia.
    • Religious preoccupations.
    • A tendency to aggressive outbursts, especially after right temporal lobectomy.
  • As well as behavioural change, temporal lobe lesions can present with visual field defects in the form of superior quadrant loss, sometimes called the 'pie in the sky defect'.
  • Temporal lobe lesions may be associated with true hypersexuality. A CVE normally reduces libido but temporal lobe lesions can increase it.[10] Lesions of the medial temporal lobe have been reported to produce the Klüver-Bucy syndrome (may present with hyperphagia, hypersexuality, hyperorality, visual agnosia and docility).[11, 12]

The problems of examining difficulties of speech and comprehension are discussed in the separate Dysarthria and Dysphasia article.

In terms of recognising the ability to recall information or to recognise faces, it is complicated if there is impairment of speech. A strange or 'temporal lobe personality' may be apparent but history from people close to the patient is more reliable and will attest to changes in personality. Accurate testing and ability to make an anatomical diagnosis may well be beyond the ability of most general practitioners when presented with such patients. The help of a neuropsychologist may be required.

If a CVE is suspected, check the cardiovascular system, including blood pressure, auscultation of the heart and carotid arteries. A brief examination of the rest of the nervous system is required.

Many conditions may be worthy of consideration including:[13]

  • Modern imaging studies can now localise lesions with great accuracy. MRI tends to be better than CT.
  • If metastatic cancer is suspected, a CXR and other further imaging of the chest and abdomen is required.
  • Visual field defects can be assessed by perimetry.
  • A possible or certain diagnosis of a CVE requires investigation, as outlined in the separate Stroke Prevention article.
  • Referral to a neuropsychologist may still be useful to elucidate the precise nature of the problem and for help with management.
  • CVE: this is similar to that for stroke rehabilitation. See the separate Cerebrovascular Event Rehabilitation article.
  • Temporal lobe tumours: tumour surgery in the temporal region is challenging due to the anatomical complexity. However, gross total tumour resection rates of 88% with neurological and surgical morbidity less than 10% have been reported.[14]

The prognosis will depend on the underlying cause and comorbidities.

Young people, especially children, have an ability to let one part of the brain take over the function of a damaged part (plasticity) but this is lost with increasing age. Hence, young patients may regain some function but this is less likely with advancing age.

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Further reading and references

  • Kiernan JA; Anatomy of the temporal lobe. Epilepsy Res Treat. 20122012:176157. doi: 10.1155/2012/176157. Epub 2012 Mar 29.

  • Zhao F, Kang H, You L, et al; Neuropsychological deficits in temporal lobe epilepsy: A comprehensive review. Ann Indian Acad Neurol. 2014 Oct17(4):374-82. doi: 10.4103/0972-2327.144003.

  1. Herlin B, Navarro V, Dupont S; The temporal pole: From anatomy to function-A literature appraisal. J Chem Neuroanat. 2021 Apr113:101925. doi: 10.1016/j.jchemneu.2021.101925. Epub 2021 Feb 11.

  2. Khan I, De Jesus O; Frontotemporal Lobe Dementia

  3. Patel A, Biso GMNR, Fowler JB; Neuroanatomy, Temporal Lobe

  4. Nagle S, Musiek FE, Kossoff EH, et al; Auditory processing following consecutive right temporal lobe resections: a prospective case study. J Am Acad Audiol. 2013 Jul-Aug24(7):535-43. doi: 10.3766/jaaa.24.7.2.

  5. Rocha Cabrero F, De Jesus O; Prosopagnosia

  6. Milner B; Visual recognition and recall after right temporal-lobe excision in man. Epilepsy Behav. 2003 Dec4(6):799-812.

  7. Milner B; The medial temporal-lobe amnesic syndrome. Psychiatr Clin North Am. 2005 Sep28(3):599-611, 609.

  8. Piolino P, Bulteau C, Jambaque I; Memory dysfunctions. Handb Clin Neurol. 2020174:93-110. doi: 10.1016/B978-0-444-64148-9.00008-9.

  9. Colak B, Ilhan RS, Duman B; Rethinking Geschwind Syndrome Beyond Temporal Lobe Epilepsy. Noro Psikiyatr Ars. 2021 Aug 2658(3):169-170. doi: 10.29399/npa.27995. eCollection 2021.

  10. Baird AD, Wilson SJ, Bladin PF, et al; Neurological control of human sexual behaviour: insights from lesion studies. J Neurol Neurosurg Psychiatry. 2007 Oct78(10):1042-9. Epub 2006 Dec 22.

  11. Al-Attas AA, Aldayel AY, Aloufi TH, et al; Kluver-Bucy syndrome secondary to a nondominant middle cerebral artery ischemic stroke: a case report and review of the literature. J Med Case Rep. 2021 Jul 1515(1):346. doi: 10.1186/s13256-021-02932-0.

  12. M Das J, Siddiqui W; Kluver Bucy Syndrome. StatPearls, Jan 2023.

  13. Santana LM, Valadares EJA, Rosa-Junior M; Differential diagnosis of temporal lobe lesions with hyperintense signal on T2-weighted and FLAIR sequences: pictorial essay. Radiol Bras. 2020 Mar-Apr53(2):129-136. doi: 10.1590/0100-3984.2018.0117.

  14. Faust K, Schmiedek P, Vajkoczy P; Approaches to temporal lobe lesions: a proposal for classification. Acta Neurochir (Wien). 2014 Feb156(2):409-13. doi: 10.1007/s00701-013-1917-4. Epub 2013 Nov 8.

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