The temporal lobe is involved in processing sensory input into derived meanings for the appropriate retention of visual memory, language comprehension, and emotion association.[4]: 21 Temporal refers to the head's temples.
The temporallobe consists of structures that are vital for declarative or long-term memory. Declarative (denotative) or explicit memory is conscious memory divided into semantic memory (facts) and episodic memory (events).[4]: 194 Medial temporal lobe structures that are critical for long-term memory include the hippocampus, along with the surrounding hippocampal region consisting of the perirhinal, parahippocampal, and entorhinal neocortical regions.[4]: 196 The hippocampus is critical for memory formation, and the surrounding medial temporal cortex is currently theorized to be critical for memory storage.[4]: 21 The prefrontal and visual cortices are also involved in explicit memory.[4]: 21
Research has shown that lesions in the hippocampus of monkeys results in limited impairment of function, whereas extensive lesions that include the hippocampus and the medial temporal cortex result in severe impairment.[5]
The temporal lobe communicates with the hippocampus and plays a key role in the formation of explicit long-term memory modulated by the amygdala.[4]: 349
Adjacent areas in the superior, posterior, and lateral parts of the temporal lobes are involved in high-level auditory processing. The temporal lobe is involved in primary auditory perception, such as hearing, and holds the primary auditory cortex.[6] The primary auditory cortex receives sensory information from the ears and secondary areas process the information into meaningful units such as speech and words.[6] The superior temporal gyrus includes an area (within the lateral fissure) where auditory signals from the cochlea first reach the cerebral cortex and are processed by the primary auditory cortex in the left temporal lobe.[citation needed]
The medial temporal lobes (near the sagittal plane) are thought to be involved in encodingdeclarativelong term memory.[4]: 194–199 The medial temporal lobes include the hippocampi, which are essential for memory storage, therefore damage to this area can result in impairment in new memory formation leading to permanent or temporary anterograde amnesia.[4]: 194–199
Individuals who suffer from medial temporal lobe damage have a difficult time recalling visual stimuli. This neurotransmission deficit is not due to lacking perception of visual stimuli, but rather to the inability to interpret what is perceived.[16] The most common symptom of inferior temporal lobe damage is visual agnosia, which involves impairment in the identification of familiar objects. Another less common type of inferior temporal lobe damage is prosopagnosia which is an impairment in the recognition of faces and distinction of unique individual facial features.[17]
Damage specifically to the anterior portion of the left temporal lobe can cause savant syndrome.[18]
Pick's disease, also known as frontotemporal amnesia, is caused by atrophy of the frontotemporal lobe.[19] Emotional symptoms include mood changes, which the patient may be unaware of, including poor attention span and aggressive behavior towards themselves or others. Language symptoms include loss of speech, inability to read or write, loss of vocabulary and overall degeneration of motor ability.[20]
Temporal lobe epilepsy is a chronic neurological condition characterized by recurrent seizures; symptoms include a variety of sensory (visual, auditory, olfactory, and gustation) hallucinations, as well as an inability to process semantic and episodic memories.[21]
Schizophrenia is a severe psychotic disorder characterized by severe disorientation. Its most explicit symptom is the perception of external voices in the form of auditory hallucinations. The cause of such hallucinations has been attributed to deficits in the left temporal lobe, specifically within the primary auditory cortex.[22][23] Decreased gray matter, among other cellular deficits, contribute to spontaneous neural activity that affects the primary auditory cortex as if it were experiencing acoustic auditory input. The misrepresentation of speech in the auditory cortex results in the perception of external voices in the form of auditory hallucinations in schizophrenic patients.[24] Structural and functional MRI techniques have accounted for this neural activity by testing affected and non-affected individuals with external auditory stimuli.[22]
^Pertzov, Y., Miller, T. D., Gorgoraptis, N., Caine, D., Schott, J. M., Butler, C., & Husain, M. (2013). "Binding deficits in memory following medial temporal lobe damage in patients with voltage-gated potassium channel complex antibody-associated limbic encephalitis". Brain: A Journal of Neurology, 136(8), 2474–2485.
^Mizuno T, Takeda K (November 2009). "[The symptomatology of frontal and temporal lobe damages]". Brain and Nerve = Shinkei Kenkyu No Shinpo (in Japanese). 61 (11): 1209–18. PMID19938677.
^Yokota O, Tsuchiya K, Arai T, Yagishita S, Matsubara O, Mochizuki A, et al. (April 2009). "Clinicopathological characterization of Pick's disease versus frontotemporal lobar degeneration with ubiquitin/TDP-43-positive inclusions". Acta Neuropathologica. 117 (4): 429–444. doi:10.1007/s00401-009-0493-4. PMID19194716. S2CID23749655.
^Lah S, Smith ML (January 2014). "Semantic and episodic memory in children with temporal lobe epilepsy: do they relate to literacy skills?". Neuropsychology. 28 (1): 113–22. doi:10.1037/neu0000029. PMID24245928.
