2 Neuroscience2.6 Neuroanatomy
2.6.3 Internal anatomy of the temporal lobes, hippocampal formation and amygdala
3 min read2 figures
Written by Resident Doctor Committee · Published
Fusiform gyrus
The fusiform gyrus, on the inferior surface in the ventral occipitotemporal cortex, is the substrate of face identity recognition.
Damage to it causes prosopagnosia, and right-sided injury alone may do so.
Hippocampal formation
The hippocampal formation comprises the cornu ammonis (CA, the hippocampus proper), the subiculum and the dentate gyrus. It lies in the medial temporal lobe, in the floor of the temporal horn.
The dentate gyrus is a subregion of the hippocampus that principally supports the formation of new episodic memories.
CA1 (Sommer's sector) is particularly vulnerable to hypoxic-ischaemic injury, as after cardiac arrest.
The entorhinal cortex forms the anterior part of the parahippocampal gyrus and links neocortex with the hippocampus.
Bilateral hippocampal injury causes severe anterograde declarative amnesia, often sparing immediate span and procedural learning.
Stage | Projection | Tract |
|---|---|---|
Entry | Entorhinal cortex to dentate granule cells | Perforant path |
First relay | Dentate gyrus to CA3 | Mossy fibres |
Second relay | CA3 to CA1 | Schaffer collaterals |
Return | CA1 to subiculum to entorhinal cortex | Subicular output |
Output axons then collect in the alveus, fimbria and fornix.
Papez circuit and the limbic system
Papez's circuit (1937) runs from the hippocampus through the fornix, mamillary bodies, anterior thalamic nucleus and cingulate gyrus, then back through the parahippocampal gyrus and entorhinal cortex.
The limbic system is the medial ring of cortex and diencephalic structures organised around this circuit; the amygdala, septum, basal forebrain and nucleus accumbens were added later.
Prefrontal association areas connect with the limbic system but are not members of it.
The amygdala
The amygdala lies in the anteromedial temporal lobe at the anterior (head) end of the hippocampus, deep to the uncus.
It appraises the emotional salience of stimuli, whether threatening, rewarding or socially significant, and starts the behavioural and autonomic response.
Nucleus | Main connections | Role |
|---|---|---|
Basolateral complex | Thalamus, cortex, hippocampus | Appraises emotional value; carries the noradrenergic, stress-hormone-driven enhancement of memory storage in hippocampus and cortex |
Central nucleus | Hypothalamus, brainstem | Main autonomic and endocrine output, producing the bodily expression of fear |
In fear conditioning, the amygdala stores the association between a neutral cue and an aversive outcome, and it takes part in extinction.
The amygdala modulates the strength of hippocampal-dependent consolidation of emotionally arousing memories, acting on hippocampus and cortex.
It is not needed for consolidation itself, so learning of neutral material survives amygdala damage.
Bilateral amygdala damage
Urbach-Wiethe disease can damage both amygdalae.
Selective bilateral amygdala damage abolishes fear processing for external threat, including recognising fear in others, yet panic induced by inhaled carbon dioxide is preserved.
Klüver-Bucy syndrome
Klüver-Bucy syndrome results from bilateral damage to the amygdalae and anterior medial temporal lobes.
It does not follow hippocampal or frontal damage, and it differs from Balint's syndrome (parieto-occipital lesion) and Kleine-Levin syndrome (no fixed lesion).
Its features are placidity with loss of fear, hyperorality, hypersexuality, hyperphagia, visual agnosia and hypermetamorphosis, which is excessive attention to and handling of visible objects.
Complete human cases are rare; partial syndromes follow herpes simplex encephalitis, temporal surgery, frontotemporal dementia, trauma, anoxia or stroke.
New hyperphagia after herpes simplex encephalitis points to Klüver-Bucy syndrome from bilateral amygdala damage, not to Cushing's syndrome.