The Papez circuit, first discovered by James Papez in 1937, is a circuit within the brain consolidates memories into the long-term store. This loop runs from the association cortex to the cingulate gyrus and hippocampal formation onto the amygdala and mammillary bodies, via the fornix; then onto the hypothalamus; from the mammillary bodies to the anterior thalamic nuclei via the mammillo thalamic tract; back to the cingulate gyrus and the prefrontal cortex. It is more commonly associated with declarative memory rather than procedural memory. Damage to the Papez circuit will lead to insufficient consolidation of memories.. Memory related diseases, such as Korsakoff’s syndrome, Kluver-Bucy syndrome and Alzheimer’s disease have all shown to have an effect on the Papez circuit.
Function of the Papez circuit edit
Consolidation of Long Term Memory edit
Long term memory is divided into two types of memory: declarative and procedural. Procedural memory refers to unconscious memories such as priming, simple forms of conditioning, skills and habits [1] . The mechanisms involved in procedural memory are not thought to be contingent with the Papez circuit. Declarative memory refers to conscious recall of facts (semantic memories) and events (episodic memory) [2]. [3]. Studies with amnesic patients who have suffered damaged to the Papez circuit, such as Patient HM have shown that patients have intact procedural memory, but impaired declarative memory. The Papez circuit can be imagined as the ‘glue’ that holds memories together. For example, when you first see a face and hear a name at the same time, the Papez circuit will consolidate those two pieces of information (i.e., auditory and visual) together. This is stored in long term memory. Repeated exposure to both stimuli, will lead to a fully consolidated memory. Note that long-term memories are not stored within the structures of the Papez circuit, they are simply retrieved from their original storage through the mechanisms of the Papez circuit (see figure 4). Damage to the Papez circuit will result in insufficient consolidation, therefore not allowing the memory to be transferred to the long term store. Research suggests that fully consolidated memories no longer rely on the Papez circuit. [4] These conclusions are heavily based on research with amnesic patients [5].
Associated Syndromes edit
Amnesia edit
There are two types of amnesia: anterograde and retrograde. Anterograde amnesia is where a person is unable to remember on going events after a head trauma. A sufferer of anterograde amnesia will not tend to forget who they are, or anything previous to the incident; however they will have severe difficulty remembering anything new. Retrograde amnesia is where a person is able to remember things after an incident, but will not remember things previous to the event. This retrograde effect has been reported to span over some years before the brain trauma. However older memories are in some cases spared. Leading to the theory that consolidation over a long period of time will result in fully consolidated memories that are no longer dependent on the Papez circuit (in particular the hippocampus). [6] [7] Damage to different components of the Papez circuit is thought to lead to different forms of memory impairment (See table 1).
| Damaged Area | Resulting Effect |
|---|---|
| Hippocampal Formation | Bilateral damage causes anterograde and in some case retrograde amnesia [8] |
| Fornix | Can cause impairments of temporal order memory for retrograde information [9] |
| Mammillary Bodies | Korsakoff’s Syndrome; Anterograde Amnesia [10] |
| Mamillothalamic tract | Markedly impaired declarative memory (both anterograde and retrograde amnesia); linked with Korsakoff’s Syndrome [11] |
| Anterior Thalamic Nuclei | Linked to Korskaoff’s syndrome; spatial memory deficits. [12] |
| Cingulate Gyrus | Schizophrenia; disorientation as a major component of dementia [13] |
| Amygdala | Klüver-Bucy syndrome (visual agnosia) [14] |
| Hypothalamus | Anterograde and to a lesser extent retrograde amnesia; verbal memory impairment (Patient B.J) [15] |
| Prefrontal Cortex | Spatial memory deficit; Working memory deficits [16] |
| Association Cortex | Working memory deficits [17] |
H.M. edit
In 1953, Patient H.M. underwent surgery to treat his epilepsy. The surgery consisted of bilateral removal of his medial temporal lobes (including the hippocampal formation and amygdala). As a direct result of this procedure H.M’s seizures decreased significantly, but more prominent was the severe anterograde amnesia that persisted. H.M showed impaired declarative memory functions for both forming new memories (anterograde amnesia) and retrieving old memories (retrograde amnesia). However the retrograde effect appeared to be on a time gradient, very old memories remained intact. Nondeclarative forms of memory appeared to be intact (i.e. priming tasks). From the hundreds of studies that H.M participated in, the general consensus implicates the medial temporal lobe as essential for the formation and temporal storage of memories, until fully consolidated. [18] [19]
Alzheimer’s edit
Alzheimer’s disease (AD) is a progressive neurodegenerative disease. Neuronal degeneration in AD begins in the medial temporal lobe structures, including the entorhinal cortex and hippocampus. Further neuroanotomic spread then incorporates other critical components of the Papez circuit, including the amygdala and anterior cingulate; which leads to the behavioural characteristics of AD. Eventually this spreads to involve the frontal regions, finally leading to death. AD is characterised by many symptoms, the most common being long-term memory loss, trouble with language, and confusion. [20]
Korsakoff’s Syndrome edit
Korsakoff’s syndrome is characterised by deficits in declarative memory, both anterograde and retrograde amnesia and confabulations and has also been linked with temporal order deficits. [21] Korsakoff’s syndrome is caused by damage to the medial thalamus and hypothalamus, in particular the mammillary bodies. [22] The most common cause of Korsakoff’s syndrome is a thiamine (vitamin B1) deficiency, through alcoholism or malnutrition. [23]
Klüver-Bucy Syndrome edit
Paul Bucy and Heinrich Klüver demonstrated that disrupting the Papez circuit by damage to the amygdala leads to profound effects on social and emotional behaviour. Klüver-Bucy syndrome is recognised by a combination of visual agnosia, placidity, hyperorality and hypersexuality. Visual agnosia is an inability to recognise objects or faces, and can lead to other memory disorders. [24]
References edit
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- ^ Tulving, E., (2002) Episodic Memory: from mind to brain, Annual Review of Psychology 53 1-25
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- ^ MedicineNet(2012) Definition on Retrograde Amnesia. Retrived from: http://www.medterms.com/script/main/art.asp?articlekey=11959
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- ^ Zola-Morgan, S., Squire, L. R., & Amaral, D. G. (1989) Lesions of the hippocampal formation but not lesions of the fornix or the mammillary nuclei produce long-lasting memory impairment in monkeys. The Journal of Neuroscience 9 (3) 898-913
- ^ Yasuno, F., Hirati, M., Takimoto, H., Taniguchi, M., Nakagawa, Y., Ikekiri, Y … Takeda, M. (1999). Retrograde temporal order amnesia resulting from damage to the fornix. Journal of Neurology, Neurosurgery and Psychiatry, 67, 102-105.
- ^ Tanaka, Y., Miyazawa, Y., Akaoka, F., & Yamada, T. (1997) Amnesia Following Damage to the Mammillary Bodies Neurology 481) 160-165
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- ^ Harding, A., Halliday, G., Caine, D., & Kril, J. (1999) Degeneration of anterior thalamic nuclei differentiates alcoholics with amnesia. Brain 123(1) 141-154
- ^ Benes, F. M., Sorensen, I., Vincent, S. L., Bird, E. D., & Sathi, M. (1992) Increased Density of Glutamate-immunoreactive Vertical Processes in Superficial Lamina in Cingulaye Cortex of Schizophrenic Brain. Cerebral Cortex 2(6) 503-512
- ^ Hayman, L. A., Rexer, J. L., Pavol, M. A., Strite, D., & Meyers, C. A. (1998) Kluver-Bucy Syndrome After Bilateral Selective Damage of Amygdala and Its Cortical Connections The Journal of Neuropsychiatry and Clinical Neurosciences 10 354-358
- ^ Dusoir, H., Kapur, N., Byrnes, D. P., McKinstry, S., Hoare, R. D. (1989) Human Memory Disorder: Evidence from a penetrating paranasal brain injury. Brain 113(6) 1695-1706
- ^ McCarthy, G., Blamire, A. M., Puce, A., Nobre, A. C., Bloch, G., Hyder, F., … Shulman, R. G. (1994) Functional magnetic resonance imaging of human prefrontal cortex activation during a spatial working memory task. PNAS 91(18) 8690-8694
- ^ Colombo, M., D’Amato, M. R., Rodman, H. R., & Gross, C. G. (1990) Auditory Association Cortex Lesions Impair Audiory Short-Term Memory in Monkeys. Science 247 336-338
- ^ Corkin, S. (2002) What’s new with the amnesic patient H.M. Nature 3 153-160
- ^ Scoville, W. B., & Milner, B. (1957) Loss of recent memory after bilateral hippocampal lesions ‘’Journal of Neurology, Neurosurgery, Psychiatry’’ ‘’20’’(11) 11-21
- ^ Jicha, G. A., & Carr, S. A. (2010) Conceptual Evolution in Alzheimer’s disease: Implications for understanding the clinical phenotype of progressive neurodegenerative disease. Journal of Alzheimer’s Disease 19(1) 253-272
- ^ Shimamura, A. P., Janowsky, J. S., & Squire, L. R. (1990) Memory for the temporal order of events in patients with frontal love lesions and amnesic patients. Neuropsychologia 28(8) 803-813
- ^ Shimamura, A.P., Jernigan, T. L., & Squire, L. R. (1988) Korsakoff’s syndrome: radiology (CT) findings and neuropsychological correlates. Journal of Neuroscience 8(11) 4400-4410
- ^ Alzheimer’s Society (2012) What is Korsakoff’s Syndrome. Retrieved from http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=98
- ^ Hooshmand, H., Sepdham, T., & Vries, J. K. (1974) Kluver-Bucy Syndrome: Successful Treatment with Carbamazepine. JAMA 229(13)