Amnesia

The profound loss of memory in the presence of relatively preserved cognitive abilities

• The inability to recall information, usually about stressful or traumatic events in persons' lives, such as a violent attack or disaster.
• The memory is stored in long-term memory, but access to it is impaired because of psychological defense mechanisms.
• Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory.

Amnesia that results from a psychological cause as opposed to direct damage to the brain caused by head injury, physical trauma or disease

• Temporary amnesia
• Persistent amnesia is often permanent

Degenerative amnesia gets worse over time (i.e. Alzheimers)

Global amnesia is amnesia for all memory, whereas material specific just relates to certain things, like names for objects

The hippocampus, or areas that deal with hippocampal input or output

• Deals with spatial and episodic memory 
• Disruption at the mammillary bodies or fornix is a common cause of amnesia 
• Hippocampus 
• Fornix 
• Mammillary bodies 
• Mammillothalmic tract 
• Anterior thalmic nucleus
• Cingulum 
• Entorhinal cortex 
• Back to the hippocampus

• Physical Damage  - head trauma or surgery
• Viral Disease – Encephalitis
• Loss of blow flow - Ischaemia
• Loss of oxygen – Anoxia Nutritional deficiency – Low Thiamine (Korsakoff’s)

• H.M. had brain surgery in 1953 when he was 27 yrs. old. The surgery involved removal of part of the brain known as the hippocampus to alleviate the severe symptoms of epilepsy in a bilateral removal of the medial temporal lobe 
• After the surgery his short-term memory was normal but he was completely unable to transfer any new information into his long-term memory.
• In many respects H.M. seemed cognitively 'normal' as he was able to learn and remember perceptual and motor skills although he needed reminding of what he was able to do.

• Van and Aggleton 2004
• Snooker cue rammed through nose into the basal regions of the brain.
• Initially, his memory disorder had the clinical features of a dense amnesic syndrome, with both anterograde and retrograde amnesia, but B.J. subsequently showed significant recovery of memory function.
• Formal memory testing was carried out 21 months after injury. This demonstrated marked verbal memory impairment, as severe as that seen in patients with the amnesic syndrome.
• On nonverbal memory tests, his impairment was relatively mild and patchy.
• His retrograde amnesia had regressed mainly to affect a 6 month period before the injury.
• On other cognitive tasks, he performed at an average or above average level, and there was no neuropsychological evidence of frontal lobe dysfunction.
• Neuroradiological investigations  failed to demonstrate a lesion in any of the thalamic nuclei.
• Magnetic resonance imaging showed a lesion in the hypothalamus in the region of the mamillary bodies.
• Shows that amnesia can occur even without direct damage to the hippocampus (but a disruption of the Papez circuit)

• Herpes damage to the anterior temporal lobe including the amygdala, hippocampus, entorhinal, and perirhinal cortices, rostral fusiform gyrus and the rostral parahippocampal cortex, bilaterally
• No loss to neurological functions like intelligence 
• STM was fine 
• Severely impaired declarative memory 
• Also severe retrograde amnesia 
• Non-declarative memory is fine 
• Failed to complete the Wisconsin Card Sorting Task

• Anoxia (loss of oxygen) due to Co2 poisoning 
• Severe damage to prefrontal cortex resulting in the loss of half of its volume 
• Led to anterograde amnesia

• Ischemia (restricted blood supply)
• Underwent left thyroid lobectomy because of loss of blood to the left lobe of the thyroid during removal of the parathyroids
• Gave no evidence of intellectual or cognitive deficit other than memory impairment. He exhibited little interest in testing, however, and this complicated the interpretation of some of his memory test scores (also had low IQ)
• Had moderately severe anterograde amnesia, but few signs of retrograde amnesia 
• Shows that damage limited primarily to the hippocampal region, even when incomplete, is sufficient to produce a clinically significant memory impairment

• IQ, Language, attention, vision, executive functions
• Short term memory
• Implicit/procedural memory

• Ask what is hidden in an image, and make it progressively more and more obvious 
• Wait until they cannot remember the process 
• Ask again, they will be way better, but won't know why

• Cards with different patterns are associated with weather 
• Amnesiacs can learn the rules in 50 trials 
• When asked again (after forgetting) they remember the rules, but don't recognise the stimuli

• 1: retrograde amnesia 
• 2: anterograde amnesia

• Rey figure 
• Tests episodic memory 
• See this, delay, then asked to recreate it in as much detail as possible

The ability to remember facts and information independently from the initial experience

• Familiarity: Feeling that something is familiar but no details about it retained. E.g. recognising someone you’ve seen before, but not knowing their name, or who they aren
• Recollection: Rich detailed remembering of past events. E.g. seeing a face and remembering who they are, where and when you last saw them

• Baddeley et al, 1994
• Asked to recall names to faces and shapes, and recognise which door they had seen amongst 4 
• Amnesiacs with hippocampal are much better at the latter suggesting that we have different memory systems for recognition and recollection, and that the hippocampus is not essential for the former

• Yes and no
• HM is impaired memory for word definitions (Gabrielli et al., 1988). Also patient GD. Squire (1992) and others – Both episodic and semantic memory affected in amnesia – declarative memory 
• However, Vargha-Khadem et al., 1997, Science  Early onset developmental amnesics. - spared semantic memory.   Late-onset cases PS (Verfaeille  et al., 2000) and RS (Kitchner et al., 1998) some degree of semantic learning
• Either: A) neocortex allows slow gradual learing or B) a small fragement of remaining hippocampus supports this function

• Old memories (childhood) still remembered
• Memories 5-10yrs before lesion lost
• Forgot death of favorite uncle in 1950
• Implies hippocampal/ MTL memories ‘consolidated’ in neocortex over time & become independent of the hippocampus

• Not often examined in studies
• Few standardized tests available
• Low motivation of patients
• Are all the stimuli as salient across time periods?
• Have the episodic memories become more semanticized?

• HPC/MTL memories usually consolidated in neocortex over time and become independent of the HPC/MTL by perseveration.
• If perseveration is interrupted then consolidation (and therefore memory) are disrupted, resulting in amnesia
• Asked amnesics and controls about news events in past 30y. Found diminishing reterograde amnesia for earlier events (i.e. older the event = better the memory), but memory for newer events was more and more impaired.
• Using fMRI found retrieval of newest memories in normal PPs cause the biggest activation in the HPC. Oldest memories cause least. Consistent w/ idea that memories are initially in HPC, before gradual transferring to neocortex.

• Episodic memories (esp. visuospatial details) never consolidated completely from HPC, but become more resistant to damage bc of repetition and rehearsal.
• Semantic memories become independent of the HPC over time.
• Patient T.T, bad retrograde amnesia, but only when using minor roads 
• Patient V.C, total amnesia, no temporal gradient, everything is just gone

• Hippocampus damaged patients asked to imagine a beach scene 
• Can't picture the scene, only hear and feel things 
• Suggests the hippocampus plays a part in mental scene construction 
• Hassabis et al, 2007