Amnesia

Amnesia

1. Studying Amnesia

   • Amnesia is a disorder of memory with preserved intellect and language. Severe forgetfulness
   • Patients have difficulty in keeping a job, maintaining relationships, looking after oneself and maintaining an independent existence
   • Anterograde Amnesia: A problem in encoding, storing or retrieving info that can be used in the future - New Memories
   • Retrograde Amnesia: A problem accessing events that happened in the past - Previous Memories

2. Causes of Amnesia

   • Alzheimer's disease (AD): the most common cause of amnesia. Not a pure form of amnesia because it is usually complicated by additional symptoms of dementia.
   • Korsakoff Syndrome (KS): usually from chronic alcoholism. Arises due to deficiency in vitamin B1 and is mainly characterised by a memory impairment. Frequently studied, relatively pure form of amnesia. Usually a gradual onset.
   • Herpes Simplex Encephalitis: a virus of the brain which can leave individuals severely amnesia. Very rare (E..G. Clive Wearing)
   • Temporal Lobe Surgery: Individuals become amnesic as a result of deliberate surgical procedures (E.G. H.M,)

3. Patient H.M.

   • Epileptic seizures at age 10
   • Quality of life was severely poor - surgery at 27 removing Medial Temporal Lobe, including the Hippocampi
   • No more seizures, but profound memory problems
   • Several decades after the surgery it was observed that he: does not know where he lives, who cares for him, or where he hate his last meal. His guesses as to the current year may be off by as much as 43 years. In 1982, he did not recognise a picture of himself taken on his 40th bday
   • Anterograde deficits extremely severe
   • Retrograde deficits extended back to age 16 (11 years before the surgery)

4. Episodic Memory

   • Typically, episodic memory tasks use free-recall or recognition
   • According to dual-processes models of memory there are 2 distinct bases for memory performance: ?

5. Recollection and Familiarity

   • Jon
     • Problems teaching him the remember/ know distinction
     • After he declared he understood the R/K, he was tested - used R/K categories as often as controls but he was unable to explain the basis of his R decisions. Used a strength rather than a recollective criterion. Lacked the R component in an ERP study of memory (Duzel et al 2001). Same deficit using a different task (PDP)
   • Hypoxic Patients: Yonelinas et al 2002 - 56 cardiac arrest patients, 55 controls. Greater deficits in recall than recognition (see recording when writing up)

6. Dual-process model of memory

   • Aggleton & Brown 1999: Hippocampus - recollection; Perirhinal regions - familiarity
   • Controversy: there are hippocampal amnesic who have deficits in recall and recognition. Also a dispute as to whether there are two processes: R & F or whether they just reflect strong vs weak memory traces

7. Retrograde Amnesia

   • Need to test items learned prior to the onset of amnesia. Researcher has no control over the learning
   • Scales have been developed to test a range of events: news, winners of classic horse races, TV shows etc
   • Probe method: river (recall a personal memory and then date it)
   • Koppelman et al 1990: developed the Autobiographical Memory Interview (AMI) - ask ps to remember specific info from a range of time periods e.g. name of their first school. Then recollect a specific event from the period
   • problems with these scales? see recording
   • Temporal Retrograde Amnesia Gradient: for those with RA memories from earlier in life are easier to recall that those later on (RIbot's Law)/. Butters & Cermak 1986 report case of P.Z.: looks like acute onset, nut P.Z. had history of alcohol abuse - progressive impairment in ability to register new memories>
   • Explanations of RA
     • Multiple Trace Hypothesis (e.g. Nadel & Moscovitch 1997;1998): Accepts many of tenets of the standard models, but assumes that the hippocampus is not only important in encoding but also in LT retrieval and that LT consolidation results in the creation of redundant races in the hippocampus, instead of the cortex (older memories have more traces, so are more robust against partial hippocampal damage; predicts that complete hippocampal damage will result in complete RA)
     • Standard Consolidation Models (e.g. Alvarez & Squire 1994): assume info is consolidated by transferring it from one brain region to another (i.e. system consolidation) - accounts for Ribot's Law

8. Semantic Memory

   • Some evidence for deficits in acquiring new semantic knowledge in patients with MTL damage
   • H.M. unable to define words introduced since the onset of his amnesia (e.g. Jacuzzi)
   • The amount of damage to MTL corresponds to the magnitude of deficits in acquiring new semantic info (Verfaellie et al 2000)
   • H.M. can learn new info when it is anchored to pre morbidly acquired knowledge. However less consistent access to semantic representations and learning can decay after a relatively short period of time (Skotko et al 2004)
   • A number of early onset hypoxic patients show relatively preserved acquisition of semantic knowledge but profound episodic deficits (e.g. Jon)
   • Because damage happens in life is there a functional reorganisation of the brain?