How Memory Works? Amnesia Cases of H.M, M.S, C.W, E.P

How Memory Works? Much of what we know today comes from the stories and real cases of amnesia (memory loss) patients result from brain damage under various different situations. Human memories have different types corresponding to the encoding, storage and retrieval of different types of information, sensual stimulation, and experience. For example, episodic memory are those used to store autobiographical facts and events, semantic memory handle the information which has contextual meanings that are part of the knowledge. Procedural memory record information how an individuals can remember to complete certain tasks such as play piano or how to do surfing (motor tasks, skills). For details of different types of memory, refer to the table in this post at the end or to the post “Types of Memory”. Different parts of the brain get involved and are responsible for the formation and retrieval of different memory types. Much of what neurobiologist and neuropsychologist know about how memory works comes from their casebooks of real life amnesia (memory loss) patients. This post describes 4 of them which is considered as the most well-known with significant value in the research studies conducted by neurobiologists.

H.M is the initial for Henry Molaiso.  H.M amnesia case has identified hippocampus as the most important brain structure responsible for new memory creation, the transfer from short-term memory into long-term memory for storage. This memorization process or memory process involves 3 phases as encoding (acquisition, consolidation) (the step to transform information into biological electrochemical signal that have the corresponding pattern that can be stored, accessed and retrieved later), storage, and retrieval. See post “memory process” for more detail. Individuals with damage to hippocampus can not form new memory which implies that they have anterograde amnesia (inability to create new memory, especially recent events after the onset of amnesia). (For different types of amnesia, see post “memory loss diseases”). H.M amnesia case is by far the most prominent case whose hippocampus was completely removed due to the surgery operation trying to treat his year’s epileptic seizures. Before H.M’s surgery operation, no one know the importance of hippocampus in the memory formation. Both of Henry Molaiso’s hippocampus within each temporal lobe was skillfully removed. Although the surgery successfully reduced Henry’s seizures, he was left with severe global memory loss in that he can not create  new conscious memories after his operation, he also suffered some retrograde amnesia for a span of 11 years of past memory before his surgery operation. His retrograde amnesia does not appear to be caused by the removal of his hippocampus, instead the complication of retrograde amnesia (can not remember past experience) may be a consequence of his chronic and large use of medications – the antiepileptic drugs which affect the other area of the brain that is responsible for memory storage and recall function. His procedural memory retain intact so that he can normally perform various motor tasks and other skilled procedural tasks as before. Since then, Henry Molaiso has been participating in numerous scientific experiments and researches led by teams of neuropsychologists and H.M became the most cited amnesia cases in the literature.

C.W is the initial for Clive Wearing. His case identified the difference between short-term and long-term memory. Clive Wearing has only short-term memory but no long-term memory (particularly the declarative or explicit memory). His procedural memory -one of the main implicit long-term memory – is till intact though. Procedural memory is affected by the region of brain that form the striatum and cerebellum. Long-term declarative memory are medicated mainly by the medial temporal lobe (hippocampus and associated cortices). Hippocampus is responsible for the transfer of information from short-term memory after being encoded and consolidate to the long-term storage in the cortex. Short-term memory is affected by angular gyrus. Clive Wearing can create new short-term memory, but the formed short-term memory can not be transferred to long-term memory.  His memory only lasts between 7 and 30 seconds. Wearing still remembers how to play the piano and conduct a choir (he is a musician) which uses his intact procedural memory, but quickly forgets that he has just played piano. His hippocampus was damaged due to encephalitis (infection of the brain). Some of the temporal lobe and some of the frontal lobe in the cerebral cortex were damaged. These damage of temporal lobe cortex wiped out some of his past stored information (past long-term memory – explicit memory) made him suffer both long-term anterograde amnesia and some degree of retrograde amnesia. He has also been showing some physical signs (shake spasmodically) of impairment in controlling memory related to emotional thoughts (e.g. some outburst of anger). These appear to be linked to the lesion in his frontal lobe cortex.

M.S’s amnesia is a very distinct case. His amnesia identified the importance of the regions of brain that store long-term visual memory as well as for visual perceptual priming. M.S suffered from sever visual perceptual priming deficit – the visual memory deficit amnesia – a distinct amnesia presentation and etiology. Visual priming is the type of implicit memory that does not require conscious effort. Visual perceptual priming refer to the ability of an individual to spontaneously increase the speed and accuracy of response (process of visual information) to a visual stimuli that he has been exposed to in the past. Visual priming require the visual-specific cortex region of the brain that also responsible for the storage and retrieval of the visual memory. He can copy images but can not recognize them later, he also can not recognize faces and many other common objects. He can not manipulate visual images including those involve color, people. The associative nature of the (visual) perceptual priming suggests that activation of past stored same or similar visual information may be involved or required in this implicit memory function. At the same time of his long-term visual memory loss, he also suffered from some semantic memory impairment. M.S manifests both a severe retrograde amnesia and moderate anterograde amnesia. The lesion in his brain was caused by infection of herpes encephalitis. Neuroimaging techniques revealed extensive damage to his occipital lobes on both sides. This is what responsible for his long-term storage problem for visual information and visual priming deficit. In addition, part of his hippocampus was damaged which made him difficult to form new memories (moderate anterograde amnesia). Part of his parietal white matter was also destroyed but the parietal lobe cortex is intact. His loss of autobiographical memory (episodic memory) is believed to be linked to his sever long-term loss of past visual memory and visual priming. The loss of visual memory storage region in the brain appear to disrupt and impair the activation in retrieval of autobiographical information.

E.P’s story is strikingly similar to the well-known case of H.M. His amnesia was also a result of encephalitis. His disease result in extensive damage to medial temporal lobe where hippocampus resides. Crucial structures – among them the amygdala and hippocampus – were eliminated. Additionally, other brain regions had atrophied. Therefore E.P does not have new memories too. In addition, he also has modest impairment in his semantic knowledge. (memories about contextual concepts, words). E.P was subject to continued study which include hundreds of different assessment and tests regarding his cognitive and memory functions. E.P’s case provides new and surprising twists in understanding how memory functions and the difference between types of amnesia. One twists is the fact that E.P does not have any residual capacity in learning anything subconsciously. Scientists has believed that besides hippocampus, there may be some other ways information can get in. E.P’s learning ability is absolutely zero, this is attributed to the fact of a total damage of all specific memory-linked brain structures.  A second twist from E.P case is to identify the different areas of brain cortex that stores episodic and semantic memory. It appears that some adjacent areas of the medial temporal lobe, not just the medial temporal lobe alone, are responsible for semantic memory storage. Finally, E.P’s retrograde amnesia is very different from other cases. His retrograde amnesia extending back 40-50 years compared to a few months or years of the past memory loss of other amnesia cases. Scientists said this effect probably is the result of lateral temporal lobe damage caused as a secondary consequence of the initial encephalitis-induced brain damage.

Types of Memory

Type And Time FrameSubtypeRegion of BrainItems Can Be HeldOther Properties
Sensory Memory

milliseconds to seconds
iconic memory (visual sense)
echoic memory (hearing)
haptic memory (touch)
smell
taste
many
Short-Term (Working) Memory

seconds to minutes
short-term memory
working memory
frontal cortex, parietal cortex, anterior cingulate, parts of basal ganglia
7+/-2disrupted by distractor
recency effect
Long-Term Memory - Declarative Memory

(days, decades, up to lifetime)
Episodic Memory (autobiographical, facts, events)medial temporal lobe (hippocampus) and associated cortexunlimitedrehearsal facilitates storage
many types of LTM mediated by different brain region
Semantic Memory (contextual meaning, knowledge)
Long-Term Memory: Nondeclarative Memory
(days, decades, up to lifetime)
Procedural Memory (motor tasks, skills)striatum and cerebellumoperate outside of awareness (consciousness)
Primingcortex
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