The hippocampus is the site of memory Essay Example

specialized areas of the brain for different memory tasks (Ramachandran, 1998).

The statement that the hippocampus is the site of memory oversimplifies this cognitive process. This knowledge has led researchers to critically examine this claim, presenting evidence to explain why the hippocampus has been labeled as such and showing that understanding of memory retrieval, categorization, and censorship requires consideration of the hippocampus's interaction with other brain structures. Insights into memory function are often derived from observations of brain-damaged individuals. The case of 'H' explored by Scoville & Millner (1957) has been particularly influential.

After studying for over 35 years (Kolb; Whishaw, 1999), M' underwent a bilateral medial temporal-lobe resection due to severe epilepsy that did not respond to medication of various forms, as described by Scoville and Milner (1957) who justified the "frankly experimental operation" because of M's total incapacitation (p. 11).

Despite reducing H.M's "incapacitating" seizures, the operation resulted in a severe loss of recent memory (now referred to as anterograde amnesia). Scoville & Millner (1957) reached this conclusion based on H.M's case.

As part of a study on normal memory function, ten patients underwent bilateral medial temporal-lobe resection, including M. The results demonstrated the significance of the hippocampal region in memory. In 1957, Scoville and Millner proposed that damage to certain parts of the anterior hippocampus and hippocampal gyrus would result in persistent recent memory impairment after this procedure. This suggests that the extent of removal from the hippocampus is associated with memory loss. It should be noted that despite their assertion about the importance of the hippocampus for memory function, only H.M. experienced impaired recent memory.

Further investigation into H. M. revealed that his long-term memory

was specifically affected by his memory impairment.

As per the findings of Wickelgren's investigation in 1868, H. M. suffered from a deficiency in transferring data from his short-term memory to his long-term memory.

While H. M. had typical short-term memory and digit span capacities, his performance in creating new long-term memories through digit span tests was inadequate - a pattern not observed in regular individuals (Parkin, 2000). This reinforces the belief that transferring short-term memories into long-term ones relies on the hippocampal region. Moreover, studies have shown that besides its importance in generating novel memories, the hippocampus is also critical for consolidating enduring memories (Gazzaniga et al.).

According to Gazzaniga et al. (1998) and Thompson (2000), the hippocampal area is vital in converting short-term memories into long-term ones and strengthening them. Hebb (1949) suggested that consolidation occurs biologically through the modification of neurons for new memory formation.

Research on H.M. indicates that patients with severe psychological disorders, like depression, may experience temporal and hippocampal consolidation through electroconvulsive therapy. While amnesia is a common side effect, it typically does not affect procedural memory (memory for actions or "knowing how") as much as declarative memory (memory for specific facts and events or "knowing that"). This aligns with Squire's 1987 proposal to distinguish between procedural and declarative memory. Many studies demonstrate individuals with amnesia can learn perceptual-motor skills, such as tracking and mirror tracing, at a similar pace to those without amnesia.

In 1976, Brooks and Baddeley, as well as Cohen and Squire in 1978, conducted research on amnesiacs. In 1980, Cohen and Squire observed that the amnesiacs were able to learn the encoding rules or procedures for acquiring skills. However, they

were only able to remember minimal or no information after applying these procedures. This supports the idea of a modular view of memory proposed by Cohen and Squire in 1980. They suggested that perceptual-motor and pattern-analyzing skills belong to a class of operations that have different memory characteristics compared to those that depend on specific declarative, data-based material. Further evidence for a modular set up of memory comes from research done on normal/non-amnesic subjects, which has shown a dissociation between kinesthetic-motor memory and spatial and verbal memory based on differences in forgetting rates and susceptibility to interference (Posner, 1966). Research carried out on amnesic patients has also revealed a separation between semantic memory (memory of knowledge, facts or meaning without any reference to 'when' it was learned) and episodic memories (memories for specific places or situations that occurred in the past) (Thompson, 2000).

Lhermitte and Serdaru (1993) conducted tests on amnesic patients in order to compare their retrieved memories to those of normal matched subjects. The tests involved four interviews over twelve days on three topics related to familiar places and itineraries. The results showed a significant improvement in memories of places and itineraries, but no improvement in autobiographical memories. The researchers concluded that the neuropsychological conditions required for activating memory are different for a day in one's life compared to places. However, if a often recalled event becomes a familiar story, then the autobiographical/episodic memory can become a semantic memory. These findings support the hypothesis that semantic and episodic memory are two independent systems that may involve different underlying anatomical structures (Tulving, 1984).

According to Gazzaniga et al. (1998), the hippocampal region does not completely

prevent new memory creation and is therefore not solely responsible for memory. They also argue that damage to the medial temporal lobe/hippocampal area does not entirely erase established memories, indicating that explicit knowledge is not limited to this region (p. 266).

Although the hippocampus is an important factor in human memory, studies indicate that it is not solely responsible for all types of memory. Furthermore, there is evidence that challenges the idea that the hippocampus is the only area accountable for memory. Damage to other neocortical regions such as those observed in Alzheimer's or herpes simplex encephalitis can lead to retrograde amnesia, including areas like the entorhinal and perihippocampal cortex situated in the lateral cortex of the anterior pole (Parkin, 1997; Gazzaniga et al., 1998; Kolb & Whishaw, 1999).

The literature covers two types of amnesia - limited scope retrograde amnesia and diencephalic amnesia. The former results in significant memory loss from before the injury, but patients can still create new long-term memories (Miller et al., 2001; DallaBarba et al., Mantovan, Ferruzza; Denes, 1997). This is typically due to damage to the anterior temporal lobe that affects memory retention more than acquisition (Miller et al., 2001). On the other hand, diencephalic amnesia refers to a different type of amnesia.

Memory loss caused by damage to midline structures of the diencephalon, such as the dorsal medial nucleus of the thalamus and mamillary bodies, is known as diencephalic amnesia. This can result from factors like strokes, tumours or metabolic issues. Evidence for this type of memory loss comes from research on Korsakoff's syndrome patients with brain damage due to a deficiency of thiamine who experience both anterograde and retrograde amnesia.

Damaging

important brain regions responsible for memory, such as the thalamus, mammillary bodies, and basal forebrain can be caused by a lack of thiamine. This deficiency may lead to Korsakoff's disease which is mainly associated with prolonged alcoholism (Parkin, 1987). The illness triggers degeneration in the diencephalon; however, it remains unclear whether amnesia results from damage to either the dorsomedial thalamic nucleus or mamillary bodies or both (Gazzaniga et al., 1998). Nevertheless, relying solely on the hippocampus cannot explain memory loss since amnesia occurs when there is harm to the diencephalon region of the brain.

According to Kolb and Whishaw (1999), the extensive literature suggests that the amygdala has a significant role in memory associated with emotions, as well as visceral and olfactory events, and arousal. Additionally, Sarter and Markowitsch's (1985) current research shows that emotional memory for both humans and animals involves the amygdala. Therefore, any amnesia caused by this brain region may stem from emotional factors. Ultimately, evidence contradicts the notion that memory is exclusively situated in the hippocampus.

While the hippocampus is essential for forming new memories, studies have revealed that other brain regions including the diencephalon, perirhinal cortex, amygdala and basal forebrain also play a significant role in human memory. Rather than solely attributing memory function to the hippocampus, it is more accurate to recognize its critical role alongside these additional regions. This discussion highlights the intricate complexity of human memory and cognitive functioning. According to Ramachandran (1998), research on amnesia suggests that although old memories are stored elsewhere in the brain, creating new memory traces heavily relies on involvement from the hippocampus.