Retrograde amnesia: causes, mechanisms, and clinical manifestations

Retrograde Amnesia

Partly because of anecdotal evidence about the manner in which retrograde amnesia is typically caused by physical trauma to the head and by the physical destruction of neurons and specific regions of the brain associated with the memory formation process, the traditional view has tended to support the theory that retrograde amnesia is substantially a function and manifestation of the physical destruction of brain matter associated with memory formation and recall. However, both traditional empirical studies of individuals suffering from amnesia and the relatively recent addition of brain imaging technology to the tools available for the study of brain-based disorders strongly suggest that retrograde amnesia (in particular) is more likely a complex function of alteration in brain processes and metabolism in addition to solely a function of the physical destruction or loss of brain matter as a the result of trauma.

Introduction

Amnesia refers to a general class of associative psychological disorders characterized by inability to of the individual to remember events, circumstances, and knowledge (Sadek, White, Taylor, et al., 2004; Staniloiu & Markowitsch, 2010). The term anterograde amnesia describes the condition as it pertains to the difficulty forming new memories; the term retrograde amnesia describes the condition whereby the individual experiences difficulty recalling past memories rather than difficulty establishing new memories (Staniloiu & Markowitsch, 2010). While volumes of prior research have identified the causal connection between damage to different regions of the brain and the formation of one type of amnesia or the other, more recent empirical evidence based largely on brain imaging studies suggests that other factors are also responsible, among them, individual metabolic and regenerative differences and the relative strength and frequency of use of specific memories prior to onset of amnesia (Staniloiu & Markowitsch, 2010).

Discussion

Differentiating Retrograde Amnesia from Anterograde Amnesia

In general, amnesia is characterized by difficulties in forming new memories or in accessing previously stored memories (James & MacKay, 2001). Typical underlying causes of amnesia fall into either: (1) organic or neurological factors, such as injuries resulting in the physical destruction of or damage to specific regions of the brain, neurological disease, or damage or alteration to the brain as the result of exposure to drugs with neurological effects; or (2) functional or psychogenic factors, such as specific mental disorders, psychological trauma, or the product of psychological defense mechanisms along the lines of those concepts originally outlined by Freud in connection with the psychological mechanics of the repression of unpleasant and challenging thoughts and memories into the unconscious mind (Staniloiu & Markowitsch, 2010).

In principle, anterograde amnesia interferes with the affected individual's ability to form new memories by virtue of a disruption to the ordinary processes by which new experiences and knowledge are transferred from short-term memory to long-term memory (Meeter & Murre, 2004). By contrast, retrograde amnesia does not typically interfere with the new memory formation processes; instead, it disrupts access to previously stored memories that were readily available to the affected individual prior to the onset of symptoms. While it is possible for anterograde amnesia and retrograde amnesia to occur together within total or global amnesia, it is much more common for them to occur separately (James & MacKay, 2001).

Identifying the Mechanics of Retrograde Amnesia

Unlike, other forms of amnesia (and unlike anterograde amnesia in particular), retrograde amnesia does not involve injury to or destruction of the hippocampal region of the brain which is known to be responsible for the initial encoding, storage, and subsequent retrieval of memories (Sadek, White, Taylor, et al., 2004). In retrograde amnesia, the processes of encoding new memories by hippocampus remain intact but the affected individual cannot recall memories that have been previously encoded. Neurological theorists originally suggested that the mechanics of retrograde amnesia, therefore, related to the fact that long-term memories are stored in the neurons and synapses of specific regions capable of sustaining injuries or of being affected by various factors that disrupt their proper functioning (Sadek, White, Taylor, et al., 2004). Brain imaging studies confirm that those factors include the efficiency of processes unrelated to the underlying cause of amnesia, such as the subsequent neurological regeneration of nerve fibers in particular (Staniloiu & Markowitsch, 2010).

As predicted, volumes of animal studies and research involving testing individuals suffering from retrograde amnesia have subsequently identified several specific regions and structures as being involved in the development of retrograde amnesia that are completely distinct from the hippocampal regions implicated in connection with anterograde amnesia. In particular, Broca's Area and Wernicke's Area have been identified in that regard (Sadek, White, Taylor, et al., 2004). The other principal importance of these findings has to do with their roles of memory in human speech and language (James & MacKay, 2001).

Retrograde amnesia is often seen in connection with injury to regions of the temporal lobe and the right temporo-prefrontal cortices (Staniloiu & Markowitsch, 2010), areas of the brain that are closely related to two specific types of memory: declarative and episodic memory (James & MacKay, 2001). Those observations would be entirely consistent with the evidence that individuals suffering from retrograde amnesia typically experience no disruption of procedural memories (such as how to drive or wash themselves) or of semantic memory (such as how to use language and understand the meaning of words in their existing vocabulary). In that regard, some of the more interesting research suggests that, unlike other forms of amnesia, the extent to which individuals suffer (and are unable to recover) from retrograde amnesia depends partially on factors other than the nature, location, and extent of the actual damage to the regions of the brain involved. Instead, the degree of retrograde amnesia and its resistance to recovery also depend substantially on factors such as the strength and frequency of use of the affected knowledge prior to the onset of retrograde amnesia (Meeter & Murre, 2004).