KS is the result of a thiamine deficiency caused by chronic alcoholism, severe malnutrition, eating disorders, chemotherapy, and rarely, Wernicke's encephalopathy (Pitel et al., 2011). KS is characterized by amnesia in a range of severity (Kessels, Kortrijk, Wester, & Nys, 2008). Because of the impairment to the ability to remember contextual information, KS patients confabulate or contrive memories (Kessels et al., 2008). Originally believed to be a correction mechanism of the brain to complete incomplete memories, confabulation does not ordinarily occur with amnesia, and this tendency is characteristic of KS, but is not of BMTL. Additionally, executive dysfunction exists in many KS patients, although this is not necessarily an effect of BMTL (Kessels, et al., 2008). Cognitive deficits characteristic of KS, such as the ability to take initiative and use abstract reasoning, accompany the memory problems typical in this condition (Paller & Acharya, 1997).
The BMTL is a procedure that was originally utilized as an experimental procedure to quell seizures in intractable epilepsy (Scoville & Milner, 1957). Typically this surgery included the removal of the medial areas of both temporal lobes (Breedlove, Watson, & Rosenzweig, 2010). In addition, the amygdala, hippocampus and parts of the adjacent cortex were removed. The amount of brain matter removed was approximately the size of a golf ball. In a bilateral resection, this amount may be slightly more (Zola-Morgan, Squire, & Amaral, 1966). Early in these experimental resections, it was believed that it was the hippocampus that lead to irreparable damage to the memory system because bilateral resection of this brain section inevitably lead to amnesia (Zola-Morgan et al., 1966). In cases of hippocampal damage, the severity of the damage was predictive of a greater amount of memory damage (Zola-Morgan et al., 1966). Scoville and Milner (1957) found similar results after a BMTL. With KS, a deficiency in thiamine causes a loss of neurons, more specifically the glial cells that nourish the central nervous system (Breedlove, Watson, and Rosenzweig, 2010). Additionally, KS causes damage to the thalamus, which may be the cause of the lack of awareness, characteristic of patients with KS (Paller & Acharya, 1997). This is especially characteristic of alcoholic KS patients. However, stroke, tumors, or head trauma can cause similar or related symptoms (Graff-Radford, Tranel, Van Hoesen & Brandt, 1990).
Symptoms of Korsakoff's Syndrome
The primary symptoms of KS are confabulation (invented memory), anterograde amnesia, which is the inability to create new memories after the amnesia-inducing event. After progression of the disease, KS patients may additionally experience retrograde amnesia, which is the loss of the ability to remember memories created before the amnesia-inducing event (Breedlove et al., 2010). KS can also cause a lack of insight as well as apathy and indifference. KS ordinarily affects declarative memory (Kessels et al., 2008), although procedural memory is not affected (Oudman, Van der Stigchel, Wester, Kessels, & Postma, 2011).
Memory Loss After BMTL
After BMTL, patients' working memory is left intact (Di Gennaro et al., 2008). In the case of H.M., the surgery caused profound anterograde amnesia, although "his overall intelligence and neurologic status (were) relatively well-preserved" (Corkin, 1992, p. 250). Other cases resulted in similar findings; anterograde amnesia was extensive (Bayley, Hopkins, & Squire, 2006). Similar to the findings of Zola-Morgan et al. (1966), Bayley, Hopkins, and Squire (2006) found that more extensive damage to the hippocampal area resulted in anterograde amnesia, although could affect retrograde amnesia as well. When damage to the hippocampal region was severe, retrograde amnesia accompanied the anterograde amnesia, sometimes for a few to several years (Bayley et al., 2006). Additionally, Corkin (1992) suggested that the procedure of BMTL can hyposexuality, although little research has been done on this effect.
Memory Loss with Korsakoff's Syndrome
Patients with KS show a loss of immediate memory as well as remote memory, and these memory deficits can worsen as the condition progresses (Pital et al., 2011). Although initially, Korsakoff patients may present with anterograde amnesia exclusively, during disease progression, the amnesia may globalize and result in retrograde amnesia as well. Paller and Acharya (1997) discovered disruptions in the normal interactions of the thalamocortical area that support the normal processes of memory. Paller and Acharya (1997) concluded the impairment of KS is not solely in the hippocampus, which is a major component of the memory loss associated with BMTL. Rather, the primary impairment of KS is in the frontal and parietal lobes as well as the cingulate (Paller & Acharya, 1997).
Although it is well established that the hippocampus and the medial temporal lobes are involved in the ability to form new episodic and semantic memories, less understood is the extent to which these brain areas are implicated in the ability to establish episodic and semantic memories long-term (Kensinger, Ullman, & Corkin, 2001). Lexical memory, which is the ability to retain information about words and their meanings is a component of semantic memory. H.M.'s lexical memory and language processing remained intact for the most part (Kensinger, Ullman & Corkin, 2001). This is similar in KS patients, who usually retain their ability to carry on normal conversation, although may forget shortly thereafter, that the conversation took place (Pitel et al., 2011).
Contextual Memory Loss in Both Types of Amnesia
Contextual memory supports the ability to recall past events and store newly acquired information. This is often referred to as target information and is commonly processed with the help of contexts (Kessels & Kopelman, 2012). Context provides meaning that is characteristic of episodic memory, without which, the memories would be meaningless (Kessels & Kopelman, 2012). It is, in fact, the context that gives episodic memory is distinct nature. Korsakoff was the first neurologist to discover contextual memory was severely challenged in his patients with KS (Pitel et al., 2011; Victor & Yakovlev, 1955). Kessels and Kopelman (2012) found it was difficult, if not impossible for KS patients to utilize contexts as retrieval cues for recalling information. However, KS patients can continue to learn new contextual information, although likely through iterative presentation (Oudman et al., 2011).
This was not the case with H.M. after damage sustained to his temporal lobes. The hippocampus, which was destroyed at the time of his surgical procedure, is implicated in the ability to retrieve episodic and contextual memories (Brian et al., 2010). Not only is the hippocampus implicated in the ability to form new contextual memories, but this brain area is necessary for retrieving episodic and contextual memories as well. This may explain why H.M. lost the ability to acquire new memories, but many of his episodic memories were inaccurate or absent (Brian et al., 2010). Although the hippocampus is implicated in the retrieval of episodic memories, this same loss is characteristic of KS patients, although KS involves more damage to the frontal and parietal lobes and the cingulate (Paller & Acharya, 1997). In KS, however, there is usually damage to the hippocampus as well. These findings, when synthesized, lead one to conclude that amnesia and various components of the memory system may not be as exactly understood as one might believe.
Korsakoff’s syndrome damages the thalamus and hypothalamus, hippocampus, cerebellum and neocortex, all of which contributes to the loss of information retrieval (Sullivan & Marsh, 2003). The BMTL procedure undergone by H. M. removed the medial areas of both temporal lobes the amygdala, hippocampus and parts of the adjacent cortex. The condition and the surgery resulted in memory loss, presumably because of the loss or damage to the hippocampus. Although patients of each condition can experience a profound loss of memory, Squire (1982) believes KS causes deficits unrelated to amnesia, and are likely the result of damage to the frontal lobe. Patients with KS experience some of the same losses as individuals who received the BLML surgical procedure. One major difference exists, however, between the two: Korsakoff's Syndrome is often preceded by alcohol abuse whereas the bilateral medial lobectomy is preceded by intractable epilepsy. The former, at least in the case of alcoholic Korsakoff's Syndrome, is preventable, the latter, is not.
Bayley, P., Hopkins, R., & Squire, L. (2006). The fate of old memories after medial temporal lobe damage. The Journal Of Neuroscience: The Official Journal Of The Society For Neuroscience, 26(51), 13311-13317.
Breedlove, S. M., Watson, N. V., & Rosenzweig, M. R. (2010). Biological psychology: An introduction to behavioral, cognitive, and clinical neuroscience. (6th ed.) Sunderland, MA: Sinauer Associates, Inc. Publishers.
Brian J., W., Miou, Z., Ying, C., J., B., Mikael Guzman, K., Sherveen N., P., & ... Alcino J., S. (2010). The Hippocampus Plays a Selective Role in the Retrieval of Detailed Contextual Memories. Current Biology, 201336-1344. doi:10.1016/j.cub.2010.06.068
Corkin, S. S. (1992). Lasting consequences of bilateral medial temporal lobectomy: Clinical course and experimental findings in H. M. In S. M. Kosslyn, R. A. Andersen (Eds.) , Frontiers in cognitive neuroscience (pp. 516-526). Cambridge, MA US: The MIT Press.
Di Gennaro, G., Grammaldo, L., Quarato, P., Esposito, V., Mascia, A., Sparano, A., & ... Picardi, A. (2006). Severe amnesia following bilateral medial temporal lobe damage occurring on two distinct occasions. Neurological Sciences, 27(2), 129-133.
Kensinger, E. A., Ullman, M. T., & Corkin, S. (2001). Bilateral medial temporal lobe damage does not affect lexical or grammatical processing: Evidence from amnesic patient H.M. Hippocampus, 11(4), 347-360. doi: 10.1002/hipo.1049
Kessels, R. C., Kortrijk, H. E., Wester, A. J., & Nys, G. S. (2008). Confabulation behavior and false memories in Korsakoff's syndrome: Role of source memory and executive functioning. Psychiatry & Clinical Neurosciences, 62(2), 220-225. doi:10.1111/j.1440- 1819.2008.01758.x
Kessels, R., & Kopelman, M. (2012). Context memory in Korsakoff's syndrome. Neuropsychology Review, 22(2), 117-131. doi:10.1007/s11065-012-9202-5
Graff-Radford, N. R., Tranel, D., Van Hoesen, G. W., & Brandt, J.P. (1990). Diencephalic amnesia. Brain, 113, 1-25.
Paller, K. A., & Acharya, A. (1997). Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome. Journal Of Cognitive Neuroscience, 9(2), 277.
Oudman, E., Van der Stigchel, S., Wester, A. J., Kessels, R. P., & Postma, A. (2011). Intact memory for implicit contextual information in Korsakoff's amnesia. Neuropsychologia, 49(10), 2848-2855. doi: 10.1016/j.neuropsychologia.2011.06.010
Pitel, A. L., Zahr, N. M., Jackson, K., Sassoon, S. A., Rosenbloom, M. J., Pfefferbaum, A., & Sullivan, E. V. (2011). Signs of preclinical Wernicke’s encephalopathy and thiamine levels as predictors of neuropsychological deficits in alcoholism without Korsakoff’s syndrome. Neuropsychopharmacology, 36, 580–538.
Scoville, W., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal Of Neurology, Neurosurgery & Psychiatry, 20(1), 11.
Squire, L. R. (1982). Comparisons between forms of amnesia: Some deficits are unique to Korsakoff's syndrome. Journal Of Experimental Psychology: Learning, Memory, And Cognition, 8(6), 560-571. doi:10.1037/0278-73184.108.40.2060
Sullivan, E.V., & Marsh, L. (2003). Hippocampal volume deficits in alcoholic Korsakoff’s syndrome. Neurology, 61, 1716-1719.
Victor, M., & Yakovlev, P. I. (1955). S. S. Korsakoff's psychic disorder in conjunction with peripheral neuritis; a translation of Korsakoff's original article with brief comments on the author and his contributions to clinical medicine. Neurology, 5394-406.
Zola-Morgan, S., Squire, L., & Amaral, D. (1986). Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus. The Journal Of Neuroscience: The Official Journal Of The Society For Neuroscience, 6(10), 2950-2967.