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Figure B-3

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Figure B-2

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Wernicke’s Encephalopathy is known as a precursor of KS, with studies finding that those who don’t receive thiamine treatment for Wernicke’s Encephalopathy can suffer hemorrhagic lesions around the diencephalon (Oscar-Berman, 2012). It was originally believed that damage to the diencephalon (Figure B-2) was the cause for amnesia in KS, however it was later found that KS involved damage to the frontal brain regions, the medial dorsal thalamic nucleus and the medial mammillary nucleus (Oscar-Berman, 2012). Additionally, more recently, KS has been linked to a loss of connectivity in the cerebellothalamocortical and limbic circuitry system.

These lesions occur due to the damaging effects of alcohol, causing loss of grey and white matter in the orbitofrontal and mesiotemporal cortex and in dienchephalic structures (Goldstein & McNeil, 2013), and the thinning of the corpus callosum (Oscar-Berman, 2012). This is demonstrated in Figure B. Harper (2009) argued that, due to the fact that the corpus callosum allows for interhemispheric exchange of sensory, motor and cognitive information, this reduction in white matter of the corpus callosum would be the responsible for changes in cognitive performance.

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Figure E

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Thiamine (Vitamin B) is an essential nutrient for tissue, required by both neurons and glia cells in the brain. Excessive consumption of alcohol can contribute to thiamine deficiency through three mechanisms; 1) poor nutrition, 2) lower levels of absorption and uptake of thiamine, 3) impaired functioning of thiamine in the cells (P. R. Martin et al., 2003). According to Martin et al. (2003), the consequences of this are:

Biochemical reactions, such as neurotransmitter reactions, are unable to occur efficiently, causing a lack of communication in the nervous system.

Enzymes that rely on thiamine can’t function, which causes oxidative stress from free radicals

Cerebellar degeneration, affecting movement, body and eye coordination and cognitive and sensory functioning.

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Figure D

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Figure C

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The d2 Test - 14 lines, each with 47 letters. Target letter ‘d’ needs to be identified against distractor letters ‘p’. Participant must identify as many target letters as possible under timed conditions.

Trail Making Test - Patients have to try and connect the dots in correct sequence under timed pressure. See example in Figure D.

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The Flexibility Test - patient given the name of an object and its common use and must come up with a series of alternative uses.

Verbal Fluency Test - Patient given 120 seconds to verbally give a list as long as possible for the target letter, semantic category, and two alternating categories (one condition at a time).

Hayling Test - sentence completion task with 15 sentences with last word omitted. In first section, patient must respond with filler word. In second section, patient must respond with a word that doesn’t belong.

BADS Battery - A 20-item questionnaire consisting of 6 subtests that assess emotional and personality changes as well motivational, behavioural and cognitive changes.

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California Verbal Learning Test - 16 words consisting of 4 words in 4 semantic categories. Asked to freely recall the words. After long delay, 28 distractor words are mixed in with 16 target words and patient must identify target words.

AB-AC Task - 12 related words are shown in pairs. Patient must remember the words as pairs, being asked later to identify the second word when shown the first.

Rey Complex Figure Task - Patients must look at figure and then try and draw it after delay. See example in Figure C

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Once a patient has passed the Wernicke's Encephalopathy stage and progress onto KS, restoration of functioning to premorbid capacity isn't accomplishable. Rather, compensatory methods are used to assist in improving cognitive function and health The following are compensatory methods as well as preventative methods to slow the progression.

Abstinence - Since KS can be caused by excessive alcohol use, abstaining from drinking would allow for a better chance at recovery. Svanberg and Evans (2013) highlight the importance of providing support by making explicit associations between concepts, such as drinking alcohol and consequential behaviour. This would allow an understanding of the consequences of drinking and thus may make abstinence easier for the patient.

Memory Aid - Diaries, lists and prompts (see Figure E)can be used to help patients in carrying out day-to-day activities. As well as this, breaking down routine activities into steps so that they can be easily followed and using the method of Errorless Learning (See video 3) will allow patients to still learn new information (Thomson, Guerrini & Marshall, 2012). This will not restore memory function, but will allow for more independence for patients.

Thiamine - Excessive drinking of alcohol prevents the absorption of Thiamine into the body. Thus, one form of treatment is Thiamine supplementation, used to improve the symptoms of KS (Sum & Brody, 2012). In most cases, thiamine administered orally, intravenously, or intramuscularly with varying dosages depending on individual's needs, two to three times per day for approximately 3-5 days (Sum & Brody, 2012).

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Figure A - Thomson, Guerrini & Marshall (2012)

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Gerridzen, I. J., & Goossensen, M. A. (2014). Patients with Korsakoff syndrome in nursing homes: characteristics, comorbidity, and use of psychotropic drugs. International Psychogeriatrics, 26(01), 115-121. doi:doi:10.1017/S1041610213001543

Goldstein, L. H., & McNeil, J. E. (2013). Clinical Neuropsychology: A Practical Guide to Assessment and Management for Clinicians (2nd ed.). West Sussex: Wiley-Blackwell.

Harper, C. (2009). The neuropathology of alcohol-related brain damage. Alcohol And Alcoholism (Oxford, Oxfordshire), 44(2), 136-140. doi:10.1093/alcalc/agn102

Kopelman, M. D., Thomson, A. D., Guerrini, I., & Marshall, E. J. (2009). The Korsakoff Syndrome: Clinical aspects, psychology and treatment. Alcohol and Alcoholism, 44(2), 148-154. doi:10.1093/alcalc/agn118

Labudda, K., Todorovski, S., Markowitsch, H. J., & Brand, M. (2008). Judgment and memory performance for emotional stimuli in patients with alcoholic Korsakoff syndrome. Journal of Clinical and Experimental Neuropsychology, 30(2), 224-235. doi:10.1080/13803390701363811

Martin, E., & McFerran, T. Korsakoff's syndrome: 'Oxford University Press'.

Martin, P. R., Singleton, C. K., & Hiller-Sturmhöfel, S. (2003). The role of thiamine deficiency in alcoholic brain disease. Alcohol Research & Health: The Journal Of The National Institute On Alcohol Abuse And Alcoholism, 27(2), 134-142.  Retrieved from

http:// ezproxy.acu.edu.au/login?url=https://search.ebscohost.com/login.aspx?direct=true&db=mdc&AN=15303623&site=ehost-live

Noel, X., Schmidt, N., Van der Linden, M., Sferrazza, R., & et al. (2001). An atypical neuropsychological profile of a Korsakoff syndrome patient throughout the follow-up. European Neurology, 46(3), 140-147. doi:10.1159/000050787

Oscar-berman, M. (2012). Function and dysfunction of prefrontal brain circuitry in alcoholic Korsakoff's Syndrome. Neuropsychology Review, 22(2), 154-169. doi:10.1007/s11065-012-9198-x

Sum, S. S.-M., & Brody, R. (2012). The link between thiamine supplementation and treatment of Wernicke-Korsakoff Syndrome in patients with alcoholism. Clinical Nutrition, 27(4), 334-338. doi:10.1097/TIN.0b013e31826f915e

Thomson, A. D., Guerrini, I., & Marshall, E. J. (2012). The evolution and treatment of Korsakoff's Syndrome. Neuropsychology Review, 22(2), 81-92. doi:10.1007/s11065-012-9196-z

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- Anterograde and retrograde amnesia

- Disorientation of place and time

- Lack of insight

- Confabulation

- Anxiety

- Apathy

- Thomson, Guerrini & Marshall (2012)

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- Definition

- Symptoms and Causes

- Neurological Profile

- Cognitive Profile

- Instruments for Assessent

- Approaches to Rehabilitation

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No single test can completely assess the presence and degree of KS, and thus multiple cognitive tests are used to get a full picture. The following are tests used for KS (Maharasingam, Macniven, & Mason, 2013; Noel, Schmidt, Van der Linden, Sferrazza, & et al., 2001)

As stated by Thomson, Guerrini & Marshall (2012), these tests need to be used in conjunction with a collateral history of the patient's premorbid functioning and alcohol use history, as well as a physical examination.

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Instruments for  Assessment of Korsakoff's Syndrome

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Instruments for  Assessment of Korsakoff's Syndrome

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Confabulations are memory distortions that occur when information is missing in ones memory (Oscar-berman, 2012). Confabulations can be divided into spontaneous (consistent erroneous memories) or provoked (distortion in memory made in response to a gap in memory) (Kopelman et al., 2009). Spontaneous is usually rare in KS, whereas provoked is more common (Kopelman et al., 2009).

An example of confabulation is demonstrated in Video 2.

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A damaged frontal lobe can lead to problems in executive functioning .A case study by Noel et al. (2001) found deficits in inhibition, flexibility and rule detection in a KS patient; However, it was also found that the patient had intact abstract reasoning.

This lack of executive function is mainly evident in one's lack of behaviour regulation (Oscar-Berman,2012)

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Kopelman, Thomson, Guerrini, and Marshall (2009) explored the damaging effects that KS has on memory. It was found that episodic memory is severely impacted in KS, with patients showing retrograde amnesia, affecting ability to freely recall memories and mentally travel back in time. Semantic memory is also affected in KS, affecting one’s ability to make new memories containing fact, concepts and language. Labudda, Todorovski, Markowitsch, and Brand (2008) found that this occurs regardless of if the stimuli are verbal or pictorial, and that the facilitation of emotion for memory that is present for healthy people is not present for those with KS. However, as found by Kopelman et al. (2009), implicit memory, such as responses to priming or procedural memory, is preserved in KS.

Thus, it appears that only secondary memory is marginally impacted by KS, whilst working memory remains in tact. Overall, Noel, Schmidt, Van der Linden, Sferrazza, and et al. (2001) suggest these memory impairments are due to the frontal lobe dysfunctioning.

An example of a KS patient with memory impairment is shown in Video 1.

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The Neurological Pathology of Korsakoff's Syndrome 

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The Neurological Pathology of Korsakoff's Syndrome 

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Impact on Cognition of Korsakoff's Syndrome 

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Impact on Cognition of Korsakoff's Syndrome 

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Figure B

A) Control brain

B) Alcoholic brain

C) Korsakoff brain

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Korsakoff’s syndrome (KS) is an organic disorder of the brain, causing brain lesions, memory impairment and confabulation (Martin & McFerran). It usually results from acute Wernicke’s encephalopathy, which tends to be brought on by alcoholism and thiamine deficiency (Gerridzen & Goossensen, 2014).