Glen Calvin
Psych 472
Neuropsychology
12-10-99
Professor Morgan

	The detrimental effects of alcohol on the human brain 
have been well known for centuries but it was not until 1878 
that Lawson made the first scientific link between alcohol 
and amnesia (Martin 362).  This link would spark new 
interest and studies in the effects of chronic alcoholism as 
well as encourage new research into the areas of amnesia and 
memory functioning.  In 1881, Carl Wernicke described a 
neurological disturbance which he called Hemorrhagic 
superior encephalitis (Knight 55).  Six years later, 
Korsakoff would describe a peripheral nervous disease which 
he called cerebropathia psychica toxaemica which he said was 
a consequence of long term alcoholism (Knight 55). The term 
korsakoff's syndrome was first used by Jolly in 1897 to 
describe a case of permanent amnesia without any mention of 
peripheral neuritis (Knight 56).  Early descriptions of 
Wernicke's encephalitis and Korsakoff's disease (KD)  
involved an inability to properly digest food as a primary 
etiologic factor and often marked people with carcinoma of 
the stomach, persistent vomiting during pregnancy, or severe 
malnutrition as beginning to develop Wernicke's 
encephalopathy (Knight 56).  We now generally describe 
Korsakoff's disease as a disorder marked by profound and 
irreversible amnesia, without any dementia symptoms, or any 
major problems with higher activities, and Wernicke's 
encephalopathy as the episode of 'acute confusion' prior to 
the onset of KD  (Knight 54). Unfortunately, the exact 
etiology of Korsakoff's disease is still unknown (Knight 
55).  Korsakoff actually believed cortical atrophy to be the 
most responsible factor for memory impairment in his cases 
(Knight 56).  He reported severe memory loss in thirty cases 
of chronic alcoholism during his study (Martin 362).  Until 
the late 1940's, it was believed that Korsakoff's disease 
was caused by pathological changes in the cortex, 
specifically the frontal lobes (Knight 56).  It should also 
be noted that Korsakoff's disease may be used to refer to 
any severe case of amnesia, but that it is primarily used to 
refer to the consequences of long term alcohol abuse (Knight 
54).  
	Korsakoff's disease is essentially, the chronic stage 
of an alcohol related brain disorder. Although the major 
symptoms of what are now known as Wernicke's Encephalopathy 
and Korsakoff's disease or syndrome are similar, they are 
far from exact.  Wernicke's encephalopathy patients exhibit 
severe confusion or delirium while Korsakoff's disease 
patients may appear quite normal.  Both conditions share 
disorientation for time and place, with Korsakoff's patients 
being more disoriented regarding time, and both include 
amnesia although KD patients suffer from a more severe and 
disabling type while Wernicke's may be masked in delirium 
(Knight 60).  Both conditions include confabulation and 
ataxia (Knight 60).  Confabulation is a rare condition in 
which Wernicke Korsakoff patients fabricate improbable 
stories or tall tales.  This behaviour is probably due to 
the memory deficit induced by the conditions which, when 
combined with poor judgment of appropriateness or 
possibility (Royce 71).  Only a small percent of Korsakoff 
Disease patients engage in confabulation, which is not 
simply a result of amnesia.  Korsakoff's Disorder patients 
are more likely to evade or be noncommittal about their 
memory impairment, simply answering "Im not interested in 
the news" or "I don't watch TV" when questioned regarding 
recent news events (Knight 61).  Ataxia is a motor 
disturbance such as Ataxic gait, a broad based staggering 
walk common in alcoholic patients (Knight 61).  Those 
patients who can still walk on their own take short, 
shuffling steps and may appear to stagger forward (Knight 
61).  This condition is attributed to alcohol related 
cerebellum damage and may appear without any signs of 
cognitive impairment (Knight 61).  
	There are many undebatable facts regarding alcohol 
consumption.  We are already destined to lose approximately 
ten percent of the billions of nerve cells we are born with, 
and alcohol consumption accelerates this aging process 
irreversibly while causing brain damage directly, not just 
through malnutrition or avitaminosis (Royce 70).  Alcohol 
related brain damage includes sludging (decrease in brain 
protein synthesis), RNA interference, nerve cell membrane 
damage, and fluid pressure leading to atrophy  (Royce 71).  
Myelinated fibers actually suffer more from alcohol induced 
lesioning than nerve cells (Victor 196).   Wernicke 
Korsakoff syndrome is a result of brain damage (Royce 71).  
Its primary symptoms are first confusion followed by 
excitement, possible double vision from palsy to the third 
and sixth cranial nerves, sleepiness, stupor, possibly 
hypothermia, illogical thinking, disorientation, severe 
memory deficits of recent events and even hallucinations 
(Royce 71).  Wernickes Encephalopathy includes ocular 
disturbances such as but not limited to hystagmus and 
paralysis of conjugate gaze (Rothschild 449).  Wernickes 
encephalopathy is characterized by morphologic lesions 
primarily localized on the thalamus, hypothalamus, brainstem 
and cerebellum, but in the early stages, the disorder is the 
result of a biochemical or neurophysiological disturbance, 
not a specific structural lesion (Rothschild 449). The 
Wernickes phase is often treatable and reversible with 
thiamine treatment, but Korsakoffs patients only show 
partial or poor recovery (Royce 71).  It has been 
established that the Wernicke Korsakoff syndrome is related 
to vitamin B deficiency but alcohol causes cerebellar 
degeneration (Royce 71).  The vitamin B complex is extremely 
important for neural functioning and its administration 
appears to dramatically improve the condition of chronically 
undernourished alcoholics (Royce 244).  Alcohol contributes 
to Korsakoffs syndrome by adding its own carbohydrate 
calories to metabolism which leads to a deprivation of B 
vitamins, specifically thiamine (Victor 195).  Thiamine is 
an organic molecule composed of a pyrimidine and thiazol 
moiety, which when combined with phosphoric acid constitutes 
thiamine pyrophosphate (TPP) (Victor 152).  Between 20 and 
40 percent of alcoholics who receive hospital care exhibit 
thiamine deficiency, which in sever cases may lead to 
peripheral neuropathy and wernickes encephalopathy 
(Rothschild 449).  Polyneuropathy or peripheral nerve 
disease is typical of alcoholics and is also evident in 
Wernickes and Korsakoffs disease patients (Knight 62).  Its 
symptoms include loss of sensation (typically in lower 
limbs), loss or reduction of ankle ore knee reflexes, 
weakness or muscle wasting in the limbs, either dull and 
aching, or paroxysmal pain in the limbs, or complaints of 
excessive sensitivity in lower limbs (making walking 
unpleasant) (Knight 61).  Immediate forced abstinence may 
result in a Wernickes patient experiencing alcohol 
withdrawal delirium including hallucinations (visual or 
tactile), autonomic hyperactivity with profuse sweating or 
tachycardia which typically goes away after three to five 
days of treatment (Knight 62).  Tachycardia of over 100 
beats per minute was recorded in 51 percent of a 245 patient 
study (Victor 14).  Although peripheral nerve disease exists 
in both, occulomotor disturbances are not as prominent in 
Korsakoff's disease patients who also do not suffer the 
alcohol withdrawal symptoms (Knight 60).  Essential DSM 
features for Wernickes Korsakoff syndrome include 1, 
impaired short term and long term memory 'following 
prolonged heavy ingestion of alcohol' with memory impairment 
in absence of delirium 2, no evidence of dementia, 
personality change, disturbance of higher cortical 
functioning or 'impairment in abstract thinking or judgment" 
and 3, memory disturbance is 'not due to any physical or any 
other mental disorder" (Knight 57).  But, Most Korsakoffs 
disease patients have some amount of high cognitive 
functioning impairment which becomes evident when testing 
problem solving skills or visuo motor tasks (Knight 58).  KD 
sufferers also have redness and or papillary atrophy of the 
tongue, dry and think skin, discoloration of the nose, 
rhinophyma, and acne rosacea (Victor 14).  About two thirds 
of the 245 patients had signs of liver disease, 17 percent 
had decompensated liver disease, jaundice, ascites, spider 
angiomata, and evidence of portal systemic shunting (Victor 
15).  Body temperatures over 99.6 degrees Fahrenheit were 
recorded in 12 percent, and two patients had hypothermia, 
one of which had a body temperature below 92 degrees F which 
could not be measured accurately with a clinical thermometer 
(Victor 15).  This hypothermia which ended when the patient 
was treated with thiamine and fluids, is attributed to 
lesions in the posterior and poserolateral portions of the 
hypothalamus (Victor 16).  KD patients have been shown to 
have a 47 percent reduction in the nucleus basalis of 
Meynert (principal source of cholinergic innervation of the 
cerebral cortex) (Knight 65), and some have been shown to 
have a reduced blood flow to the hypothalamus and basal 
forebrain, while some show metabolic disruption in anterior 
brain areas and in the right posterior white matter (Martin 
363).  Korsakoffs disease has been implicated in loss of 
olfactory discrimination (Victor 59).  Major gross 
neuropathalogic changes in Wernickes Korsakoffs sufferers 
include widening of sulci, enlarged ventricles, lesion of 
mammillary bodies, lesion of walls of third ventricle, 
atrophy of superior cerebellar vermis, and hemorrhages in 
diencephalon and brain stem (Victor 62).  Korsakoffs 
sufferers also exhibit the cerebrospinal fluid abnormality 
of elevation of total protein from 50 to 91 mg per 100ml 
(Victor 26).  Also, most sufferers exhibit what is called 
'Global confusional state', a state of confusion, 
disorientation, apathy, and memory derangement (Victor 16).  
Few sufferers recognize their illness and those that do tend 
to minimize or 'explain away' its seriousness with weak 
rationalizations or apathetic responses (Knight 90).  Post 
mortem KD patients brain studies have helped develop three 
competing hypothesis regarding which diencephalic structures 
are involved in amnesia.  One theory states that the 
damaging lesions are in the medial thalamic nuclei, 
specifically the dorsomedial nuclei, the second attributes 
KD amnesia to the mamillary bodies alone, and the third, 
based on Mishkin's 1982 dual memory circuit model insists 
that bilateral lesions must occur on both the medial 
portions of the thalamus, and the mamillary bodies (which 
would disrupt memory circuits from both the Amygdala and 
hippocampus). (Knight 69).  Korsakoffs disease patients show 
sever anterograde amnesia (AA) (capacity to learn new info), 
and variable degrees of retrograde amnesia (RA) (inability 
to retrieve info acquired before onset of brain injury) 
(Knight 72).  The anterorade amnesia is the most striking 
feature of KD and it may take a patient weeks or months of 
practiced repetition to learn the names of the doctors 
treating him (Knight 73).  Kd patients have functional 
deficits in such tasks as delayed free recall of verbal 
material, recall of prose passages, delay recall of visual 
location, recognition of words, pictures, sentences, and 
meaningless designs, and memory of complex designs due to 
anterograde amnesia (Knight 75).  Korsakoffs patients can 
learn new motor skill normally and are unimpaired on 
semantic priming tasks which suggests that memory may exist 
in a few separate systems which may be damages or treated 
independently (Knight 87).

Bibliography

Knight, Robert G.  The Neuropsychology of Degenerative Brain 
Diseases 1992 Lawrence Erlbaum associates publishers, 
Hillsdale

 Martin, Neil G.  Human Neuropsychology  Prentice Hall,  
London. 1999.

Rothschild, Marcus A. editor  Alcohol and Abnormal Protien 
Biosynthesis biochemical and Clinical  1975, Pergamion Press 
Inc.  new York 1975

Royce, James E  Alcoholism and other Drug Problems  1996  
The Free Press, New York

Victor, Maurice  The Wernicke Korsakoff Syndrome  1989  F.A. 
Davis Company, Philadelphia

Copyright © 1999, Dr. John M. Morgan, All rights reserved - This page last edited 13 - December, 1999
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