Wernicke encephalopathy

Wernicke encephalopathy (WE), also Wernicke's

Wernicke encephalopathy
encephalopathy,[1] or wet brain is the presence of
neurological symptoms caused by biochemical lesions Other Wernicke's disease
of the central nervous system after exhaustion of B- names
vitamin reserves, in particular thiamine (vitamin B1 ).[2]
The condition is part of a larger group of thiamine
deficiency disorders that includes beriberi, in all its
forms, and alcoholic Korsakoff syndrome. When it
occurs simultaneously with alcoholic Korsakoff
syndrome it is known as Wernicke–Korsakoff
syndrome.[3][4]

Classically, Wernicke encephalopathy is characterised

by a triad of symptoms: ophthalmoplegia, ataxia, and Hypothalamus
confusion. Around 10% of patients exhibit all three
features, and other symptoms may also be present.[5] Specialty Neurology
While it is commonly regarded as a condition peculiar Symptoms Ataxia, ophthalmoplegia,
to malnourished people with alcohol misuse, it can be confusion
caused by a variety of diseases.[3][6] It is treated with Causes Thiamine deficency
thiamine supplementation, which can lead to
improvement of the symptoms and often complete Risk factors Alcohol use disorder,
resolution, particularly in those where alcohol misuse is malnutrition
not the underlying cause.[7] Often other nutrients also
need to be replaced, depending on the cause. Medical literature notes how managing the condition in a
timely fashion can avoid worsening symptoms.[6][8][9]

Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is
considered underdiagnosed; probably, many cases are in patients who do not have commonly-associated
symptoms.[10]

Signs and symptoms

The classic triad of symptoms found in Wernicke encephalopathy is:[11]

ophthalmoplegia (later expanded to other eye movement disorders, most commonly

affecting the lateral rectus muscle.[11] Lateral nystagmus is most commonly seen although
lateral rectus palsy, usually bilateral, may be seen).
ataxia (later expanded to imbalance or any cerebellar signs)
confusion (later expanded to other mental changes. Has 82% incidence in diagnosis cases)

Other symptoms found in patients with this condition include:

pupillary changes, retinal hemorrhage, papilledema,[12] impaired vision and hearing,[13]

vision loss[14][15]
 hearing loss,[16]
fatigability, apathy, irritability, drowsiness, psycho and/or motor slowing[17]
dysphagia,[18] blush, sleep apnea, epilepsy[19] and stupor
lactic acidosis[20]
memory impairment,[11] amnesia,[21] depression,[22] psychosis[23][24]
hypothermia,[14][25][26] polyneuropathy,[27] hyperhidrosis.[18][28]

Although hypothermia is usually diagnosed with a body temperature of 35 °C (95 °F), or less, incipient
cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can
promote the development of an infection.[18] The patient may report feeling cold, followed by mild chills,
cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques
are advised to prevent hypothermia.

Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest
pain, orthostatic hypotension, changes in heart rate and blood pressure.[29] The lack of thiamine sometimes
affects other major energy consumers, the myocardium, and also patients may have developed
cardiomegaly.[30] Heart failure with lactic acidosis syndrome has been observed.[31] Cardiac abnormalities
are an aspect of the WE, which was not included in the traditional approach,[4][32] and are not classified as
a separate disease. Infections have been pointed out as one of the most frequent triggers of death in
WE.[33][32] Furthermore, infections are usually present in pediatric cases.[34][35]

In the last stage other symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic
dyskinesias and coma.

Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to
call it Wernicke disease rather than simply encephalopathy.[4][36]

Early symptoms are nonspecific,[37][38] and it has been stated that WE may present nonspecific
findings.[39] In Wernicke Korsakoff's syndrome some single symptoms are present in about one-third.[40]

Location of the lesion

Depending on the location of the brain lesion different symptoms are more frequent:

Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy:
nystagmus.
Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunction: temperature;
cardiocirculatory; respiratory.
Medulla: vestibular region. Cerebellum. - Ataxia.
Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.

Mamillary lesion are characteristic-small petechial hemorrhages are found.

Diffuse cerebral dysfunction.- Altered cognition: global confusional state.

Brainstem: periaqueductal gray.- Reduction of consciousness[41]
 Hypothalamic lesions may also affect the immune system, which is known in people who
consume excessive amounts of alcohol, causing dysplasias and infections.

Korsakoff syndrome

Korsakoff syndrome, characterised by memory impairment, confabulation, confusion and personality

changes, has a strong and recognised link with WE.[3][42] A very high percentage of patients with
Wernicke–Korsakoff syndrome also have peripheral neuropathy, and many people who consume excess
alcohol have this neuropathy without other neurologic signs or symptoms.[43] Korsakoff's occurs much
more frequently in WE due to chronic alcoholism.[42] It is uncommon among those who do not consume
excessive amounts of alcohol. Up to 80% of WE patients who misuse alcohol develop Korsakoff's
syndrome.[39] In Korsakoff's, is usually observed atrophy of the thalamus and the mammillary bodies, and
frontal lobe involvement.[39] In a study, half of Wernicke–Korsakoff cases had good recovery from the
amnesic state, which may take from 2 months to 10 years.[2]

Risk factors
Wernicke encephalopathy has classically been thought of as a disease solely of people who drink excessive
amounts of alcohol, but it is also found in the chronically undernourished, and in recent years had been
discovered post bariatric surgery.[11][39] Without being exhaustive, the documented causes of Wernicke
encephalopathy have included:

pancreatitis, liver dysfunction, chronic diarrhea, celiac disease, Crohn's disease, uremia,[39]
thyrotoxicosis[44]
vomiting,[6] hyperemesis gravidarum,[44] malabsorption, gastrointestinal surgery or
diseases[6]
incomplete parenteral nutrition,[44] starvation/fasting[6]
chemotherapy,[39] renal dialysis,[44] diuretic therapy,[44] stem cell/marrow transplantation[6]
cancer, AIDS,[45] Creutzfeldt–Jakob disease,[11][46] febrile infections[6]
this disease may even occur in some people with normal, or even high blood thiamine
levels, are people with deficiencies in intracellular transport of this vitamin.[11] Selected
genetic mutations, including presence of the X-linked transketolase-like 1 gene, SLC19A2
thiamine transporter protein mutations, and the aldehyde dehydrogenase-2 gene, which may
predispose to alcohol use disorder.[39] The APOE epsilon-4 allele, involved in Alzheimer's
disease, may increase the chance of developing neurological symptoms.[39]

Pathophysiology
Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke
encephalopathy. Thiamine, also called B1 , helps to break down glucose. Specifically, it acts as an essential
coenzyme to the TCA cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more
active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine
reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic
inflammatory states or in diabetes.[11][39] Thiamine is involved in:[39][47]

1. Metabolism of carbohydrates, releasing energy.

2. Production of neurotransmitters including glutamic acid and GABA.
 3. Lipid metabolism, necessary for myelin production.
4. Amino acid modification. Probably linked to the production of taurine, of great cardiac
importance.[48][49]

Neuropathology

The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: oxidative

damage, mitochondrial injury leading to apoptosis, and directly stimulating a pro-apoptotic pathway.[50]
Thiamine deficiency affects both neurons and astrocytes, glial cells of the brain. Thiamine deficiency alters
the glutamate uptake of astrocytes, through changes in the expression of astrocytic glutamate transporters
EAAT1 and EAAT2, leading to excitotoxicity. Other changes include those to the GABA transporter
subtype GAT-3, GFAP, glutamine synthetase, and the Aquaporin 4 channel.[51] Focal lactic acidosis also
causes secondary oedema, oxidative stress, inflammation and white matter damage.[52]

Pathological anatomy

Despite its name, WE is not related to Wernicke's area, a region of the

brain associated with speech and language interpretation.

Brain lesions in WE are usually credited to focal lactic acidosis. An

absence of thiamine can lead to too much pyruvate within the cells
since it's not available to help convert pyruvate through the TCA
cycle. An increase in pyruvate causes an increase in lactate
concentration leading to focal lactic acidosis.[53]

Lesions can be reversed in most cases with immediate supplementation

of thiamine.
Cerebellum
Lesions are usually symmetrical in the periventricular region,
diencephalon, the midbrain, hypothalamus, and cerebellar vermis.
Brainstem lesions may include cranial nerve III, IV, VI and VIII nuclei, the medial thalamic nuclei, and the
dorsal nucleus of the vagus nerve. Oedema may be found in the regions surrounding the third ventricle, and
fourth ventricle, also appearing petechiae and small hemorrhages.[54] Chronic cases can present the atrophy
of the mammillary bodies.[55]

In 1949, the idea that WE lesions are a result of a disruption to the blood-brain barrier was introduced.[53]
Large proteins passing into the brain can put neurological tissue at risk of toxic effects. The blood-brain
barrier junctions are typically found to have WE lesions located at that region of the brain.[53]

An altered blood–brain barrier may cause a perturbed response to certain drugs and foods.[56]

Diagnosis
Diagnosis of Wernicke encephalopathy or disease is made clinically.[6][57] Caine et al. in 1997 established
criteria that Wernicke encephalopathy can be diagnosed in any patient with just two or more of the main
symptoms noted above.[58] The sensitivity of the diagnosis by the classic triad was 23% but increased to
85% taking two or more of the four classic features. These criteria are challenged because all the cases he
studied were people who drank excessive amounts of alcohol. Some consider it sufficient to suspect the
presence of the disease with only one of the principal symptoms.[5] Some British hospital protocols suspect
WE with any one of these symptoms: confusion, decreased consciousness level (or unconsciousness, stupor
or coma), memory loss, ataxia or unsteadiness, ophthalmoplegia or nystagmus, and unexplained
hypotension with hypothermia. The presence of only one sign should be sufficient for treatment.[59]

The sensitivity of magnetic resonance imaging (MR) was 53% and the specificity was 93%. The reversible
cytotoxic edema was considered the most characteristic lesion of WE. The location of the lesions were
more frequently atypical among people who drank appropriate amounts of alcohol, while typical contrast
enhancement in the thalamus and the mammillary bodies was observed frequently associated with alcohol
misuse.[55] These abnormalities may include:[11]

Dorsomedial thalami, periaqueductal gray matter, mamillary bodies, tectal plate and
brainstem nuclei are commonly affected.[60] Involvement is always bilateral and symmetric.
Value of DWI in the diagnosis of WE is minimal. Axial FLAIR MRI images represent the best
diagnostic MRI sequence. Contrast material may highlight involvement of the mamillary
bodies.

There appears to be very little value for CT scans.[6]

Thiamine can be measured using an erythrocyte transketolase activity assay,[6] or by activation by

measurement of in vitro thiamine diphosphate levels.[6] Normal thiamine levels do not necessarily rule out
the presence of WE,[6] as this may be a patient with difficulties in intracellular transport.

Prevention
There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of
alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent
diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and
others.[59][61][62]

Some experts advise parenteral thiamine should be given to all at-risk patients in the emergency
department.[6]

In the clinical diagnosis should be remembered that early symptoms are nonspecific,[37][38] and it has been
stated that WE may present nonspecific findings.[39] There is consensus to provide water-soluble vitamins
and minerals after gastric operations.

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases.
Improvement is difficult to quantify because they applied several different actions. Avoiding or moderating
alcohol consumption and having adequate nutrition reduces one of the main risk factors in developing
Wernicke–Korsakoff syndrome..

Treatment
Most symptoms will improve quickly if deficiencies are treated early. Memory disorder may be
permanent.[43]

In patients suspected of WE, thiamine treatment should be started immediately.[39] Blood should be
immediately taken to test for thiamine, other vitamins and minerals levels. Following this an immediate
intravenous or intramuscular dose of thiamine should be administered[36] two or three times daily. Thiamine
administration is usually continued until clinical improvement ceases.[6]
Considering the diversity of possible causes and several surprising symptomatologic presentations, and
because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic
from the first day, some qualified authors indicate parenteral thiamine if WE is suspected, both as a resource
for diagnosis and treatment.[6] The diagnosis is highly supported by the response to parenteral thiamine, but
is not sufficient to be excluded by the lack of it.[63] Parenteral thiamine administration is associated with a
very small risk of anaphylaxis.[64]

People who consume excessive amounts of alcohol may have poor dietary intakes of several vitamins, and
impaired thiamine absorption, metabolism, and storage; they may thus require higher doses.[37]

If glucose is given, such as in people with an alcohol use disorder who are also hypoglycaemic, thiamine
must be given concurrently. If this is not done, the glucose will rapidly consume the remaining thiamine
reserves, exacerbating this condition.[39]

The observation of edema in MR, and also the finding of inflation and macrophages in necropsied
tissues,[54] has led to successful administration of antiinflammatories.[65][66]

Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease.[33][32] In
particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease.[39]

Other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide,
zinc,[67][68] phosphorus (dicalcium phosphate)[69] and in some cases taurine, especially suitable when there
cardiocirculatory impairment.[70][71] Patient-guided nutrition is suggested. In patients with Wernicke–
Korsakoff syndrome, even higher doses of parenteral thiamine are recommended. Concurrent toxic effects
of alcohol should also be considered.[42][69]

Epidemiology
There are no conclusive statistical studies, all figures are based on partial studies.

Wernicke's lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% of people
with an alcohol use disorder. This figure increases to 35% of such individuals if including cerebellar
damage due to lack of thiamine.[72]

Most autopsy cases were from people with an alcohol use disorder. Autopsy series were performed in
hospitals on the material available which is unlikely to be representative of the entire population.
Considering the slight affectations, previous to the generation of observable lesions at necropsy, the
percentage should be higher. There is evidence to indicate that Wernicke encephalopathy is
underdiagnosed.[17][73] For example, in one 1986 study, 80% of cases were diagnosed postmortem.[17] Is
estimated that only 5–14% of patients with WE are diagnosed in life.[72][74]

In a series of autopsy studies held in Recife, Brazil, it was found that only 7 out of 36 had consumed
excessive amounts of alcohol, and only a small minority had malnutrition.[75] In a reviewed of 53 published
case reports from 2001 to 2011, the relationship with alcohol was also about 20% (10 out of 53 cases).[11]

WE related to alcohol misuse is more common in males and is more common in females when not related
to alcohol misuse.[53] In alcohol-related cases, WE patients average the age of 40, and non-alcohol-related
cases typically occur in younger people.[53]

History
WE was first identified in 1881 by the German neurologist Carl Wernicke, although the link with thiamine
was not identified until the 1930s.

Carl Wernicke discovered the sensory center of speech. Wernicke figured out that Broca's area was not the
only center of speech, it was also able to distinguish motor aphasia from sensory aphasia.[76] He also
pointed to the possibility of conduction aphasia since he came to understand the arrangement of the brain's
extrinsic and intrinsic connections. He demonstrated that the sensory information reached its corresponding
area in the cerebral cortex through projection fibers. From there, this information, following the association
system, would be distributed to different regions of the cortex, integrating sensory processing.[76]

He reported three patients with WE, including two men (aged 33 and 36) who were alcoholics and one
woman (aged 20) who ingested sulfuric acid, leading to pyloric stenosis. All three had ocular motor
abnormalities and he performed an autopsy on each, providing a clinical-pathological correlation.[77]

A similar presentation of this disease was described by the Russian psychiatrist Sergei Korsakoff in a series
of articles published 1887–1891;[11] where the chronic version of WE was described as Korsakoff's
Syndrome, involving symptoms of amnesia.[78][79][9]

References
1. "Wernicke Encephalopathy" (https://meshb.nlm.nih.gov/record/ui?ui=D014899). MeSH
Browser. U.S. National Library of Medicine.
2. Oudman E, Oey MJ, Batjes D, van Dam M, van Dorp M, Postma A, Wijnia JW (December
2022). "Wernicke-Korsakoff syndrome diagnostics and rehabilitation in the post-acute
phase" (https://doi.org/10.1016%2Fj.addicn.2022.100043). Addiction Neuroscience. 4:
100043. doi:10.1016/j.addicn.2022.100043 (https://doi.org/10.1016%2Fj.addicn.2022.10004
3). ISSN 2772-3925 (https://www.worldcat.org/issn/2772-3925). S2CID 253296206 (https://a
pi.semanticscholar.org/CorpusID:253296206).
3. Sullivan EV, Fama R (June 2012). "Wernicke's encephalopathy and Korsakoff's syndrome
revisited" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723427). Neuropsychology
Review. 22 (2): 69–71. doi:10.1007/s11065-012-9205-2 (https://doi.org/10.1007%2Fs11065-
012-9205-2). PMC 4723427 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723427).
PMID 22588370 (https://pubmed.ncbi.nlm.nih.gov/22588370).
4. Ropper A, Brown R. Princ. of Neurology, Adams & Victor. 8º ed. McGraw Hill 2007.
5. Cook CC (2000). "Prevention and treatment of Wernicke-Korsakoff syndrome". Alcohol and
Alcoholism. 35 (1): 19–20. doi:10.1093/alcalc/35.Supplement_1.19 (https://doi.org/10.1093%
2Falcalc%2F35.Supplement_1.19). PMID 11304070 (https://pubmed.ncbi.nlm.nih.gov/1130
4070). S2CID 45726575 (https://api.semanticscholar.org/CorpusID:45726575).
6. Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA (December 2010).
"EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy".
European Journal of Neurology. 17 (12): 1408–1418. doi:10.1111/j.1468-1331.2010.03153.x
(https://doi.org/10.1111%2Fj.1468-1331.2010.03153.x). PMID 20642790 (https://pubmed.nc
bi.nlm.nih.gov/20642790). S2CID 8167574 (https://api.semanticscholar.org/CorpusID:81675
74).
7. Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent
advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455.
doi:10.1016/s1474-4422(07)70104-7 (https://doi.org/10.1016%2Fs1474-4422%2807%2970
104-7). PMID 17434099 (https://pubmed.ncbi.nlm.nih.gov/17434099). S2CID 15523083 (http
s://api.semanticscholar.org/CorpusID:15523083).
 8. Arts NJ, Pitel AL, Kessels RP (1 January 2021), Swaab DF, Kreier F, Lucassen PJ, Salehi A
(eds.), "Chapter 29 - The contribution of mamillary body damage to Wernicke's
encephalopathy and Korsakoff's syndrome" (https://www.sciencedirect.com/science/article/p
ii/B978012820107700029X), Handbook of Clinical Neurology, The Human Hypothalamus,
Elsevier, 180: 455–475, doi:10.1016/b978-0-12-820107-7.00029-x (https://doi.org/10.1016%
2Fb978-0-12-820107-7.00029-x), ISBN 9780128201077, PMID 34225949 (https://pubmed.n
cbi.nlm.nih.gov/34225949), S2CID 235746125 (https://api.semanticscholar.org/CorpusID:23
5746125), retrieved 18 November 2022
9. Oudman E, Wijnia JW, Oey MJ, van Dam M, Postma A (July 2021). "Wernicke-Korsakoff
syndrome despite no alcohol abuse: A summary of systematic reports" (https://doi.org/10.101
6%2Fj.jns.2021.117482). Journal of the Neurological Sciences. 426: 117482.
doi:10.1016/j.jns.2021.117482 (https://doi.org/10.1016%2Fj.jns.2021.117482).
PMID 34000679 (https://pubmed.ncbi.nlm.nih.gov/34000679). S2CID 234769882 (https://ap
i.semanticscholar.org/CorpusID:234769882).
10. Isenberg-Grzeda E, Kutner HE, Nicolson SE (2012). "Wernicke-Korsakoff-syndrome: under-
recognized and under-treated" (https://doi.org/10.1016%2Fj.psym.2012.04.008).
Psychosomatics. 53 (6): 507–516. doi:10.1016/j.psym.2012.04.008 (https://doi.org/10.1016%
2Fj.psym.2012.04.008). PMID 23157990 (https://pubmed.ncbi.nlm.nih.gov/23157990).
11. Lough ME (June 2012). "Wernicke's encephalopathy: expanding the diagnostic toolbox".
Neuropsychology Review. 22 (2): 181–194. doi:10.1007/s11065-012-9200-7 (https://doi.org/
10.1007%2Fs11065-012-9200-7). PMID 22577001 (https://pubmed.ncbi.nlm.nih.gov/225770
01). S2CID 18884274 (https://api.semanticscholar.org/CorpusID:18884274).
12. Mumford CJ (June 1989). "Papilloedema delaying diagnosis of Wernicke's encephalopathy
in a comatose patient" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429353).
Postgraduate Medical Journal. 65 (764): 371–373. doi:10.1136/pgmj.65.764.371 (https://doi.
org/10.1136%2Fpgmj.65.764.371). PMC 2429353 (https://www.ncbi.nlm.nih.gov/pmc/article
s/PMC2429353). PMID 2608577 (https://pubmed.ncbi.nlm.nih.gov/2608577).
13. Chitra S, Lath KV (May 2012). "Wernicke's encephalopathy with visual loss in a patient with
hyperemesis gravidarum". The Journal of the Association of Physicians of India. 60: 53–56.
PMID 23029727 (https://pubmed.ncbi.nlm.nih.gov/23029727).
14. Truswell AS (June 2000). "Australian experience with the Wernicke-Korsakoff syndrome".
Addiction. 95 (6): 829–832. doi:10.1046/j.1360-0443.2000.9568291.x (https://doi.org/10.104
6%2Fj.1360-0443.2000.9568291.x). PMID 10946433 (https://pubmed.ncbi.nlm.nih.gov/1094
6433).
15. Flabeau O, Foubert-Samier A, Meissner W, Tison F (August 2008). "Hearing and seeing:
Unusual early signs of Wernicke encephalopathy" (https://doi.org/10.1212%2F01.wnl.00003
24599.66359.b1). Neurology. 71 (9): 694. doi:10.1212/01.wnl.0000324599.66359.b1 (https://
doi.org/10.1212%2F01.wnl.0000324599.66359.b1). PMID 18725598 (https://pubmed.ncbi.nl
m.nih.gov/18725598).
16. Jethava A, Dasanu CA (2012). "Acute Wernicke encephalopathy and sensorineural hearing
loss complicating bariatric surgery". Connecticut Medicine. 76 (10): 603–605.
PMID 23243762 (https://pubmed.ncbi.nlm.nih.gov/23243762).
17. Harper CG, Giles M, Finlay-Jones R (April 1986). "Clinical signs in the Wernicke-Korsakoff
complex: a retrospective analysis of 131 cases diagnosed at necropsy" (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC1028756). Journal of Neurology, Neurosurgery, and Psychiatry.
49 (4): 341–345. doi:10.1136/jnnp.49.4.341 (https://doi.org/10.1136%2Fjnnp.49.4.341).
PMC 1028756 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1028756). PMID 3701343 (htt
ps://pubmed.ncbi.nlm.nih.gov/3701343).
18. Puiggros C (1994). Tratado de Neurología. Madrid: Editorial Libro del Año. pp. 823–824.
ISBN 9788487748547.
19. Meierkord H, Boon P, Engelsen B, Göcke K, Shorvon S, Tinuper P, Holtkamp M (March
2010). "EFNS guideline on the management of status epilepticus in adults" (https://doi.org/1
0.1111%2Fj.1468-1331.2009.02917.x). European Journal of Neurology. 17 (3): 348–355.
doi:10.1111/j.1468-1331.2009.02917.x (https://doi.org/10.1111%2Fj.1468-1331.2009.02917.
x). PMID 20050893 (https://pubmed.ncbi.nlm.nih.gov/20050893).
20. Kondo K, Fujiwara M, Murase M, Kodera Y, Akiyama S, Ito K, Takagi H (August 1996).
"Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy
with 5-fluorouracil and cisplatin: case report and review of the literature" (https://doi.org/10.1
093%2Foxfordjournals.jjco.a023220). Japanese Journal of Clinical Oncology. 26 (4): 234–
236. doi:10.1093/oxfordjournals.jjco.a023220 (https://doi.org/10.1093%2Foxfordjournals.jjc
o.a023220). PMID 8765181 (https://pubmed.ncbi.nlm.nih.gov/8765181).
21. Becker JT, Furman JM, Panisset M, Smith C (1990). "Characteristics of the memory loss of a
patient with Wernicke-Korsakoff's syndrome without alcoholism". Neuropsychologia. 28 (2):
171–179. doi:10.1016/0028-3932(90)90099-A (https://doi.org/10.1016%2F0028-3932%289
0%2990099-A). PMID 2314572 (https://pubmed.ncbi.nlm.nih.gov/2314572).
S2CID 41693535 (https://api.semanticscholar.org/CorpusID:41693535).
22. Zhang G, Ding H, Chen H, Ye X, Li H, Lin X, Ke Z (January 2013). "Thiamine nutritional
status and depressive symptoms are inversely associated among older Chinese adults" (htt
ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521461). The Journal of Nutrition. 143 (1): 53–
58. doi:10.3945/jn.112.167007 (https://doi.org/10.3945%2Fjn.112.167007). PMC 3521461 (h
ttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521461). PMID 23173173 (https://pubmed.nc
bi.nlm.nih.gov/23173173).
23. Worden RW, Allen HM (2006). "Wernicke's encephalopathy after gastric bypass that
masqueraded as acute psychosis: a case report". Current Surgery. 63 (2): 114–116.
doi:10.1016/j.cursur.2005.06.004 (https://doi.org/10.1016%2Fj.cursur.2005.06.004).
PMID 16520112 (https://pubmed.ncbi.nlm.nih.gov/16520112).
24. Jiang W, Gagliardi JP, Raj YP, Silvertooth EJ, Christopher EJ, Krishnan KR (January 2006).
"Acute psychotic disorder after gastric bypass surgery: differential diagnosis and treatment".
The American Journal of Psychiatry. 163 (1): 15–19. doi:10.1176/appi.ajp.163.1.15 (https://d
oi.org/10.1176%2Fappi.ajp.163.1.15). PMID 16390883 (https://pubmed.ncbi.nlm.nih.gov/163
90883).
25. Lindberg MC, Oyler RA (April 1990). "Wernicke's encephalopathy". American Family
Physician. 41 (4): 1205–1209. PMID 2181837 (https://pubmed.ncbi.nlm.nih.gov/2181837).
26. Mann MW, Degos JD (1987). "[Hypothermia in Wernicke's encephalopathy]" [Hypothermia
in Wernicke's encephalopathy]. Revue Neurologique (in French). 143 (10): 684–686.
PMID 3423584 (https://pubmed.ncbi.nlm.nih.gov/3423584). INIST 7514445 (https://pascal-fr
ancis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7514445).
27. Reinhard R (2004). Color Atlas of Neurology. Thieme. ISBN 978-1-58890-191-0.
28. Biller J (2008). The Interface of Neurology & Internal Medicine. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-7906-7.
29. Rohkamm R (2004). "Hemodynamic abnormalities" (https://books.google.com/books?id=EK
08J953yzgC&pg=PA148). Color Atlas of Neurology. Thieme. p. 148. ISBN 978-1-58890-
191-0.
30. Ishiko T, Taguchi T, Takeguchi M, Saito H, Nanri K (September 2009). "[Case of Wernicke's
encephalopathy and subacute combined degeneration of the spinal cord due to vitamin
deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to
beriberi heart disease]" (http://medicalfinder.jp/ejournal/openUrl.do?issn=18816096&genre=
article&volume=61&issue=9&spage=1069) [Case of Wernicke's encephalopathy and
subacute combined degeneration of the spinal cord due to vitamin deficiency showing
changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease].
Brain and Nerve = Shinkei Kenkyu No Shinpo (in Japanese). 61 (9): 1069–1073.
PMID 19803406 (https://pubmed.ncbi.nlm.nih.gov/19803406).
31. Harper C, Fornes P, Duyckaerts C, Lecomte D, Hauw JJ (March 1995). "An international
perspective on the prevalence of the Wernicke-Korsakoff syndrome". Metabolic Brain
Disease. 10 (1): 17–24. doi:10.1007/BF01991779 (https://doi.org/10.1007%2FBF01991779).
PMID 7596325 (https://pubmed.ncbi.nlm.nih.gov/7596325). S2CID 9751459 (https://api.sem
anticscholar.org/CorpusID:9751459).
32. Zarranz JJ (2007). Neurologia (in Spanish) (4th ed.). Madrid, España: Harcourt Brace De
Espana SA. p. 821. ISBN 978-8480862288.
33. Brown AH, Ropper RH (2007). Principios de neurología de Adams y Victor (in Spanish)
(8th ed.). México: McGraw-Hill. p. 1132. ISBN 978-9701057070.
34. Vasconcelos MM, Silva KP, Vidal G, Silva AF, Domingues RC, Berditchevsky CR (April
1999). "Early diagnosis of pediatric Wernicke's encephalopathy". Pediatric Neurology. 20
(4): 289–294. doi:10.1016/s0887-8994(98)00153-2 (https://doi.org/10.1016%2Fs0887-899
4%2898%2900153-2). PMID 10328278 (https://pubmed.ncbi.nlm.nih.gov/10328278).
35. Fattal-Valevski A, Kesler A, Sela BA, Nitzan-Kaluski D, Rotstein M, Mesterman R, et al.
(February 2005). "Outbreak of life-threatening thiamine deficiency in infants in Israel caused
by a defective soy-based formula" (https://doi.org/10.1542%2Fpeds.2004-1255). Pediatrics.
115 (2): e233–e238. doi:10.1542/peds.2004-1255 (https://doi.org/10.1542%2Fpeds.2004-12
55). PMID 15687431 (https://pubmed.ncbi.nlm.nih.gov/15687431).
36. Hauser S (2010). Harrison's Neurology in Clinical Medicine (2nd ed.). New York: McGraw-
Hill Publishing. ISBN 978-0-07-174123-1.
37. Current Medical Diagnosis & Treatment 2012 (48th ed.). New York: McGraw-Hill Medical.
2009. ISBN 978-0-07-176372-1.
38. Johnson LE (November 2022). "Thiamin Deficiency" (http://www.merckmanuals.com/profess
ional/nutritional_disorders/vitamin_deficiency_dependency_and_toxicity/thiamin.html?qt=w
ernicke%20encephalopathy&alt=sh). Merk Manuals.
39. Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent
advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455.
doi:10.1016/S1474-4422(07)70104-7 (https://doi.org/10.1016%2FS1474-4422%2807%2970
104-7). PMID 17434099 (https://pubmed.ncbi.nlm.nih.gov/17434099). S2CID 15523083 (http
s://api.semanticscholar.org/CorpusID:15523083).
40. Shand F, Gates J, Fawcett J, Mattick R (October 2003). "Wernicke Korsakoff's syndrome".
Guidelines for the Treatment of Alcohol Problems (https://web.archive.org/web/20140214092
650/http://www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/2C3FC9166082567D
CA257260007F81F8/$File/alcprobguide.pdf) (PDF). National Drug and Alcohol Research
Centre, Commonwealth of Australia. p. 48. ISBN 978-0-642-82383-0. Archived from the
original (http://www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/2C3FC91660825
67DCA257260007F81F8/$File/alcprobguide.pdf) (PDF) on 14 February 2014.
41. Haberland C (2007). Clinical neuropathology: text and color atlas. Demos Medical
Publishing. p. 200. ISBN 978-1-888799-97-2.
42. Thomson AD, Guerrini I, Marshall EJ (June 2012). "The evolution and treatment of
Korsakoff's syndrome: out of sight, out of mind?" (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3545191). Neuropsychology Review. 22 (2): 81–92. doi:10.1007/s11065-012-9196-z (h
ttps://doi.org/10.1007%2Fs11065-012-9196-z). PMC 3545191 (https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC3545191). PMID 22569770 (https://pubmed.ncbi.nlm.nih.gov/22569770).
43. Goldman L, Ausiello DA, Arend W, Armitage JO, Clemmons D, Drazen J, et al., eds. (2007).
"Chapter 443". Cecil Medicine (23rd ed.). Saunders, Elsevier. ISBN 978-1-4160-4478-9.
44. MedlinePlus Encyclopedia: Wernicke-Korsakoff syndrome (https://medlineplus.gov/ency/arti
cle/000771.htm)
45. Ng KL, Nguyễn LT (April 2013). "The role of thiamine in HIV infection" (https://doi.org/10.101
6%2Fj.ijid.2012.11.019). International Journal of Infectious Diseases. 17 (4): e221–e227.
doi:10.1016/j.ijid.2012.11.019 (https://doi.org/10.1016%2Fj.ijid.2012.11.019).
PMID 23274124 (https://pubmed.ncbi.nlm.nih.gov/23274124).
46. Rosen A, van Kuilenburg A, Assmann B, Kuhlen M, Borkhardt A (May 2011). "Severe
encephalopathy, lactic acidosis, vegetative instability and neuropathy with 5-Fluorouracil
treatment - pyrimidine degradation defect or beriberi?" (https://www.ncbi.nlm.nih.gov/pmc/arti
cles/PMC3177792). Case Reports in Oncology. 4 (2): 371–376. doi:10.1159/000328803 (htt
ps://doi.org/10.1159%2F000328803). PMC 3177792 (https://www.ncbi.nlm.nih.gov/pmc/artic
les/PMC3177792). PMID 21941485 (https://pubmed.ncbi.nlm.nih.gov/21941485).
47. Martin PR, Singleton CK, Hiller-Sturmhöfel S (2003). "The role of thiamine deficiency in
alcoholic brain disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668887). Alcohol
Research & Health. 27 (2): 134–142. PMC 6668887 (https://www.ncbi.nlm.nih.gov/pmc/articl
es/PMC6668887). PMID 15303623 (https://pubmed.ncbi.nlm.nih.gov/15303623).
48. Soukoulis V, Dihu JB, Sole M, Anker SD, Cleland J, Fonarow GC, et al. (October 2009).
"Micronutrient deficiencies an unmet need in heart failure" (https://doi.org/10.1016%2Fj.jacc.
2009.08.012). Journal of the American College of Cardiology. 54 (18): 1660–1673.
doi:10.1016/j.jacc.2009.08.012 (https://doi.org/10.1016%2Fj.jacc.2009.08.012).
PMID 19850206 (https://pubmed.ncbi.nlm.nih.gov/19850206).
49. Lee JH, Jarreau T, Prasad A, Lavie C, O'Keefe J, Ventura H (2011). "Nutritional assessment
in heart failure patients" (https://doi.org/10.1111%2Fj.1751-7133.2011.00239.x). Congestive
Heart Failure. 17 (4): 199–203. doi:10.1111/j.1751-7133.2011.00239.x (https://doi.org/10.11
11%2Fj.1751-7133.2011.00239.x). PMID 21790970 (https://pubmed.ncbi.nlm.nih.gov/21790
970).
50. Hirsch JA, Parrott J (2012). "New considerations on the neuromodulatory role of thiamine".
Pharmacology. 89 (1–2): 111–116. doi:10.1159/000336339 (https://doi.org/10.1159%2F000
336339). PMID 22398704 (https://pubmed.ncbi.nlm.nih.gov/22398704). S2CID 22555167 (ht
tps://api.semanticscholar.org/CorpusID:22555167).
51. Hazell AS (2009). "Astrocytes are a major target in thiamine deficiency and Wernicke's
encephalopathy". Neurochemistry International. 55 (1–3): 129–135.
doi:10.1016/j.neuint.2009.02.020 (https://doi.org/10.1016%2Fj.neuint.2009.02.020).
PMID 19428817 (https://pubmed.ncbi.nlm.nih.gov/19428817). S2CID 12615886 (https://api.s
emanticscholar.org/CorpusID:12615886).
52. Hazell AS, Todd KG, Butterworth RF (June 1998). "Mechanisms of neuronal cell death in
Wernicke's encephalopathy". Metabolic Brain Disease. 13 (2): 97–122.
doi:10.1023/A:1020657129593 (https://doi.org/10.1023%2FA%3A1020657129593).
PMID 9699919 (https://pubmed.ncbi.nlm.nih.gov/9699919). S2CID 25130884 (https://api.se
manticscholar.org/CorpusID:25130884).
53. Kohnke, Sara; Meek, Claire L (January 2021). "Don't seek, don't find: The diagnostic
challenge of Wernicke's encephalopathy" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC77
91272). Annals of Clinical Biochemistry: International Journal of Laboratory Medicine. 58 (1):
38–46. doi:10.1177/0004563220939604 (https://doi.org/10.1177%2F0004563220939604).
ISSN 0004-5632 (https://www.worldcat.org/issn/0004-5632). PMC 7791272 (https://www.ncb
i.nlm.nih.gov/pmc/articles/PMC7791272). PMID 32551830 (https://pubmed.ncbi.nlm.nih.gov/
32551830).
54. Powell SZ, Schochet Jr SS (March 2003). "Intoxications and Metabolic Diseases of the
Central Nervous System". In Nelson JS, Mena H, Parisi JE, Schochet SS (eds.). Principles
and Practice of Neuropathology. Oxford University Press. p. 193. ISBN 978-0-19-802907-6.
55. Zuccoli G, Pipitone N (February 2009). "Neuroimaging findings in acute Wernicke's
encephalopathy: review of the literature". AJR. American Journal of Roentgenology. 192 (2):
501–508. doi:10.2214/AJR.07.3959 (https://doi.org/10.2214%2FAJR.07.3959).
PMID 19155417 (https://pubmed.ncbi.nlm.nih.gov/19155417). S2CID 32749934 (https://api.s
emanticscholar.org/CorpusID:32749934).
56. Cernicchiaro L (September 2017). "Wernicke's Disease (or Wernicke's Encephalopathy).
Symptoms and new treatments. Clinical and practical approach. Daily monitoring for twelve
years of a reversed severe case" (http://enfermedad-de-wernicke.weebly.com/).
57. McPhee SJ, Papadakis MA, Rabow MW, eds. (12 September 2011). Current medical
diagnosis & treatment 2012 (https://archive.org/details/currentmedicaldi00step) (51st ed.).
New York: McGraw-Hill Medical. ISBN 978-0-07-176372-1.
58. Caine D, Halliday GM, Kril JJ, Harper CG (January 1997). "Operational criteria for the
classification of chronic alcoholics: identification of Wernicke's encephalopathy" (https://ww
w.ncbi.nlm.nih.gov/pmc/articles/PMC486695). Journal of Neurology, Neurosurgery, and
Psychiatry. 62 (1): 51–60. doi:10.1136/jnnp.62.1.51 (https://doi.org/10.1136%2Fjnnp.62.1.5
1). PMC 486695 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC486695). PMID 9010400 (ht
tps://pubmed.ncbi.nlm.nih.gov/9010400).
59. Protocol for: The management of the alcohol withdrawal syndrome and Wernicke
encephalopathy. East Kent Hospitals NHS Trust (Report).
60. Hegde AN, Mohan S, Lath N, Lim CC (2011). "Differential diagnosis for bilateral
abnormalities of the basal ganglia and thalamus". Radiographics. 31 (1): 5–30.
doi:10.1148/rg.311105041 (https://doi.org/10.1148%2Frg.311105041). PMID 21257930 (http
s://pubmed.ncbi.nlm.nih.gov/21257930). S2CID 207707771 (https://api.semanticscholar.org/
CorpusID:207707771).
61. Attard A, Torrens N, Holvey C (June 2012). "Clinical Guideline: The Management of
Wernicke's Encephalopathy (WE)" (https://web.archive.org/web/20150709175514/http://ww
w.guysandstthomas.nhs.uk/resources/our-services/acute-medicine-gi-surgery/elderly-care/al
cohol-withdrawal-syndrome.pdf) (PDF). Guy's and St. Thomas Hospitals. Archived from the
original (http://www.guysandstthomas.nhs.uk/resources/our-services/acute-medicine-gi-surg
ery/elderly-care/alcohol-withdrawal-syndrome.pdf) (PDF) on 9 July 2015.
62. Wood VM (June 2006). "Guidelines for the Management of Alcohol Issues in the Acute
Hospital Setting" (https://web.archive.org/web/20130921054552/http://www.alcohollearningc
entre.org.uk/_library/17__Doncaster_Guidelines_For_The_Management_Of_Patients_with_
Alcohol_Misuse_In_The_Acute_General_Hospital_Setting.pdf) (PDF). Doncaster and
Bassetlaw Hospitals. Archived from the original (http://www.alcohollearningcentre.org.uk/_lib
rary/17__Doncaster_Guidelines_For_The_Management_Of_Patients_with_Alcohol_Misuse
_In_The_Acute_General_Hospital_Setting.pdf) (PDF) on 21 September 2013.
63. Thomson AD, Cook CC, Guerrini I, Sheedy D, Harper C, Marshall EJ (2008). "Wernicke's
encephalopathy revisited. Translation of the case history section of the original manuscript
by Carl Wernicke 'Lehrbuch der Gehirnkrankheiten fur Aerzte and Studirende' (1881) with a
commentary" (https://doi.org/10.1093%2Falcalc%2Fagm144). Alcohol and Alcoholism.
Oxford, Oxfordshire. 43 (2): 174–9. doi:10.1093/alcalc/agm144 (https://doi.org/10.1093%2Fal
calc%2Fagm144). PMID 18056751 (https://pubmed.ncbi.nlm.nih.gov/18056751).
64. Thomson A, Guerrini I, Marshall EJ. "Incidence of Adverse Reactions to Parenteral Thiamine
in the Treatment of Wernicke's Encephalopathy, and Recommendations." Alcohol and
Alcoholism. 2019 Nov;54(6):609-614. doi:https://doi.org/10.1093/alcalc/agy091
65. Iwamoto Y, Okuda B, Miyata Y, Tachibana H, Sugita M (June 1994). "[Beneficial effect of
steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]".
Rinsho Shinkeigaku = Clinical Neurology. 34 (6): 599–601. PMID 7955722 (https://pubmed.
ncbi.nlm.nih.gov/7955722).
66. Warot P, Lesage R, Dupuys P (February 1962). "[Corticotherapy of the severe forms of the
Gayet-Wernicke encephalopathy]". Lille Medical. 7: 123–124. PMID 14005025 (https://pubm
ed.ncbi.nlm.nih.gov/14005025). (article in French)
67. Harrison TR, Braunwald E, Agud Aparicio JL (2002). Medicina Interna. p. 2462.
68. Kelley WN, DeVita VT, DuPont HL, Harris ED, Hazzard WR (1990). Medicina Interna
(1st ed.). Buenos Aires: Médica Panamericana. pp. 621, 974. ISBN 9789500612401.
69. Thomson AD, Cook CC, Touquet R, Henry JA (2002). "The Royal College of Physicians
report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and
Emergency Department" (https://doi.org/10.1093%2Falcalc%2F37.6.513). Alcohol and
Alcoholism. 37 (6): 513–521. doi:10.1093/alcalc/37.6.513 (https://doi.org/10.1093%2Falcal
c%2F37.6.513). PMID 12414541 (https://pubmed.ncbi.nlm.nih.gov/12414541).
70. Lourenço R, Camilo ME (2002). "Taurine: a conditionally essential amino acid in humans?
An overview in health and disease" (http://www.nutricionhospitalaria.com/pdf/3337.pdf)
(PDF). Nutricion Hospitalaria. 17 (6): 262–270. PMID 12514918 (https://pubmed.ncbi.nlm.ni
h.gov/12514918).
71. Iwamoto Y, Okuda B, Miyata Y, Tachibana H, Sugita M (June 1994). "[Beneficial effect of
steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]".
Rinsho Shinkeigaku = Clinical Neurology (in Japanese). 34 (6): 599–601. PMID 7955722 (ht
tps://pubmed.ncbi.nlm.nih.gov/7955722).
72. Torvik A, Lindboe CF, Rogde S (November 1982). "Brain lesions in alcoholics. A
neuropathological study with clinical correlations". Journal of the Neurological Sciences. 56
(2–3): 233–48. doi:10.1016/0022-510x(82)90145-9 (https://doi.org/10.1016%2F0022-510x%
2882%2990145-9). PMID 7175549 (https://pubmed.ncbi.nlm.nih.gov/7175549).
S2CID 26100578 (https://api.semanticscholar.org/CorpusID:26100578).
73. Harper C (March 1979). "Wernicke's encephalopathy: a more common disease than
realised. A neuropathological study of 51 cases" (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC490724). Journal of Neurology, Neurosurgery, and Psychiatry. 42 (3): 226–231.
doi:10.1136/jnnp.42.3.226 (https://doi.org/10.1136%2Fjnnp.42.3.226). PMC 490724 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC490724). PMID 438830 (https://pubmed.ncbi.nlm.ni
h.gov/438830).
74. Blansjaar BA, Van Dijk JG (July 1992). "Korsakoff minus Wernicke syndrome". Alcohol and
Alcoholism (Oxford, Oxfordshire). 27 (4): 435–7. doi:10.1093/oxfordjournals.alcalc.a045269
(https://doi.org/10.1093%2Foxfordjournals.alcalc.a045269). PMID 1418116 (https://pubmed.
ncbi.nlm.nih.gov/1418116).
75. Lana-Peixoto MA, Dos Santos EC, Pittella JE (September 1992). "Coma and death in
unrecognized Wernicke's encephalopathy. An autopsy study" (https://doi.org/10.1590%2FS0
004-282X1992000300012). Arquivos de Neuro-Psiquiatria. 50 (3): 329–333.
doi:10.1590/S0004-282X1992000300012 (https://doi.org/10.1590%2FS0004-282X1992000
300012). PMID 1308411 (https://pubmed.ncbi.nlm.nih.gov/1308411).
76. Bem Junior, Luiz Severo; Lemos, Nilson Batista; de Lima, Luís Felipe Gonçalves; Dias,
Artêmio José Araruna; Neto, Otávio da Cunha Ferreira; de Lira, Carlos Cezar Sousa; Diniz,
Andrey Maia Silva; Rabelo, Nicollas Nunes; Barroso, Luciana Karla Viana; Valença,
Marcelo Moraes; de Azevedo Filho, Hildo Rocha Cirne (28 June 2021). "The anatomy of the
brain – learned over the centuries" (http://surgicalneurologyint.com/surgicalint-articles/the-an
atomy-of-the-brain-learned-over-the-centuries/). Surgical Neurology International. 12: 319.
doi:10.25259/SNI_200_2021 (https://doi.org/10.25259%2FSNI_200_2021). ISSN 2152-
7806 (https://www.worldcat.org/issn/2152-7806). PMC 8326080 (https://www.ncbi.nlm.nih.go
v/pmc/articles/PMC8326080). PMID 34345460 (https://pubmed.ncbi.nlm.nih.gov/34345460).
77. Isen, Danielle R.; Kline, Lanning B. (30 June 2020). "Neuro-ophthalmic Manifestations of
Wernicke Encephalopathy" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335288). Eye
and Brain. 12: 49–60. doi:10.2147/EB.S234078 (https://doi.org/10.2147%2FEB.S234078).
PMC 7335288 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335288). PMID 32636690
(https://pubmed.ncbi.nlm.nih.gov/32636690).
78. Isenberg-Grzeda E, Kutner HE, Nicolson SE (1 November 2012). "Wernicke-Korsakoff-
syndrome: under-recognized and under-treated" (https://doi.org/10.1016%2Fj.psym.2012.04.
008). Psychosomatics. 53 (6): 507–516. doi:10.1016/j.psym.2012.04.008 (https://doi.org/10.1
016%2Fj.psym.2012.04.008). PMID 23157990 (https://pubmed.ncbi.nlm.nih.gov/23157990).
79. Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent
advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455.
doi:10.1016/S1474-4422(07)70104-7 (https://doi.org/10.1016%2FS1474-4422%2807%2970
104-7). PMID 17434099 (https://pubmed.ncbi.nlm.nih.gov/17434099). S2CID 15523083 (http
s://api.semanticscholar.org/CorpusID:15523083).

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