Wernicke Encephalopathy + Korsakoff Syndrome + TBI

Question 1

why does WKS occur

Answer 1

due to NECROTIC lesions in the MAMILLARY BODIES, THALAMUS and BRAINSTEM

Question 2

what is the prevalence of WKS

Answer 2

up to 12.5% in those with AUD

2% in general population

*frequently underdiagnosed in life, often dx for first time in post mortem (up to 80% of cases dx first time post mortem)

Question 3

what % of those who are not treated for wernicke encephalopathy die

Answer 3

up to 20%

Question 4

what % of those with untreated wernicke’s encephalopathy go on to develop korsakoff syndrome

Answer 4

up to 75%

Question 5

what is korsakoff syndrome

Answer 5

irreversible cognitive impairment

Question 6

list risk factors for WKS

Answer 6

AUD

cancer patients

GI surgery i.e gastric bypass

hyperemesis gravidarum

starvation/fasting

Question 7

how do you dx WKS

Answer 7

clinical diagnosis

Question 8

what is the WKS triad

Answer 8

oculomotor abnormalities

cerebellar dysfunction

altered mental state

Question 9

what are the Caine criteria for WKS

Answer 9

In 1997, Caine et al. proposed that a diagnosis can be made when patients have any 2 of the following 4 features:

Nutritional deficiency
Ocular signs
Cerebellar signs
Altered mental status or mild memory impairment

Question 10

how does korsakoff syndrome usually present

Answer 10

often is late, chronic manifestation of wernicke’s enccephalopathy

anterograde and retrograde amnesia with preserved long term memory

Question 11

symptoms of korsakoff syndrome

Answer 11

anterograde amnesia

confabulations

personality changes

Question 12

how quickly does the body’s thiamine store deplete

Answer 12

between 4-6 weeks

Question 13

how does thiamine deficiency lead to brain dysfunction

Answer 13

Thiamine is a cofactor in the decarboxylation of pyruvate. Thiamine is needed for pyruvate to enter the citric acid cycle, which allows for aerobic metabolism of glucose to adenosine triphosphate (ATP).

Lack of ATP production in areas of the brain susceptible to thiamine depletion thus leads to neuronal death

This can result in damage to the limbic system, specifically the mammillary bodies and anterior/medial thalamus.

Question 14

what might you see on MRI in WKS

Answer 14

mamillary body atrophy

volume loss in thalamus

volume loss in corpus callosum

–> lesions from wernicke’s often characterized by petechial hemorrhage and can be found in symmetrical distribution

Question 15

list some neuropsychi sx associated with mild TBI

Answer 15

depression, irritability, fatigue, headache, photosensitivity, sleep disturbance

Question 16

how quickly do sx from mild TBI generally resolve

Answer 16

within days to weeks, usually resolved by 3 months

Question 17

moderate to severe TBI are associated with increased risk of what neuro/psych disorders

Answer 17

depression, PTSD, aggression, and possibly neurodegenerative diseases such as Alzheimer’s disease

Question 18

what population has the highest risk of TBI of any group

Answer 18

those above 75 –> falls from standing height and MVAs

in younger people, Men>women but in older cohort theres more women with TBI

Question 19

how does substance use change after TBI

Answer 19

tends to be high BEFORE the onset of TBI but in fact DECLINES after injury

Question 20

what is chronic traumatic encephalopathy

Answer 20

Chronic traumatic encephalopathy (CTE) is a term used to describe brain degeneration likely caused by repeated head trauma. CTE is thought to significantly increase the risk for dementia.[12] A diagnosis of CTE can only be made during autopsy. CTE is a rare condition and usually found in individuals who play contact sports.

Question 21

is there a biomarker for acute concussion

Answer 21

yes, approved by FDA

ubiquitin carboxy-terminal hydrolase L1 (UCH-L1)

Question 22

are there any approved pharmacologic tx for TBI

Answer 22

no, all are used off label

Question 23

list meds that can be used to treat aggression/agitation in TBI

Answer 23

VPA
carbamazepine

propanolol
pindolol

lithium

clozapine
quetiapine
ziprasidone

Question 24

list meds that can be used to treat cognitive deficits in TBI

Answer 24

amantadine

cholinesterase inhibitors

stimulants like methylphenidate