This document discusses alcohol related brain damage (ARBD), a spectrum of neurological and cognitive conditions caused by chronic alcoholism. It describes several specific conditions under the ARBD umbrella, including Wernicke's encephalopathy and Korsakoff's syndrome. Wernicke's encephalopathy is an acute neurological disorder caused by thiamine deficiency, with symptoms including eye movement abnormalities, gait issues, and altered consciousness. Korsakoff's syndrome is a chronic memory disorder that can develop after Wernicke's encephalopathy, characterized by anterograde amnesia and confabulation. The document outlines the molecular mechanisms, neuroimaging features, and neural substrates of these conditions.

1. ALCOHOL RELATED BRAIN DAMAGE
(ARBD)

2. ARBD
• Alcohol related brain damage (ARBD) is a term used to cover a
spectrum of conditions and disorders induced by chronic
alcoholism which leads to a constellation of neurological,
cognitive, behavioural and neuropsychiatric symptoms.
• These disease entities merge into each other, clinically overlap
and combine synergistically to contribute to the phenomena of
neurological and cognitive dysfunction resulting in alcohol
related brain damage.
• The clinical features and neuroradiologic (functional
neuroimaging) distinctive features help in differentiating these
entities.

3. THE MULTIFACTORIAL SPECTRUM- ARBD
• Wernicke’s encephalopathy (WE)
• Korsakoff’ syndrome (KS)
• Marchiafava Bignami Disease (MBD)
• Alcohol related dementia (ARD)
• Alcohol and Dysexecutive syndrome (DES)
• Acquired non-Wilsonian hepatocerebral degeneration (AHD)
• Vitamin B12 deficiency and Leucoencephalopathy
• Central/Extrapontine myelinolysis (CPM/EPM)
• Pellegra encephalopathy
• Alcohol related brain injury (ARBI)

4. MOLECULAR MECHANISMS-ARBD
• Neuronal membrane protein / receptor alterations
• Abnormalities in intracellular signal transduction cascades
Ion channels, second messengers: c-AMP, G proteins,
chaperonins
• Abnormalities in neurotransmitters & neuromodulator functions;
receptor abnormalities (GABAa; NE, DA 2, 5HT3; Ach); EAA NMDA,
Glutamate, Aspartate; Adenosine A2
• Brain dysmorphology: neuronal loss; dendritic & synaptic
changes; loss of white matter & cerebral atrophy
• Alcohol metabolism: ADH & ALDH (genetic functional
polymorphisms)
• Ethanol responsive genes (GABAa; Opoid receptors; molecular
chaperones); Neurotransmitter & Neuroanatomical systems: Brain
Reward Circuitry: Addiction

5. CELLULAR PATHOPHYSIOLOGY

6. BRAIN REWARD CIRCUITRY
• Brain Reward Circuitry : network of four circuits involved in drug
abuse and addiction
• Reward circuit _Nucleus Accumbens DA-regulated reward circuit
• Motivation circuit _Orbitofrontal cortex, Subcallosal cortex
• Memory circuit _Amygdala (Conditioned-learned associations )
and Hippocampus (memory of expected reward)
• Cognitive Control circuit _Prefrontal cortex and Cingulate gyrus
• OFC-Amygdala-NA reward circuit
Without the inhibitory frontal cognitive control, a positive-
feedback loop is set forth that result in compulsive drug intake.
The prefrontal cortex is involved in self-monitoring, decision-
making processes, and in inhibitory control. The disruption of the
prefrontal cortex leads to loss of self-directed/willed behaviour in
favour of automatic sensory-driven behaviour (high reward
dependence).

7. BRAIN REWARD CIRCUITRY

8. WERNICKE’S ENCEPHALOPATHY
• Acute neurologic disorder secondary to nutritional Thiamine
deficiency ; Mortality 20%; WE KS (80%)
• Triad [10%]: Opthalmoplgeia , Ataxia, Disturbances of
consciousness
• Opthalmoparesis [30%]: (Bilateral; Asymmetrical) Horizontal
nystagmus, LR palsy, Gaze palsy, Ptosis, INO; Pupils:
Anisocoria, sluggish reaction to light
• Ataxia: LL; gait disturbances
• Alterations in level of consciousness: acute confusional state;
inattention, disorientation, drowsiness, stupor, pre-coma, coma
• Hypotension, hypothermia, tachycardia: Hypothalamic
involvement
• Axonal Polyneuropathy
• Gratifying and prompt response to Thiamine

9. THIAMINE & B COMPLEX VITAMINS
• Thiamine dependent enzymes in HMP & Kreb’s cycle
• B2, B6, Niacin: coenzymes in glucose/ lipid/ production of
glucose derived neurotransmitters (GABA)
• Daily requirement: 1.5mg
• Body stores: 25-30mg
• Deficiency: 2-3 weeks
• Alcoholics: malnourished; derive 50% calories from ethanol
• Alcoholics: 50-70% decreased GI absorption; reduced intake;
impaired utilization, decreased hepatic storage
• Low circulating thiamine levels: 30-80% alcoholics
• Folate deficiency: 60-80% alcoholics
• B6 deficiency: 50% alcoholics
• B2/Niacin deficiency: 15% alcoholics
• Magnesium: cofactor for thiamine dependent enzymes

10. LAB MARKERS-THIAMINE STATUS
• Red Blood Cell Thiamine Pyrophosphate (RBCTPP)
• Red Blood Cell Transketolase (RBCTTK)
• Blood Pyruvate
• GGTP (gamma-glutamyl transferase)
• ALT/AST ratio
• Alcoholic toxic neuropathy- Small fiber- Predominant sensory-
Axonal
• Thiamine deficient Neuropathy- Large fiber- Predominantly motor-
Demyelinating
• Thiamine deficiency Screening Test : Thiamine Deficiency
Questionnaire (TDQ)
Sgouros X. Alcohol & Alcoholism 2004; 39:227-232

11. WKS-SUSCEPTIBILITY
• Variation in Transketolase biochemical activity
• Variation in Transketolase-like 1 gene (TKTL1 gene)
• GABA-A subunit receptor gene-chr 5q33; susceptibility to alcohol
dependence and Korsakoff’s syndrome
• Genetic variants of Thiamine Transporter Protein gene; Thiamine
transport systems

12. THIAMINE DEPENDENT ENZYMES
MECHANISMS FOR BRAIN DAMAGE
Thiamine-dependent enzymes: (1) transketolase; (2) pyruvate
dehydrogenase complex; (3) α-ketoglutarate dehydrogenase
complex.

13. PARENTERAL THIAMINE
Active transport is saturable at low Thiamine levels
High plasma:CNS concentration gradient is needed for passive diffusion
for rapid correction of CNS thiamine levels

14. PABRINEX
• Vitamin B1 (Thiamine) = 250mg
• Vitamin B2 (Riboflavin) = 4mg
• Vitamin B6 (Pyridoxine) = 50mg
• Nicotinamide = 160mg
• Vitamin C = 500mg
• Prophylaxis: 250mg IV OD 3-5 days
• Established WE: 500mg IV TID 3-5 days; then 250mg IV/IM OD
continued until clinical response
Supplement with 10-30mEq Mg, 60-180mEq K, 10-
40mmol/L PO4
Alcohol & Alcoholism 2005; 40:155-156 / 2002; 37:513-521

15. WE: ANATOMIC SUBSTRATES
• Symmetrical lesions
• Paraventricular-Thalamus,
Hypothalamus, Midbrain,
Pons, Medulla, Cerebellum,
Fornix
• Mamillary body, Medial
dorsal nucleus of thalamus,
Periaqueductal GM, Pontine
tegmentum, Superior
cerebellar vermis
Karl Wernicke
“ Polioencephalitis
hemmorhagica superioris”

16. Multiple, small, new haemorrhages in the brainstem and the thalamus, with some spongiosis
(characteristic loosening of the neuropil) between the haemorrhages without interstitial infiltration
of macrophages; capillary proliferation, reactive astrocytes

17. A 57-year-old alcoholic man was admitted for nausea,
vomiting, and diarrhoea for 1 month, and confusion, imbalance,
and auditory and visual hallucinations for 1 week. His daughter
noticed that he had “funny eye movements” over the previous
week. A diagnosis of Wernicke’s encephalopathy was made.
Despite treatment with IV thiamine and nutritional
supplementation, the patient progressed 2 days later to coma
with total ophthalmoplegia. Two weeks after admission, the
patient was oriented to person, had recovered some horizontal
eye movements, remembered the names of his children, and
could follow simple commands.
WE CASE I

20. WE:NEUROIMAGING
FLAIR MR images demonstrated increased signal around the third
and fourth ventricles, Sylvian aqueduct, mamillary bodies (indicated
by arrow), and tectum.

21. A 61-year-old man was admitted with slight confusion. He had
been a heavy drinker for several years and had general fatigue.
A doctor who examined him first considered the possibility of
electrolyte disturbance and gave him an infusion including
electrolytes and glucose. After starting IV injection, the patient
fell into a deep coma. On neurologic examinations, he had
diminished doll’s head eye phenomenon and weakened deep
tendon reflexes. Laboratory findings showed severe vitamin B1
deficiency, an elevation of -glutamyl transpeptidase, and
macrocytic anemia. MRI was typical for Wernicke
encephalopathy. Although thiamine was started 5 days after
admission, the patient died of pneumonia without recovery
after 3 months. We should not forget that the activation of
glycolysis consumes vitamin B1 and that an infusion including
glucose to patients with vitamin B1 deficiency is fatal.
WE CASE II

22. WE:NEUROIMAGING
Fluid-attenuated inversion recovery brain MR images show
hyperintensity lesions around the fourth ventricle (A), in the
mamillary bodies (B), and around the third ventricle and
hypothalamus (C).

23. A 26-year-old woman presented with a 4-day history of
progressive lateral ophthalmoplegia, inability to stand, gait
ataxia, apathy, and confusion. The diagnosis of acute
Wernicke encephalopathy was consistent with characteristic
changes seen on her admission MRI.Three hours after
initiating IV thiamine, her lateral gaze returned, Romberg
test was negative, and cognition improved dramatically. Her
clinical improvement was correlated with normalization of
hyperintense T2 MRI signals 5 days later. This dramatic
turnaround underscores the necessity of IV thiamine in
acute Wernicke encephalopathy.
WE CASE III

24. WE:NEUROIMAGING
T2W MR images:
Hyperintense SI
periaqueductal GM &
Dorsomedial thalamic nuclei
Improvement after 5 days of
100mg IV Thiamine

25. WE:NEUROIMAGING
Complete resolution within
2 weeks of IV Thiamine
T2WI
DWI

26. WE:NEUROIMAGING
ATYPICAL
Unusual sites of MR involvement
Hyperintense SI : Red Nucleus;
MB tectum; periaqueductal GM
Symmetrical hyperintense SI:
facial, vestibular, abducens, and
dentate nuclei
T1WI: Atrophy of Mamillary body

27. KORSAKOFF SYNDROME
• Pure amnestic-confabulatory disorder secondary to Thiamine
deficiency
Short term memory impairment
Dense anterograde memory deficits; new learning
deficits,declarative/episodic memory impairment
Confabulation
Variable duration of retrograde memory impairment
• Recovery pattern:25% complete recovery; 25% no demonstrable
recovery; 50% mild to moderate improvement
• Neural substrates: Papez circuit
Hippocampus vs. Diencephalic

28. KORSAKOFF SYNDROME
Decreased volumes on
MR volumetric studies
Hippocampus; mamillary
body mediodorsal
nucleus of thalamus,
anterior thalamic nucleus,
nucleus basalis of
Meynert

29. WK SYNDROME
WE
KS

30. KORSAKOFF SYNDROME
• Possible role of the cholinergic system in the memory deficit of
Wernicke-Korsakoff syndrome
• Morphometric measurements of the volume of magnocellular
neurones had been documented to be decreased in the NBM
(Cortex 1988; 24:367-388)
• AChEI in Korsakoff Syndrome
Increased attention and working memory abilities as evidenced
by improved scores in TMT B and logical memory on the WMS-R;
improvement in MMSE, cognitive, memory, behavioural
outcomes and QOL
Galantamine (Psychosomatics 2004; 45:4)
Donepezil (Alcohol & Alcoholism 2001; 36:553-555; Alcohol
& Alcoholism 2004; 40:151-154)

31. MARCHIAFAVA-BIGNAMI DISEASE
• Progressive demyelination and central necrosis of corpus
callosum
• Extra-callosal white matter involvement: frontal, parietal,
anterior-posterior commissures, middle cerebellar peduncles,
corona radiata
• Extracallosal cortico-cortical association fibers; cortico-
subcortical projection fibers involved; disruption of white matter
connectivity and distributed neural circuits/networks within and
between hemispheres (Hemispheric disconnection syndromes)
• Widespread cerebral functional involvement (PET, SPECT
studies)
• Acute onset MBD
• Chronic MBD

32. MARCHIAFAVA-BIGNAMI DISEASE
• Acute MBD: delirium, stupor, coma, seizures, long tract signs,
aphasia, ataxia
• Chronic MBD: frontal type dementia, paratonic rigidity, frontal
release reflexes, signs of callosal disconnection

33. MBD
The corpus callosum degenerates and splits into three layers
(“layered necrosis”). Central layer: necrosis;dorsal & ventral layers
spared; ‘Sandwich sign’
Callosal involvement Extra-callosal involvement:
deep frontal WM, corona
radiata

34. PONTINE/EXTRAPONTINE MYELINOLYSIS
• Characteristic symmetrical demyelination of central portion of
the base of the pons
• Clinical features CPM: spastic paraparesis/tetraparesis,
pseudobulbar palsy (dysphagia, dysarthria, mutism, emotional
lability, locked in syndrome, bilateral/unilateral abducens palsy,
conjugate gaze palsies; altered mental status; Horner’s
syndrome
• Sites of EPM: cerebellum, cerebral peduncles, lateral geniculate
body, thalamus, lentiform nuclei, caudate & internal capsule and
cerebral white matter
• EPM: extrapyramidal signs, cerebellar ataxia, dystonia;
behavioural abnormalities

35. PONTINE MYELINOLYSIS

36. CPM/EPM
CT BRAIN

37. EXTRAPONTINE MYELINOLYSIS
Cerebellum
Caudate & Lentiform
nuclei
Cortical & subcortical

38. ALCOHOL RELATED COGNITIVE DETERIORATION /
IMPAIRMENT
ACD/ARCI
• Ethanol/metabolites-neurotoxic per se (ARD)
• Frontal Dysexecutive Syndrome (DES)
• Alcohol related encephalopathies
WKS
MBD
Pellegra encephalopathy
Acquired hepatocerebral degeneration
• Alcohol related brain injury (ARBI)
• Co morbid substance abuse

39. ALCOHOL RELATED DEMENTIA
Oslin D, Atkinson RM, Smith DM, et al: Alcohol-related dementia: proposed clinical
criteria. Int J Geriatr Psychiatry 1998; 13:203–212
Oslin DW,Cary MS. Alcohol related dementia: Validation of diagnostic criteria. Am J
Geriatr Psychiatry 2003; 11:441-447

40. ARD
• Ventricular enlargement, selective loss of subcortical white
matter, gray matter loss, cerebral atrophy, alterations on
neuronal size, number, architecture, and synpatic & dendritic
complexity (graded brain dysmorphology)
• Lack of distinctive, well defined neuropathology
• Personality changes, apathy, poor judgement, poor memory,
cortical signs (aphasia, apraxia, agnosia)
• Alcohol + ApoE4 MCI AD
• Risk of dementia (AD, VaD) increased with increasing alcohol
consumption only in those individuals carrying the
apolipoprotein e4 allele
• There is a J or U shaped relation between alcohol drinking and
cognitive impairment or dementia
• In patients with mild cognitive impairment, up to 1 drink/day (15
g) of alcohol or wine may decrease the rate of progression to
dementia (AD, VaD) Neurology 2007; 68:1790-1799

41. FRONTAL LOBE VULNERABILITY
Potential reversibility of frontal lobe changes after
alcohol abstinence

42. DYSEXECUTIVE SYNDROME
• Frontal lobe vulnerability : increased susceptibility of frontal
brain systems to alcohol related brain damage; selective
neuronal loss in superior frontal association cortex, loss of
frontal lobe volume (white matter loss); grey matter loss
• DES characterised by three categories of cognitive dysfunction
(Berrios GE. JNNP 2000; 68:731-737)
 Isolated impaired executive functions with preserved
intelligence and memory
 modified dysexecutive pattern in which memory as well as
executive functions were impaired with intelligence preserved
 general cognitive deterioration

43. FrDES
 Maladaptive behaviour; loss of control, inability to abstain from
alcohol, repetitive habitual behaviour, and lack of forward
planning, regulating behaviour, goal directed behaviours, poor
judgement, poor problem solving abilities; poor short term
memory planning, problem solving, impulsivity, apathy, social &
personal neglect,lack of insight
 Abnormal frontal neuropsychological tests (TMT B, WCST,
CWST,FAB, Verbal Fluency Test, BADS)
 Vulnerability of right hemisphere: Impaired emotional
processing; decreased empathy; impairment in recognising facial
expression of emotions; emotionally flat, loss of insight etc
similar to Frontotemporal dementia syndrome

44. PELLEGRA ENCEPHALOPATHY
o Niacin deficiency encephalopathy
Encephalopathic pellegra- acute form
Insidious onset pellegra- chronic form
o Acute form:
Confusion, delirium,generalised cogwheel rigidity,Gegenhalten
phenomenon, dysarthria, myoclonus,
peripheral neuropathy,seizures
o Chronic form:
Dementia (apathy, memory failure, depression),
Dermatitis (Casal’s necklace rash, stomatitis, glossitis)
Diarrhoea
o Co-exist with WKS, MBD
o Thiamine and Vit B6 treatment can trigger development of
encephalopathic pellegra: imperative to supplement niacin
along with vitamin B complex; 300-1000mg/day acute form, 50
100mg/day after recovery

45. ALCOHOLIC CEREBELLAR DEGENERATION
• Related to Thiamine deficiency
• Loss of cerebellar cortical neurones: anterior and superior
vermis
• Gait ataxia (broad based, unstable) , Signs of limb
incoordination LL>UL

46. VITAMIN B12 RELATED NEUROLOGIC DISORDER
• Dementia
• Neuropsychiatric symptoms: personality changes, depression,
affective syndromes, psychosis (“megaloblastic madness”),
delusions, hallucinations, mania, ataxia
• Optic neuropathy, peripheral neuropathy, SCD
• Symptoms occur commonly in the absence of anemia, or
elevated MCV, a borderline low serum cobalamin: not rare and
should not be considered as evidence against the diagnosis of
cobalamin deficiency
• Useful confirmatory evidence of cobalamin deficiency: elevated
serum levels of methylmalonic acid (MMA) and total
homocysteine (Hcy) [100% specificity] ; with treatment MMA &
Hcy levels normalises (Lindenbaum J. NEJM 1988; 318:1720-
1728)

47. VITAMIN B12 RELATED LEUCOENCEPHALOPATHY
• Selective white matter involvement: diffuse
leucoencephalopathy; Disruption of WM tracts-Dysfunction of
distributed neural networks- “ White matter dementia”;
neurobehavioural syndrome
• Detrimental effect of cobalamin deficiency on the integrity of
myelin
• Leukoencephalopathy, evidenced by confluent white matter
abnormalities on MRI, is increasingly recognized as a possible
presenting sign of cobalamin deficiency, even in the absence of
anemia or myelopathy (Organic psychosis without anemia/
SCD)
• Reversible with treatment
• Diffuse supratentorial leucoencephalopathy; supratentorial WM
loss; severe periventricular/paraventricular WM bulk loss;
hydrocephalus (mimics central demyelination syndromes)
• Remarkable confluent white matter abnormalities on MRI

48. B12 LEUCOENCEPHALOPATHY
Before & After treatment

49. SCD
Before & After treatment

50. ALCOHOL RELATED FOLATE DEFICIENCY
• Folate related Dementia
• Neuropsychiatric symptomatology
• Spasticity; folate induced SCD
• Vit B12 and folate deficiency can co exist
• The treatment of cobalamin deficiency with folic acid will
result in deterioration in the neuropsychiatric status, while
improving the haematological indices (CH3 TH4 trap
hypothesis)

51. ACQUIRED NON-WILSONIAN HEPATOCEREBRAL
DEGENERATION (AHD)
• Chronic brain disorder caused by liver dysfunction and long-
standing portal-systemic shunting; repeated episodes of
hepatic insufficiency leading to CNS dysfunction; irreversible
neurological condition
• Dementia, frontotemporal cognitive dysfunction, cerebellar
signs (ataxia, intention tremors), extrapyramidal signs:
symmetric akinetic-rigid syndrome (Parkinsonian features),
movement disorders (chorea, athetosis, orobuccal dyskinesia,
myoclonus, tremors), corticospinal signs (progressive spastic
paraparesis), axonal / autonomic peripheral neuropathy
(myeloneuropathy)
• Cirrhosis-related Parkinsonism, post-shunt myelopathy and
cerebellar degeneration
• Normal serum/ urine copper & ceruloplasmin; absent KF ring
• Elevated serum Manganese levels

52. ACQUIRED NON-WILSONIAN HEPATOCEREBRAL
DEGENERATION
• MRI: Symmetrical hyperintense SI in T1WI in Globus pallidus,
midbrain (crus cerebri, substantia nigra) with sparing of red
nuclei, tectum of pons with normal T2WI
• AHD + CPM/EPM

53. OPTIC NEUROPATHY
 Visual acuity; symmetrical central/centrocecal scotomas,
papillomacular bundle involvement in optic chaisma

54. ARBD: SUMMARY
• ARBD: THE DISEASE SPECTRUM, pleomorphic effects of ethanol
with multifactorial causative factors
• Specific distinctive subsyndromes; alcoholic encephalopathies
(WE, KS, MBD)
• Overlaps, commonalities, produce a synergistic clinical picture,
continuum of disorders with no specific laboratory diagnostic
tests/markers (Lab tests, EEG, CSF)
• Dx: Clinical features + Distinctive neuroimaging characteristics
• Ethanol neurotoxicity or toxic metabolites; nutritional, genetic,
adaptive biochemical factors, altered brain neurochemistry,
ethanol-induced changes in gene expression (disorder of
behaviour)
• ARBD: Potentially treatable disorder “No more alcohol means no
more cerebral damage”
• Recovery pattern: 25% (complete recovery), 25%(No recovery),
25% (Slight recovery) & 25% (significant recovery)

55. ARBD SUMMARY
• Membrane dependent events (protein trafficking, intracellular
signalling, membrane receptor systems, ion channels, receptors,
NT, second messengers); specific vulnerabilities of
topographical brain systems; genetic vulnerability (ethanol
responsive genes; alterations in gene expression); alcohol/ drug
seeking behaviour (Reward circuitry): Co morbid substance
abuse
• Altered cerebral energy metabolic derangements
(intramitochondrial energy kinetics, cytotoxic edema, Glutamate
exicitoxicity); The B-Complex
• Nutritional related neurologic disorders
• Alcohol related brain injury (ARBI): frontotemporal contusions,
post traumatic epilepsy, head injuries, subdural & intracerebral
hematomas, SAH, communicating hydrocephalus, meningitis

56. ALCOHOL RELATED NEUROLOGIC DISORDERS-I
• Alcoholic intoxication
• Alcohol withdrawal syndrome
• Alcohol withdrawal seizures
• Delirium tremens
• Nutritional diseases of the nervous system secondary
to alcoholism
Wernicke-Korsakoff’s syndrome-thiamine
deficiency
Pellagra encephalopathy- niacin deficiency
Vitamin B12 & folate deficiency-
leucoencephalopathy, peripheral neuropathy,
myelopathy
• Marchiafava-Bignami Disease
• Frontal dysexecutive syndrome
• Optic neuropathy/ Tobacco-alcohol ambylopia
• Fetal alcohol syndrome
• Alcoholic myopathy, rhabdomyolysis
• Cerebellar degeneration
• Alcoholic polyneuropathy
• Alcohol induced epileptic seizures
• AIP (porphyria), PRES
• Subacute encephalopathy with seizure activity/SESA
syndrome

57. ALCOHOL RELATED NEUROLOGIC DISORDERS-II
SYSTEMIC DISORDERS
• Liver disease
Hepatic encephalopathy, stupor, coma
Acquired chronic hepatocerebral degeneration
• Gastrointestinal disease
Malabsorption syndrome
Post gastrectomy syndrome
Pancreatic encephalopathy (with WE) dysphoria,
disturbance of orientation, delirium, lethargy, illusion,
raised ICP, coma, elevated CSF amylase
• Cardiovascular disease
Cardiomyopathy, cardiogenic embolism and stroke
Arrythymias-Holiday heart syndrome leading to stroke
• Hematologic disorders
Anemia, leucopenia, thrombocytopenia-leading to
hemorrhagic stroke
• Infectious disease
Meningitis (pneumococcal, meningococcal)

58. ALCOHOL RELATED NEUROLOGIC DISORDERS-III
SYSTEMIC DISORDERS
• Hypothermia and hyperthermia
• Respiratory depression and hypoxia
• Toxic encephalopathies due to co-morbid substance abuse
• Dyselectrolytemia
Hypoglycemia
Hyperglycemia
Hyponatremia (beer potomania)
Hypercalcemia
Hypomagnesemia
Hypophosphatemia
• Increased incidence of trauma
• Extradural/subdural, intracerebral hematoma, SAH, contusions
• Post traumatic, symptomatic communicating hydrocephalus
• Spinal cord injury
• Post traumatic seizure disorders
• Compressive neuropathies, brachial plexus injuries (Saturday
night palsies)
• Muscle crush injuries, compartmental syndromes