OS  212  Neurology

    Neuro Consultants
SGD 2: Altered Sensorium Exam 1

Outline o (-) dental caries, (-) tonsillopharyngeal congestion

I. The Case
II. The Questions
Hi Block A. Considering the rush job we put together in an
attempt to get this trans out in a timely manner, not to
mention the fact that this case is different from last year’s,
we hope you’ll pardon whatever errors and omissions are
exposed in this trans during your SGD sessions. I hope
we’re at least on the right track with our diagnosis and
differentials, but there’s a chance our preceptors will point
out something totally different. Hopefully that won’t be the
case. The ‘answers’ to the questions are based solely on
our research, and in anticipation of additional points we
might have missed, there are boxes below each tentative
answer so that you can fill in the blanks. Good luck on the
exam, everyone!
I. The Case
General Data
R. D. is a 26 year-old male, right-handed, single, born and
residing in Manila, admitted for the chief compliant of
unarousability
History of the Present Illness
The patient was apparently well and of good functional
capacity until…
36 hours prior to admission, the patient had a drinking
spree with friends consuming several bottles of brandy
and several bottles of beer. After the binge, the patient
went to sleep without eating his dinner.
24 hours prior to admission, the patient was noted to be
unarousable despite vigorous verbal and tactile
stimulation. The patient then had 1 episode of stiffening of
both upper and lower extremities, with upward rolling of
eyeballs, drooling of saliva, and involuntary micturition,
lasting for approximately 20 seconds. The patient was
then brought to a local hospital, where he was given 1 vial
of D50-50 IV and 1 ampoule of Vitamin B complex IV. He
was then transferred to PGH for further evaluation and
management.
Review of Systems
o equal chest expansion, clear breath sounds, (-)
adventitious sounds
o (-) heaves/thrills, apex beat at the 4th intercostal
space midclavicular line, normal heart rate and
regular rhythm, (-) murmurs
o Flat abdomen, normoactive bowel sounds, soft, (-)
masses/tenderness/organomegaly
o Full and equal pulses, pink nailbeds,
o (-) Pallor/edema/cyanosis
Neurologic Examination Findings
o Drowsy but arousable by tapping, no verbal output,
uncooperative, restless and does not follow
commands
o Pupils 2-3 mm equal, briskly reactive
o (+) ROR, clear media, (-) papilledema, (-) retinal
hemorrhages/exudates,
o (-) preferential gaze, roving, conjugate eye
movements,
o (+) brisk corneal reflexes, (-) facial asymmetry
o (+) brisk gag reflex
o unable to protrude tongue on command
o (-) preferential movement
o Withdraws to pain in all extremities
o DTRs +++ in all extremities; (-) Babinski sign; (-)
clonus
o (-) nuchal rigidity, (-)Brudzinski sign, (-) Kernig’s sign
o (-)nystagmus, (-) tremors
o (-)Horner syndrome
II. The Questions
1) Give a 3-sentence summary of the pertinent
features of the case.
The case features R.D., a 26 year old male who
was well and of functional capacity until an evening of
binge drinking 36 hours prior to admission. 24 hours prior
to admission, the patient was found to be somnolent and
unresponsive to verbal and tactile stimulation, with
stiffening of the upper and lower extremities, upward
rolling of the eyeballs and involuntary micturition. Physical
examination showed no significant abnormalities and the
neurologic examination findings were normal other than
the patient’s episode of altered sensorium.
Notes:

Past Medical History

o No other known illnesses or co-morbidities
o No previous hospitalizations or surgeries

Family Medical History

o (+) pulmonary tuberculosis (maternal), (+)
hypertension (father)
o (-) asthma, heart disease, stroke

Personal and Social History

o Regular alcoholic beverage drinker (2-4 sessions per
week)
2) What neural structures are involved? What is your
o Smoker: consumes 1 stick per day for 1 year
localization?
o MAP user 1995-1996; not known if still presently
using shabu
Mamillary bodies - The mammillary bodies are parts of
the brain known to be significantly damaged by alcohol
Physical Examination Findings
intoxication, especially by chronic alcohol abuse and
o Received at the ER drowsy but arousable, not in
associated deficiency of thiamine. They, along with the
cardiorespiratory distress
anterior and dorsomedial nuclei in the thalamus, are
o BP120/80, HR 70/min, RR 20/min, T 37.2°C
involved with the processing of recognition memory.
o Pink palpebral conjunctivae, anicteric sclerae, no
cervical lymphadenopathy, no jugular venous
CN III, IV, VI – Damage to these cranial nerves which
distention, no carotid bruit;
serve the extra-ocular muscles can explain the upward

November
  10, 2008, | Thursday   Page 1 of 5 
Ikey and Lee 
 

OS  212  Neurology
   
SGD 2: Altered Sensorium
rolling of the eyes noted prior to R.D.’s admission.
Thalamus - The thalamus plays an important role in
regulating states of sleep and wakefulness. Thalamic
nuclei have strong reciprocal connections with the cerebral
cortex, forming thalamo-cortico-thalamic circuits that are
believed to be involved with consciousness. The thalamus
plays a major role in regulating arousal, the level of
awareness, and activity. Damage to the thalamus can lead
to permanent coma.
Many different functions are linked to the system to which
thalamic parts belong. This is at first the case for sensory
systems (which excepts the olfactory function) auditory,
somatic, visceral, gustatory and visual systems where
localized lesions provoke particular sensory deficits. A
major role of the thalamus is devoted to "motor" systems.
This has been and continues to be a subject of interest for
investigators.
Cerebellar Vermis - It is the site of termination of the
spinocerebellar pathways that carry subconscious
proprioception.
Recent research on the posterior cerebellar vermis
indicates that this particular area of the brain may be
linked to the brain's natural ability to integrate and analyze
inertial motion. Specialized cells in this area, known as
Purkinje cells, are now thought to receive sensory
information from the vestibular system of the inner ears
and use this to compute information about the body's
movement through space.
Notes:
3) What is the etiology of the illness? What are the
differential diagnoses?
Wernicke’s Encephalopathy – A syndrome
characterised by ataxia, ophthalmoplegia, confusion, and
impairment of short-term memory. It is caused by lesions
in the medial thalamic nuclei, mammillary bodies,
periaqueductal and periventricular brainstem nuclei, and
superior cerebellar vermis, often resulting from inadequate
intake or absorption of thiamine (Vitamin B1), especially in
conjunction with carbohydrate ingestion. Its most common
correlate is prolonged alcohol consumption resulting in
thiamine deficiency. Alcoholics are therefore particularly at
risk, but it may also occur with thiamine deficiency states
arising from other causes, particularly in patients with such
gastric disorders as carcinoma, chronic gastritis, and
repetitive vomiting.
It should be noted that although Wernicke’s
encephalopathy is defined by classic triad of symptoms
(encephalopathy, ataxic gait, oculomotor dysfunction), all
three features of the triad are observed in only about one-
third of cases. Consideration for Wernicke
encephalopathy should be given to patients with any
November
  10, 2008, | Thursday
Neuro Consultants
Exam 1
evidence of long-term alcohol abuse or malnutrition and
any of the following: acute confusion, decreased
conscious level, ataxia, ophthalmoplegia, memory
disturbance, hypothermia with hypotension, and delirium
tremens.
Long-term alcohol abuse is the most common cause of
Wernicke encephalopathy. In long-term alcoholics,
malnutrition can reduce intestinal thiamine absorption by
70%, decreasing serum levels of thiamine from between
30% and 98% below the lower level established for normal
subjects. Alcohol alone can also decrease absorption by
50% in one third of patients who are not malnourished.
R/I:
o Alcohol abuse (2-4 drinking sessions per week)
o Oculomotor dysfunction
o Altered sensorium
o Ataxia (not entirely certain, but the stiffening of
extremities may correlate with an overall lack of
coordination in muscle movements)
o An effective Vitamin B complex treatment would
suggest improvement of possible thiamine
deficient state
R/O:
o Does not directly explain involuntary micturition
or drooling
o Stupor and coma are rare symptoms
o No nystagmus
o Usually does not present with seizure-like
symptoms
Hypoglycemia due to excessive alcohol consumption
(Note: for this differential, we found this abstract of a
recently published study explaining the possible
pathophysiology of alcohol-induced hypoglycemia)
Hypoglycemia induced by alcohol ingestion is a well-
known clinical problem in diabetic patients. However, the
mechanisms underlying this phenomenon have largely
remained elusive. Since insulin secretion can be rapidly
tuned by changes in pancreatic microcirculation, scientists
at the Stockholm South Hospital Diabetes Research
Center, Karolinska Institutet, evaluated the influence of
alcohol administration on pancreatic islet blood flow and
dynamic changes in insulin secretion and blood sugar
levels.
"We have now found that alcohol exerts substantial
influences on pancreatic microcirculation by evoking a
massive redistribution of pancreatic blood flow from the
exocrine into the endocrine (insulin-producing) part via
mechanisms mediated by the messenger molecule nitric
oxide and the vagus nerve, augmenting late phase insulin
secretion, and thereby evoking hypoglycemia" says lead
investigator Åke Sjöholm.
In general, symptoms of hypoglycemia include hunger,
nervousness, tremors, perspiration, sleepiness, confusion,
difficulty speaking, generalized weakness, seizures and
anxiety.
R/I:
o Sleepiness
o Excessive alcohol intake
o Altered sensorium
o Can cause single or multiple focal or generalized
seizures
o Pt did not eat before drinking
R/O:
o Does not account for opthalmoplegia, ataxia
  Page 2 of 5 
Ikey and Lee 
      
OS  212  Neurology
    Neuro Consultants
SGD 2: Altered Sensorium Exam 1

Stroke - Stroke should be considered in any patient
presenting with an acute neurologic deficit (focal or global)
or altered level of consciousness. Common symptoms of
stroke include abrupt onset of hemiparesis, monoparesis,
or quadriparesis; monocular or binocular visual loss; visual
field deficits; diplopia; dysarthria; ataxia; vertigo; aphasia;
or sudden decrease in the level of consciousness.
R/I:
o Decreased level of consciousness
o Ataxia (not entirely certain, but the stiffening of
extremities may correlate with an overall lack of
coordination in muscle movements)
R/O:
o PE findings are not suggestive of stroke
o No history of CV disease
o No hemi/mono/quadriparesis
o No strong correlation linking alcohol as a risk
factor for ischemic stroke.
o No family history
respiratory paralysis 
500 
death 
R/I:
o Stupor
o Can cause seizures
R/O:
o Cannot be ruled out completely but pattern of
symptoms suggest a more specific syndrome
Epileptic seizure - An epileptic seizure is caused by
excessive and/or hypersynchronous electrical neuronal
activity, and is usually self-limiting. It can manifest as an
alteration in mental state, tonic or clonic movements,
convulsions, and various other psychic symptoms (such
as déjà vu). This needs to be differentiated from epilepsy,
which is the medical syndrome of recurrent, unprovoked
seizures, but seizures can occur in people who do not
have epilepsy.

Ethanol Intoxication Seizures are often associated with a sudden and

SERUM LEVELS  involuntary contraction of a group of muscles and loss of
MANIFESTATIONS  consciousness. However, a seizure can also be as subtle
(mg/dL)  as marching numbness of a part of the body, a brief - long
term loss of memory, sparkling or flashes,
euphoria or dysphoria  sensing/discharging of an unpleasant odor similar to
alcohol base is produced by internal organs, a strange
shy or expansive  epigastric sensation or a sensation of fear and total state
of confusion which in some case leads to suicide during
50 – 150*  friendly or argumentative  seizure. Other common symptoms of seizure include:
chewing movements, difficulty talking, drooling, eyelid
impaired concentration and judgment  fluttering, eyes rolling up, falling down, hand waving,
inability to move, incontinence, lip smacking, making
sexual inhibitions 
sounds, staring, stiffening, twitching movements, breathing
difficulty, sweating and teeth clenching.
slurred speech 
Checking glucose levels, for example, is a mandatory
ataxic gait 
action in the management of seizures as hypoglycemia
may cause seizures, and failure to administer glucose
diplopia 
would be harmful to the patient.
nausea 
R/I:
150 – 250 
-Altered mental state, loss of consciousness
tachycardia 
-Drooling
drowsiness  -Incontinence
-Stiffening of extremities
labile mood with sudden bursts of anger or  -Eyes rolling upwards

antisocial acts  R/O:
-Often associated with concurrent cardiac or endocrine
stupor alternating with combativeness or  diseases
incoherent speech 
Notes:
300 
heavy breathing 

vomiting 

400  coma 

November
  10, 2008, | Thursday   Page 3 of 5 
Ikey and Lee 
 

OS  212  Neurology
   
SGD 2: Altered Sensorium
4) Based on your main working diagnosis, what is the
pathophysiology of the signs and symptoms seen in
this patient?
Epileptic seizure and altered sensorium induced by
binge drinking, is the diagnosis which offers the most
complete explanation for the patient’s symptoms. Seizures
can be caused by sever hypoglycemia, and in this case
there are two possible explanations for a hypoglycemic
state. Firstly, after a night of binge drinking, the patient
went to sleep with no additional food intake. A prolonged
period of fasting can induce low blood sugar. Secondly,
R.D. may have been functionally hypoglycemic, even if his
blood sugar levels were normal, due to thiamine
deficiency. Thiamine deficiency, common in patients
suffering from alcohol abuse, affects the body’s ability to
metabolize carbohydrates, so a lack of Vitamin B1 can
induce a situation similar to actual hypoglycemia.
Furthermore, as a general depressant of the nervous
system, the state of unarousability described in the case
can also be attributed to excessive alcohol intake.
The precipitating event in this case is excessive
consumption of alcohol (ethanol). The presence of large
amounts of ethanol has an adverse effect on the
absorption of Vitamin B1 (thiamine). Acute alcohol
exposure interferes with the absorption of thiamine from
the gastrointestinal tract at low, but not at high, thiamine
concentrations. Furthermore, in studies using rats, the
activity of the TPK (thiamine diphosphokinase) enzyme
from various tissues decreased with acute alcohol
exposure to about 70 percent of the activity level in control
animals, and with chronic alcohol exposure to about 50
percent. Although no studies have addressed whether
alcohol directly affects TPK in humans, indirect analyses
have found that the ratio of phosphorylated thiamine
(primarily ThDP, the form utilized in cell metabolism) to
thiamine is significantly lower in alcoholics than in
nonalcoholics - that is, that less thiamine is converted to
ThDP. This finding suggests that TPK is less active in the
alcoholics.
Thiamine malabsorption could become clinically significant
if combined with the reduced dietary thiamine intake that is
typically found in alcoholics, when other aspects of
thiamine utilization are compromised by alcohol, or when a
person requires increased thiamine amounts because of
his or her specific metabolism or condition (in pregnant or
lactating women).
Thiamine in its metabolically active form, called thiamine
pyrophosphate (TPP), is vital in the metabolism of
carbohydrates. It serves a critical role in 3 enzyme
systems: (1) conversion of pyruvate to acetyl coenzyme A
by pyruvate dehydrogenase, (2) conversion of a-
ketoglutarate to succinate by a-ketoglutarate
dehydrogenase in the Krebs cycle, and (3) catalysis by
transketolase in the pentose monophosphate shunt. In the
presence of thiamine deficiency, these cellular systems
dependent on thiamine begin to fail, leading eventually to
cell death.
Diminished transketolase activity results in failure of the
maintenance of the myelin sheaths in the nervous system,
metabolism of lipids and glucose, and production of
branched chain amino acids.
Lack of a-ketoglutarate dehydrogenase activity in the
Krebs cycle alters cerebral energy utilization. If cells with
high metabolic requirements have inadequate stores of
thiamine to draw from, energy production drops, and
November
  10, 2008, | Thursday
Neuro Consultants
Exam 1
neuronal damage ensues. Increased cell death then feeds
the localized vasogenic response (Buscaglia, 2005).
Additionally, the reduced production of succinate, which
plays a role in GABA metabolism and the electrical
stimulation of neurons, leads to further CNS injury.
As for the pathophysiology of a seizure itself, two sets of
changes can determine the epileptogenic properties of
neuronal tissues. Abnormal neuronal excitability is thought
to occur as a result of disruption of the depolarization and
repolarization mechanisms of the cell (this is termed the
"excitability of neuronal tissue"). Aberrant neuronal
networks that develop abnormal synchronization of a
group of neurons can result in the development and
propagation of an epileptic seizure (this is termed the
"synchronization of neuronal tissue").2
A hyperexcitability of neurons that results in random firing
of cells, by itself, may not lead to propagation of an
epileptic seizure. Indeed, both normal and abnormal
patterns of behavior require a certain degree of
synchronization of firing in a population of neurons.
Epileptic seizures originate in a setting of both altered
excitability and altered synchronization of neurons.
The membrane properties and microenvironment of
neurons, which maintain potential differences of electrical
charge, are determined by selective ion permeability and
ionic pumps. Excitatory neurotransmitters usually act by
opening Na+ or Ca2+ channels, whereas inhibitory
neurotransmitters usually open K+ or Cl- channels. The
mechanism of action of certain anticonvulsant medications
is by Na+ or Ca2+ channel blockade, which likely prevents
repetitive neuronal firing. Extracellular ionic concentrations
also can contribute to neuronal excitability; for example,
an increase in extracellular K+ concentrations (such as in
rapid neuronal firing or dysfunction of glia, which are
mainly responsible for K+ reuptake) causes membrane
depolarization.
Various intracellular processes are controlled by genetic
information. Neuronal excitability can be preprogrammed
by DNA-controlled effects on cell structure, energy
metabolism, receptor functions, transmitter release, and
ionic channels. The mechanisms that induce these
changes, either phasic or long-term, appear to be linked to
ionic currents, especially Ca2+ influx. Intracellular Ca2+
mediates changes in membrane proteins to initiate
transmitter release and ion channel opening; it also
activates enzymes to allow neurons to cover or uncover
receptor sites that alter neuronal sensitivity. Various
plastic or persistent changes in excitability can result by
influencing the expression of genetic information through
Ca2+ influx. This may occur by selectively inducing genes
to synthesize a protein for a specific reason. One example
is the induction of the c-fos gene to produce c-fos protein
in neurons involved in an epileptic seizure by the
administration of pentylenetetrazol. The exact effects of
this coupling are not known, but it provides a means to
study the effects of neuronal excitation on cell growth and
differentiation as a model for epilepsy, learning, and
memory.
Notes:
  Page 4 of 5 
Ikey and Lee 
      
OS  212  Neurology
    Neuro Consultants
SGD 2: Altered Sensorium Exam 1

GREETINGS:

Ikey: Hello to the footballers of 2012 (championship #4,

5) What diagnostic procedures are you going to
facilitate for this patient?
o Blood Alcohol levels
 Alcohol toxicity can cause neural
symptoms and seizures
o Blood Glucose
 To rule out alcohol-induced
hypoglycemia
o Thiamine levels
 Wernicke encephalopathy – low
thiamine levels
 Pt was already given B Complex – an
improvement supports a Dx of
Wernicke’s encephalopathy
o Drug Screen
 Check if the patient still has MAP in his
system which can cause unpredictable
results when mixed with ethanol
o CT Scan
 To check for focal lesions
here we come!), to Lee (happy birthday), to Gillian, Kris,
Ivan, Mean, Errol, Chard (for settling their accounts), to
Raphy (for also settling his account and for writing the
TRP song that’s going to win our class first place this
year!), to Maddie and Adrian (for already paying part of
nd
the 2 sem funds way ahead of schedule), to Barre (car-
talk buddy), Nobel Neonates (get well soon, CO). Hello
to Block B, good luck with GI! 5 weeks until Christmas
break!
Lee: Thanks for all the birthday greetings! Happy birthday
to the fellow November celebrants: Jay, Mike Perez,
Suzie, Nemo, Borgy, Alex, Noems, Jay-R, Diane,
Butch, Laura, Kenneth, Gio, NiÑo, Aimee, Dane,
Crystal, and Mitch (and any other Nov b-days I missed).
Raphy et al, nice job on the TRP song! Congrats to Nobel
Neonates on our successful weekend. Good luck to all
our Palarong Med teams this weekend! Hi Lyz! To my
Brods & Sisses, AFTG!

6) What is the value of each of the diagnostic tests

done on this patient?

See Question 5

7) What are the initial approaches to therapy?

o Thiamine 100mg IV or IM
 Given daily until patient resumes a
normal diet
 Should be given prior to treatment with
IV glucose solutions
o Glucose IV –
 Standard treatment (along with
Thiamine) for alcohol related toxicity.
 Not to be given w/o Thiamine due to risk
of precipitating or worsening Wernicke’s
disease

8) What is the prognosis for this patient?

o Dependent on time before beginning treatment

 Untreated Wernicke’s can progress to
Korsakoff’s syndrome affecting memory
 Prolonged and severe hypoglycemia
can cause global insult to the neurons of
the brain

Notes:  

November
  10, 2008, | Thursday   Page 5 of 5 
Ikey and Lee