SGD: Neuromuscular

System

02/02/2021
Prepared by: SGD Group 8 Case 1
Prepared for: Dr. Gulane Southwestern University
PHINMA
School of Medicine
 SGD Group 8

Members:
• MUMTAZ, MUHAMMAD
• PETALLO, KIMBERLY VERGARA
• PULAW, FATNUHARDA ASGALI
• REJUSO, ARNOLD JESFEL MORALES
• RODRIGUEZ, KATREEN YNNA MARRI
COJAMCO
• ROSALES, ZYRA JOYCE GOC-ONG
The
Case
Chief complaint:

Left-sided body
weakness

General Data:

Name: MR
Age: 37-year-old
Sex: female
Nationality: Filipino
Religion: Roman Catholic
Address: Subangdaku mandaue
Occupation: Institutional worker
admitted for the first time at Vicente
Sotto Memorial Medical Center
History of Present Illness:
8 hours PTA, the patient noted sudden onset of
dizziness, which is rotatory, described as swaying in
motion, associated with vomiting, of previously-
ingested food, x3 episodes ~½ cup per episode, non
projectile, nonbilious, non-bloody. Dizziness not
relieved by vomiting. Self-medicated with
Betahistine 16mg/tab x 1 dose with minimal relief.
The patient then fell asleep.
30 minutes PTA, after waking up, recurrence of
dizziness was noted with the same character, now
associated with left-sided weakness and numbness,
slurring of speech, and inability of right eye to
move to the right.

The patient then was immediately

brought to the ED, and was subsequently
admitted.
Past Medical History:

➔ June 2015 – dizziness and vomiting –

diagnosed with Benign Paroxysmal
Positional Vertigo at CCMC ED –
prescribed 16mg/tab PRN,
Metoclopramide 10mg/tab PRN
➔ Non-asthmatic, non-hypertensive,
nondiabetic
➔ No maintenance medications other
than multivitamin supplementation
➔ No known food and drug allergies
➔ No previous surgery
Family Medical History:

(+) Hypertension – both paternal and maternal sides

(+) CVD – maternal (aunt, age 43 y.o.)
(-) DM, BA, Malignancy, Thyroid disease, Mental/Psychiatric
disorder

Personal and Social History:

Smoker: 25 pack years (25 sticks/day for 20

years)

Alcoholic Beverage Drinker: occasional, once a

week, 3 bottles/session
 General:
Physical Examination:
★ Awake,
★ Conscious,
★ Coherent,
★ Wheelchair-borne,
★ Not in respiratory distress

Vital signs:
BP: 140/90 mmHg
HR: 99 bpm
RR: 22 cpm
T: 37˚C

O2 sat: 98% Wt.: 88 kg Ht.: 166 cm

BMI: 31.9
Physical Examination:
SKIN: brown in color, warm to touch, fair skin turgor, no
lesions
HEENT: anicteric sclerae, pink palpebral conjunctivae,
moist lips and oral mucosa, no tonsillopharyngeal
congestion, no neck vein distention, no cervical
lymphadenopathies, no palpable masses, no audible
bruit
RESPIRATORY: No fractures, lesions or hematoma,
symmetrical chest expansion, clear breath sounds, no
adventitious sound, no use of accessory muscles for
respiration, no retractions, resonant on percussion.
CARDIOVASCULAR: Adynamic precordium, normal
rate, regular rhythm, distinct S1 and S2, no murmurs,
apex beat at 5th ICS MCL, no bruits
GASTROINTESTINAL: globular abdomen, no visible
veins or visible peristalsis; normoactive bowel sounds;
tympanitic on percussion, no palpable masses or
organomegaly appreciated, no abdominal bruit noted
 • Cortical
Neurologic Examination: o Frontal – good attention span, (-) Broca’s aphasia
o Parietal – (-) right/left disorientation, finger agnosia
o Temporal – (-) Wernicke’s Aphasia
o Occipital – Able to identify color and object

o MSE – Conscious, coherent; Oriented to person, place, and time; Able to

subtract serial 7s; Intact immediate, recent, and remote memory

• Sensory

o 100% sensation to light touch, pain, pressure, and temperature on the

right upper and lower extremity

o 80% sensation to light touch, pain, pressure, and temperature on the left
upper and lower extremity

• Motor
o 5/5 right upper and lower extremities
o 3/5 left upper and lower extremities
• DTR • Cerebellar
o +2 on all extremities o (+)dysdiadochokinesia,
o (+) Babinski, bilateral left
o (+) dysmetria, left
Neurologic Examination:
• Cranial Nerves o CN I – able to smell and identify scent

o CN II, III – pupils equally and briskly reactive to light, 3-4mm;

on fundoscopy, (+) red-orange reflex (-) hemorrhages,
neovascularization, AV ratio 2:3; Near Vision: OS 20/20, OD
20/50-1

o CN III, IV, VI – primary gaze to the left; right eye cannot move
laterally; horizontal and vertical nystagmus

o CN V – V2, V2, V3: intact sensory and motor

o CN VII – facial asymmetry, left

o CN VIII – intact gross hearing

o CN IX, X – intact gag reflex, uvula midline; (+) dysarthria

o CN XI – good shrug, SCM and trapezius muscle symmetric

with muscle strength of 5/5

o CN XII – tongue deviated to the left

 LABORATORY RESULTS
Urinalysis: yellow, slightly cloudy,
CBC:
pH 5.5,
WBC-18.29
N-0.84 SG 1.025,
L-0.13 RBC 1-2 hpf,
M-0 E-0 B-0
Stabs-0.03 Pus cells 1-2 hpf,

HGB-168 EC-few
HCT-0.48
IMAGING STUDIES
PLT-336,000
Chest X-ray: Normal Chest Prothrombin Time-11.3,
ECG: NSR; Non-specific ST-T wave changes
Control-11.21sec, INR-
Cranial CT Scan 1.01,
Protime Activity 98.2%,
Impression: Chronic infarct, right
APTT- 28.2, Control-
cerebellar hemisphere, suggests delayed
32.5
contrast-enhanced cranial CT study for
further evaluation.
Physical Diagnosis:
Neurologic
Examination
Bates Guide to Physical
Examination & History Taking
 Motor System

1. Muscle Bulk
2. Muscle Tone
3. Muscle Strength

Plantar Response
Motor:
o 5/5 right upper and lower extremities
o 3/5 left upper and lower extremities

Bates Guide to Physical

Examination & History Taking
Motor System
1. Coordination
● Rapid alternating
Movement
● Point-to-point movements
● Gait
● Stance

• Cerebellar
o (+) dysdiadochokinesia, left
o (+) dysmetria, left

Bates Guide to Physical

Examination & History Taking
CC: left sided weakness

Bates Guide to Physical

Examination & History Taking
 Diagnostic Tests

Neuroimaging:
● CT Scan
● MRI
“Time is brain”: time is of
essence when it comes to
stroke.

MRI of Acute Stroke

CT Scan of an Acute left MCA stroke

 Diagnostic Tests

Advantages Disadvantages
Neuroimaging:
CT Widespread availability; Infarct may not be seen
● CT Scan Scan rapid scan times; lower reliably for 24-48 h
cost; differentiate
● MRI ischemic from
hemorrhagic stroke

“Time is brain”: time is of

essence when it comes to MRI More sensitive than Higher cost; limited
noncontrast CT availability & access;
stroke.
patience intolerance or
incompatibility
GUIDE QUESTIONS
WHAT IS STROKE ?

Definition: A stroke, or Risk Factors:

cerebrovascular accident, is defined ● Hypertension
as an abrupt onset of a neurologic ● Cigarette smoking
deficit that is attributable to a focal ● Dyslipidemia
vascular cause. ● Obesity/Lack of
physical exercise
● High-risk diet
Middle Cerebral Artery ● Family history
- Most common artery involved
in stroke
- Largest branch & 2nd terminal
Statistics: Stroke is the
branch of internal carotid artery
second leading cause of death
- Supplies a large area of lateral
worldwide, with 6.2 million
surface of brain & part of basal
dying from stroke in 2015, and
ganglia, and the internal
an increase of 830,000 since
capsule via 4 segments (M1,
the year 2000.
M2, M3, M4)
WHAT ARE THE CATEGORIES OF STROKE?

● Ischemic (80%)
- Typically resulting from thrombosis or embolism

● Hemorrhagic (20%)
- Resulting from vascular rupture

● Transient ischemic attack

- Typically lasting for <1 hour
WHAT ARE THE RISK FACTORS FOR STROKE IN THE YOUNG?
❖ Although the incidence of ischaemic stroke increases with age, an
estimated 10% to 20% of these events occur in young people aged
18 to 50 years
❖ In contrast to stroke in older adults, the incidence of ischaemic
stroke among young adults is rising globally

Common factors: Underlying illnesses:

● Hypertension ● Moya moya disease
● Cigarette smoking ● Rheumatic heart disease
● Dyslipidemia ● HIV
● Obesity/Physical inactivity ● Arterial dissection
● Alcohol consumption

National Library of Medicine, 2015

Journal of Neurology, Neurosurgery
& Psychiatry, 2019
 Stroke Severity
● important predictor of patient outcomes and is
commonly measured with the National Institutes of
Health Stroke Scale (NIHSS) scores
○ the sum of 15 individually evaluated elements,
and ranges from 0 to 42

moderate
Stroke no stroke minor moderate severe
to severe
Severity symptoms stroke stroke stroke
stroke

NIHSS
Score
0 1–4 5–15 16–20 21–42
Treatment &
Management
What is the primary goal for the acute management of
stroke?

● ABC, treat reversible conditions

● Confirm vascular pathology and exclude stroke
mimics
● Acute Stroke Unit
● Reperfusion Therapy
● Early Antiplatelet Therapy
ABC, treat reversible conditions
 Confirm vascular pathology and
exclude stroke mimics

● History and Physical

Examination
● Emergency CT/MRI
brain scan
● Laboratory studies
● Cardiac studies
 Acute Stroke Unit

● Acute Stroke Unit is an acute neurological ward

providing specialist services for people who have
had a new suspected stroke.
● Allows close monitoring
● Lowers mortality, improves function, reduces
complications and reduces rehospitalizations
 Reperfusion Therapy

● Intravenous thrombolysis
● Intra arterial thrombolysis
● Endovascular technique for clot retrieval
 Early antiplatelet therapy

● Starting aspirin within 48 hours of presumed

ischemic stroke onset reduced the risk of early
recurrent ischemic stroke without a major risk of
early hemorrhagic complication and improved long
term outcome
● Aspirin is the only antiplatelet agent that has been
established as effective for the early treatment of
acute ischemic stroke
What is the approach to acute management
of stroke?

The first goal is to prevent or reverse brain

injury.

Attend to the patient’s airway, breathing, and

circulation (ABCs), and treat hypoglycemia or
hyperglycemia if identified by finger stick testing.

Perform an emergency noncontrast head CT

scan to differentiate between ischemic stroke
and hemorrhagic stroke.

Harrisons, Internal Medicine

 Process of treatment

(1) medical support

(2) IV thrombolysis
(3) endovascular revascularization
(4) antithrombotic treatment
(5) neuroprotection
(6) stroke centers and rehabilitation

Harrisons, Internal Medicine

The National Institute of Neurological IV thrombolysis
Disorders and Stroke (NINDS) rtPA Stroke
Study showed a clear benefit for IV rtPA in
selected patients with acute stroke.

● rtPA is approved in the 3- to 4.5-h

window in Europe and Canada
● Only approved for 0–3 h in the United
States.
● Dose of 0.6 mg/kg is typically used in
Japan and other Asian countries based
on observation of >600 patients given
this lower dose, and observing similar
outcomes to historical controls and a
lower rate of intracranial hemorrhage.

Use of IV tPA is now considered a central

component of primary stroke centers.
Harrisons, Internal Medicine
Alteplase (formerly known as tissue
plasminogen activator or tPA)
● serine protease originally derived from
cultured human melanoma cells. It is
now obtained as a product of
recombinant DNA technology.
● MOA: act either directly or indirectly to
convert plasminogen to plasmin, which,
in turn, cleaves fibrin, thus lysing
thrombi
● Alteplase is approved for the treatment
of Ml, massive PE, and acute ischemic
stroke.

Katzung, Basic and Clinical Pharmacology

Lippincott, Pharmacology
Platelet Inhibition ANTITHROMBOTIC
● Aspirin TREATMENT for
➔ the only antiplatelet agent that
has been proven to be
ISCHEMIC STROKE
effective for the acute
treatment of ischemic stroke.
● MOA: inhibit the activity of
cyclooxygenase (COX), impair
platelet aggregation via
inhibition of platelet
thromboxane A2 synthesis,
thus reducing thrombus
formation on the surface of the
damaged arterial wall.
Anticoagulants

Warfarin
● Coumarin anticoagulants/ Vitamin K antagonists
● MOA: Coumarin anticoagulants block the γ-
carboxylation of several glutamate residues in
prothrombin and factors VII, IX, and X as well as
the endogenous anticoagulant proteins C and S ,
● Effects: the blockade results in incomplete
coagulation factor molecules that are biologically
inactive.
● Clinical applications: used in the prevention and
treatment of DVT and PE, stroke prevention,
stroke prevention in the setting of atrial
fibrillation and/or prosthetic heart valves, protein
C and S deficiency, and antiphospholipid
syndrome

Katzung, Basic and Clinical Pharmacology

Lippincott, Pharmacology
 Neuroprotective therapy

Are therapies designed to interrupt the

cellular, biochemical, and metabolic
elaboration of injury during or following
exposure to ischemia; they encompass
a rapidly expanding array of
pharmacologic interventions.
 Blood glucose and pressure control

Hypertension is the most important

modifiable risk factor for stroke
High blood pressure can cause the
arteries that supply blood and oxygen to
the brain to burst or be blocked. causing
a stroke.

Blood glucose is often elevated in acute

stroke, and higher admission glucose levels
are associated with larger lesions, greater
mortality and poorer functional outcome. In
patients treated with thrombolysis,
hyperglycemia is associated with an increased
risk of hemorrhagic transformation of
infarcts.
Non-pharmacologic Interventions

• healthy diet
• regular physical activity/ exercise
• low-normal body mass index
• smoking abstinence
• moderate drinking of alcohol

It is essential to inform patients on the importance, value and benefits of non-pharmacological stroke
prevention, in particular when it remains the only therapeutic option in case of adverse side effects of
pharmacotherapy prevention. Numerous studies demonstrated that even small lifestyle modifications could
significantly reduce the risk of stroke. -Planjar-Prvan M. (2010)
 Concept Map
Chief Complaint:
Left-sided body weakness

NEUROLOGICAL EXAM
NEUROLOGICAL EXAM NEUROLOGICAL EXAM
CN III, IV, VI – primary gaze to the left;
Coordination Motor System right eye cannot move laterally;
● Rapid alternating 1. Muscle Bulk horizontal and vertical nystagmus
Movement 2. Muscle Tone CN VII – facial
3. Muscle Strength asymmetry, left CN XII – tongue
● Point-to-point movements deviated to the left
● Gait
● Stance
STROKE

GOALS FOR MANAGEMENT TREATMENT

DIAGNOSTIC TESTS ● (1) medical support
● ABC, treat reversible conditions
Neuroimaging: ● Confirm vascular pathology and
● (2) IV thrombolysis
● (3) endovascular revascularization
● CT Scan exclude stroke mimics ● (4) antithrombotic treatment
● MRI ● Acute Stroke Unit ● (5) neuroprotection
● Reperfusion Therapy ● (6) stroke centers and rehabilitation
● Early Antiplatelet Therapy
 References

● Bates’ Guide to Physical Examination and History Taking, 13th edition

● Robbins and Cotran Pathologic Basis of Disease, 10th edition
● Henry’s Clinical Diagnosis and Management by Laboratory Methods 24th
edition
● Katzung Basic and Clinical Pharmacology 15th edition
● Harrison’s 20th edition
 SGD: Neuromuscular
System

02/02/2021
Prepared by: SGD Group 8 Case 2
Prepared for: Dr. Gulane Southwestern University
PHINMA
School of Medicine
The
Case
Chief complaint:

Altered
Sensorium

General Data:

Name: MJ
Age:3-year-old
Sex: Male
Nationality: Filipino
Status: Married
Admitted for the first time at SWU –
Medical Center
 History of Present Illness:
1 month PTC, initially complained of low grade,
recurrent ear infection. Consulted school physician
and prescribed Co-Amoxiclav 228.5mg/5mL, given
3mL 3x a day, Paracetamol 250mg/5mL syrup 2.5mL
every 6hrs as needed for fever >38C. Meditations
initially taken but unfortunately with poor
compliance and patient eventually lost to follow up.
5 days PTA, complains of fever and altered
sensorium, mother remarked had increased
sleepiness over the past days.

He was then admitted to the SWU-MC

Past Medical History:

Delivered with unclear

vaccination history.

Physical Examination

Delivered with unclear

vaccination history.
 Diagnostic findings

CBC: WBC 18,000 (neu: 79%, lym 12%, eos: 2%)

The following lumbar puncture cerebrospinal fluid

(CSF) results (normal ranges) are reported from the The patient is diagnosed with
biochemistry and pathology laboratories within 4 suspected meningitis and the
hours of admission. treatment plan are as follows:
• Ceftriaxone IVTT
White blood cells: 23000 cells/mm3 (<5 cells/mm3), • Paracetamol IVTT
90% polymorphs

CSF protein 1.31 g/L (<0.4 g/L)

CSF glucose 1.4 mmol/L (2.2–4.4 mmol/L)

CSF:blood glucose ratio 0.22 (>0.6)

Gram-negative coccobacilli were identified in the

CSF
Clinical Impression
Bacterial meningitis
 Ali

1. What are the important pathogens?

a. Characteristic/description of culprit microorganism in Meningitis

i. Bacterial pathogens

ii. Viral Pathogens

iii. Fungal Pathogens

Antibiotic options for each of the causative agents

I. Bacterial Pathogens

Goal is to begin antibiotic therapy

within 60 minutes of a patient’s arrival
in the ER. Empirical antimicrobial
therapy is initiated in patients with
suspected bacterial meningitis before
the results of CSF gram stain and
culture are known.

Empiric therapy:
Dexamethasone + 3rd or 4th-generation
cephalosporin + vancomycin
 Antibiotic options for each of the causative agents

II. Viral Pathogens

CA: HSV -1 or -2, EBV, VZV
Oral or intravenous acyclovir
● Severely ill patients: IV Acyclovir (15-30 mg/kg per day in 3 divided
doses), followed by oral drug Acyclovir (800 mg five times daily, famciclovir
(500 mg TID), or Valacyclovir (1000 mg TID) for a total of 7-14 days.
● Less ill patients: Oral drugs alone

Acyclovir
MOA: activated by viral thymidine kinase (TK) to forms that inhibit viral DNA polymerase
Clinical Applications: Treatment & prophylaxis for HSV-1, HSV-2, & VZV
Pharmacokinetics: Topical, oral, and IV
Toxicities: oral forms cause nausea, diarrhea, & headache; IV acyclovir may cause renal &
CNS toxicity
 Antibiotic options for each of the causative agents
III. Fungal Pathogens
Cryptococcal infection: induction therapy with amphotericin B (AmB) (0.7 mg/kg IV per day)
plus flucytosine (100 mg/kg per day in four divided doses) for at least 4 weeks if CSF culture
results are negative after 2 weeks of treatment.
Coccidioidal infection: treated with either high-dose fluconazole (100 mg daily) as monotherapy
or intravenous AmB (0.5-0.7 mg/kg per day) for > 4 weeks.

Amphotericin B Flucytosine
MOA: Binds to ergosterol in fungal cell MOA: inhibits DNA & RNA polymerases
membranes, forming leaky pores Pharmacokinetics: Oral; enters CSF
Pharmacokinetics: Multiple forms, IV for Toxicities: Bone marrow suppression
systemic infections; topical for ocular/bladder
infections
Toxicities: Nephrotoxicity is dose-limiting, Fluconazole
additive with other nephrotoxic drugs; MOA: inhibits fungal P450-dependent enzymes by
infusion reactions (chills, fever, muscle blocking ergosterol synthesis
spasms, hypotension Pharmacokinetics: various topical & oral forms
Toxicities: less toxic; may cause GI upsets & rash
Which antibiotic regimens achieve therapeutic concentrations
in the cerebrospinal fluid and which ones should be avoided?

Achieved therapeutic concentrations in CSF Avoid:

• Ceftriaxone, cefotaxime, ● Cefuroxime
ceftazidime,cefixime & cefepime
• Penicillins
• Meropenem & imipenem
• Aztreonam
• Chloramphenicol &
sulfamethoxazole/trimethoprim
• Linezolid
• Metronidazole
• Rifampin
• Vancomycin
• Isoniazid, pyrazinamide &
streptomycin

National Library of Medicine, 201

3
Dexamethasone
• glucocorticoid , adjunctive therapy
improves the outcome in adults with
acute bacterial meningitis
• MOA: suppressing the migration of
neutrophils and decreasing
lymphocyte colony proliferation.
• Adverse effect: Stomach upset,
heartburn, headache, trouble
sleeping, or increased appetite may
occur.
Ceftriaxone
• broad-spectrum third-generation
cephalosporin antibiotic

MOA: inhibiting the mucopeptide

synthesis in the bacterial cell wall. The
beta-lactam moiety of ceftriaxone binds to
carboxypeptidases, endopeptidases, and
transpeptidases in the bacterial
cytoplasmic membrane. These enzymes
are involved in cell-wall synthesis and cell
division. Binding of ceftriaxone to these
enzymes causes the enzyme to lose
activity; therefore, the bacteria produce
defective cell walls, causing cell death.

Adverse effects:Black tarry stools, chest

pain, chills, cough, fever, painful or difficult
urination, and shortness of breath
Acyclovir
• used to treat infections caused by
certain types of viruses. It treats
cold sores around the mouth (caused
by herpes simplex), shingles (caused
by herpes zoster), and chickenpox.

MOA: competitively inhibits viral DNA

polymerase by acting as an analog to
deoxyguanosine triphosphate (dGTP).
Incorporation of acyclovir triphosphate into DNA
results in chain termination since the absence
of a 3' hydroxyl group prevents the attachment
of additional nucleosides.

Adverse effect: Nausea, diarrhea, headache,

or vomiting may occur.
Amphotericin B
• belongs to the polyene class of
antifungals, been used for the
treatment of invasive fungal
infections

MOA: acts by binding to ergosterol in the cell

membrane of most fungi. After binding with
ergosterol, it causes the formation of ion
channels leading to loss of protons and
monovalent cations, which results in
depolarization and concentration-dependent
cell killing.

Adverse effect: Loss of potassium, loss of

magnesium, anaphylaxis, fevers, and
nephrotoxicity.
Ceftriaxone IVTT
Recommended dose: 80-100mg/kg
Childs weight:
 Concept Map (AJ)
Pertinent Data: Chief Complaint: right-sided weakness Clinical features:
● 56 y/o ● Right-sided hemiparesis
● Male ● Facial asymmetry
● Chronic Hypertension ● Slurring of speech
● Diabetic ● Stage 2 Hypertensive
● Chronic Smoker: 80 pack years Cardioembolic Stroke ● Tachycardic
● Paternal history of hypertension & ● Irregular rate & rhythm
diabetes ● + grade 3 soft, decrescendo
● No formal diet or exercise
regimens
murmur, heard best at 2nd ICS,
Pertinent Diagnostic Findings: right sternal border
● ECG: Atrial fibrillation with rapid ● VII: prominent facial droop &
ventricular response flattening of right nasolabial fold
● Increased PT ● Motor: 1/5 strength right upper &
lower extremities

Ischemic (Cardioembolic) Stroke

Amyotrophic Lateral Sclerosis Bell’s Palsy with Right-sided Hemiparesis
Ruled out: Ruled out:
(-)significant reflex hyperactivity (-) decreased tearing, altered sense of taste,
(-) muscle cramp & fasciculations drooling, pain in or behind the ear & hyperacusis Management & Prevention:
● IV Thrombolysis - Alteplase
(-) exaggeration of motor expressions -> (-) no muscle weakness in both upper & lower ● Antithrombotic Treatment- Aspirin
pseudobulbar affect extremities ● Anticoagulants- Warfarin
(-)CVS consequences are not pronounced ● Neuroprotection- Citicoline
 References

● Bates’ Guide to Physical Examination and History Taking, 13th edition

● Robbins and Cotran Pathologic Basis of Disease, 10th edition
● Henry’s Clinical Diagnosis and Management by Laboratory Methods 24th
edition
● Katzung Basic and Clinical Pharmacology 15th edition
● Harrison’s 20th edition