CASE

STUDIES ON
MAJOR
CONCEPTS
NEUROLOGICAL
 BELL’S PALSY
By: ALCE

Case Scenario – Mrs. Seaborn is a 43-year-old woman who presents to the emergency department with complaints of
weakness of the left side of her face. She is married and is an interior decorator who owns her own business. Earlier
today she was working at a client’s home when she started to have increased facial weakness and was unable to taste
her lunch. She states a history of two days of numbness in her forehead.

History of Present Illness – Mrs. Seaborn’s vital signs are temperature 98.2°F, blood pressure 148/60, pulse 83, and
respiratory rate of 26. She is fearful, crying, and states, “My mother died of a stroke, I am sure that is what is going on.
Am I going to die?” She complains of pain behind and in front of her left ear. She is exhibiting unilateral facial paralysis.
Her left eye is drooping and she says it feels dry. Her inability to raise her eyebrow, puff out her cheeks, frown, smile or
wrinkle her forehead is suspicious for Bell’s palsy. A healing cold sore is observed on her lower lip.
Pathophysiology

The precise pathophysiology of Bell palsy remains an area of debate. The facial nerve courses through a
portion of the temporal bone commonly referred to as the facial canal. A popular theory proposes that
edema and ischemia result in compression of the facial nerve within this bony canal. The cause of the
edema and ischemia has not yet been established. This compression has been seen in MRI scans with
facial nerve enhancement.
Concept Map

Causes
Causes

•• herpes
herpes simplex,
simplex, which
which causes
causes cold
cold
sores
sores and
and genital
genital herpes
herpes
•• HIV,
HIV, which
which damages
damages the
the immune
immune
system
system
•• sarcoidosis,
sarcoidosis, which
which causes
causes organ
organ
inflammation
inflammation
Risk
Risk factors
factors Signs
Signs and
and Symptoms
Symptoms

••are
are pregnant
pregnant ••drooling
drooling
••have
have diabetes
diabetes ••difficulty
difficulty eating
eating and
and drinking
drinking
••have
have aa lung
lung infection
infection ••an
an inability
inability to
to make
make facial
facial expressions,
expressions,
••have
have aa family
family history
history of
of the
the condition
condition such
such as
as smiling
smiling oror frowning
frowning
••facial
facial weakness
weakness
••muscle
muscle twitches
twitches inin the
the face
face

Bell's
Palsy
 MENINGITIS
By: ADUNA
A 25 year old female client presented to the ED with the chief complaint of a generalized throbbing headache, accompanied by mild neck
pain and stiffness, as well as a general feeling of malaise. She has a fever of 102 degrees F. She stated that it hurts to rotate or flex her
neck. Upon examination, she was found to have a positive Kernig and Brudzinski sign. Client seems irritable during his examination and
also complains that she is not able to look at any light, as both artificial and sunlight cause her discomfort.
Chief complain: generalized throbbing headache, accompanied by mild neck pain and stiffness, as well as a general feeling of malaise.
Past Medical History: Mother passed away from breast cancer at the age of 40 while her father has type 2 DM and hypertension but
otherwise alive and well at the age of 55. Brother is alive and well at age 18. Sister is alive and well at age 23. No known history of viral
meningitis. She was diagnosed to have Type 1 Diabetes Mellitus at age of 17. Non smoker and non alcoholic.
Present history: It was late afternoon and she was watching the television when she felt dizzy and cold. She told her mother about it and
she took her temperature and it was 38 degree. She was given a warm blanket and was asked to lay down on the sofa. She then started
to feel throbbing headache. As time goes by her neck started aching as well. After an hour, she complain that it hurts to rotate or flex her
neck and that she feels weak. Her mother call 911 and she was sent to the emergency room.
Pathophysiology

The infection is spread through contaminated saliva, respiratory tract secretions and respiratory droplets.  Infection
occurs when these pathogens are inhaled. The bacteria will then attach to the epithelial cells in the nasopharynx, cross
the mucosal barrier and enter the blood stream. After the bacteria enters the blood stream it will travel to the cerebral
blood vessels where it will cross the blood brain barrier and infect the meninges. After the bacteria crosses the blood
brain barrier it will multiply rapidly and lyse in the subarachnoid space releasing bacterial endotoxins. This rapid
multiplication will attract a large number neutrophils to the area where they will release inflammatory cytokines to fight
the infection. This release of endotoxins and cytokines increases the permeability of the blood brain barrier causing
cerebral edema and brain tissue damage. The exudate from the inflammatory response will also thicken the CSF,
obstructing flow around the brain and spinal cord. This paired with edema will increase the intracranial pressure which
if not corrected will lead to cerebral ischemia, necrosis and subsequent cerebral infarction (References: McCance &
Heuther, 2019).
Concept Map
 ACUTE SPINAL CORD INJURY
By: BAYAUA
Case Scenario: John is a 19-year-old student, who had an accident while on holidays with his friends when his head hit a sandbank as he dived into
the waves. His friends were experienced first aiders and were first responders to the accident. Paramedics arrived at the scene within 15 mins. John
was lying in the supine position, he reported severe pain in his neck and was unable to move his arms and legs. He was drowsy but, oriented to his
current location, and some details of the accident. He complained that he could not feel his arms and legs. His pupils were equal and reactive to light.
He showed no other signs of injury but paramedics were concerned as John may have inhaled some water during the accident. His vital signs
revealed a blood pressure of 100 / 72, heart rate of 82 beats per minute, respirations of 22 per minute. The paramedics applied a cervical collar,
placed him on Ferno Scoop Stretcher, immobilized his head, provided 100% Oxygen and transported him to the trauma center by helicopter. He
arrived at the hospital and underwent an initial assessment within 120 mins of the accident.
History Of Present Illness: John hit his head and was floating on the water for approximately 30 seconds, his friends initially thought he was joking
around but one friend realised that John was having trouble and went to check on him. He called to his other friends to assist with turning John and to
call for an ambulance. John was turned face up in the water. He was awake and had a weak cough, he had swallowed some water but was breathing.
John was taken out of the water by six individuals, including two lifeguards who arrived on the scene who supported his neck throughout. He was
positioned lying on his back, supported at the neck and covered with a blanket to try to maintain his body temperature as they waited for assistance to
arrive.
Pathophysiology

The primary phase involves the initial mechanical injury during

which failure of the spinal column (fracture and/or dislocation)
directly imparts force to the spinal cord, disrupting axons, blood
vessels, and cell membranes.
spinal cord injury can be categorized as acute impact or
compression. Acute impact injury is a concussion of the spinal
cord. This type of injury initiates a cascade of events focused in
the gray matter, and results in hemorrhagic necrosis.
Concept Map

His pupils were equal He was awake

and reactive to light and had a weak
cough, he had
swallowed some
John hit his water but was
head and was ACUTE SPINAL CORD
INJURY
breathing
floating on the
water for
approximately
30 seconds
  He was drowsy but,
he reported oriented to his current
severe pain in his location, and some details
neck and was of the accident. He
unable to move complained that he could
his arms and legs not feel his arms and legs
 MIGRAINE
By: BERNABEO

Case Scenario: A 25-year-old single woman presented with the chief complaint of “daily headaches for the past 30 days.” 
She has a previous history of allergies and depression and currently is on treatment with Zoloft. She started having
migraines at 12 years old at the same time she started her menstrual cycles (menarche).  She reports that the time her
usual migraine lasts is 7 days.  Using the International Classification of Headache Disorders (ICHD) check list for
diagnosing migraine she had all the features of migraine without aura except nausea.

History of Present Illness: She’s experiencing daily headaches for the past 30 days.
Pathophysiology

A migraine attack can be divided into phases on the basis of its temporal relationship to headache: the premonitory phase (precedes
headache), the aura phase (immediately precedes or accompanies headache), the headache phase, and the postdrome phase
(after resolution of headache). Although this description of a migraine attack is practical, the phases of an attack can be overlapping
and variable. Some symptoms of a migraine attack (sensory sensitivity and neck pain) might be present throughout an attack,
whereas others (aura symptoms) might come and go. The different phases of a migraine attack represent an opportunity to
characterize and distinguish the physiological changes that are occurring at the start of a migraine attack, those that are responsible
for headache, and those involved in the process of recovery. In the premonitory phase, a variety of symptoms, including yawning,
polyuria, mood change, irritability, light sensitivity, neck pain, and concentration difficulties, among others, commonly occur hours
before onset of headache during a migraine attack. Although some of these symptoms are subjective, others, particularly sensory
sensitivity, can be objectively quantified. For example, changes in quantitative sensory thresholds occur hours before headache,
consistent with the occurrence of subjective sensory symptoms in the premonitory phase
Concept Map:

SIGNS &
RISK FACTORS
SYMPTOMS

Overuse of
Severe Visual effects or
Family History migraine
Headache aura
medications

Sensitivity to light
Nausea & or sound Age first occurs History of head
vomiting during adolescence injury
 

Frequent Common in Stressful life

Vision loss
yawning women events

Mood changes
Weakness or from depression Drinking
Hormonal
numbness in the to euphoria caffeinated
changes
face beverages
 
 OTOSCLEROSIS
By: COCUSA

A male patient, aged 11 years, presented at our unit complaining of unilateral progressive hearing loss for 5 years, and moderate,
intermittent, whistle-like tinnitus; there were no vestibular symptoms. The patient reported repeated episodes of otitis media with effusion
during the past 5 years that was resistant to the usual medical treatment. The patient had a family history of otospongiosis (mother and
maternal grandmother). The otorhinolaryngological exam revealed a reddish hue seen by transparency through the tympanic membrane
in the promontory of the left ear (Schwartze’s sign) and no right ear alterations. Pure tone audiometry showed mild left ear conductive
hearing loss; the right ear hearing thresholds were within normal limits. Immitance testing revealed decreased left tympanic membrane
complacency and bilateral absence of the stapedian reflex Computed tomography of the temporal bones showed anterior otosclerosis in
the right and left oval windows bilateral cochlear pericochlear foci with no endosteal involvement, and thickening of the stapes footplate
to the left.
Medical treatment with sodium fluoride (10 mg/day) was started, but the patient developed pharmacodermy, which required interrupting
the use of this drug. Surgery (stapedotomy) and a hearing aid were suggested. A choice was made for waiting and programmed
outpatient monitoring (pure tone audiometry, voice audiometry and immitance testing) every six months.
 Pathophysiology

Bony changes vary according to the duration of diseases

 First: the normal bone is absorbed and replaced by vascular, spongy osteoid tissue and
advanced with blood vessels.
 Later: bone become thicker and less vascular
 Then: new bone formation takes place at annular ligament of the oval window fixing the
stapes and leads to conductive deafness.
 Spread to footplates of the stapes
Also affect the bony-capsule of the labyrinth, resulting sensory-neural deafness.
Concept Map
Risk Factors:
•Age
•Sex
Sign and Symptoms include: •Family history
•Hearing loss •Medical History
•Dizziness, vertigo, or balance problems •Race and Ethinicity
•Tinnitus, or ringing, roaring, or hissing in
your ears

Otosclerosis

Treatment
•Monitoring
•Device (Hearing Aids)
•Surgery
 MYASTHENIA GRAVIS
By: DELA CRUZ

Case Scenario: The patient is a 35 year old woman who works as a librarian in a high school. She lives with her husband and dog
in a two-story house in the suburbs near the high school. The patient decided to try an outpatient physiotherapy clinic for her
increasing shoulder pain over the past 3 weeks. She also hopes to get some help with her generalized muscle weakness and
fatigue that is preventing her from completing her daily activities and work.
History of Present Illness: Patient reported an aching pain in her right shoulder with occasional shooting pain when reaching too
high overhead on bookshelves. She reports having little to no pain at the beginning of the day but it progressively gets worse and
by her lunch break she is unable to unload a full cart of books. After taking a 30 minute lunch break, her fatigue and pain
improves and she prefers finishing the rest of her day with computer work. By the end of the day, she notices her vision becomes
slightly blurred and finds it worsens when driving home. Patient reports feeling frustrated with her exhaustion at the end of the day
and is unable to do her normal activities with her husband including cooking and walking the dog because of arm weakness.
Patient reports having a nap when she gets home from work and sleeping well through the night. No red flags were detected.
Pathophysiology

The normal neuromuscular junction releases acetylcholine (ACh) from the motor nerve terminal in
discrete packages (quanta). The ACh quanta diffuse across the synaptic cleft and bind to receptors
on the folded muscle end-plate membrane. Stimulation of the motor nerve releases many ACh
quanta that depolarize the muscle end-plate region and then the muscle membrane causing
muscle contraction. In acquired myasthenia gravis, the post-synaptic muscle membrane is
distorted and simplified, having lost its normal folded shape. The concentration of ACh receptors
on the muscle end-plate membrane is reduced, and antibodies are attached to the membrane.
ACh is released normally, but its effect on the post-synaptic membrane is reduced. The post-
junctional membrane is less sensitive to applied ACh, and the probability that any nerve impulse
will cause a muscle action potential is reduced.
Concept Map

Signs and Symptoms Risk Factors

Weakness of the eye muscles

Weakness in the arms, hands, Men over 60 and

fingers, legs, and neck women under 40

Impaired speech MYASTEHNIA Family history of

GRAVIS autoimmune diseases
A change in facial expression

Shortness of breath

Difficulty swallowing Ptosis Diplopia

INCREASED INTRACRANIAL PRESSURE
By: MUNGCAL

Case Scenario: W.C. is a 50-year-old man initially diagnosed with a glioblastoma involving the right temporal lobe after
presenting with headaches and reduced short-term memory in May, 2006. He was placed on corticosteroids and
underwent a gross total resection. Following surgery, he received 60 Gy of external beam irradiation with concurrent
daily temozolomide at 75 mg/m2; he completed the regimen in August 2006. W.C.’s course was com- plicated by
fatigue, hair loss, and deep venous thrombosis for which he was placed on anticoagulation with Lovenox (enoxaparin
sodium injection, sanofiaventis). He was subsequently placed on adjuvant temozolomide at 200 mg/m2 for five days
every 28 days.
History of Present Illness: After completing two months of adju- vant treatment, W.C. presents to the emergency room
with a one-day history of in- creasing headaches and somnolence. This morning, his wife was unable to wake him and
called 911. She reports that W.C. fell yesterday while walking his dog, hitting his head on the sidewalk. He did not lose
consciousness at the time of the fall. Upon evaluation, he is arousable to sternal rub only and unable to follow
commands.
Pathophysiology
 
 Insult to brain
 Tissue edema
 Increase ICP
 Compression of ventricles
 Decreased blood flow
 Decreased oxygen with death of brain cells
 Edema around necrotic tissue
 Increased ICP with compression of brainstem and respiratory
center
 Accumulation of carbon dioxide
 Vasodilation
 Increased ICP resulting from increased blood volume
 Death
Concept Map

SIGNS AND
RISK
SYMPTOM
DEFINITION FACTORS
S
Increase in intracranial pressure can also be Changes in mental status such
due to a rise in pressure within the brain as disorientation, restlessness,
infections.
itself. This can be caused by a mass (such mental confusion tumors.
as a tumor), bleeding into the brain or fluid Purposeless movement stroke.
around the brain, or swelling within the brain Increased respiratory effort aneurysm.
itself. An increase in intracranial pressure is
a serious and life-threatening medical
problem.
Pupillary changes epilepsy.
Weakness in one extremity or seizures.
on one side of the body
hydrocephalus, which is an
Nausea and vomiting accumulation of spinal fluid in
Seizures the brain cavities.
 HYDROCEPHALUS
By: OMLANG

Jerod is the name Joanna and Jim chose for their first child. Jim accompanied Joanna to all of her prenatal visits. When the
routine ultrasound was performed at 32 weeks’ gestation, Jerod was diagnosed with hydrocephalus and a myelomeningocele. His
parents were initially devastated, but remained very excited about their son’s birth. Joanna was scheduled for a caesarean section
at 38 weeks’ gestation and the couple were anxious about Jerod’s condition and his treatment following birth.
Jerod is delivered by caesarean section and transferred to the pediatric intensive care unit (PICU). On admission to the nursery he
weighs 3.4 kg (7.5 lb) and is 8 cm (20 in.) in length. His vital signs are: Temperature: 37° C (98.6° F) Pulse: 144 beats/minute
Respirations: 40 breaths/minute He has bulging fontanels and a high-pitched cry. His head circumference is 40 cm (15.8 in.) and
his chest circumference is 34 cm (13.4 in.). In the lumbar region of his spine, the nurse notes a sac-like projection. When Joanna
and Jim visit the nursery, they stroke Jerod and caress his fingers and toes. Joanna begins to cry and comments to the nurse, “I
so wanted to breastfeed Jerod, but now I guess I can’t.”
Pathophysiology:

ICP rises if production of CSF exceeds absorption. This occurs if CSF is overproduced, resistance to CSF flow is increased, CSF
resorption is decreased, or venous sinus pressure is increased. CSF production falls as ICP rises. Compensation may occur
through transventricular absorption (subependymal flow) of CSF and also by absorption along nerve root sleeves (which may
result in enlarged optic nerve sheaths). The temporal and frontal horns dilate first, often asymmetrically. This may result in
elevation of the corpus callosum, stretching or perforation of the septum pellucidum, thinning of the cerebral mantle, or
enlargement of the third ventricle downward into the pituitary fossa (which may cause pituitary dysfunction) as well as dorsal
midbrain compression resulting in Parinaud's syndrome (analysis of upgaze, Pseudo-Argyll Roberson pupils, convergence-
retraction nystagmus, eyelid retraction, and setting sun sign).
 The mechanism of NPH has not been elucidated completely. Current theories include increased resistance to flow of CSF within
the ventricular system or subarachnoid villi; intermittently elevated CSF pressure, usually at night; and ventricular enlargement
caused by an initial rise in CSF pressure. The enlargement is maintained despite normal pressure because of the Laplace law.
Although pressure is normal, the enlarged ventricular area reflects increased force on the ventricular wall.
Concept Map

Hydrocephalus Risk Factors Signs and

Symptoms

• Hydrocephalu • Being born

prematurely
• Large Head
s can be • Problems during • Prominent
defined pregnancy veins over the
• Lesions & Tumors
broadly as a • Infections of the head
disturbance of nervous systsem • Bulging of
formation, • Bleeding in the the eyes with
brain
flow, or dowanward
absorption of gaze (Sunset
cerebrospinal eyes)
fluid (CSF) •
that leads to Measurement
an increase in of the head at
volume the largest
occupied by part (head
this fluid in circumference
the CNS. )
 AMYOTROPHIC LATERAL SCLEROSIS (LOU GEHRIGS DISEASE)
By: ONIA

CASE SCENARIO: A 57-year-old male with no known past medical history presented two months after the onset of bilateral lower extremity
weakness. The weakness initially affected his right leg, with subsequent progression to his left leg. He then noted 'muscle twitching'. There
had been no preceding illness or insect bites.

HISTORY OF PRESENT ILLNESS: 2 months prior to his illness he had been painting his house and reportedly was exposed to mold.

2 hours prior admission His weakness worsened with progressive decreased movement in the legs as well as weakness in the arms
associated with atrophy in intrinsic hand muscles.

VITAL SIGNS: BP 128/80 HR: 72 RR 18 TEMP 36.5c

FAMILY HISTORY: He has a family history of heart disease in his maternal side
Pathophysiology

Destruction of anterior horn cells by glutamate>calcium influx>non

modifiable risk factors such as age> dysphagia, dyspnea, nasal
speech, weakness>Degeneration of: Upper Motor Neuron (Spasticity,
Hyper reflexia, + Babinski) Lower Motor Neuron (Muscle Atrophy,
Fasciculations)> No Action potential transmitted
Concept Map:

AMYOTROPIC SIGNS AND SYMPTOMS

LATERAL - Difficulty walking - Spasticity - Muscle Weakness
- Tripping and falling - Slurred Speech – Cramps
SCLEROSIS
- Difficulty swallowing - Difficulty maintaining posture

TREATED WITH: RISK FACTORS

- Riluzole - Gene Mutation - Diet
50mg bid - Protein Mishandling - Behavioral Factors
- Anti - Chemical Imbalance - Occupational factors
glutamate (increased glutamate) - Viruses
properties - Exposure to toxic or infectious agents
- Vitamin E
 
and C
- Physical
Therapy
- Tricyclic
antidepressa
nts
 H
By: PANOPIO
 H
By: PERENA
 Friedreich’s ataxia (FRDA)
By: SANTOS
Case Csenario: The patient is a 25 year-old female who was referred to physical therapy after being diagnosed with FRDA. She complains that around a year ago, she began to
lose coordination of her hands eat, write and complete other activities of daily living. She also felt a loss of sensation in her lower extremities, with problems initiating movement
and in balance. Progressive difficulties led to issues with ambulating in a straight line and multiple falls. She indicates that she tires easily and is often short of breath. The patient is
currently an office worker at an architectural firm who lives with her boyfriend in a 5th floor apartment with elevator access. She would like to return to her normal activities at home
and community, including walking without falling and being productive at work again. The initial part of the physical therapy program will begin with a review of the patient’s medical
history and profile; in this scenario, she offers additional information that she has DM II. A thorough subjective assessment will then be conducted, whereby the location of
symptoms will be ascertained with the details listed in the excerpt above.
Next an objective examination will be conducted; her postural assessment reveals a slight postural tremor and it appears she has a right thoracic scoliosis and bilateral pes cavus.
In addition her sitting and standing balance are both poor in static and dynamic conditions, requiring moderate assistance to maintain. In her systems review, integumentary and
cardiovascular functions are unimpaired. Her gross muscle strength in the bilateral upper and lower extremities is 4/5 on a MMT while ROM is within functional limits for upper and
lower extremities, though she demonstrates some tightness in her bilateral hamstring groups and heel cords. Her light touch sensation is diminished in her right lower extremity.
Knee and ankle jerk reflexes are also diminished at 1+. The patient exhibits bilateral cerebellar signs of dysmetria, disdiadochokinesia, and intention tremor in her upper
extremities. She demonstrates considerable difficulty in gait, using a wide base of support without a steady cadence and consistency in her steps. Her transfer from sit <-> stand
requires min assist while supine <-> sit requires close supervision due to significant difficulties in maintaining her balance. Her vital signs reveal a resting heart rate of 90 BPM and
a blood pressure of 110/80.
An assessment will determine that the patient has a problem list that includes functional limitations in gait and ADL due to poor balance and coordination. The patient has primary
impairments in: motor control, gait, locomotion, balance, posture, muscle performance, and sensation. She currently is functionally limited in some aspects of self-care, home
management, and community activities.
History of Present Illness: The initial part of the physical therapy program will begin with a review of the patient’s medical history and profile; in this scenario, she offers additional
information that she has DM II. A thorough subjective assessment will then be conducted, whereby the location of symptoms will be ascertained with the details listed in the excerpt
above.
Family History: when the patient asking about family history, the patient tells that her grandmother is also have a FRDA.
 Sign & Symptoms
High cholesterol is a common medical condition,
but it's often the result of unhealthy lifestyle
choices, and thus preventable and treatable.
With familial hypercholesterolemia, a person's
risk of high cholesterol is higher because a
defect (mutation) in a gene changes how the
body processes cholesterol. This mutation
prevents the body from removing low-density Manifestation
lipoprotein (LDL) cholesterol, the "bad"
cholesterol, from the blood. As a result, plaques Familial
can cause your arteries to narrow and harden, hypercholesterolemia (FH)
increasing the risk of heart disease. Genetic is a genetic disorder
testing can reveal whether you have this
mutation.
Risk factors characterized by high
cholesterol levels,
The risk of familial
specifically very high levels
These gene mutations are passed from parent to hypercholesterolemia
child. To have the condition, children need to
of low-density lipoprotein
 is higher if one or
inherit an altered copy of the gene from one (LDL, "bad cholesterol"), in
both of your parents
parent. Most people with familial the blood and early
hypercholesterolemia have one affected gene have the gene defect
cardiovascular disease. The
and one normal gene. In rare cases, a person that causes it. Most
inherits an affected copy from both parents,
most common mutations
people who have the
which can lead to a more severe form of the diminish the number of
condition got one
condition. functional LDL receptors in
affected gene.
the liver.