Don Peter S.

Dator
Group 4
Neurology Case Questions (please cite sources if needed):

1. Differentiate upper motor neuron signs vs lower motor neuron signs.

An upper motor neuron lesion is a lesion of the neural pathway above the
anterior horn of the spinal cord or motor nuclei of the cranial nerves. A lower motor
neuron lesion is a lesion which affects nerve fibers traveling from the anterior horn of
the spinal cord to the associated muscles.
Upper motor neurons control the lower motor neurons through the pyramidal
and extrapyramidal tracts. They originate from the primary motor area of the cerebral
cortex where they will descend to the spinal cord. Upper motor neuron signs include
loss of voluntary movements, muscle weakness, positive Babinski sign, hyperreflexia,
pseudobulbar palsy, and spasticity which is the hallmark of an UMN lesion.
Lower motor neurons on the other hand innervate the skeletal muscle fibers and
they function as the final common pathway between the CNS and skeletal muscles.
LMNs are classified based on the type of muscle fiber they innervate. Alpha-motor
neurons innervate extrafusal muscles fibers which are involved in muscle contraction.
Gamma-motor neurons innervate intrafusal muscle fibers, which compose of muscle
spindles and involved in proprioception. LMN signs include flaccid paralysis, muscle
atrophy and hyporeflexia, hypotonicity, fasciculations.
Paralysis in UMN lesions affect movement of muscle groups rather than affecting
direct specific muscles seen in LMN lesions. Therefore, muscle wasting is greatly seen in
LMN lesions, although UMN lesions can also develop muscle wasting, this is only due to
disuse of the muscle from movement paralysis.

2. What are the salient features of the patient?

a. 54-year-old male, married, right-handed, Roman catholic, high school graduate,
farmer from Batanes
b. Chief complaint of left sided weakness (March 28, 2019)
c. Slurring of speech and left sided facial asymmetry
d. Non-throbbing headache 6/10, non-radiating right occipital in location
e. No dizziness, vomiting, nor loss of consciousness
f. No changes in behavior, delay of responses, memory lapses, nor disorientation
g. Persistence of symptoms with no progression from March 28 to April 23, 2019
h. Twitching of left side of the face accompanied with jerking of the left UE lasting for
approximately 1 to 2 minutes (April 23, 2019)
i. No eye deviation, version of the neck, drooling of saliva, nor loss of consciousness
j. No bowel and bladder incontinence and post-ictal confusion
k. No recurrence of seizure but still with persistence of left sided weakness, facial
asymmetry, slurring of speech, and headache; can still perform ADL
l. Recurrence of left facial twitching and left upper extremity jerking, no head version
or gaze deviation, now accompanied with urinary incontinence, which lasted for 1
minute.
m. Batanes General Hospital admission - assessment of seizure disorder secondary to
CVA
Don Peter S. Dator
Group 4
n. Review of systems – no fever, rashes, dysphagia, neck limitation of motion
o. Hypertensive since 2017
p. Previous smoker with ½ pack year history; No exposure to irritants, toxins,
radiations, nor chemicals; No history of travel outside the Philippines
q. No family history of DM, CVD stroke, food or drug allergies.
r. Physical examination –
i. conscious coherent, not in cardiorespiratory distress
ii. BP 120/80 PR 69 RR 20 Temp 36.5 O2 97%
iii. Negative tracheal deviation; uvula midline
s. Neurological Examination
i. GCS 15 (E4V5M6)
ii. Word finding difficulty and slow response
iii. Intact repetition, registration and attention; delayed recall and impaired
calculations
iv. MMSE 20/35, MCA 20/25 mild cognitive impairment
v. Cranial nerves
1. 10% sensory deficit on left V1, V2, and V3
2. Left central facial palsy
3. No tongue deviation, atrophy nor fasciculations
vi. Negative dysmetria, dyssynergia, dysdiadochokinesia
vii. 10% sensory deficit on light touch, pain, and temperature on left UE and LE;
intact vibration sense
viii. DTR – hyperreflexia on left side
ix. Negative Babinski, right; negative nuchal rigidity
3. Given the historical data:
a. Give your main clinical impression and why?
Acute cerebral infarct, probably right due to the presence of left sided UMN
signs of weakness, hyperreflexia, slurring of speech and left sided facial asymmetry

b. Give your differential diagnoses.

i. Acute ischemic infarct
ii. Intracerebral hemorrhagic stroke
iii. Subarachnoid hemorrhage

c. Give the reasons for your differential diagnoses.

i. Acute ischemic infarct – Most common type of stroke with global incidence of
68%. presence of left sided UMN signs of weakness, hyperreflexia, slurring of
speech and left sided facial asymmetry. Symptoms lasting for more
ii. Intracerebral hemorrhagic stroke – 2nd most common type of stroke at 32%
incidence rate. Patient is hypertensive since 2017, previous smoker. Presence of
focal neurologic symptoms and headache can also be seen.
iii. Subarachnoid hemorrhage – Due to headache, focal neurologic symptoms
although can be ruled out due to the chronicity of disease and no loss of
consciousness
Don Peter S. Dator
Group 4
d. Management for each differential diagnosis.
i. Acute ischemic stroke - Assess vital signs and ensure stabilization of airway,
breathing, and circulation. Assess NIHSS score. Check blood glucose levels.
Neuroimaging studies such as CT scan or MRI. Laboratory ancillaries, ECG, and
EEG. Fluid resuscitation due to intravascular fluid depletion such as isotonic
saline. Resume antihypertensive medications with included statin therapy.
Observe for progression of symptoms and administration of AED if with
recurrence of seizure.
ii. Intracerebral hemorrhagic stroke – Primary management of stroke. Maintain
blood pressure at normal levels. Discontinue anticoagulants and antiplatelets if
any. VTE prophylaxis to prevent an embolic stroke. Hemostatic therapy such as
recombinant factor VIIa and tranexamic acid may prevent further hemorrhage.
Surgical removal of hemorrhage may be done if the diameter is greater than 3
cm.
iii. Subarachnoid hemorrhage – Primary management of stroke. Grade the
severity of SAH. The most important goal of SAH management is the prevention
of rebleeding by early repair of the aneurysm with surgical clipping or
endovascular coiling. DVT and seizure prophylaxis

4. If you were to see the patient in the emergency room:

a. Which neuroimaging modality will you request and why?
I would opt for a non-contrast CT scan due to its quick nature so that I
can determine the cause and type of stroke in the patient.

b. What other diagnostic and laboratory procedures would you want to request
and why?
I would request for a 12L ECG and 2D echocardiography to rule out
cardiac arrhythmia or cardioembolic cause and to assess heart function. An EEG
would also be warranted to assess brain activity since the patient presented with
seizure like symptoms and to assess brain function since the symptoms have
been present for more than 24 hours. Serum electrolytes is needed to rule out
metabolic causes of weakness. Clotting parameters to assess risk of
thromboembolism. Lipid profile because the patient is known to have
hypertriglyceridemia.

5. Enumerate the cranial nerves involve in the movement of the extraocular muscles and
the specific muscles they innervate.
 Cranial nerve III (oculomotor) – superior, inferior, and medial rectus; inferior
oblique, levator palpebrae superioris, sphincter pupillae, and ciliaris muscles
 Cranial nerve IV (trochlear) – superior oblique
 Cranial nerve VI (abducens) – lateral rectus

6. What is Gertsman syndrome? And if a patient has this syndrome, which part/s of the
brain is/are involved?
Don Peter S. Dator
Group 4
It is a rare neurological disorder that can result from a traumatic brain injury or
as a developmental disorder. The syndrome is characterized by the absence of four
cognitive abilities such as agraphia, acalculia, finger agnosia, and inability to distinguish
between the right and left sides of one’s body.
The lesion mostly affects the posterior lobe of the parietal lobe of the dominant
hemisphere.

7. What are the roles of doing a Mini Mental State Examination and a Montreal Cognitive
Assessment-Philippine version? And given the results, what could they represent?
MMSE and MoCA are used to identify cognitive impairments in elderly patients
or those presenting with neurologic symptoms. The scoring systems are done to stratify
the patient’s level of cognitive impairment.

Reference:
1. Fix, James D., High yield neuroanatomy / James D. Fix, Jennifer K. Brueckner. — 4th ed.
2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update
to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American
Heart Association/American Stroke Association. Stroke 2019; 50:e344.
3. Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2015; 21:1263.
4. The WHO STEPwise approach to stroke surveillance
5. Altabakhi IW, Liang JW. Gerstmann Syndrome. [Updated 2019 Dec 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519528/