Examination of Motor System: Nerurological Exam & Theoreticals

SAN BEDA COLLEGE OF MEDICINE
NEUROLOGY:
BATCH 2019 A/Y 2015-2016 MINI OSCE REVIEWER
EXAMINATION OF MOTOR SYSTEM: NERUROLOGICAL EXAM & THEORETICALS

Part I: Motor examination
1. Inspection including station and gait testing
2. Palpation
3. Percussion
4. Muscle tone via passive movements
5. Strength Testing
6. Muscular stress reflex Examination
7. Test for Clonus
8. Other additional motor NE
9. Sources
10. Authors
Part II: Theoreticals portion:

- De Myer’s, Lectures, Snell/Bates, Recordings etc.
- Authors
Tips
1. In history taking, the Ex must be mindful of the info the Pt will give because it may hint where and what is /are the lesion/s
2. Before anything else, show to the Pt that you have sanitized the part you are about to use in NE
3. Always ask for the permission to conduct the NE
4. Start first with the good side and then compare it to the other
5. Memorize the NAMES, STEPS PER EXAM, NORMAL & ABNORMAL RESULTS
6. In reporting the results, start also with the good side
7. MEMORIZE THE GRADING SYSTEM. Do not forget to mention the description of the grade the Ex is about to report.
8. NE will always start from head to toe
9. Kung time pressured ka, test all the reflexes/strength test applicable in the particular area
10. Pagbunot mo ng question or station. READ THE QUESTION FIRST! DO NOT PANIC! BREATHE! Good luck.
LEGEND: NR- normal reports, AR- abnormal Reports
Texts in Red- must know and memorize
I. INSPECTION
 Habang papalapit kayo sa pasyente, papalapit ang pasyente sa inyo or sa history taking ay na may mga na
OBSERBAHAN NA KAYO
 Kung hindi nyo lubos makita, magpaalam kayo sa Pt kung pwede iangat niya ang manggas ng kanyang damit
Body Position
 Observe the patient’s body position NR: Patient stands/walks/sits erect Abnormal positions alert you to
during movement and at rest. Pt has vertical posture and is conditions such as mono- or hemiparesis
 Posture & gestures steady from stroke.
 Asymmetry: face, trunk, upper and The Pts body is symmetrical
lower extremities Pts body build is the same in comparison AR: Patient drags left leg while walking.
 Compare the Pt’s body type/ build to a to _______
normal person: family members or
examiner itself (comparison must be of
same age, height, weight)
Range of motion
 Allow the Pt to extend his arms NR: Pt able to extend fully his arms and AR: Pt not able to extend his arms fully.
upwards, side wards, over the head forearms Only up to an angle approximately ____
 Inspect for Lateral Rotation- ask the pt NR: Pt able to rotate his neck freely. Able AR: Pt able to rotate his neck but with
to move his neck side to side & rotate to move his neck side to side freely difficulty/ Pt not able to move his neck at
all / PT able to move his neck but up to an
angle of ____
Involuntary Movements
 Watch for involuntary movements such NR: No tremors, tics, fasciculation. AR: Resting tremor on right hand.
as tremors, tics, or fasciculation.
 Note their location, quality, rate,
rhythm, and amplitude, and their
relation to posture, activity, fatigue,
emotion, and other factors.
 Scrutinize the contours of the Pts
muscles
SBCM 2019 SECTION A Page 1 of 31

NEUROLOGY:
Station & Gait Testing

 Observe the Pts station: stance and NR: PT is steady when standing and
verticality walking
 Ask the Pt to walk in tandem, in toes Verticality of the PT is equal
and heels NR: Pt walks in tandem
II. PALPATION
 Hahawakan at oobserbahan nyo po mismo yung mga body part ng Pt, remember to ask permission
 Kung hindi mo makita ang ibang parts ask the Pt na itaas niya ang manggas ng kanyang damit
 Always compare one part from the other, observe the normal first if the Pt shows sign of neurololgic deficits
Muscle Bulk
 Inspect the size and contours of R: Normal contours R: Presence of atrophy, hypertrophy, or
muscles. Always state the laterality and the part pseudohypertrophy in the left/right leg,
 Do the muscles look flat or concave, tested (e.g. right forearm etc.) etc.
suggesting atrophy?
 If so, is the process unilateral or Note their location, quality, rate, rhythm,
bilateral? and amplitude, and their relation to
 Is it proximal or distal? posture, activity, fatigue, emotion, and
 When looking for atrophy, pay other factors.
particular attention to the hands, Scrutinize the contours of the Pts muscles
shoulders, and thighs.
Joint & other abnormalities
 Look for Joint misalignment NR: Pts ____ joint is aligned and does AB: Pts ____ joint is misaligned
 Again: tremors, fasc, fibrillation & other NR: No noticeable tremors, fasciculations If possible, state if it shows some signs of
involuntary movements etc on the (laterality) of the (part) fracture etc.)
III. PERCUSSION
A. Self demonstration percussion irritability
 Normal Result: faint dimple or ripple at the percussion site
 Bare your biceps, flex your arms and strike the belly of your biceps with a sharp blow point of the neurohammer
B. Percussion myoedema
 Result: tiny hump
 myoedema occurs in some debilitating or sysmetabolic states (e.g. uremia or myxedema)
C. Muscle contraction myotonia
 NR: can rapidly flip open the palm on command
 AR: cannot flip the fingers open on command, wrist involuntary flexes bec of sustained contraction
 Ask the pt to make a fist, hold for 10 secs and ask the pt to flip open as rapidly as possible when you sa “Go”
IV. MUSCLE TONE VIA PASSIVE MOVEMENTS

 Ask the Patient to relax completely then move the limbs of the patient
 Do not the Pt move voluntarily
 “Mam/ Sir, relax lang po kayo. Hayaan nyo pong ako ang gumalaw mismo ng inyong mga kamay at mga binti”
V. STRENGTH TESTING
Numerical Scale to Record Muscle Strength MEMORIZE THE NUMERICAL SCALE!!!

5- Normal Strength Upon reporting again mention to the preceptor the number and
4- Move joint through full range against definition of the findings
ROSTROCAUDAL SEQUENCE WHEN TESTING
resistance greater than gravity but the examiner
Test the muscles in the natural rostrocaudal order because it
can overcome
requires no memorization.
3- Moves part full range against gravity but not Simply continue in the neck-shoulderarm- forearm-hand-chest-
against any resistance abdomen-thigh-leg-foot-toe sequence and continually-compare
2- Moves part only when positioned to right and left sides
eliminate gravity
1-Only a flicker of contraction of muscle but
cannot move joint
0-Complete paralysis

NEUROLOGY:
A. BICEPS & TRICEPTS STRENGTH TESTS

BICEPS & TRICEPS STRENGTH TESTING
Biceps: Position of examiner’s hands to test NR: 5/5 Normal strength of the right AR: 4/5 or lower of the right or left biceps
biceps strength. The examiner pulls with the or left biceps
right hand, exactly matching strength with the
patient’s biceps.The left hand braces the
patient
Triceps: The examiner presses just above the NR: 5/5 Normal strength of the right AR: 4/5 or lower of the right or left biceps
patient’s elbow with the right hand and or left biceps
presses in the opposite direction with the left
The inserts show the length of the

triceps with the arm extended or
flexed. You must actually do these
tests on another person with the arms
extended and flexed to appreciate the
great difference in strength in the two
positions
B. NECK FLEXION AND NECK EXTENSION

 Flexion: Trapezius, SCM, Spinal Accessory nerve, root C6
 Extension: Trapezius, SCM, Spinal Accessory nerve, root C9
Neck Flexors
1. Place on hand on the patient’s forehead or R: 5/5 strengths Neck flexion and R: 3/5 neck flexion and extension.
occiput and the other on the front or back extension
of the patient’s chest to provide bracing
and counter pressure
2. Flexors: Start with the patient’s head
strongly extended. The examiner resists the
neck flexion with the hands. Ex place one
hand on the forehead, the other at the
back.
Neck Extensors
Extensors: Patient starts with the head tightly R: 5/5 strength of Neck flexion and R: 3/5 neck flexion and extension
flexed, chin on chest. Then examiner tries to extension
extend it. one hand at the occiput, the other
at the chest

NEUROLOGY:
C. TESTING THE STRENGTH OF THE SHOULDER GIRDLE

 Arm elevation: Deltoid, Axillary nerve, root C5, C6
 Arm adduction
o Initiation: Supraspinatus, Brachial Plex, Root C5, C6
o Flexed: Latissimus dorsi, Brachial Pleaxus, Toot C6-C8
 Arm adduction using pec muscles: Pectoralis major, brachial pleus, Root C5/C6
 Scapular adduction: Rhomboid major, Dorsal scapular, root C5
 Scapular winging
o Medial winging: Serratus anterior, long thoracic nerve, root C5-C7
o Lateral winging: Trapezius, spinal accessory never, root C9
Arm Elevation
 Request Test requiring supraspinatus action to Weakness or inability to perform and
the patient to initiate the act and deltoid action to maintain act.
hold the arms carry the arm to shoulder.
straight out to R: Patient was unable/weak to perform
the sides. Press R: Patient was able to perform act act. <5/5 on right/left arm.
down on both with 5/5 strength on both upper
arms at a point extremities.
where you expect your strength to
approximate the patient’s.
Arm Adduction Downward

 With Test for latissimus dorsi strength. Weakness or inability to perform and
the arms Patient should be able to perform and maintain act.
extended to the maintain the act.
sides, the R: Patient was unable/weak to perform
patient resists R: Patient was able to perform act act. <5/5 on right/left arm.
your efforts to with 5/5 strength on both upper
elevate them. extremities.
Arm Adduction Across The Chest

 With the arms extended right in front, the Test for pectoralis muscle. Weakness or inability to perform and
patient cross the wrists. maintain act.
 You try to pull them apart. R: Patient was able to perform act
with 5/5 strength on both upper R: Patient was unable/weak to perform
extremities. act. <5/5 on right/left arm.
Scapular Adduction
 With the hands on the hips, the patient The serratus anterior and trapezius Weakness or inability to perform and
forces the elbows backward as hard as muscles hold the scapula in place maintain act.
possible. against the chest wall.
 Standing behind the patient, the examiner R: Patient was unable/weak to perform
tries to push them forward. R: Patient was able to perform act act. <5/5 on right/left arm.
with 5/5 strength on both upper
extremities.
Scapular Winging
 Have the The serratus anterior and trapezius Serratus anterior paralysis (long thoracic
patient try a push-up or muscles hold the scapula in place nerve) results in winging of the scapula
lean forward against a against the chest wall. away from the chest wall.
wall, supporting the
body with outstretched R: Negative sign for scapular winging.
arms.

NEUROLOGY:
D. TESTING FOR THE STRENGTH OF THE ELBOWS

 Elbow flexion: Biceps & Brachialis muscle, Musculocutaneous nerve, roo C5/C6
 Elbow Extension: Triceps brachii, Radial Nerve, root C6-C8
Elbow Flexors (Biceps)
 Starting position: Pt tightly flexes the You should have difficulty straightening A weak elbow flexion is seen in Pt having
forearm. pt’s forearm. problems with innervations of C5 and C6
 Brace one hand against the Pt’s nerve roots via the musculocutaneous
shoulder. R: 5/5 elbow flexion on both extremities. nerve.
 With the other hand, grasp the Pt’s
wrist and attempt to straighten Pt’s R: 3/5 elbow flexion on the R/L forearm.
forearm.
Elbow Extensors (Triceps)

Start with the Pt’s elbow flexed, as in You should have difficulty opposing A weak elbow extension is seen in Pt
testing the elbow flexors, but this time extension of pt’s forearm. having problems with innervations of C6
grasp the wrist and oppose extension of and C7 nerve roots via the radial nerve.
the forearm by the Pt R: 5/5 elbow flexion on both extremities.
R: 3/5 elbow extension on the R/L
forearm.
E. TESTING THE STRENGTH OF THE FOREARM MUSCLES: Wrist and fingers

 Wrist flexors: flexor carpi ulnaris, flexor carpi radalis, Palmaris longus, median & ulnar neve
 Wrist extensors: extensor carpi ulnaris, extensor carpi radialis brevis & longus, radial nerve
 Finger flexion: flexor digitorum, flexor policis longus, flexor digiti minimi, median & ulnar nerve
 Finger extension: extensor digitorum, extensor indicis, extensor pollicis longus and brevis, extensor digiti minimi,
median & ulnar nerve

Wrist Flexors
 Pt makes a The patient should be able to resist R: 3/5 flexion on the R/L wrist.
fist and holds the your force.
wrist flexed against
your efforts to R: 5/5
extend it.
 Hook Your
fingers around the
Pt’s fist and flex
your own wrist.
 Brace the wrist with your other hand.
Wrist Extensors
 For The patient should be able to resist R: 3/5 extension on the R/L
support, rest the your force. wrist.
Pt’s forearm flat
on his thigh or a R: 5/5
tabletop.
 Pt holds
the wrist forcefully
dorsiflexed as you
try to press it
down with the butt of your palm on the Pt’s knuckles.

NEUROLOGY:
Finger Extension
 Pt hold Patient should be able to Weakness or inability to perform and
out the hands with perform act without maintain act.
palms down and difficulty.
fingers hyper R: Patient was unable/weak to perform
extended. R: Patient was able to act. <5/5 on right/left hand.
 Turn your perform act with 5/5
hand over so that strength on both upper
the dorsum of your extremities.
fingernail presses
against the dorsum
of the Pt’s.
Finger Flexion
 Ask the patient You should have difficulty A weak grip is seen in cervical
to squeeze your fingers. removing your fingers from radiculopathy, de Quervain’s
 Grasp the the patient’s grip. tenosynovitis, carpal tunnel syndrome,
patient’s wrist with one arthritis, and epicondylitis.
hand to steady the arm R: 5/5 finger flexions on
and offer two fingers of both hands R: 3/5 finger flexion on the right/left hand
your hand for the
patient to grasp.
Finger Abduction and Adduction

Press the terminal phalanx Patient should be able to Weak finger abduction occurs in ulnar
of your right index finger perform act without nerve disorders.
alongside the resisting difficulty.
terminal phalanx of the R: Patient was unable/weak to perform
patient’s right index R: Patient was able to act. <5/5 on right/left hand.
finger, matching muscle to perform act with 5/5
muscle, which is an ideal strength on both upper
test extremities.
F. TESTING FOR THE ABDOMINAL MUSCLES & LARGE BACK MUSCLES

Testing of Abdominal Muscles
Patient is able to assume and maintain Patient is unable to assume the position
the position stated and integrity of the stated. Change in shape being a possible
abdominal muscles is present. Typically side effect from ascites and umbilical
lies at a vertical level corresponding to the hernias. If some abdominal muscles are
junction between the L3 and L4 vertebrae weak, umbilicus will migrate towards the
intact muscle during contraction
R: Patient was able to assume position
and there is 5/5 abdominal muscle R: Patient was not able to assume the
strength without umbilical deviation. position and there was an umbilical
deviation to the R/L.
Testing of the Large Back Muscles
Patient is able to assume and maintain Patient is unable to assume the position
the position stated and integrity of the stated. Weak back muscle may also cause
paraspinal muscle is present. muscle pain.
R: Patient was able to assume position, R: Patient was not able to assume
5/5 back muscle strength with intact position, 3/5 muscle strength
paraspinal muscles

NEUROLOGY:
G. TESTING FOR HIP GIRDLE

 Hip flexion: sartorius muscle & iliopsoas, (femoral nerve), rectus femoris-minor (femoral nerve)
 Hip Extension: gluteus maximus, inferior gluteal nerve
 Thigh abduction: gluteus medius & minimus, superior gluteal nerve
 Thigh adduction:
Hip Flexion
The patient should be able to resist your R: Patient was unable/weak to perform
force. act. <5/5 on right/left hand.
R: 5/5
 Ask the patient to sit.

 Ask Pt to lift knee off the table surface
and to hold thigh in a flexed position.
 Try to push the knee back down with
the butt of your palm.
Hip Extension
 With the Pt prone, have the pt lift the The patient should be able to resist your R: Patient was unable/weak to perform
knee from the table surface and hold it force. act. <5/5 on right/left hand.
up.
R: 5/5
 Place your hand on the popliteal space

and try to press the knee back down.
Thigh Abduction and Adduction
The patient should be able to resist your Symmetric weakness of the proximal
force. muscles suggests a myopathy
or muscle disorder; symmetric
R: 5/5 weakness of distal muscles suggests
a polyneuropathy, or disorder
of peripheral nerves.
 With the Pt sitting, have the Pt hold the

legs abducted as you try to press them
together with your hands on the lateral
sides of knees.
 Have the patient try to hold the legs

adducted (squeezed together) as you
place your hands on the medial sides of
the knees to try to pull the knees apart.

NEUROLOGY:
H. TESTING KNEE STRENGTH

 Knee Flexors: Biceps femoris, Semitendinosus, Semimembranosous, Sciatic nerve, root L5-S2
 Knee Extensors: Tensor facia latae & Quadriceps femoris, Femoral nerve, L2-L4
Knee Flexors (Hamstrings)
 Starting position: Pt prone; Pt holds the You should have difficulty straightening A weak leg flexion is seen in Pt having
knee at an angle of 90 degrees. pt’s leg. problems with innervations of L5 and S1
 Try to straighten pt’s leg by grasping the nerve roots via the sciatic nerve.
Pt’s ankle. R: 5/5 elbow flexion on both extremities.
R: 3/5 knee extension on the R/L leg.
Knee Extensors (Quadriceps)
 Starting position: Pt prone; pt tries to You should have difficulty opposing A weak leg extension is seen in Pt having
touch the heel to the buttock to induce extension of pt’s leg. problems with innervations of L3 and L4
extreme flexion of the knee. nerve roots via the femoral nerve.
 Grasp the Pt’s ankle and oppose R: 5/5 elbow flexion on both extremities.
extension. R: 3/5 knee extension on the R/L leg.
 Compare the extensor strength of two
legs.
I. ANKLE & TOE STRENGTH

 Dorsiflexion
o Foot (medial): anterior tibial muscle, deep peroneal neve, root L4 & L5
o Toes (proximal & distal phalanges): extensor digitorum longus & brevis, deep peroneal nerve, root L5 & S1
o Great toe: extensor hallucis longud, deep peroneal nerve, root L5-S1
 Plantar flexion: gastrocnemius, soleus, tibial nerve, root S1-S2
 Eversion: peroneus longus and brevis, superficial peroneal nerve, L5-S1
 Inversion: tibialis posterior, tibial nerve, root L4-L5
Testing of the Ankle and Toe Movements
Dorsiflexion
1. Test dorsiflexion and plantar flexion at the ankle by asking the patient to
pull up and push down against your hand R: 5/5 on both ankle and R: 3/5 or lower on
toes both ankle and toes
As well as of the great toe.

Plantar Flexion
R: 5/5 on both ankle and R: 3/5 or lower on

toes both ankle and toes
Eversion
Ask the patient to evert the foot, the examiner tries to move it to the original
position but the patient opposes R: 5/5 on both ankle and R: 3/5 or lower on
 Itutulak nyo po pabalik yung paa pero sasabihin nyo sa pasyente na toes both ankle and toes
pigilan niya

NEUROLOGY:
Inversion
Ask the patient to invert the foot, the examiner tries to move it to the original
position but the patient opposes R: 5/5 on both ankle and R: 3/5 or lower on
 Itutulak nyo po pabalik yung paa pero sasabihin nyo sa pasyente na toes both ankle and toes
pigilan niya
VI. TESTING THE MUSCLE STRETCH REFLEX
Numerical Scale to Record Muscle

IN TESTING MUSCLE STRETCH REFLEX:
Stretch Reflex
Memorize the numerical scoring
0- Areflexia
Memorize all procedures or maneuver. Refer to the Theoreticals portion to learn
1- Hyporeflexia more about the purpose of these tests
2- NORMAL
3- Hyper reflexia Always ask the Pt’s permission and start with the good par
4- clonus
NEUROHAMMER: Master the art of swinging and not pecking it.
- Dangle the hammer handle loosely between thumb and
forefinger. Allow the hammer to swing like a pendulum
- Avoid gripping it tightly or hanging it very loose.
- Learn to approximate your own. PRACTICE!!
-
STICK FIGURE from De Myer’s that must

be mastered accdng kay Doc Paragua.
Example po ito ng scoring. MEMORIZE!!
Now practice drawing and mastering
where to put the number.

NEUROLOGY:
A. JAW REFLEX
 Masseter, motor trigeminal nerve, root C5
Jaw Reflex
Starting position: Pt’s mouth sag loosely Usually absent or Exaggerated and pathologically brisk with
Rest a finger across the tip and strike it weakly present. lesions affecting the pyramidal pathways
with a crisp blow. above the 5th motor nucleus, especial if
R: 0+/ 1+/ 2+/ the lesions are bilateral.
R: 3+/ 4+/ 5+
B. BICEPS REFLEX
 Biceps muscle, musculocutaneous nerve, root C5(C6)
Biceps Reflex
Place thumb with slight tension on the Flexion at the elbow Areflexia in LMN lesions and hyperreflexia
patients bicep tendon and bicipital & contraction of or presence of clonus in UMN lesions.
aponeurosis. biceps muscle.
Repeat on the other arm. R: 1+ biceps reflex on the right/ (+) clonus
Observe and grade the response R: 2+ on both on the left
extremities.
C. TRICEPS REFLEX
 Triceps, radial nerve, root c7
Triceps Reflex
 Dangle the patient’s forearm over your hand and strike the Contraction of the Diaschisis or neural shock, such as after
triceps tendon. triceps muscle and acute spinal cord transection, the MSRs
 Cradle the patients forearm in your hand and strike the extension at the may be inactive.
triceps tendon. elbow. Symmetrically
 Repeat on the other arm. diminished or even R: 0/1+ triceps reflex on the right/ (+)
 Observe and grade the response absent reflexes may clonus on the left
be found in normal
people.
R: 2+ Normal
D. BRACHIORADIALIS REFLEX
 Brachioradialis, radial nerve, root C6 (C5)
Brachioradialis Reflex
 Cradle A normal reflex will Abnormal reflex will not elicit reaction.
the patient’s cause the lower arm May indicate damage in the C5 and C6
forearm in one to flex at the elbow nerve roots
hand, placing the and the hand to
thumb on top of supinate (turn palm R: 0, 4, 5 on both or
the radius. upward). 1/ 2/ 3, asymmetric
 The
hammer strikes R: 1/ 2/ 3 on both,
the examiner’s symmetric
thumbnail rather than the patient’s radius. Don’t whack
away on the patient’s unprotected bone.
 The examiner may cradle both forearms side by side for
accurate comparison of the responses of the two arms.

NEUROLOGY:
FINGER FLEXION REFLEXES

 Flexor digitorum profundus & superficialis muscles, medial & ulnar nerve, root C8
Finger flexion reflex (Tromner’s)
1. Support the patient completely relaxed hand. No response (+) Tromner’s sign: flexion of the thumb
2. Briskly flip the patient’s distal phalanx upward. and index finger in response to tapping or
3. Observe and grade the response. flicking the volar surface of the distal
phalanx of the middle finger held partially
flexed between the examiner’s finger and
thumb. And suggests upper motor neuron
lesions above the fifth or sixth cervical
segments of the spinal cord.
Finger Flexion Reflex (Hoffmann’s Method)

The examiner depresses the No reaction from The other fingers respond by also flexing,
distal phalanx and allows it to other fingers. This is a positive sign confirming
flip up. Hoffmann’s Reflex.
The extension of the phalanx R: Negative for Positive Hoffmann’s reflex reflects
stretches the flexor muscles, Hoffmann’s reflex. presence of an upper motor neuron lesion
causing the fingers and thumb from spinal cord compression.
to flex.
This method is effective only R: Positive for Hoffman’s reflex.
with very brisk muscle stretch
reflexes.
E. Quadriceps Femoris
 4 methods: patient is sitting, supine, with Jendrassik & Counterpressure
 Quadriceps femoris, femoral nerve, L2-L4
Quadriceps Femoris Reflex (Sitting)
 Starting position: Pt A little one swing May be diminished by abnormalities in
seated, with legs dangling over the forward and one back. muscles, sensory neurons, lower motor
edge of a table. neurons, and the neuromuscular
 Place hand on the R: 1+/ 2+/ 3+ on both, junction; acute upper motor neuron
patient’s knee (to feel and see the symmetric lesions; and mechanical factors such as
magnitude of the response) and joint disease. Abnormally increased
strike the patellar tendon with a reflexes are associated with upper
crisp blow. motor neuron lesions.
(Spinal nerve root: L4)
R: 0/4+on both, asymmetric

hyperreflexia
Quadriceps Femoris Reflex (Supine)
 Bend the patient’s leg to place slight tension on the patellar The blow will deform Diaschisis or neural shock, such as after
tendon. the tendon and transmit acute spinal cord transection, the MSRs
 Notice if the blow will deform the tendon and transmit a a stretch to the muscle. may be inactive.
stretch to the muscle. Symmetrically
 Observe and grade the response diminished or even R: +1 quadriceps reflex on the right/ (+)
absent reflexes may be clonus on the left
found in normal people.
R: 2+ Normal
Pull Method (of Jendrassik) for Reinforcing the Quadriceps Reflex

Instruct the patient to lock his Contraction of the AR: Areflexia in LMN lesions and
hand and pull it apart hard. quadriceps with hyperreflexia or presence of clonus in
Strike the tendon. extension at the knee. UMN lesions.
Observe and grade the
response. R: 2+ on both AR: +1 quadriceps reflex on the right/
extremities. (+) clonus on the left
Other Jendrassik: Clench teeth
or tighten the gastrocnemius
muscle

NEUROLOGY:
Counter-Pressure Method for Quadriceps Femoris Reflex

1. Apply slight thumb pressure against patient’s tibia. AR: Hyperactive reflex and clonus is
2. (The patient will counteract the pressure by exerting Knee jerk present. Indicates lesions of the UMNs
slight tension in the quadriceps femoris muscle) R: 2+/4 (normal) Or no response at all which results
3. Strike the quadriceps tendon. from LMN lesions.
4. Observe and grade the response. R: 0/4 (no response) or 4+/4
(hyperactive with clonus)
F. Triceps Surae & Toe Flexion Reflex

 Triceps surae muscle, tibial nerve, S1-S2
Triceps Surae Reflex (Sitting)

 With the patient sitting, A weak reaction is No reaction or hyper-reaction. Hyper-
have the pt. relax the leg. observed. Response may reaction is difficult to obtain. Reflex
 Dorsiflex the foot then be minimal or absent in suggest presence of corticospinal tract
apply slight tension on the triceps normal individuals. Tends disease.
surae muscle. to diminish with age.
 Try reinforcement if no R: 0, 4+ on both or asymmetric
reflex occurs. R: 1+/2+ on both feet,
symmetric
Triceps Surae Reflex (Supine)
 Bend the patient’s knee and allow it to relax. Symmetrically diminished Diaschisis or neural shock, such as after
 Dorsiflex the patient’s foot to place slight tension on or even absent reflexes acute spinal cord transection, the MSRs
the triceps surae muscle. may be found in normal may be inactive. Lesion of the S1 segment.
 Observe and grade the response. people.
 Reinforce if no response occurred. R: +1 triceps surae reflex on the right/ (+)
R: 2+ Normal clonus on the left
(Plantar) Toe Flexion ROSSOLIMO’S SIGN

 Tap/percuss the Absent Toe flexion (+) Rossolimo sign. This is
ball of the foot. indicative of an upper motor neuron
 Identical with R: (-) Rossolimo sign lesion.
finger flexion
R: (+) Rossolimo sign
G. Plantar Reflex
 The following are test of plantar reflexes that shows changes in the stimulus of plantar reflex after UMN lesion.
 Normal patients should have a NEGATIVE reflex for this tests
 Segments S1-S2
Plantar Toe Reflex: Babinski
1. Move an Plantar Flexion Babinski response: pathological in
object along the adults, indicates upper motor
lateral aspect of Graded as PRESENT or neuron lesion.
the sole. ABSENT.
(+) Babinski: Dorsiflexion of great
toe with fanning of other toes.
Chaddock’s Maneuver
 Move an object along R: Absent. Extension of the great toe occurs in
the lateral side of the foot. cases of organic disease of the
 From the level of the corticospinal reflex paths.
heel going to (down) small toe
R: Dorsiflexion of the right/left big
toe.

NEUROLOGY:
Gonda, Stransky (Toe-Pull Reflex)

 Pull the fourth There should be no Dorsiflexion of the big toe.
toe outward and dorsiflexion of the big toe.
downward for a brief R: Positive for Gonda, Stransky (toe-
time and release R: Negative for Gonda, pull reflex). Dorsiflexion of right/left
suddenly. Stransky (toe-pull reflex). big toe.
Gordon (Calf-Toe Reflex)

 Squeeze the calf R: Absent. Fanning of toes (+) Babinski sign,
muscles momentarily. indicative of an upper motor
neuron lesion.
R: Dorsiflexion of the right/left big

toe.
Oppenheim (Shin-Toe Reflex)
 Press your No reaction occurs. This reflex When reaction of the foot occurs,
knuckles (or use a is normal in children up to 2 there is a positive Babinski sign. A
pointed object) on years old. It disappears as the positive Babinski's sign is indicative
the patient’s shin or child gets older. It may of an upper motor neuron lesion.
the anterior tibial disappear as early as 12 Positive sign indicates a damage to
region and move months. the pyramidal tract.
them down
R: Absent. R: (+) Babinsiki reflex
Schaeffer (Achilles-toe Reflex)
 Squeeze There should be no Dorsiflexion of the big toe.
hard on the Achilles dorsiflexion of the big toe.
tendon. R: Positive for Gonda, Stransky (toe-
R: Negative for Schaeffer pull reflex). Dorsiflexion of right/left
(Achilles-toe Reflex). big toe.
Bing (Pinprick-Toe Reflex)

1. Make multiple Plantar Flexion Dorsiflexion of great toe and
light pinpricks on the fanning of other toes. Indicates
dorsolateral surface of the Graded as PRESENT or UMN lesion.
foot. ABSENT.
VII. TEST FOR CLONUS

 Clonus is a repetitive muscle stretch reflex thus a normal person must not have these
 Included here also is the test used to determine clasp knife
Technique for Eliciting Clonus

Ankle Clonus
 Induce the patient R: (-) for ankle clonus If the foot oscillates between flexion and
to relax completely. extension for as long as you maintain
 To elicit ankle pressure, the patient has the sustained
clonus, flex the Pt’s knee type of clonus.
slightly to relax the triceps
surae muscle. R: (+) ankle clonus on right/left ankle
 Hold the patient’s
foot.
 Gently but briskly jerk the foot upward and a little
outward.
 After the upward jerk, maintain finger pressure against
the sole of the patient’s foot.
Wrist Clonus
 To elicit wrist clonus, simply jerk quickly up on the R: (-) for wrist clonus R: (+) wrist clonus on right/left wrist
patient’s hand.
Patellar Clonus
 To elicit patellar clonus, have the patient’s lower R: (-) for patellar clonus R: (+) for patellar clonus on right/left leg
extremity straight and relaxed.
 Grasp the patella between your thumb and index finger
and displace it briskly downward in line with the

NEUROLOGY:
patient’s thigh, stretching the quadriceps femoris

muscle.
 Maintain the downward pressure to sustain the clonus.
Technique for Eliciting Clasp-Knife Rigidity
 The examiner lifts the patient’s leg with one hand, R: (-) for clasp-knife The spastic leg catches and then molds to
placing the other under the patient’s knee. rigidity the flexed position, like a clasp-knife
 As briskly as possible, in fact with a jerk, the examiner closing.
simultaneously pushes down with the ankle hand and up
with the other. R: (+) for clasp-knife rigidity on right/left
leg
VIII. ADDITIONAL MOTOR EXAMINATION

A. Writing- watch the Pt write spontaneously through copying a text or dictation (if the Pt cannot read).
B. Finger tapping speed test- place an audiocassette case in the table. Ask the pt to grasp the case in between the thumb
and third digit leaving index finger then tap. (NR: 50 taps/10secs)
C. Archimedes spiral- the e places a pen & paper printed with a spiral. The pt traces the spiral line from the center out to
the periphery
D. Tasks of daily living- the ex should watch the Pt button, use scissors, tie shoelaces, drink glass of water and arrange
clothes as if to put them on. Ex eat for tremors, incoordination etc.
IX. SOURCES
 De Myer Neurological Exam Textbook
 Notes from upper years
 Anatomy Lab manual
 Pictures: De Myer & internet sources
AUTHORS
Garay, Shirley (Editor)
De La Rosa, Jessah
De Villa, Yhana
Guererro, Reissa
Bautista, Ronel Mark
Asturiano, Argie
Gaoat, Gerard
NEUROSCIENCE I PRECEPTORIALS
EXAMINATION OF MOTOR SYSTEM AND CEREBELLUM
SAN BEDA COLLEGE, MANILA
COLLEGE OF MEDICINE
S.Y 2015-2016

NEUROLOGY:
TERMS TO REMEMBER! ➔ Epilepsy is any change in the mental, motor, or sensory

➔ Akathisia refers to motor unrest manifested by state of the Pt caused by an abnormal
continual shifting of positions and sometimes by hypersynchronous discharge of neurons
restlessly moving about.
➔ Essential (familial) tremor appears during a sustained
➔ Aplasia (amyoplasia) – muscle failed to develop posture but may appear during voluntary movements.
affects the hands predominantly but may affect the
➔ Areflexia — pathologic, except in toe and finger MSRs,
head, bulbar muscles,and voice
and in some particular muscles in infants and females
who lack prominent tendons ➔ Fasciculations – contractions of muscle fascicles,
detected by clinical inspection or by characteristics
➔ Asterixis consists of sudden lapses of a sustained
EMG waves. They indicate a hyperexcitable state of the
posture, which may have a periodic or pseudo
cell membrane of the LMNs, which depolarize
rhythmic frequency.
spontaneously, causing contraction of all muscle fibers
➔ Athetosis — slow, writhing movement of fingers and of a motor unit.
extremities
➔ Fibrillation – random, spontaneous contractiom of an
➔ Atrophy – muscle was once in its normal size but then individual denervated muscle fiber
lost its bulk
➔ Flaccidity – lacking in force or vigor
➔ Benign fasciculations: Fasciculations appear
➔ Hemiballismus — violent flinging movements of one
particularly after exercise. Example twitching of an
half of the body
eyelid
➔ Hyperactive child: Hyperactive children display
➔ Chorea — incessant, random, quick movement
incessant, rapidly changing motor activity, often
➔ Clonus – is a to-and-fro, 5 to 8 cycles per second, starting in infancy
rhythmic oscillation of a body part elicited by a quick
➔ Hypertonia — too much tone
stretch
➔ Hypoplasia – muscle failed to develop to its normal
➔ Clasp-knife spasticity — generally greater in flexors of
size.
upper extremities and extensors of lower extremities.
➔ Hypotonia – too little tone
➔ Cramps – sustained contractions that last seconds to
minutes, often brought on by exercise and relieved by ➔ Involuntary movement — person does not start and
stretching the muscle cannot stop at the person’s own or an observer’s
command
➔ Deficit phenomena are sensorimotor functions loses
after a neurologic lesion loss of movement or loss of ➔ Isometric tremor appears during a sustained muscular
vision. contraction against a stationary object
➔ Denervation atrophy – muscle deprived of / loses its ➔ Kinetic tremor or intention tremor (also called ataxic
nerve supply tremor) appear during any voluntary movement
➔ Diaschisis – distant impairment of function beyond the ➔ Locked-in syndrome —UMN paralysis of all volitional
confines of the acute lesion movements except vertical eye movements. The Pts
remain conscious and not demented but are “locked-
➔ Disuse atrophy – normal muscle put to rest for
in” to themselves by the paralysis.
prolonged periods.
➔ Mixed tremors: A particular type of mixed tremor that
➔ Double hemiplegia: The lesion interrupts both
appears at rest, while maintaining a posture, and that
pyramidal tracts. The lower part of the face and all four
becomes severe during voluntary movement often
extremities are paralyzed bilaterally.
follows trauma to the midbrain or other midbrain
➔ Drug-induced and toxic tremors: A number of tremors, lesions
as with hyperthyroidism,lithium treatment, delirium,
➔ Monoplegia — A small lesion of the motor cortex or
and drug over dosage or withdrawal (including
internal capsule, where thepyramidal fibers have a
alcohol), share features of one or more of the
discrete somatotopic arrangement, may cause
foregoing types of tremors or come from an
contralateral weakness of one arm or one leg. A lesion
enhancement of physiologic tremor.
of the leg area of its projection fibers will cause a
➔ Dystonia — prolonged slow, alternating contraction contralateral lower extremity monoplegia.
and relaxation of agonist and antagonist muscles Interruption of the pyramidal tract on one side of the
thoracic spinal cord causes a monoplegia of the
➔ Electromyography - a needle is inserted into a normal
ipsilateral leg.
resting muscle and wired to an amplifier and
oscilloscope records no electrical activity in most ➔ Motor unit – one LMN, its axon, and all of muscle
skeletal muscles at rest fibers it innervates.
➔ Emotional tremor distinguished from psychogenic ➔ Muscle spindles – stretch-sensitive receptors for the
tremor, is an enhanced physiologic tremor. It occurs at muscle-stretch reflex (MSRs), which consists of small
rest, but it worsens during volitional movement bags and small muscle fibers. (Remember muscle
spindles as “muscle within a muscle”)

NEUROLOGY:
➔ Muscle tone – muscular resistance that the Ex feels ➔ Reflex – consists of a relatively invariant response to a
when manipulating a Pt’s resing joint, apart fro gravity specific stimulus.
or joint disease
➔ Reflexogenous zone (zone from which a reflex can be
➔ Myoclonic jerks sudden, brief, shock-like, involuntary elicited), is the first sacral dermatome (S1) for the
twitches of individual muscles or sets of muscles. normal plantar reflex.
➔ Myoclonus means shock-like, lightning fast ➔ Release phenomena are sensorimotor functions that
contractions of parts of muscles or groups of muscles. increase after a neurologic lesion. Consist of an
Individual movements are very brief but may be exaggeration of a normal action, e.g., hyperactive
repetitive MSRs
➔ Myokemia – visible, rippling, worm-like action of the ➔ Rest (or resting) tremor is a tremor when the body
muscle caused by prolonged periods of discharge of parts are at complete rest
motor units. Muscles go into continuous spasms that
➔ Restless-legs syndrome (Ekbom’s syndrome) When
may appear focally or segmentally.
attempting to rest or sleep, Pts feel an irresistible
➔ Neural shock – is a stage of hypotonic total paralysis urge, a necessity, to move their legs around
and total areflexia that immediately follows an acute,
➔ Rhythmic myoclonus shows intermittent brief jerks,
severe UMN lesion. The term shock in this context
irregular or rhythmic, of slow frequency and often
designates the disastrous disorganization of acutely
limited to segmental levels
injured nervous system
➔ Rigidity – increased muscular resistance felt
➔ Neuropathic tremor:This tremor,usually an action
throughout the entire range of movement
type,occurs with a variety of acquired or hereditary
peripheral neuropathies, more commonly with ➔ Self-mutilation: The Pt compulsively inflicts self-injury
demyelinating than with axonal types by biting, scratching, or pounding despite punishments
or rewards
➔ Orthostatic tremor —a very fine, rapid, 16-cps tremor
of the legs appears mainly when the Pt stands, usually ➔ Summation and the Plantar Reflex — A stimulus that
combined with a general feeling of unsteadiness. requires increasing application to elicit a response is
said to summate or undergo summation.
➔ Pain and plantar reflex — The plantar stimulus results
in a somewhat noxious feeling of tickling, pressure, ➔ Spastic diplegia — Bilateral pre- or perinatal cerebral
and pain. lesions may result in a bilateral pyramidal syndrome,
but with the legs more affected than the arms, and the
➔ Paraplegia: paralysis of the legs, with loss of bladder
bulbar muscles relatively spared.
and bowel control but spares the arms
➔ Spasticity – initial catch or resistance and then a
➔ Paratonia – is the resistance, equal in degree and
yielding
range. Also known as Gegenhalten meaning “Hold
against or resist” ➔ Stereotyped behavioral mannerisms: Many retarded,
autistic, and some other- wise normal children and
➔ Parkinsonian tremor appears when the part is at rest,
psychotic adults display repetitive behaviors, including
increases during mental and emotional tension, but
spinning, rocking, patting, touching, grimacing, licking,
disappears or dampens during intentional movement,
and mouthing
and is absent during sleep
➔ Synkinesis is an involuntary or automatic movement
➔ Partial continual epilepsy shows contin-uous low-
that accompanies a voluntary movement. Example if
frequency jerks of one muscle group days and nights
you close your eyes, your eyeballs automatically roll up
for weeks, months to years
(Bell’s phenomenon). Walk and your arms swing
➔ Physiologic tremor arises from a combination of
➔ Task-specific tremors appear during defined tasks,
neurally mediated oscillations and the ballistic effects
such as writing.
of respiratory and cardiac actions
➔ Tics — quick, lightning-fast movements of face and
➔ Postural or position maintenance tremor occurs
upper extremities
during the maintenance of any intentional posture,
such as holding the head up, the trunk erect, or the ➔ Tremors — rhythmic, involuntary, oscillations of one or
arms out stretched more regions of the body
➔ Pseudobulbar palsy — bilateral weakness of the ➔ Voluntary movement person can start or stop at the
oropharyngeal muscles with dysphagia, dysarthria, and person’s own command or an observer’s command.
spas-tic dysphonia, but the Pt shows exaggerated
➔ Wallerian degeneration – When a neuronal perikaryon
smiling and crying
dies, its axon dies. The axon also dies after complete
➔ Quadriplegia (tetraplegia) — paralysis the volitional separation from its perikaryon. The process of
movements of the trunk and all four extremities but dissolution of the dead axon and its myelin sheath is
spares the face called the Wallerian degenerative disease
REVIEW!
GENERAL ORGANISATION
The central nervous system (CNS)

NEUROLOGY:
— includes the cerebrum, cerebellum. brain stem, and spinal cord (Fig. 1) the diencephalon (Which includes everything with the
name " thalamus;" i.e. the thalamus, hypothalamus. epithalamus and subthalamus) and the basal ganglia (which includes the
caudate nucleus. the globus pellidus, the putamen, claustrum, and amygdala).
— The basic functional unit in the CNS is the neuron (Fig. 2).
The Neuron
— Electrophysiological impulses travel down a neuron from its dendrites to the cell body and axon.
— Information then is chemically transmitted to other neurons via connections known as synapses.
— A chain of such communicating neurons is called a pathway, Within the CNS. a bundle of pathway axons is called a tract,
fasciculus, peduncle, or lemniscus.
— Outside the CNS (i.e.• in the peripheral nerves, which connect the CNS with the skin. muscles. and other organ systems),
bundles of axons are called nerves.
The Nerves
— There are 31 pairs of spinal nerves and 12 pairs of cranial nerves.
— Cervical nerves CI-C7 exit over their corresponding vertebrae. but that thoracic nerve 1 and the remainder of the nerves exit
below their correspondingly numbered vertebrae (fig3)
— Cervical nerve 8 is unique since there is no correspondingly numbered vertebra (fig3)
— Also. note that the spinal cord is shorter then the vertebral column so that the spinal nerve roots extend cau- dally when
leaving the spinal cord. This disparity increases at more caudal levels of the cord. The spinal cord ends at about vertebral level
1..2 but nerves 1..2-55continuecaudallyasthecauda equina("borse'stail")toexitbytheir corre sponding vertebrae (Fig. 3)
Subdivisions of the Cerebrum
— Cerebrum subdivides into frontal, parietal, occipital and temporal lobes (fig4)
— These are further subdivided into bulges. called gyri, and indentations called sulcus and fissures (small and large.
respectively)
The Brain Stem
— The brain stern contains three parts - the midbrain. pons and medulla (Fig. 1).
— The pons lies squashed against the clivus. a region of bone resembling a slide that extends to the foramen magnum. the hole
at the base of the skull where the spinal cord becomes the brain stem (Fig5).
— Sometimes the brain stem does " slide down" the clivus, herniating into the foramen magnum. This is a serious clinical
condition. generally resulting from a pressure differential between cranial and spinal cavities. Many clinicians therefore are wary
in removing cerebrospinal Fluid during a spinal tap in patients with high intracranial pressure.
— Note the close proximity or the clivus to the nasal passages. Sometimes rare invasive tumors or the nasal passages erode and
break through the clivus and damage the brain stem.
— Pituitary tumors may be reached surgically via the nasal passages by producing a hole in the sphenoidal bone, which houses
the pituitary gland- the”transsphenoidal approach”.
— A spider named Willis lives on the pons and its nose fils into the pituitary fossa.
THE MOTOR PATHWAY
• The motor (corticospinal) pathway is relatively simple. It extends from the motor area of the cerebral cortex down through the
brain stem, crossing over at approximately the same level as the medial lemniscus (at the junction between brain stem and spinal
cord), (Figs. 15. 17). (There is an uncrossed cornponent that will not concern us here.)
• The corticospinal pathway synapses in the anterior hom (motor grey matter) of the spinal cord just prior to leaving the cord.
• Motor neurons above the level of this synapse (connecting the cerebral cortex and anterior hom) are termed upper motor
neurons(UMN). whereas those beyond this level (the peripheral nerve neurons) are termed lower motor neurons (LMN).
• These terms are actually somewhat misleading and probably would better have been phrased as first order motor neurons
(UMN) and second order motor neurons (LMN). as either of these categories may have axons that lie in the upper or lower part
of the body.
• Upper and lower motor neuron injuries result in different clinical signs. Although both result in paralysis. they differ as follows:

SAN BEDA COLLEGE OF MEDICINE NEUROLOGY:
NEUROLOGY:
BATCH 2019 A/Y 2015-2016 MINI
MINI OSCE
OSCE REVIEWER
REVIEWER
Upper MN Defect Lower MN Defect

• spastic paralysis • flaccid paralysis
• no significant muscle atrophy fasciculations • significant atrophy fasciculations
• fibrillations not present • fibrillations present
• hyperreflexia
• hyporeflexia
• Babinski reflex may be present
• Babinski reflex not present
For unknown reasons various disease processes affect different portions of the spinal cord.
— Amyotrophic lateral sclerosis (Fig. 18A) is characterized by a combination of upper and lower motor neuron signs - muscle
weakness. atrophy, fibrillations. and fasciculations combined with hyperreflexia. The lesion involves both the anterior horns
(motor) of the grey matter (causing a lower motor neuron lesion) as well as the corticospinal tracts (resulting in an upper motor
neuron lesion).
—Tertiary syphilis (tabes dorsalis) includes propioceptive loss and pain (posterior root irritation), particularly affecting the lower
extremities. The lesion involves the posterior columns of white matter (Fig. 18B) and may extend to me posterior roots and root
ganglia.
— Pernicious anemia (Fig. 18C), there is proprioceptive loss and upper motor neuron weakness. The lesion involves the
posterior columns and corticospinal tracts.
— Polio auackes me anterior hom cells (Fig. 180) leading to lower motor neuron involvement. with weakness, atrophy.
fasciculatlons, fibrillations. and hyporeflexla,
— Patients with Guillatn-Barre syndrome (Fig. 18E) experience sensory and lower motor neuron loss because of peripheral
nerve involvement.
Motor cortex → corona radiata (ponytail) → internal capsule → cerebral peduncle → brainstem → cervicomedullary
junction → corticispinal tract → anterior horn cell → ventral root → peripheral nerve → NMJ → muscle
NOTE: (1) Certain muscle groups may be affected more than others in an upper motor neuron lesion. In the typical cerebral
hemisphere stroke secondary to carotid artery occlusion. the patient develops decorticate posturing, characterized by flexion of the
wrist and elbow and extension (straightening) of the ankle and knee. In midstrokes, the posturing is similar. except that the elbow is
extended (decerebrate posturing). The mechanisms apparently involve injury to other motor pathways (extrapyramidal) outside the
corticospinal (pyramidal) system. "Pure" lesions of the corticospinal tract result predominantly in difficulty with skilled movements
of the distal aspect of the extremities (2) all axons will radiate to corona radiate to gather into internal capsule then into the cerebral
peduncle down the midbrain, pons and medulla and will decussate and descend into lateral corticospinal tract. It will descend to the
white matter of the spinal cord then to the gray matter into the ventral horn where the 1st neuron will synapse to the 2nd neuron.
Another axon will come out (ventral root: motor) tat joins the (dorsal root:sensory) to form a single peripheral nerve. This will go to
the neuromuscular junction and finally to the muscle

BEFORE MOVING ON TO THE NEXT!!

PLEASE MEMORIZE THE DERMATOMES!!

TIPS IN HISTORY TAKING
1. As much as possible, use 5-6 sentences while reporting

a. 1st sentence- includes patient’s general information (Name, Age, Sex, Address, Dominant hand) + with a chief
complaint of _____________
b. 2nd and 3rd sentences- HPI (Use (eg. “Last January 2013..” instead of “ 2 years ago”)
c. 4th and 5th- Past Medical History, Treatment, Relieving Factors
d. 6th- additional relevant information such as Social History of the patient (kapag kay doc Abella, mas gusto niyang
kasama ang social history)
2. Never give diagnosis if it was not mentioned by the patient
3. Construct sentences that are simple and precise
4. For references and techniques, use only DEMYER (magagalit si Doc Terencio and si Doc San Diego kung di yan galing sa
demyer. Ayaw nilang makarinig na galing sa Youtube etc.
EVALUATION OF MOTOR SYSTEM
History
Physical Examination
Neurologic Examination
Laboratory Work-up
LOCALIZATION
DIFFERENTIAL DIAGNOSIS
History - taking
 Onset : acute, chronic
 Course : progressive, remissions and exacerbations
 Distribution : proximal, distal, hemiparetic, paraplegic
 Associated neurologic symptoms : dysphagia, dysarthria, diplopia, ataxia, numbness, paresthesias, seizures
 Others : fever, exposure to toxins, medications
Physical Examination
 Tachycardia
 Signs of hyperthyroidism
 Evidence of liver and renal dysfunction
 Skin lesions
 Neoplastic
Neurologic Examination  Vascular
 Distribution of weakness  Metabolic / Toxic
 Muscle bulk  Degenerative
 Muscle tone  Congenital / Developmental
 Key muscles involved  Infectious
 Sensory features  Immunologic
 Deep tendon reflexes
Etiologies of lesions affecting the motor tract

 Traumatic

EXAMINATION OF THE MOTOR SYSTEM

INSPECTION
— Motor examination begins the moment the patient MUSCLE TONE
walks into your clinic — Muscular resistance apart from gravity or joint disease the
— Have the patient undress examiner feels when manipulating a patient’s resting joint
— Determine the patient’s gestalt, somatotype or body
— Muscle tone is due to:
build
— Inspect the size and contour of muscles  Elasticity of the muscle (ordinarily is
slight, unless muscle is fibrotic)
▪ Look for atrophy vs hypertrophy
 Number and rate of motor discharges
▪ Body asymmetry which depend on:
▪ Joint malalignment • -LMNs stimulation by muscle spindles and other
receptors in skin, tendons, joints, and bone.
▪ Fasciculations
• -LMNs stimulation or inhibition by pyramidal and
▪ Tremors
extrapyramidal pathways
▪ Involuntary movements
•
STATION AND GAIT
HYPERTONIA
— Look for
— spasticity (increased tension in extensor joint
1. Unsteadiness that gives resistance to passive flexion, e.g. clasp
2. Wide-based gait knife spascticity), rigidity(increased muscle tone
3. Lack of arm swing that is resistance to passive extension of joint, eg.
Lead pipe rigidity), paratonia(involuntary
— Ask the patient to walk on toes, heel, in tandem
resistance to movement or inability to relax)
NOTE: (1) Station – steadiness and verticality of the standing

▪ SPASTICITY
posture (2) Gait – walking
— Initial catch or resistance and then a yielding
when the examiner manipulates the patient’s
PRINCIPLE OF STRENGTH TESTING resting extremityis briskly manipulated, which
1. Matching principle- select movements that matches resembles pulling the blade of an ordinary
your arm and hand strength. Match your strength with pocketknife open. When first opened, blade
pt’s strength resists but quickly yield as it straightens out
2. Length-strength principle- “muscles are strongest (clasp-knife spasticity).
when acting from their shortest position, and little or — Clasp knife spasticity
no strength when in their longest position” (mas
malakas ang flexors than extensors)
3. Antigravity muscle principle- muscles work in ▪ RIGIDITY
opposing, agonist-antagonist pairs; one of the — Increased muscular resistance felt throughout
opposing pairs is stronger than the other (e.g. neck the entire range of movement when the
extension is stronger than neck flexion). examiner slowly manipulates a patient’s resting
joint. The steady resistance feels like bending
➔ Antigravity Muscle system – the muscles that
solder or a lead pipe (lead-pipe rigidity). It
support / lock standing posture against
involves agonists and antagonists at the joints.
collapse by pull of gravity and that leap,
propel, or locomote against gravity. — Lead-pipe rigidity
➔ Antigravity Muscle Theory predicts the

strongest muscles and how much stronger NOTE: (1) Presence of a lead-pipe rigidity indicates an
they are. extrapyramidal lesion in the basal motor circuitry, more
specifically in the dopaminergic projection from the substantia
 Antigravity Muscle Theory
nigra to the striatum in Parkinsonism.
explains the posture, decerebrate
rigidity (Pt assumes the position
dictated by contraction of the entire
antigravity muscles; the ▪ PARATONIA
vestibulospinal tract controls — Resistance equal in degree and range that the
antigravity muscles) patient presents to the examiner as he tries to
move a part in any direction; pari passu response
NOTE: (1) Antagonistic pairs: As one of the muscles in ▪ FLACCIDITY
a pair contracts, the other relaxes (e.g. Biceps and
Triceps) (2) In other words: Antigravity muscles are the ▪ Hypotonia
muscles that stabilize / maintain posture by opposing ▪ Decreased resistance the Ex feels when
gravity. manipulating a Pt’s resting joint; an increased
range of joint movement, as with
4. Engagement principle-( dapat isipin palagi ni patient hyperextensible knees
na nakikipagcompete siya sa strength ni examiner)

▪ Increased range of motion of the joint MUSCLE STRETCH REFLEXES

movement i.e. hyperextensible knees or ➔ Muscle spindles – stretch-sensitive receptors for the
flaccid heel cords muscle-stretch reflex (MSRs), which consists of small bags and
small muscle fibers. (Remember muscle spindles as “muscle
▪ Lesions at the level of the reflex arc or
within a muscle”).
peripheral neuro-muscular system.
▪ Interruption of afferent fibers in peripheral A. Stretch in muscle spindles:
nerves or dorsal roots reduces muscle tone by
— Muscle fibers of the spindle originate and insert into
removing the inflow of excitatory afferent
the perimystal (pertaining to perimysium) connective
impulses.
tissue, which is continuous with tendons. If the joint
▪ Section of ventral roots would cause extends, the tendon pulls on the perimysium and
hypotonia because no nerve impulses could stretches the muscle spindles. Flexion, on the other
reach the muscles. Primary myopathies cause hand, would cause relaxation.
hypotonia by reducing the ability of the — Muscle spindles must readjust their length whenever
muscles to respond to tonic nerve impulses. the muscle length changes (to remain sensitive
throughout the entire range of the muscle length).
— Flexion momentarily relaxes the muscle spindle
NOTE: Central Causes (1) Although cerebral, cerebellar, and
tension. Muscle fibers of the spindle contracts slightly to
brainstem lesions sometimes cause hypotonia, pathyphysiology
maintain original tension.
is elusive. (2) Many congenital brain disorders, such as Down’s
— Extension slightly lengthens the spindles to maintain
syndrome and Prader-Willi syndrome cause profound
original tension.
hypotonia. Patients with spastic cerebral palsy may present as
a) hypotonic infants before spasticity evolves, or b) may remain
hypotonic. B. Innervation:
— Each muscle spindle has its own afferent and efferent
From cerebral or spinal (neural) shock: axons that maintains its constant tension.
— In response to stretch, the spindles send afferent
signals into the neuraxis via the afferent axon.
➔ Neural shock – is a stage of hypotonic total paralysis
and total areflexia that immediately follows an acute, severe NOTE: (1) In response to slow stretch, spindles send signals
UMN lesion. The term shock in this context designates the intermittently and asynchronously. The spindles quickly adapt
disastrous disorganization of acutely injured nervous system. to the new length and resume to baseline activity level. (2) In
➔ Diaschisis – distant impairment of function beyond the response to rapid stretch, essentially instantaneous, all
confines of the acute lesion. After an acute lesion, signs and spindles of the muscle synchronously send a strong afferent
symptoms often exceed the actual tracts interrupted or neurons volley into the central nervous system (CNS), which stimulates
destroyed. For example, acute and strictly unilateral occipital the lower motor neurons (LMNs) of the regular muscle fibers.
lobe infarction may result in complete (bilateral) cortical The resultant discharge of the LMNs causes clinically evident
blindness for hours or days. After that period, Pt will show only muscle contraction, the muscle stretch reflex.
the expected hemianopia.
— The event that initiates the MSR is stretch of the
➔ Causes of neural shock or diaschisis: large, acute, and muscle spindles, but the resultant twitch of the entire
catastrophic, including trauma, spinal cord transection, and muscle is the result of the contraction of the regular
large brain infarcts or hemorrhages. muscle fibers.
— When the MSR acts, the muscular contraction pulls
NOTE: If a Pt originally in a stage of neural shock begins to the two ends of the muscles closer together. The tension
recover movement, recovery usually parallels the emergence of is momentarily reduced. Hence, the spindles cease firing
the MSRs, spasticity, and clonus. After most slow-onset UMNLs, and MSR ends abruptly.
most Pts present increase in MSRs, clonus, and spasticity early
in the course without going through the hypotonic phase. Thus, AREFLEXIA AND THE REFLEX ARC
clinical signs of UMNLs depend on: (a) Rapidity of onset (b) Size — Areflexia is pathologic, except in toe and finger MSRs, and in
of lesion (c) Stage in the CNS recovery after an acute lesion some particular muscles in inafnts and females who lack
prominent tendons.
MUSCLE WEAKNESS — Some people who have generalized hyporeflexia or
— Lack or diminution of muscle strength hyperreflexia fall at one end of the normal range; they will have
— Leads to inability to perform the usual function of a normal muscle size and strength, and sensation.
given muscle or group of muscles — Ballet dancers and women who wear very high heeled shoes
— “Fatigue” – subjective perception may lose their quadriceps and triceps surae stretch reflexes.
— Usually referable to a dysfunction of the corticospinal — To determine cause of areflexia, we must think through the
tract Reflex Arc:
— Could be associated with gait disturbances or muscle 1. Start with the stimulus and receptor (by NE)
atrophy but not all the time! 2. Next, the integrity of muscle spindles and afferent limb
/ arm of the arc (also by NE)
3. The Lower Motor Neuron (LMN) cell body
➔ The LMN includes the cell body and its axons.
Many diseases attack the cell bodies of LMNs:
a.) Poliomyelitis destroys LMNs with less
effect on the dorsal horns or afferent fibers. A NEUROMUSCULAR DISEASE, MOTOR UNITS, AND ELECTROMYOGRAPHY
Pt with poliomyelitis loses MSRs because of ➔ Motor unit – one LMN, its axon, and all of muscle
destruction of the efferent arc but retains fibers it innervates. Each efferent axon may innervate one (in
sensation. some small fibers such as EOMs) or more (in large muscles such
4. The Efferent Axon as gluteus maximus) muscle fibers. If a normal LMN discharges a
nerve impulse, all muscle fibers contract.
➔ Through the ventral root and peripheral
nerve; the efferent axon may be interrupted ➔ The muscle fibers of motor units are grouped together
by mechanical lesions such as cuts or in a fascicle of the muscle.
compression. Many toxic and metabolic
disorders (lead poisoning) may predominantly
affect efferent axons, causing motor ➔ Myokemia – visible, rippling, worm-like action of the
neuropathy. Toxins (such as arsenic) regularly muscle caused by prolonged periods of discharge of motor
affect afferent and efferent axons causing units. Muscles go into continuous spasms that may appear
sensorimotor neuropathy. focally or segmentally.
5. The Neuromyal Junction (Neuromuscular junction –
NMJ) ➔ Cramps – sustained contractions that last seconds to
➔ Two disease of the NMJ that cause defective minutes, often brought on by exercise and relieved by
impulse transmission: Myasthenia Gravis - a stretching the muscle.
disease of fluctuating intensity. Complete
areflexia is unusual; Botulism
➔ Electromyography - a needle is inserted into a normal
➔ Lambert – Eaton myasthenic syndrome (LEMS) resting muscle and wired to an amplifier and oscilloscope
records no electrical activity in most skeletal muscles at rest.
➔ Congenital conditions: end-plate
When motor units discharge, oscilloscope screen displays
acetylcholinesterase deficiency, acetylcholine
numerous electrical potentials caused by muscle fiber
receptor deficiency, slow channel syndrome,
depolarization.
fast channel syndrome)
➔ Several other autoimmune, genetic, toxic, NOTE: The surface membrane of a disease LMN
drug-related conditions. becomes unstable. The neuron may then discharge
6. The Effector (Muscle) spontaneous, random impulses, rather than
discharging only in response to appropriate stimuli. All
➔ Final level of the reflex arc.
the muscle fibers connected to the axon of the motor
➔ Many myopathies, including the muscular neuron contract, resulting in spontaneous
dystrophies and myositides, may cause fasciculations.
areflexia. The afferent and efferent limbs of
the reflex arc are preserved, but the diseased
muscle cannot respond. ➔ Wallerian degeneration – When a neuronal perikaryon
dies, its axon dies. The axon also dies after complete separation
from its perikaryon. The process of dissolution of the dead axon
EFFECTS OF NEUROMUSCULAR DISEASE ON MUSCLE SIZE
and its myelin sheath is called the Wallerian degeneration.
➔ The size of normal muscle depends on use. If used, the
muscle undergoes hypertrophy. If not used, the muscle
NOTE: After the axon is severed from its perikaryon
undergoes disuse atrophy
and after Wallerian degeneration, the denervated
➔ UMN lesions that result in paresis or paralysis reduce muscle will not contract in response to volition,
muscle use. The muscle, therefore, undergoes some afferent stimuli, or direct electrical stimulation of the
degree of disuse atrophy, but atrophy is slight in peripheral nerve trunk.
relation to LMN lesion effect or myopathies.
➔ If deprived of axons by LMN lesions, muscle fibers ➔ Fibrillations - random, spontaneous contraction of an
undergo denervation atrophy, a severe atrophy that individual denervated muscle fiber. After denervation muscle
results to muscle fiber death, unless reinnervation fiber. After denervation by Wallerian degeneration of the motor
occurs. axon, the muscle fiber undergoes a period of hyperexcitability.
➔ Myopathies also may result in death of muscle fibers ➔ Fasciculations – contractions of muscle fascicles,
(myopathic atrophy). detected by clinical inspection or by characteristics EMG waves.
They indicate a hyperexcitable state of the cell membrane of
➔ In some myopathies, notably Duchenne’s muscular the LMNs, which depolarize spontaneously, causing contraction
dystrophy, some muscles go through a stage of of all muscle fibers of a motor unit.
pseudohypertrophy, appearing enlarged for the first ➔ Clonus – is a to-and-fro, 5-to-8-cycles per second (cps),
years, then eventually undergoing atrophy. rhythmic oscillation of a body, elicited by a quick stretch.

SUPERFICIAL REFLEXES (SKIN-MUSCLE REFLEXES) CLINICAL VARIATIONS IN THE PYRAMIDAL (UPPER MOTORNEURON)
A. Superficial vs. Deep Reflexes SYNDROME
— Because stimulation of receptors deep to the skin — Standard hemiplegic distribution: Unilateral
elicits the MSRs, the MSRs are classed with the deep interruption of the pyramidal tract at any level from the
reflexes. Stimulation of receptors in skin and mucous cortex to the pontomedullary junction causes weakness
membranes elicits superficial or skin-muscle reflexes. of the contralateral side of the body, from the lower
— The superficial skin-muscle reflexes commonly elicited facial muscles on down
in the NE consist of:
1. Corneal reflex
NOTE: Magpractice ng correct technique ng paggamit ng
2. Gag reflex neurohammer! Dapat mag-elicit ng force and power
3. Abdominal skin-muscle reflexes
4. Anal wink and bulbocavernosus reflexes OTHER NOTES FROM RECORDING AND LECTURES
PLANTAR REFLEX
➔ Reflex – consists of a relatively invariant response to a Lower Extremities
specific stimulus. Reproducibility is the goal in eliciting any a. Plantar toe reflex- blunt end of the neuro hammer →
reflex, either toe flexion or extension (in case of plantar reflex). lateral aspect of the toe
➔ Criterion for Successful in Eliciting a Reflex: b. Chaddock’s maneuver- blunt end of the neuro
REPRODUCIBILITY of toe movement, either flexion or extension. hammer → lateral side of the foot
c. Gonda, Strasky- pull the 4th toe outward and
➔ Characteristics of the Plantar Reflex: Length, Velocity,
downward and release suddenly
Pressure
d. Gordon- squeeze the calf muscle
e. Oppenheim- press your knuckles on the patient’s shin
A. Anatomy of the Plantar Reflex Arc
and move them down
— The reflexogenous zone (zone from which a reflex can
f. Schaeffer- squeeze hard the Achilles tendon
be elicited), is the first sacral dermatome (S1) for the
normal plantar reflex. g. Bing- multiple light pricks on the dorsolateral surface
— Because of the skin / contains nerve endings, the of the foot
plantar reflex is classed as a superficial reflex. Deficit Phenomenon
B. Plantar Reflex Arc: ▪ Are sensorimotor functions that are lost after a
— Reflexogenous zone: S1 dermatome neurologic lesion
— Afferent nerve: Tibial nerve (branch of Sciatic nerve)
▪ i.e. loss of movement, loss of vision
— L4 – L5 and S1 – S2 levels of the spinal cord mediates
the plantar reflex. Release Phenomenon
— The sciatic nerve divides into two branches proximal
to the knee. Tibial branch innervates toe flexors, ▪ Are sensorimotor functions that become increased or
peroneal branch innervates toe extensors. first emerge after a neurologic lesion
▪ i.e. hyperactive MSRs, Babinski sign

C. Physiology of the Plantar Stimulus
— Pain and plantar reflex: The plantar stimulus results ▪ The lesion has interrupted inhibitory connections
in a somewhat noxious feeling of tickling, pressure, and
pain. An effective plantar stimulus presumably acts Involuntary Movements
mainly through the pain receptors in the skin, but the
stimulus activates several types of afferent endings. ▪ Tremors: rhythmic oscillations of a body part
— Summation and the Plantar Reflex: A stimulus that
requires increasing application to elicit a response is said ▪ Chorea: incessant, random, quick movement
to summate or undergo summation. Certain minimum
number of afferent impulses has to add up (hence, ▪ Athetosis: slow, writhing movement of fingers and
summation) to fire the LMNs to the muscles. When a extremities
stimulus must act over a finite time to cause the reflex,
▪ Dystonia: prolonged slow, alternating contraction and
temporal summation has occurred.
relaxation of agonist and antagonist muscles
NOTE: (1) When the plantar reflex, the toe may not
▪ Hemiballismus: violent flinging movements of one half
move until the object reaches the instep or ball of the
of the body
foot. This response delay is indicative of some type of
summation. (2) Moving the object from the heel to the ▪ Tics: quick, lightning-fast movements of face and upper
instep requires a finite amount of time suggests extremties
temporal summation. Moving the object stimulated
successively more receptors suggests spatial

summation. (3) Thus, for the toe muscles to contract,
the central excitatory state of the motor neurons was
increased by temporal and spatial summation.

QUESTIONS  Tongue deviated to the L

1. When the muscle comes to rest at a new length, what  Hemiplegia, right
adjustment takes place in the tension of the muscle
spindles?  DTRs : ++ L, +++ R
A: They reset their tension to baseline level.  Babinski, R

Diagnosis: Left frontal infarct
2. Explain why only a quick stretch elicits an MSR. Case 3:
A: All muscle spindles must fire rapidly and  22 / M gradually progressive right-sided weakness and
synchronously to discharge the LMNs. If stretch is too headache
slow, spindles fire slowly and asynchronously, and
 Aphasic
adapt to new resting length without sending a
sufficiently strong signal to discharge LMNs.  R homonymous hemianopsia
 Motor strength R 2/5, L 4/5
3. Muscle fibers contract in response to stimulation of the  Spastic extemities R
muscle membrane by percussion. This is called the
________ of the muscle.  Hyperreflexia R
A: Percussion irritability Diagnosis : Left frontal arteriovenous malformation
4. ________depends on a strong volley of afferent Case 4

impulses initiated by the stretch of the specialized  35/ M
stretch receptors (muscle spindles).
 L-sided weakness
A: Reflex irritability
 Frequent jerking of the L extremities
5. After interruption of all efferent axons to a muscle,  Headache x 3 mos
what would be lost, percussion or reflex irritability?  Vomiting
Explain.
 Increased sleeping time
A: MSRs. Denervation of a muscle abolishes the MSRs,
because it depends on the integrity of the reflex arc, Diagnosis: Right frontal tumor (glioblastoma)
while percussion irritability depends on the intrinsic
property of the muscle fibers. Case 5
6. Would interruption of sensory afferents from the  55/F with gradually progressive bilateral lower
muscle cause paralysis? Explain. extremity weakness x 6 months
A: NO. As long as UMN and LMN pathways to regular  (+) incontinence, behavioral changes, headache
muscle fibers are intact, movement is possible. (but with
 Focal seizures R leg with secondary generalization
areflexia)
 Both LE spastic, hyperreflexic
7. What nerve, if cut, would interrupt the afferent and
efferent arcs of the normal plantar response, leaving  55/F with gradually progressive bilateral lower
the toe extensor muscles innervated? extremity weakness x 6 months
A: tibial  (+) incontinence, behavioral changes, headache
CASES  Focal seizures R leg with secondary generalization
Case I  Both LE spastic, hyperreflexic
 72/F with three month history of headache and left- Diagnosis : Falcine Meningioma
sided weakness NOTE: MULTIPLE SCLEROSIS (1) Demyelinating disease (2)
 Also had two episodes of focal seizures described as Involves the cerebral hemispheres, brainstem, cranial nerves
jerking of the left arm lasting for a few seconds and spinal cord (3) With remissions and exacerbations
 On PE, R 5/5, L 3/5 Case 6
 65 / M with gradually progressive weakness of all
o DTR: ++/+++, Babinski L
extremities
o spastic L extremities  Generalized atrophy and fasciculations
Diagnosis: Right frontal tumor  Hyperrflexic all extremities
 Bilateral Babinski and clonus
 No sensory deficits
Case 2
Diagnosis : Amyotrophic Lateral Sclerosis
 70/F known hypertensive and diabetic with no meds
Case 7
 3 hours prior to admission sudden onset of right -
 3 month-old boy
sided weakness, decrease in sensorium
 Born with lumbosacral mass
 BP = 150/100 HR = 90-100 (irregular)
 Hypoplastic, flaccid bilateral LE
 Drowsy, aphasic
 Areflexic both LE
 Hemianopsia R
 Urinary incontinence
 Shallow R nasolabial fold
Diagnosis: Lumbar myelomeningocoele

Case 8
• 14 / F with history of fever and cough x 2 weeks
• Developed acute ascending lower extremity weakness
and numbess
• Arreflexic and flaccid all extremities
• Hypoesthesia from waist down
Diagnosis: Guillain-Barre Syndrome
Case 9
 22 / F with fluctuating bilateral extremity weakness
 Bilateral ptosis
 (+) dysphagia , dysarthria
 Symptoms worse at nighttime
 No sensory deficits
 Normal reflexes
 Enlarged thymus on CXray
Diagnosis : Myasthenia gravis
Case 10
• 8 year-old boy with difficulty of breathing
• Started walking at 4 y.o.
• (+) waddling gait
• (+) Gower’s sign
• Weak proximal muscles
• Normal reflexes
• Similar illness in maternal uncle
Diagnosis: Myopathy

MINIATLAS



APPENDIX A
Table 1. UMN vs LM
LOCATION of the lesion UMN LMN
Motor strength weak weak
Atrophy Mild atrophy present

DTR (deep tendon reflex) hyperactive hypoactive
Muscle tone Spastic (drawing, pulling or Flaccid (reduced muscle tone,

may stiffness) overly relaxed)
Abnormal movements Withdrawal of spasms, Fasciculations (spontaneous

abnormal reflexes contraction affecting a small
number of muscle fibers, often
causing a flicker of movement
under the skin)
Table 2. Neuropathy vs Myopathy
Site of Lesion Motor Strength Atrophy Deep Tendon Muscle Tone Abnormal
Reflexes Movements
PERIPHERAL Weak Present Hypoactive or Flaccid Fasciculations

NERVE (Proximal < Distal) absent
Table 3. Strength Scale

Table 4. MSR Grading
Table 5. Plantar Reflex Maneuvers
REFERRENCES:
1. Demyer’s The Neurologic Examination, 6th ed. by Biller, Gruener, Brazis
2. Clinical Neuroanatomy: Made Ridiculously Simple by Stephen Goldberg, MD
3. Dr. Katherine San Diego’s PPT Lecture “Examination on Motor System”
4. Notes from previous preceptorials
5. Recordings
AUTHORS
Duabe, Katherine (Editor)
Grasparin, Danica
Danez, Dara
Bandayrel, Eunice
Alvaran, Karla
Domalanta, Mary Rose
Jacaban, Paul
Barcelon, Jonriey

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SAN BEDA COLLEGE OF MEDICINE

EXAMINATION OF MOTOR SYSTEM: NERUROLOGICAL EXAM & THEORETICALS

Part II: Theoreticals portion:

SBCM 2019 SECTION A Page 1 of 31

Station & Gait Testing

IV. MUSCLE TONE VIA PASSIVE MOVEMENTS

Numerical Scale to Record Muscle Strength MEMORIZE THE NUMERICAL SCALE!!!

SBCM 2019 SECTION A Page 2 of 31

A. BICEPS & TRICEPTS STRENGTH TESTS

The inserts show the length of the

B. NECK FLEXION AND NECK EXTENSION

SBCM 2019 SECTION A Page 3 of 31

C. TESTING THE STRENGTH OF THE SHOULDER GIRDLE

Arm Adduction Downward

Arm Adduction Across The Chest

SBCM 2019 SECTION A Page 4 of 31

D. TESTING FOR THE STRENGTH OF THE ELBOWS

Elbow Extensors (Triceps)

E. TESTING THE STRENGTH OF THE FOREARM MUSCLES: Wrist and fingers

SBCM 2019 SECTION A Page 5 of 31

Finger Abduction and Adduction

F. TESTING FOR THE ABDOMINAL MUSCLES & LARGE BACK MUSCLES

SBCM 2019 SECTION A Page 6 of 31

G. TESTING FOR HIP GIRDLE

 Ask the patient to sit.

 Place your hand on the popliteal space

 With the Pt sitting, have the Pt hold the

 Have the patient try to hold the legs

SBCM 2019 SECTION A Page 7 of 31

H. TESTING KNEE STRENGTH

I. ANKLE & TOE STRENGTH

As well as of the great toe.

R: 5/5 on both ankle and R: 3/5 or lower on

SBCM 2019 SECTION A Page 8 of 31

VI. TESTING THE MUSCLE STRETCH REFLEX

Numerical Scale to Record Muscle

STICK FIGURE from De Myer’s that must

SBCM 2019 SECTION A Page 9 of 31

SBCM 2019 SECTION A Page 10 of 31

FINGER FLEXION REFLEXES

Finger Flexion Reflex (Hoffmann’s Method)

R: 0/4+on both, asymmetric

Pull Method (of Jendrassik) for Reinforcing the Quadriceps Reflex

SBCM 2019 SECTION A Page 11 of 31

Counter-Pressure Method for Quadriceps Femoris Reflex

F. Triceps Surae & Toe Flexion Reflex

Triceps Surae Reflex (Sitting)

(Plantar) Toe Flexion ROSSOLIMO’S SIGN

SBCM 2019 SECTION A Page 12 of 31

Gonda, Stransky (Toe-Pull Reflex)

Gordon (Calf-Toe Reflex)

R: Dorsiflexion of the right/left big

Bing (Pinprick-Toe Reflex)

VII. TEST FOR CLONUS

Technique for Eliciting Clonus

SBCM 2019 SECTION A Page 13 of 31

patient’s thigh, stretching the quadriceps femoris

VIII. ADDITIONAL MOTOR EXAMINATION