Pediatric Neurologic Exam PEDIATRICS 1

Dr. Ignacio Rivera | March 21, 2018

Transcribers: Acosta, Adelan, Agpi, Aguinaldo
Editor: Bertumen | 09989982691
2.04
OUTLINE • static vs. progressive
I. Elements of a Complete Neurologic Assessment cerebral palsy (clinical term: static
encephalopathy) is an example of a static problem
II. Clinical History
A. Developmental History  Progressive: gets worst over time, Inborn error of
metabolism- is usually the findings for patients that
B. Neurologic History
C. Pregnancy, Perinatal and Neonatal History manifest with progressive signs and symptoms
o Developmental milestones must always be recorded. It
III. Neurologic Exam
determines if development is at par, delayed, or
IV. General Physical Exam
regressive.
V. Head
VI. Neurologic Exam: MSE, CN  Regression (loss of skills over time) suggests a
VII. Motor Examination neurodegenerative disease of the CNS such as inborn errors
VIII. Gait Abnormalities of metabolism.
IX. Sensory Examination
X. Tendon Reflexes Review of systems (ROS)
XI. Superficial Reflexes
XII. Milestone Guidelines: Motor o Focuses on the major childhood illnesses, immunizations
XIII. Cerebellar Functions (reactions), injuries, hospitalization, change in school
XIV. Newborn Reflexes performance.
XV. Autonomic Functions  frequent injuries suggest hyperactivity or poor
XVI. Soft Neurological Signs coordination
XVII. Milestone Guidelines: Social and Behavior Measles over time is SSPE-debilitating
XVIII. Milestone Guidelines: Language encephalitis
XIX. Conclusion o Also include feeding problems, respiratory difficulties,
XX. References and other ambulatory problems
XXI. Quiz
Temporal Profile
LEGEND
Remember Book Lecturer Other Trans
Trans Comm  Temporal profile – gives you an idea what kind of illness you
are dealing with
 Document duration of symptoms:
OBJECTIVES o constant
o episodic
No objectives given
o static
o progressive
I. ELEMENTS OF A COMPLETE NEUROLOGIC
o resolving
ASSESSMENT
 Focused clinical history
Neuroanatomical Localization
 Detailed neurological examination
 Additional parts of the general physical examination that are
relevant to child neurology Table 1. Localizing Neurological Manifestations
Manifestations Localization
II. CLINICAL HISTORY 1. Cognitive dysfunction or seizures Cerebral Cortex
Developmental History 2. Double vision, dizziness, dysphagia, Brainstem
 Development is a continuous process from conception to hoarse voice, disequilibrium
maturity 3. Bowel/bladder dysfunction, motor and Spinal Cord
sensory level
 The acquisition of various developmental and intellectual
functions coincides with neuromaturational processes in the 4. Weakness Motor Unit
CNS Some of the signs and symptoms that will help in localization of
affected area.
 The mode of presentation is age-dependent
o Normal presentations in infants may not be normal in Effect of the Problem on Daily Function
pediatrics of older ages.
For every age, there is a different set of milestones and  Inquire whether and to what extent, the problem has impacted
standards that are relevant to child neurology on:
o cognition
 Early identification of neurological and developmental o behavior and language
problems is important because of the potential for treatment o activities of daily living
and improvement through education and rehabilitative migraine or headaches are so intense and debilitating
services that it will stop you from your activity and would make
you find a dark and quiet environment
Neurologic History  Medications
 Identifying the children at risk  One common paroxysmal event that occurs in children is
o Unusual sleep patterns EPS presented acute stiffening of neck, back muscles in
o Determine whether the problem is: the ER due to inadvertent intake of psychotropic
• acute vs. chronic medications.
rupture vascular malformation is an example of Treatment: IV Diphenhydramine
acute problem while migraine is a chronic problem
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 Allergies o Basal ganglia (e.g. hyperbilirubinemia)
 Family History: o Cerebellar (e.g. tumors, ataxia)
o consanguinity  Spinal cord (usually weakness with bowel/ bladder
• Jews, a part of their culture is marrying a family dysfunction, sensory deficit)
member causing increase cases of Tay-sach’s  Peripheral nerve (e.g. Guillian-Barre syndrome presents as
disease and other congenital defects ascending paralysis)
o heredofamilial disorders  Neuromuscular junction (e.g. Myasthenia gravis, in children –
• e.g., PKU- 25% chance of having PKU if 1 parent is congenital muscle dystrophy)
a carrier; 50% if both parents  Muscle
o developmental problems
o epilepsy/seizures Ordered Sequence
o migraine 1. Vital signs
 may show symptoms of bigger problems because
Pregnancy, Perinatal and Neonatal History children show nonspecific symptoms (e.g headache,
• Mother’s age during pregnancy vomiting, irritability) for common systemic illness
• History of previous pregnancies (e.g hypertension)
• Prenatal exposure to prescription or illicit drugs, alcohol, 2. Anthropometric measurements
radiation, infections and timing of exposure 3. General examination
• Babies may experience withdrawal syndrome if 4. Mental status examination
the mother was taking illicit drugs during 5. Cranial nerves
pregnancy 6. Motor examination
• Maternal weight gain (excessive gain seen in 7. Cerebellar examination (including gait)
preeclampsia, causes placental insufficiency; poor weight 8. Sensory examination (peripheral and cortical)
gain leads to fetal growth restriction)
• Fetal movements (increased or reduced) Unquestionable Neurologic Signs and Symptoms
• Prenatal ultrasound • Altered sensorium: somnolent, stupor, obtunded, coma
• most routine, important as a source of • Seizures:
information in congenital screening. • focal vs generalized
• Recently, surgeons can operate congenital • Focal- involves localized part of the
abnormalities prenatally brain
• Generalized- involve the whole of
Perinatal Events both hemispheres
Labor and delivery history: • convulsive vs non-convulsive
• Gestational age; spontaneous or induced • Convulsive- involves motor
• Fetal presentation, length of labor; vacuum or forceps component; tonic clonic
• Apgar scores • Nonconvulsive- blank stare
• Norwegian registry study: NB over 2500 grams • Developmental delays / regression
with a 5-minute Apgar score of 0-3 was • Language problems
associated with a 125-fold increase risk of • Speech delay-the most common reason of
cerebral palsy, as compared with those with a consult
score of more than 8 • Causes:
• Need for resuscitation • Autism
• Birth weight, length and head circumference • Mental retardation
• Average hospital stay is 2days • Learning disabilty
• deafness
Review of System • Disorders of cognitive function
• Feeding problems
• Respiratory difficulties Subtle Signs of Increased ICP
• Ambulatory problems – clumsiness, falls • Increasing head size; bulging fontanels, widely split sutures
 These are common in children with global • Diminished Venous pulsation on fundoscopy
developmental delays and cerebral palsy. • Abducens nerve (CN VI) palsy
III. NEUROLOGIC EXAMINATION
Questions to answer during a neurologic examination:
 Is there a neurologic disorder?
o If so, where is the lesion, or as the case in many
pediatric neurologic cases, does it involve all parts of
the brain to an equal degree?
 What pathologic lesions are most likely to produce lesions at
this site or sites?
 Does the child have neurological problem?
o Signs and Symptoms of increased ICP
o Signs and Symptoms of Meningeal irritation
Figure 1. Abducens Nerve (CN VI) Palsy
o Signs and Symptoms of neurologic deficits which
includes the presence of delays, arrest or regression of
• Head tilt / Stiff neck
previously acquired milestones.
• “sun setting” eyes
o The sclera are visible between the upper eyelid and
 Where is the lesion? the iris. Sun setting sign is seen usually in
o Cortical (e.g. epilepsy, cerebral palsy can be hydrocephalus due to loss of upward conjugate
subcortical) gaze caused by raised intracranial pressure (ICP)
o Subcortical (e.g. spasticity)

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Figure 2. Sun setting Eyes

Signs of Meningeal Irritation

• Nuchal rigidity
• Spinal rigidity
• Kernig’s and Brudzinski’s signs
• Head tilt
• Photophobia

Figure 4. Localization of the different patterns of breathing

Table 2. Patterns of Respiration

Type Pattern of Respiration Description
Normal

Cheyne- Periodic hyperpnea

Stokes alternating with
apnea;
bihemispheric
Figure 3. Kernig’s sign (left). Sever stiffness of the hamstrings
dysfunction
causes an inability to straighten the leg when the hip is flexed to 90
Central Sustained rapid and
degrees. Brudzinski’s neck sign (Right). Severe neck stiffness
Hyper- deep hyperpnea;
causes a patient’s hips and knees to flex when the neck is flexed.
ventilation lower midbrain and
upper pons
NOTES: Apneustic Prolonged pause at
breathing full inspiration; mid
“Kernig’s (K for knee) and Brudzinski’s (B for batok) signs.” to lower pons
Cluster Disordered
breathing sequence of breaths
IV. GENERAL PHYSICAL EXAMINATION
with irregular
1. Vital signs
pauses; lower pons
2. Anthropometric measurements: plotted against norms
and upper medulla
3. General appearance particularly facial configuration or major
Ataxic Completely irregular
dysmorphism
breathing with random and
4. Careful exam of skin (neurocutaneous stigmata), scalp whorls
shallow breaths;
and palmar creases
central medulla
5. Teeth (antenatal reasons, hyperbilirubinemia)
Odine’s Loss of automatic
Vital Signs curse breathing; preserved
by voluntary
• Temperature instability could be due to brainstem breathing; medulla
dysfunction; Fever or hypothermia maybe due to CNS or lower cervical
infection cord
• HYPERTENSION, BRADYCARDIA, IRREGULAR
BREATHING: Cushing’s triad; increased ICP along with
General Appearance
altered sensorium
• Quality of scalp hair, eyebrows, and nails
Abnormal respiratory patterns: • Corneas and lenses for opacities
1. Cheyne-Stokes: periodic hyperpnea alternating with • Presence of cataract is a red flag
apnea; bihemispheric dysfunction • Inspect the midline of the neck, back, and pilonidal areas
2. Central hyperventilation: sustained rapid and deep • Compare thumb nail sizes and convexity
hyperpnea;lower midbrain and upper pons • Heart, chest and abdominal exam, and palpation of femoral
3. Apneustic breathing: prolonged pause at full pulses
inspiration; mid to lower pons • Unusual body odors
4. Cluster breathing: disordered sequence of breaths with
irregular pauses; lower pons and upper medulla
5. Ataxic breathing: completely irregular with random deep
and shallow breaths; central medulla

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Table 3. Urine Odors Associated with Inborn Errors of  Petechial hemorrhages – Cyotmegalovirus (CMV)
Metabolism  Macular rash – Systmic Lupus Erythematosus (SLE)
Odor Compound Disorder  Vitiligo – may suggest an autoimmune disease like
Musty, Phenylacetate Classic phenylketonuria myasthenia gravis
mousy
Maple 2-oxolsocaproic Maple syrup urine disease V. HEAD
Syrup acid Inspection
Sweaty Isovaleric acid Isovaleric acidemia  Macrocephaly - open and large fontanelles
feet Multiple acyl-CoA  Microcephaly - closed fontanels
dehydrogenase deficiency  Craniosynostosis - palpable ridgy sutures
(glutaric aciduria type II)  Venous distention (prominent scalp veins) suggesting
3-Hydroxy-3-methylglutaric increased intracranial pressure
aciduria  Flattened occiput suggest a developmentally delayed child
Cat urine 3-hydroxylsovaleric 3-Methylcrotonyl-CoA o Child is not pulling or turning over thus weight of the
acid carboxylase deficiency head is at the back of the scalp 
Multiple carboxylase  Bulging occiput suggest a Dandy-Walker cyst/malformation
deficiency  Biparietal (Devil’s horns) enlargement suggest bilateral
Cabbage- 2-hydroxybutyric Tyrosinemia type 1 chronic subdural hematomas
like acid Methionine malabsorption
Rancid 2-oxo-4- Tyrosinemia type 1
butter methiolbutyric acid NOTES: 
Acid smell Methylmaloric acid Methylmalonic academia Anterior Fontanelle closes at 18 months.
Posterior Fontanelle closes at 6 to 8 months
Sulfurous Hydrogen sulfide Cystinuria

Fish Trimethylamine Trimethylaminuria

market

Phenylketunuria (PKU) treatment: change the formula milk to a

special formulation for PKU

Dysmorphic Features
 Hypotelorism
narrowness of the interorbital distance
• seen in holoprosencephaly and Trisomy 13
 Hypertelorism
increased interorbital distance
• seen in Sotos syndrome, cleft palate, Apert
 Inner epicanthal folds
• Down syndrome, Rubistein Taybi, Zellweger
 Slanted palpebral fissure
• Down syndrome, Apert, DiGeorge, Miller Dieker
 Low set ears
• helix of the ear meets the cranium at a level below
that of a horizontal plane through both inner canthi
• seen in Noonan, Treacher Collins, Pena Shokier,
Trisomy 9 and 18
Skin examination: Neurocutaneous stigmata
 Hypopigmented patches
• pathognomonic of tuberous sclerosis, one of
the common causes of infantile spasm
 Café-au-lait spots
• uniformly hyperpigmented, sharply demarcated
macular lesions; varies in size
• Check the inguinal area and axilla for
freckling
• Seen in neurofibromatosis1
 Port-wine stain
• Facial capillary malformation
• Seen in Sturge Weber Syndrome
Figure 5. Port-wine Stain
Figure 6. Flattened occiput
Macrocephaly
 Open and enlarged fontanels
 Head circumference >2 standard deviations from the normal
population caused by:
o Hydrocephalus (communicating/non-obstructive vs.
non-communicating or obstructive)
o Excessive brain material
o Megancephaly
 Having big brains means that either you
are smart or mentally retarded 
 Mental retardation is due to storage
disorder, a genetic inborn metabolic
disorder wherein there’s excessive fat and
sugar that gets stored in all different
organs that’s why hepatomegaly and
splenomegaly are also present 
o Thickening of the skull
o Chronic subdural /epidural hemorrhage – skull will
assume a square or box-like shape
Microcephaly
 Strong predictor of mental retardation 
 closed fontanels
 head circumference < 2 standard deviation from normal
 Causes:
o congenital brain defect
o congenital TORCHS (Toxoplasmosis, others,
rubella, 6 of 18 CMV, herpes and syphilis) infection
o perinatal brain injuries
o malnutrition

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 If HC at birth is < 3 standard deviations from NL, mental
retardation is a strong possibility in the future
NOTES: 
Stunting is the most common manifestation of malnutrition not
microcephaly.
Palpation
 Cranial Sutures and Fontanelles
 Head circumference (serial): one of the most valuable
parameters for assessing hydrocephalus or microcephaly
Figure 7. Proper way of measuring head circumference 
 Tenderness
 MacEwen sign ( cracked pot sound)
 Cranial Sutures: Normal gap – 1 to 2 mm apart in the unfused
skull

Figure 8. Cranial Sutures. Sagittal, Coronal, Metopic and
Lambdoid sutures are the main cranial sutures. 
NOTES: Bone in the skull must grow perpendicular to the
suture (normal growth pattern). 
Craniosynostosis
 From cranio, + syn, together; + ostosis relating to bone
 Condition in which one or more of the fibrous sutures in an
infant skull prematurely fuses by turning into bone
(ossification), thereby changing the growth pattern of the skull
 Because the skull cannot expand perpendicular to the fused
suture, it compensates by growing more in the direction
parallel to the closed sutures
 Sometimes the resulting growth pattern provides the
necessary space for the growing brain, but results in an
abnormal head shape and abnormal facial features
 If sutures are ridged on one side there is premature lesion of
the sutures: scaphocephaly (midline), brachiocephaly (one
side), trigocephaly
Figure 9. Scaphocephaly. Premature fusion of the sagittal suture.
B. Sutures are already fused but the lambdoid and coronal sutures
are open thus head grows forward to backward, backward to
forward linking the anterior and posterior diameter. 
Figure 10. Crainiosynostosis pre and post-reconstruction
Figure 11. Brachiocephaly X-ray. (A-E): Bilateral (A-D) and
unilateral partial (E) coronal synostosis 3DCT volume rendered
images (A-C, E) and coronal CT scan (D). There is complete
fusion of the coronal suture (white arrows) with a prominent frontal
bone and flattened occiput. Coronal reconstruction (D)
demonstrates prominent bilateral elliptical orbits, known as the
"harlequin sign" deformity. Note the early partial fusion of the right
coronal suture (arrowheads in E)
Head Circumference Rate and Growth
 1st 3 months of life: 1.5 cm/month
 4 to 6 months of life: 1 cm/month
 7-12 months of life: 0.5 cm/month
VI. NEUROLOGIC EXAM: MSE, CN
Mental Status
 Age dependent
o Do not say that a 6 month old baby is oriented to
space and time 
 Glasgow coma scale
o Assess the Level of consciousness – If patient is
Awake, Somnolent, Stuporous, Obtunded or
Comatose
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o Normal awake = 15
o Brain dead = 3
o Traumatic Brain Injury = less than 8
 Orientation to person, place and time
 Higher cortical functions are intact
 Language functions
 Praxis: learned movements or behaviors
 Grapho-motor/visio-motor skills
 Example: Asking a 10-12 y/o to do serials of seven-digit span
Cranial Nerve I: Olfactory Nerve 
 Not usually tested
 Functional by 5-7 months of age
 Smell can be tested reliably as early as the 32nd week of
gestation by presenting a stimulus and observing for an
alerting response, withdrawal or both
 Each nostril should be tested individually by pinching shut the
opposite side
o Transient anosmia, usually is an association with
upper respiratory tract infection or allergies
 Permanent causes of anosmia include:
o Head trauma with damage to the ethmoid bone or
shearing of the olfactory nerve fibers as they cross
the cribriform plate
o Tumors of the frontal lobe
o Intranasal drug use
o Exposure to toxins
 Aromatic substances (perfumes, vanilla) should be used
instead of volatile substances (ammonia), which irritate the
nasal mucosa and stimulate the trigeminal nerve. 
Cranial Nerve II: Optic Nerve
 Visual Acuity
o Difficult to assess
o Can be grossly assessed by ability to follow or pick
small objects of varying sizes
o 20/20 is achieved by about 6 months of age
o A newborn has approximately 20/200 vision
o Standard visual charts displaying pictures instead of
letters can be used to assess visual acuity in
toddlers 
 Peripheral vision is tested by surreptitiously bringing objects
into the visual field from behind. A reduced pupillary reaction
to light suggests anterior visual pathway lesions, including the
retina, optic nerves, and chiasm 
 Blink reflex
o Appears as early as 28 weeks gestation
o Blinking of eyes in response to light – sign that a
newborn could see
o 32 weeks: maintains eye closure until the light
source is removed
o 37 weeks: turns the head and the eyes to a soft light
o Full Term: visual fixation and the ability to follow a
brilliant target are present; 20/200, but at 6 months:
20/20
o Hard to assess
 Visual Field
o Difficult to assess
o Introduction of non-audible stimulus from side, such
as a brightly colored object with the physician at the
back; double simultaneous presentation
o See if the baby will turn his eyes towards the
direction of the object
o Two objects can be presented at the same time. if
the baby prefer to look at one object, switch the
objects and see if the baby still looks at it. if the baby
does not follow the object, there might be a problem
 Fundoscopy
o Attention to optic disc (color, size, margins, venous
pulsations, retina (hemorrhage) and macula)
o Look for Red-orange reflex (normal)
o Things to watch out for: Retina hemorrhage,
papilledema, optic neuritis
o Retina hemorrhage is pathognomonic of “shaken
infant syndrome” where child is shaken violently
 Shaken infant syndrome can cause
contusions/linear lacerations in the brain
due to cutting from the sharp edges of the
bones.
 Presentation: No fever, bulging
fontanelles, pallor, depressed sensorium,
somnolence or irritability, lethargy and
seizures
Figure 12. (Left) Retinal Hemorrhage. (Right) Papilledema.
 Pupillary Light Reflex
o Direct and consensual
o CN II is the afferent limb
o CN III is the efferent limb
 Afferent papillary defect (Marcus Gunn pupil)
o Lesion in the optic nerve
o Slow pupillary dilation rather than quick pupillary
dilatation rather than quick pupillary constriction on
the affected side when consensual reflex is tested.
o both pupils constrict when light is directed into the
normal eye. When light is swung over to the
abnormal eye, both pupils dilate inappropriately 
o Unilateral optic nerve lesions are identified by the
swinging flashlight test 
 Horner’s syndrome (ptosis, miosis, and unilateral facial
anhidrosis) 
o In this instance, anisocoria (unequal pupils) is more
pronounced in a dark room, because the affected
pupil is unable to dilate appropriately
Cranial Nerve III (Oculomotor), IV (Trochlear), VI (Abducens)
 These three cranial nerves control eye movement and are
most easily examined with the use of a colorful toy to capture
the child’s attention 
 Position of the eyes at rest - check for Eyelids symmetry
(ptosis: Myasthenia gravis)
Figure 13. (Left) Unilateral ptosis is caused by Myasthenia gravis
(Right) Bilateral and not progressive maybe caused by Congenital
problem
 Eye movement and Doll’s phenomenon
o conjugate eye movements seen by 25 weeks
gestation
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 Doll’s eye Maneuver
o assesses oculocephalic vestibular reflexes
o for infants too young to fix and follow it is done by
rotating the infant’s head 
o If the brainstem is intact, rotating a newborn or
comatose patient’s head to the right causes the
eyes to move to the left, and vice versa 
 Diplopia
1. Unilateral third cranial nerve oculomotor nerve palsy 
o The involved eye deviates down and out
(infraducted, abducted), with associated ptosis and
a dilated, mydriatic pupil
2. Vertical Diplopia
o Trochlear Nerve Palsy
o Object targeted seems to be doubled but the other  Swinging Flashlight Test
object is higher or lower than the other; looking up o Use to check Marcus Gunn pupil
and down 1
3. Horizontal Diplopia
o Abducens Nerve Palsy
o Object is seen side by side or they are seeing
double
o Results in the inability to move the eye outward 
o Because cranial nerve VI has a long intracranial
route within the subarachnoid space, failure of
abduction of one or both eyes is a frequent, but
nonspecific, sign of increased ICP 
 Penlight Reflection
o To determine if eyeballs are aligned,
o Shine a penlight from a distance then observe the
position of the reflection of the light on the cornea, if
they fall on the same spot in both eyes, they are Figure 15. Swinging Flashlight Test. When you swing the
aligned penlight from one eye to the other, the normal eye will constrict
o Note: baby must be at his primary gaze and abnormal will dilate when light is turned away from abnormal
eye 

Cranial Nerve V: Trigeminal Nerve

 Action of muscles of mastication
o can be observed as an infant sucks and swallows

 Jaw movements and deviation
 Jaw jerk- exaggerated in lesions above the level of the pons
 Corneal Reflex
o abnormal if asymmetric or absent
o should not be done if patient is awake
o test cranial nerves V ophthalmic division and VII at
any age 
o Frequency of blinking increases with maturation and
decreases in toxic illnesses
 Facial sensation (V1, V2, V3) - tested and compared by light
touch demarcated by Ophthalmic branch (V1), Maxillary
branch (V2) and Mandibular branch (V3)
Figure 14. Penlight Reflection  Facial sensation of light touch and pain
o Determined with cotton gauze and pinprick 
Table 4: Penlight Reflection (alignment)  Facial sensation can be functionally assessed in an infant by
Penlight Reflection Interpretation gently brushing the cheek, which will produce the rooting
(position) reflex (turns head and neck with mouthing movement, as if
A. Middle Normal (but is not completely seeking to nurse) 
correct since eyes are slightly
deviated Cranial Nerve VII: Facial Nerve
B. Lateral to the Eyes are medially or nasally  UMN paresis (Stroke) – lower quadrant of the face
cornea deviated
 LMN paresis (Bell's palsy) – whole half side of the face
C. Nasal Side Eyes are laterally deviated
D. Below the cornea Eyes are deviated upward  Weakness accentuated by volitional movements
 Distinguish from Hypoplastic Depressor Anguli Oris
 McCarthy reflex- ipsilateral blinking when tapping the
supraorbital ridge- diminished with LMN lesions and
exaggerated with UMN lesions.
 Head Tilt Check for symmetry at rest and movement (during crying)
o Seen in Superior and Inferior Oblique Palsy
o Compensatory mechanism for double vision Check the size and symmetry of palpebral fissures, nasolabial
o Tilting of head for the alignment of eyeballs folds, position of the corners of the mouth 

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If necessary, taste can be tested by placing a solution of saline
or glucose on one side of the extended tongue. Normal children
can identify the test substance in < 10 seconds. 
 Vestibular function

Figure 16. Hypoplastic depressor anguli oris. When the baby cries,
only one part of the face or mouth curls downward (right side of the
baby is abnormal)
 Habituation – cessation of response by normal neonates if
 b. An isolated lesion of CN IX is rare, because it runs in
Figure 17. Peripheral Facial Palsy or Bell’s Palsy of the Right Side.
Right side is unable to fully close the eye and there is absent wrinkling
of the forehead. Usually, patients with this recover spontaneously (at
least 2 to 3 weeks, 3 months at most). Protection of the eye, however,
is of importance to prevent drying and exposure keratitis. Protection
may be done with artificial tears, Vitamin B complex, and sometimes
Acyclovir is given since keratitis is usually viral in origin.
 regurgitation of fluids, pooling of secretions, and an

Figure 18. Localization of Bell’s Palsy (Facial nerve lesion) and Stroke
(Supranuclear lesion)
Cranial Nerve VIII: Vestibulocochlear Nerve
 Hearing
o For infants: ring a bell or click ballpoint pen (localize)
o For older children: repeat whispered word or use tuning fork
(256 cps)
o Turning with eyes and head appears by 3 to 4 months when
infants begin to orient to the source of sound
Newborns have subtle responses to auditory stimuli, such as
changes in breathing, cessation of movement, or opening of the
eyes and/or mouth
o Hold child vertically facing you then turn child several times
in full circle (clockwise and counter clockwise)
o Note deviation of eyes during turn towards the direction of
rotation and on stopping quick phase nystagmus backwards
(optokinetic nystagmus)
o Abnormality suggests impaired brainstem function: valuable
in perinatal asphyxia
 Caloric Test- may also be used to further evaluate vestibular
function
a. On examination, patients with vestibular nerve dysfunction
typically have nystagmus, in which the fast component is
directed away from the affected nerve.
b. With their arms outstretched and eyes closed, their limbs tend
to drift toward the injured side.
same stimulus is presented repeatedly
Hearing impaired toddlers are visually alert and appropriately
responsive to physical stimuli but might have more frequent temper
tantrums and abnormal speech and language development
Cranial Nerve IX, X: Glossopharyngeal and Vagus
• Position of uvula at rest, quality of voice, palatal movements
during phonation
• Gag reflex absent in 1/3 of healthy individuals
• Swallowing and drooling
• Taste sensation (posterior 3rd of tongue), not worth the effort
• CN IX
a. Potential causes of injury and/or dysfunction to CN IX:
birth trauma, ischemia, mass lesions, motor neuron
disease, retropharyngeal abscess, and Guillain-Barre
syndrome
proximity to CN X.
 CN X
a. Unilateral injury of the vagus nerve results in weakness
of the ipsilateral soft palate and a hoarse voice
b. Bilateral lesions can produce respiratory distress as a
result of vocal cord paralysis, as well as nasal
immobile, low-lying soft palate.
c. Isolated lesions to the vagus nerve may be a
complication of thoracotomies or may be seen in
neonates with type II Chiari malformations
Cranial Nerve XI: Spinal Accessory
• Note movements of head side-to-side and shrugging of
shoulders in young children (remember the developmental age of
the client)
• Strength of muscles (through palpation) and against resistance
in older children
• Lesions to the accessory nerve results in atrophy and paralysis
of the ipsilateral SCM and trapezius muscles, with resultant
depression of the shoulders
Unilateral SCM paresis might not be evident unless the
patient is asked to rotate the head against resistance
Congenital torticollis is associated with SCM hypertrophy
Cranial Nerve XII: Hypoglossal
 Position of tongue at rest
 Deviation during protrusion the tongue also deviates towards
the weak side and is often seen in brainstem syndromes. 
 If the injury is unilateral, the tongue deviates toward the side of
the injury; if it is bilateral, tongue protrusion is not possible and the
patient can have difficulty in swallowing (dysphagia) 
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 Fasciculations (twitching of the muscles of the tongue) should
be observed in a relaxed child; cannot be determined with any
reliability if the youngster is crying 
a. Fasciculations should only be seen in the dorsum.
b. Abnormal fasciculations are seen in the lateral aspect of
the tongue
Infantile Spinal Muscular Atrophy Type 1/ Werdnig-
Hoffmann Disease
a. Fatal disease which involves progressive loss of anterior
horn cell function
b. Fasciculations on lateral areas of the tongue + hypotonic
+ weak + unable to suck normally + weak cry and floppy
c. Will not survive beyond 2 years of age but is very rare
Figure 19 . Tongue deviation. Tongue deviates to the weaker side
VII. MOTOR EXAMINATION
Observation
 Child’s station (i.e., posture while standing) should already
have been noticed when the child walked into the office, similarly
walking and running should also be observed. E.g. hemiparetic
gait
 These observations sometimes defer examination of the actual
strengths of the muscles as normal findings suggest muscles are
strong and are of normal tone
 Observation is very important in how they walk, they stand, to
give you an idea on their tone also by gently flapping the joints,
pull-to-sit, vertical and horizontal suspension.
 Check TONE, POWER (STRENGTH), and BULK
 -
Palpation
Muscle Tone
 Gently flapping joints: grab hold of the wrist and flap the
hands to check for resistance.
 Scarf Sign
 Pull-to-sit or Traction response: Normally, head lags slightly
behind the body and then falls forward upon reaching the sitting
position
 Vertical suspension (holding the child vertically by the
armpits): if the legs cross, it’s a sign of spasticity or hypertonia, e.g.
cerebral palsy
 Horizontal suspension (prone position, holding on abdomen):
if they droop over your hand like an inverted “U”, it’s a sign of
hypotonia.
Popliteal angle – useful method for documenting tone in the
lower extremities
a. Hip is flexed and the knee is extended
b. Normal term infants: knee extension to approximately 80°
Figure 20. Left: Pull-to-sit (notice the head lag indicating hypotonia)
Right: Horizontal suspension (an inverted “U” position may indicate
hypotonia)
Figure 21. Vertical suspension. When a baby slides in your hands
during Vertical Suspension, hypotonia is present.
Muscle Tone in Infants
 First few months: normal hypertonia of the flexors of elbows,
hips and knees (flexor dominance). This tone decreases markedly
during the 3rd month, cephalad-caudad
 At the same time, tone in neck and trunk increases allowing
the child to have head control.
 Between 8 and 12 months, a further decrease occurs in flexor
tone with an accompanying increase in extensor tone
 Passive tone best judged by passive movements of the joints,
while the infant is awake and not crying (head must be straight to
avoid influence of tonic-neck reflex)
Abnormalities of Tone
 Hypotonia – will be elicited through the following:
o Scarf sign
- Infant’s arm is pulled laterally across the chest
- Hypotonic infant: the elbow will cross the midline
Normal tone: elbow will not reach the midline
o U-shape on horizontal/ ventral suspension
- Pick up Infant on prone position: back just bends over
- Normal tone: head should rise and limbs should flex
o Slipping through armpit on vertical suspension
- Slipping through armpit; everything droops
- Normal tone: infant remains suspended; lower limbs
flexion
o Head lag on pull-to-sit (no traction response)
- Pull infant to sitting position: no traction response or
there is head lag.
- Normal tone: infant’s head lags slightly then falls
forward upon reaching sitting position
 Hypertonia
o Notable resistance to passive movements on joints (knee
or ankle joint)
o Varying degrees of posture (e.g. opisthotonus, etc);
“scissoring” of the legs on vertical suspension
o Fisting: “buried” or “cortical” thumbs (thumb is apposed
against the palm and is closed over by other fingers)
o Babies 4-6 months of age should be capable of playing
“close open” with their hands. If not, meaning there is
perinatal stroke.
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o Upper motor sign- baby continues to have cortical or
persistent fisting
o Babies with cerebral palsy have spasticity and hypotonia

Power
 Muscle power in infants and small children relies on age
appropriate gross and fine motor milestones
 Symmetries of movement
 Pronator sign: sensitive test for weakness for older children -
hypotonic hand hyperpronates
a. With palms up and elbows locked straight, ask patient to
close his eyes.

b. If the hand drifts downward and turns inward, that is a
Figure 23. Brachial Plexus Palsy
pronator drift suggesting weakness of the pronator
muscles.
 Arm roll  Abnormalities
a. ask the child to roll his hands in midline clockwise and o Should be able to determine the handedness of a
counterclockwise, you can tell the handedness of the child child at 2 years of age, earlier than that, it’s a sign of
by looking at the hand that is rolling faster than the other weakness.
b. If for instance, the left hand is fixated and only the right o Determined by seeing a preferential hand use.
hand is rolling or barely moving, then the left hand is weak. o One arm is weaker so the other hand seems
 Various muscle groups should be tested if child is old enough to dominant.
cooperate; young children through observation of their o Asymmetry at rest in infants
movements. o Opisthotonus (brainstem release phenomenon due
 to bilateral cerebral cortical dysfunction)
0 No muscle contraction
1 Flicker or trace of contraction
2 Active movement; gravity eliminated
3 Active movement against gravity
4 Active movement against gravity and resistance
5 Normal power
Table 5. Muscle contraction grading. Record the motor strength as
1/5, 2/5, 3/5 etc.


Figure 24. Opisthotonus in a brain-injured infant

o “Frog-legged” posture (abducted hips) – Hypotonia,

LMN lesion


Figure 22 . At 8 to 9 months of age, a baby should normally be able
to hold a milk bottle with both hands. In the figure above, observe
that the baby only holds the bottle of milk in his left hand. There is an
observed preference involving one upper extremity over the other. The
right hand may be weak relative to the left hand. In cases such as this,
order an MRI scan right away. It wouldn’t be surprising to find an old
stroke.

 Brachial plexus birth injury (paralysis of the upper extremity
due to birth injury)
a. Erb’s-Duchenne palsy (C5-6): “waiter’s tip” posture;
arm adducted, internally rotated, elbow extended,
forearm pronated and wrist flexed
b. Klumpke’s palsy (C8-T1): arm supinated, elbow bent,
unable to move the wrist and is extended. This is a more Figure 25. Frog-legged
distal injury which indicates a poorer prognosis.
 o Fisting of the hand (“cortical thumb”) – Hypertonia,
indicative of a cortical problem: UMN lesion

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o Polio
- Affected part: Anterior horn cell
- Not seen any more in this country at least.
o Myopathy/muscular dystrophy (Duchenne’s, Becker’s)
- Affected part: Muscle
- Older children may have difficulty climbing or
descending steps, jumping, or hopping.
- They might also use their hands to “climb up” their
legs when asked to rise from a prone position, a
maneuver called Gowers sign.
o Neuromuscular Blockade (Toxins)
- ex. Ingestion of saxitoxin, usually by consumption of
shellfish contaminated by toxic algal blooms, is
responsible for the human illness known as paralytic
shellfish poisoning (PSP)
Figure 26. Cortical thumb o Stroke
- Manifests as seizures in pediatric patients
o Tremors - Incidence of strokes in infants is almost the same as
- Resting: Parkinson’s; Lesion at Basal ganglia the incidence of strokes in older patients – in the form
- Intentional: Cerebellar lesion of acute ischemic arterial stroke or hemorrhagic
- Myoclonus stroke.
- The incidence of strokes in the middle childhood age
is not that common – except in this country where
they are secondary to TB meningitis and it is highest
in the newborn period.
- Hemorrhagic strokes are commonly caused by
defects in coagulation.
- Babies naturally need Vitamin K at birth to prevent
bleeding spontaneously
- Without Vitamin K, within a month the patient can
have spontaneous intracranial hemorrhage
- Acute Presentation: vomiting, seizures, pallor, and a
bulging tense fontanel leading to hemorrhagic
strokes.
o Demyelinating Diseases – more common in older children
- Multiple Sclerosis = prime example; presents with stroke
like symptoms
Table 6. Cervical and Lumbosacral Dermatomes and Myotomes
(Source: ppt)

 Movement Disorders
o Athetosis – contralateral putaminal lesion; seen as
sequelae in kernicterus
o Chorea – involuntary contractions mostly associated with
rheumatic heart disease
o Tics - may be facial twitching, involuntary blinking,
involuntary movement of the neck or shoulders;
o Presence of vocal and motor tics suggests Tourette
Syndrome
o Muscle atrophy, pseudohypertrophy and
fasciculation

Motor Weakness
 UMN vs LMN lesion Figure 27. Gower’s sign (left) and Pseudohypertrophy: Duchenne
muscular dystrophy (right)
 Generalized vs Focal
a. Hemiparesis/Hemiplegia
- CVA, acute ischemic stroke, hemorrhagic stroke VIII. GAIT ABNORMALITIES
(APCD), demyelinating disease ● Is it due to cerebellar neuropathy or problem in muscles?
 Always look for abnormalities involving movement: tremor, ● Circumduction: spasticity- persistently tiptoeing, seen early
myoclonic jerking aside from patterns of weakness. in Duchenne’s, if persistent, spastic diplegia
● Broad-based ataxia: cerebellar
 Examples of motor weakness
o Acute Polyradiculoneuropathy (Guillain-Barre ● High steppage gait: peripheral neuropathy with foot drop
syndrome) ● Waddling gait: myopathies like DMD, children with proximal
- If the weakness presents proximally, the disease is muscle weakness
myopathic. If the weakness initially presents distally ☝ MYOPATHIES: PROXIMAL MUSCLE INVOLVEMENT
going from the most distal portion up, the disease is NEUROPATHIES: DISTAL MUSCLE INVOLVEMENT
neuropathic. The prototype for this is Guillain-Barre ● Dystonia: normal while walking but at rest, feet turn inward
Syndrome. and walk on outer edges of the feet
o Myasthenia gravis ● Other causes: Acute Cerebellar Ataxia secondary to post
- Affected part: Neuromuscular junction viral infection
- Present with ptosis most of the time
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IX. SENSORY EXAMINATION Eversion of foot L5-S1 Superficial peroneal
● Light touch: T4 (nipple area), T10 (umbilicus), S4-5
(perianal) XIII. CEREBELLAR FUNCTIONS
● Cortical sensory: 2-point discrimination, stereognosis, ● Dysmetria and Ataxia: pathognomonic of cerebellar
graphesthesia dysfunction, sustained clonus is always pathologic.
● Joint sense: related to peripheral nerve, test done to school- ● Dysmetria can be demonstrated by having the child reach for
age children and manipulate toys
● Romberg test: test for Positional sense, therefore a sensory ● Abnormal if the baby ignored the toy or there is
test not cerebellar a struggle for the baby to reach the toy
● Tandem gait is expected to be performed well by 6 years of
X.TENDON REFLEXES age
● Jaw Jerk reflex ● Ataxia with tremor of the extremities can be demonstrated in
● Biceps reflex: C5-6 the older child on finger-to-nose and heel-to-shin testing
● Triceps reflex: C7-8 ● Accentuation of the tremor (intention) as the extremity
● Brachioradialis: more on the distal side approaches the target is characteristic of cerebellar
● Knee (patellar) reflex: L3-4 dysfunction
● Ankle (Achilles) reflex: S1-2 ● Basal ganglia tremor: resting tremor
-Nerve roots responsible for these stretch reflexes that ● Cerebellar tremor: action tremor
can aid in lesion localization ● Involuntary movements can be observed as child walks or
executes some movements
XI.SUPERFICIAL REFLEXES ● Assess rapid alternating movement, tandem
● Plantar reflex (S1) gait, fine finger movement
● Conjunctival reflex (afferent loop-CN V; efferent loop-CN IV, ● take note of involuntary movements and
VI, VII) tremors
● Superficial abdominal reflexes (T8-9, T11-12- near the ● important in maintaining muscle tone
umbilicus, stroke the skin in the abdomen, from the side to the
abdomen. Normal response: contraction of ipsilateral muscles XIV. NEWBORN REFLEXES
● Cremasteric reflex (L1-2) ● Hypoactive reflexes: lower motor neuron or cerebellar
dysfunction
XII.MILESTONE GUIDELINES: MOTOR ● Hyperactive reflexes: upper motor neuron
1. GROSS MOTOR ● The younger the child, the less the informative the deep
tendon reflexes
Table 7: Gross Motor Developmental Milestone ● Reflex inequalities are common and less reliable than
Function Expected Age Referral inequalities of muscle tone in terms of ascertaining presence
Head control 2 months 4 months of an UMN lesion
Sitting 6 months 8 months ● Routine: biceps, triceps, brachioradialis, patellar, ankle jerks
Crawling 9 months 12 months ● Patellar reflex is accompanied by adduction of the opposite
Walking 12 months 18 months thigh- known as crossed adductor reflex
o disappears by 9 to 12 months, normal in newborn up
2. MOTOR EXAM: Nerve supply of muscles to 8 months (UMN dysfunction of +)
● Anal reflex (contraction of anal sphincter upon irritation of
Table 8: Nerve Supply and innervation in the Upper anal skin): present at birth and should be elicited if spinal cord
Extremities lesion is suspected
Muscle Spinal Nerve Innervation ● Sustained clonus suggests a pyramidal tract lesion
Deltoid C5-6 Axillary ● newborn clonus is abnormal if sustained. if 2-3
Triceps C6-8 Radial beats of clonus are observed, it might be
normal especially in newborns
Biceps C5-6 Musculocutaneous
● ankle clonus beyond 5-7 beats is normal
Supination C5-7 Radial (post cord)
Pronation C6-7 Median (lateral cord) PRIMITIVE REFLEXES
Wrist Flexion C6-7 Median ● Primitive reflexes appear and disappear at specific times
Wrist Extension C7-8 Radial during development, and their absence or persistence
Interossei C8-T1 Ulnar (med cord) beyond those times signifies CNS dysfunction
Hand extension C6-T1 Radial
MORO REFLEX
3. MOTOR SYSTEM

Table 9. Nerve Supply and innervation in the Lower

Extremities
Muscle Spinal Nerve Innervation
Iliopsoas L1-3 Femoral
Quadriceps L2-4 Femoral
Adduction, thigh L2-3 Obturator
Abduction, thigh L4-S1 Superior gluteal
Hamstring L4-S2 Sciatic (trunk)
Tibialis anterior L4-5 Deep peroneal
Gastrocnemius L5-S2 Tibial Figure 28: Moro Reflex
Tibialis posterior L5-S1 Tibial

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 First appears between 28-32 weeks of gestation, present  Reappears in frontal lobe dysfunction (in adults,
in all newborns usually seen in those with severe dementia or
 Absent in very small prematures and in depressed Alzheimer’s)
newborns
 Fades out between 3 to 5 months RIGHTING REFLEX
 This reflex is elicited by supporting the infant in a semi-
erect position and then allowing the infant’s head to fall
backwards onto the examiner’s hand.
 normal response: symmetric extension and abduction of
the fingers and upper extremities, followed by flexion of
the upper extremities and audible cry
 Abnormal response:
o Asymmetric response that can signify a
fractured clavicle, brachial plexus injury, or
hemiparesis.
o Absence suggests significant dysfunction of the
CNS.
o Persistence beyond 6 months is abnormal
Figure 31: Righting reflex
TONIC NECK REFLEX
 Correction of the body whenever it is taken out of
position
 Infant supine, turn head to one side, infant rotates the
shoulder to same direction, followed by the trunk, and
finally the pelvis
 Obligatory (shoulder, trunk and pelvis rotate
simultaneously, like rolling a log) is always abnormal
 Delay in its appearance and asymmetries is significant
indicating neurologic dysfunction

PALMAR AND PLANTAR GRASP REFLEX

Figure 29: Tonic Neck Reflex

 Present at birth, but usually begin to emerge by the 1st

week, fully well developed by 1 month
 Disappears by 6 months, persistence beyond is
abnormal
 Produced by laying the patient flat and manually rotating
the infant’s head to one side
 Normal response: observing for the characteristic
fencing posture (extension of one arm on the side to
which the face is rotated and flexion of the contralateral
arm) “fencing-like” posture Figure 32: Palmar reflex
 Abnormal response: An obligatory tonic neck response
(infant is “stuck” in fencing posture) implies a CNS  Pressure on the palm or sole
disorder  Plantar is weaker than palmar
 Obligatory is abnormal irrespective of age  appears by 28-32 weeks of gestation, becomes weak
and wanes by 5-6 months (replaced by voluntary activity)
SUCKING AND ROOTING REFLEX  By 37 weeks of gestation, the reflex is strong enough that
the examiner can lift the infant from the bed with gentle
tractions
 Persistence beyond 6 months is abnormal

BABINSKI REFLEX

Figure 30: Sucking and Rooting Reflex

 Automatically turning the face towards the stimulus and

make sucking (rooting) motions with the mouth when the
cheek or lips is touched
 Starts at 28 weeks and persist till 3 months, replaced by
voluntary sucking/rooting Figure 33: Babinski Reflex
 Absent in depressed or septic babies
 Persistent in CP or in neurodegenerative disorders

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 Characterized by extension of the great toe and fanning o Jerky ocular pursuit (eyes are moving sideways or
of the remaining toes; it indicates an UMN lesion back and forth)
 Babinski response useful only in older kids o Motor impersistence (inability to sustain a
 May be present normally up to 2 ½ year old children movement)
 Modifications o Reflex asymmetry (in deep tendon reflexes)
o Oppenheim (stroking the shin) o Gross and fine motor incoordination
o Gordon (squeezing calf muscles) o Right/Left disorientation (unable to tell which is left
o Chaddock (stroking lateral malleolus) or right)
o Gonda (flicking one of the toes, usually the o Inability to distinguish double tactile stimulation
little) o synkinesia (disappear by 9 years) - involuntary
o Bing (poking a relatively sharp object on the movement accompanying a voluntary one
dorsum of the big toe)
XVII. MILESTONE GUIDELINES: SOCIAL AND BEHAVIOR
DEVELOPMENTAL REFLEXES
BUTTRESS RESPONSE Fine Motor/ Social
 Infant in sitting position: displace center of gravity with a Function Expected age Referral
gentle push on one shoulder - infant extends the Smiling 6 weeks 3-4 months
contralateral arm and spreads the fingers Reaching 4 months 5-6 months
 Normally appears by 5 months
Transfer 6 months 8 months
 Delay in its appearance and asymmetries is significant
indicating neurologic dysfunction Pincer 8 months >12 months
* pincer: if the infant is an 11 month old child, still drags the object
PARACHUTE RESPONSE before picking it up, it may be sign of delay.

Common Patterns of behavior necessitating referral if

persistent
Behavior Emerges Disappears Referral
Hand regard 12 weeks 6 months 6 months
Mouthing birth 13 months 18 months
Casting 12 months 18 months 20 months

Figure 34: Parachute response MODE OF PRESENTATION OF DEVELOPMENTAL DELAYS

● First months: Poor suck, hypotonia, or hypertonia, lack
 Child suspended horizontally (around the waist, face of visual tracking or poor auditory response to name
down),infant suddenly projected toward the floor; calling or sound
● Through 18 months: Motor delays (gross and
 Normal response: consequent extension of the arms
fine/adaptive)
and spreading of fingers ← automatic response ● ≥2 years: Speech delay and aberrant behavior
 Emerges after 6 months, well-developed by 8-10 months, ● School-age: Academic underachievement and ADHD
 Abnormal if not expressed by 1 year or if asymmetric symptomatology
 The reason why you want to do this is you want to pick
up any trace asymmetry in the response; to check if there XVIII. MILESTONE GUIDELINES: LANGUAGE
is pain, weakness, or any disability
Average age Observed behavior
XV. AUTONOMIC FUNCTIONS (months)
 As far as the autonomic functions are concerned, the 6-10 canonical babble (dada, mama)
CNS also involves this system, with problems such as:
9-10 word comprehension
o dysreflexia
o Salivation 12-13 word production
o Lacrimation 18 vocabulary
o Sweat pattern 20 word combination
o Skin color and temperature
o Bowel and bladder symptoms 24-36 grammatization (>3 word phrases)
 Vital signs: may go haywire due to sympathetic
dysfunction Early signs of impairment: Language Development
 Horner’s syndrome: miosis, ptosis, anhydrosis, Average age Observed behavior
enopthalmos (months)
11-12 no giving, showing or pointing
XVI. SOFT NEUROLOGICAL SIGNS 18 comprehends <60 words; produced <5
 Red flags words
 Non-localizable and age-dependent 24 produced no 2-word phrase
 Cut-off age for most is at 6 years
 Persistence is generally considered abnormal XIX. CONCLUSION
 The most common are the following: ● Neurological assessment involves detailed history,
o Choreiform movements (abnormal jerky complete physical examination, complete neurological
movements of the hands or the feet) = Often seen in examination and conjunction with developmental
Sydenham’s Chorea patients with Rheumatic screening this allows you to make an early identification
Fever and early implementation of management

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● Developmental screening should be performed as part of Answer key: D, C, D, C, T, C, B, C, B, B, A
health maintenance visits
● Early identification of neurological and developmental
disorders is crucial to the management
● With early implementation of appropriate intervention, the
chances of a better outcome are greatly increased with
children attaining their maximum potential.

XX. REFERENCES
1. Dr. Rivera’s powerpoint slides
2. Navarro’s Fundamentals of Pediatrics
3. Audio recordings
4. 2019 ABC
XXI. QUIZ
1. Which of the following symptoms suggest a neurologic
disorder?
a. Cafe au lait spots
b. Hypopigmentation
c. Port wine stain
d. All of the above
2. Sun-setting eyes can be seen in patients with:
a. Neurofibromatosis I
b. Neurofibromatosis II
c. Hydrocephalus
d. Systemic Lupus Erythematosus
3. A facial capillary malformation that is seen in patients
with Sturge Weber Syndrome
a. Vitiligo
b. Macular Rash
c. Café-au-lait spots
d. Port-wine stain
4. Pathognomonic of shaken infant syndrome
a. Papilledema
b. Cataract
c. Retina Hemorrhage
d. All of the above
5. T/F: Myasthenia gravis causes Unilateral Ptosis
6. For cerebellar testing, the tandem gait is expected to be
well performed by what age?
a. 2 years
b. 5 ½ years
c. 6 years
d. 7 years
7. Large newborn baby, NSD, vaginal delivery, + complication
of shoulder dystocia on the Upper left limb. Most appropriate
maneuver to evaluate the problem is?
a. elicit parachute reflex
b. elicit moro reflex
c. elicit tonic neck reflex
8. New onset progressive gait ataxia over a period of 1 months
in a previously healthy 3yo is most like due to:
a. sensory disorder
b. cerebellar disturbances
c. cerebellar tumor
9. Sucking and rooting reflex is seen in infants as young as:
a. 25 weeks old
b. 28 weeks old
c. 30 weeks old
d. 32 weeks old
10. Head control should be established by:
a. 3 months
b. 4 months
c. 6 months
d. 7 months
11. 9 yo with waddling gait, pseudo-hypertrophy of the calf
muscles and difficulty standing up from a sitting position most
likely has:
a. DMD
b. peripheral hemiplegia
c. cerebral palsy

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