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Detailed neurologic assessment of infants and children
AUTHORS: Suresh Kotagal, MD, Anne Marie Morse, DO
SECTION EDITOR: Douglas R Nordli, Jr, MD
DEPUTY EDITOR: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2023.
This topic last updated: Aug 03, 2022.
INTRODUCTION
Infants and children who present with or who are found to have neurologic or neuromuscular
abnormalities on a general physical examination should undergo a complete neurologic
assessment [1,2]. The elements of a complete neurologic assessment are:
●
Focused clinical history
●
Detailed neurologic examination
●
Additional parts of the general physical examination that are relevant to child neurology
In some cases, developmental screening tests are also helpful.
These steps are detailed in this topic review. The neurologic assessments of neonates and
adults are discussed separately. (See "Neurologic examination of the newborn" and "The
detailed neurologic examination in adults".)
THE CASE HISTORY
The objectives of taking a clinical history are to establish rapport and trust with the child and
family, understand the nature of their health concerns regardless of whether or not they
pertain to the nervous system, and anatomically localize the neurologic symptoms. A skilled
clinician is often able to arrive at a diagnosis by the time a complete history has been taken and
uses the examination to confirm the diagnosis and determine the extent of impairment.
History of present illness — The clinician should attempt to fully characterize the patient's
symptoms, including:
●
The duration of symptoms.
●
Whether symptoms are constant or episodic (episodic symptoms are characteristic of
transient ischemic attack, syncope, seizure, or migraine).
●
Whether symptoms are static, progressive, or resolving.
●
Whether there is a pattern that suggests localization to a specific anatomic region. As
examples:
• Involvement of the cerebral cortex should be suspected in patients with cognitive
dysfunction and/or seizures
• Involvement of the brainstem may be accompanied by double vision, dizziness,
dysphagia, hoarseness of voice, or impaired equilibrium
• Cerebellar disorders may be associated with altered equilibrium and coordination in
the trunk or extremities
• Disorders of the spinal cord may result in dissociation of motor and sensory function
below a certain altitudinal plane and/or bowel and bladder dysfunction
• Disorders of the motor unit (anterior horn cells, peripheral nerve, neuromuscular
junction, muscle) should be suspected in patients with weakness manifested by
inability to climb stairs, raise the arms, grasp, stand, or walk
●
Whether and to what extent the child's cognition, behavior, and language are impacted
and whether these symptoms represent developmental delay or regression.
●
Whether activities of daily living have been compromised.
●
Whether rehabilitative measures have been put in place and the specific types.
It is a common practice to inquire about activities a child cannot carry out or finds challenging.
However, it is equally important to ask about activities that the patient can do and enjoy
because these skills can be targeted for further development.
Medications — The clinician should note:
●
Current medications, nutritional supplements, and alternative therapies, including:
• Indication
• Form of the medication (capsule, tablet, suspension)
• Strength in milligrams/grams
• Route of administration
• Frequency
●
Past medications and reason for discontinuation
●
Response to current and past medications
Allergy history — Allergies to medications and the nature of the allergic reaction should be
recorded. This information may inform the choice of therapies.
Family history — Many childhood neurologic disorders are inherited. Thus, the clinician should
inquire about the health status of all first-degree relatives (parents, siblings) and whether there
is a family history of neurologic conditions, systemic disorders, or consanguinity. If other family
members have neurologic disease, a pedigree chart is often helpful.
Social history — Housing status, including the age of the home and possible lead exposure,
can be relevant to neurodevelopmental status.
Clinicians should also inquire about any safety or vulnerability concerns, including whether child
and youth services have been involved for either the patient or other children in the home,
especially if there are any concerns for nonaccidental trauma or neglect contributing to
symptoms.
Pregnancy, perinatal, and neonatal history
●
Prenatal history – The prenatal history should include the following elements:
• Mother's age at the time of pregnancy
• History of mother's previous pregnancies (gravida, para, miscarriages, and gestational
age at the time of miscarriages), including history of preterm labor or delivery and
reason
• Review of all maternal laboratory and other testing, if available, including fetal
deoxyribonucleic acid (DNA) or any other genetic testing if done
• Prenatal exposure to prescription and illicit drugs, alcohol, radiation, and infections and
the fetus's gestational age at the time of exposure
• Amount of maternal weight gain during the pregnancy; both inadequate and excessive
weight gain increase the risk of pregnancy complications and adverse outcomes in the
fetus (see "Gestational weight gain")
• Exposure to systemic illnesses or infections that could affect the developing fetal brain
(eg, cytomegalovirus, Zika virus, and other TORCH infections) (see "Overview of TORCH
infections")
• Whether fetal movements were reduced (as seen in infantile spinal muscular atrophy)
or exaggerated (as seen in intrauterine seizures associated with pyridoxine
dependency)
• Results of prenatal head ultrasound studies
●
Labor and delivery – The labor and delivery history should include the following:
• Gestational age at the time of onset of labor and whether labor was spontaneous,
induced, or caesarean, and indication if induced or caesarean
• Fetal presentation, length of the labor, and whether vacuum or forceps extraction was
used
• The infant's weight, length, and head circumference at birth
• Apgar scores at 1, 5, and 10 minutes (see "Overview of the routine management of the
healthy newborn infant", section on 'Apgar score')
• Whether the infant needed resuscitation
• Whether the infant required neonatal intensive care and, if so, for how long and
whether there were any complications
●
Newborn period – Significant events in the first few weeks of life include the need for
neonatal intensive care and, if so, whether the infant required ventilatory support, oxygen
therapy, vasopressor therapy, resuscitation medications, exchange transfusion, or
extracorporeal membrane oxygenation. In addition, it is important to inquire about
seizures in the neonatal period and other signs of neonatal encephalopathy and/or use of
therapeutic hypothermia. Poor feeding, impaired sucking and swallowing, and sleep-wake
difficulties in the first month of life may be subtle markers of brain dysfunction. If cranial
ultrasounds and/or other neuroimaging studies were performed during the neonatal
period, the results should be reviewed. Results of newborn screening also should be
reviewed. (See "Newborn screening".)
Some of the factors listed above are risk factors for cerebral palsy, which is discussed in greater
detail in a separate topic review. (See "Cerebral palsy: Epidemiology, etiology, and prevention".)
Developmental history — The clinician should record the child's age at acquisition of
developmental milestones, such as social smiling, developing adequate head control, gurgling,
reaching out for objects, rolling over, being able to maintain a sitting position, coming to a
sitting position independently, crawling, walking independently, babbling, and using first words,
phrases, and sentences (
table 1) [3].
Some parents and caregivers are unable to recall the exact age at which these milestones were
achieved. They may, however, have a good recollection of events surrounding the child's first
birthday; thus, one can help jog their memory by asking about the child's abilities at that time,
for instance, "Did this happen by the first birthday?" The examiner should be aware that in
neurodegenerative disorders, a plateau in development may precede the start of
developmental regression.
Early identification of children with autism spectrum disorders is accomplished through routine
developmental surveillance at well-child visits, with additional developmental screening tests at
specific visits or when developmental concerns are raised [4]. This is discussed separately. (See
"Autism spectrum disorder in children and adolescents: Surveillance and screening in primary
care".)
Review of other systems — The clinician should inquire about underlying medical conditions,
some of which may have neurologic symptoms. If any disorder is present, the clinician should
document the symptoms, treatment, and status of these disorders (ie, resolving, static, or
deteriorating).
Many regions require comprehensive newborn screening. An inquiry into the results of the
newborn screen is important. Although screening programs are designed for high sensitivity,
false-negative results may occur, particularly in premature or medically complicated infants.
Some forms of congenital hypothyroidism are not consistently captured by newborn screening,
so testing should be repeated if there is a clinical suspicion for this disorder. (See "Newborn
screening" and "Clinical features and detection of congenital hypothyroidism", section on
'Newborn screening'.)
Infants and children with cerebral palsy often have a variety of problems attributable to their
neurologic dysfunction, including dysphagia, gastroesophageal reflux, chronic constipation,
respiratory difficulties, chronic aspiration into the tracheobronchial tree, sleep initiation and
maintenance problems, impaired ambulation, scoliosis, deformities around joints of the
extremities, and strabismus. In such children, the clinical history should include review of their
current management. (See "Cerebral palsy: Classification and clinical features", section on
'Associated conditions'.)
NEUROLOGIC EXAMINATION
General concepts — The examination begins with observation of the child during the visit,
even before starting the examination. This observation can provide insight into the
spontaneous ability of the child and can guide prioritizing certain components of the
examination if the child becomes less compliant with hands-on examination. When examining
toddlers, the initial phase of inspection is best conducted while the child is seated in the
parent's lap. This minimizes apprehension, which tends to alter the assessment of higher
cortical functions, muscle tone, and tendon reflexes. It is also advisable to defer uncomfortable
and anxiety-provoking procedures until the end of the session, such as otoscopy and checking
of the gag reflex.
A collection of videos depicting elements of the neurologic examination in infants and children
can be viewed on the
Pediatric NeuroLogic Exam website [5].
Higher cortical functions — Observations of infants and toddlers during play (eg, while
stacking blocks or playing with an age-appropriate toy) can provide valuable information about
the patient's attention span, gross and fine motor coordination, and problem-solving abilities. It
allows the clinician to evaluate the higher cortical functions, and it provides clues to specific
learning difficulties, attention deficit hyperactivity disorder, and mild developmental delays
(
table 2). Joint attention, which requires eye contact with the parent or caretaker and making
nonverbal or verbal affectual responses from the infant, develops by the age of nine months.
The lack of development of joint attention may be an early clue to autism [6]. (See "Autism
spectrum disorder in children and adolescents: Clinical features", section on 'Impaired social
communication and interaction'.)
Cranial nerves — Each cranial nerve (CN) is tested by performance of a specific motor or
sensory test. Testing in infants is often by observation for specific movements and responses
and is less reliable. Multiple observation sessions may be helpful.
I (olfactory) — The sense of smell, mediated by CN I, can be tested by ability to detect alcohol
or peppermint. This sense may be impaired after closed head injury and in infants with
arhinencephaly-holoprosencephaly.
II (optic) — The function of CN II is assessed by the following tests of visual function:
●
Testing visual acuity – In an infant, visual acuity can be tested by observing the infant
reach for objects of varying size. Infants older than six months of age will usually reach for
scraps of paper less than 5 mm in size when they are placed on a dark background.
Standard tests can be used in older children who can recognize objects, letters, or
numbers. The narrow, alternating black and white stripes painted onto a rotating drum
should elicit optokinetic nystagmus (OKN), with quick jerks of the eyes in a direction
opposite to the movement of the drum or tape. (See "Vision screening and assessment in
infants and children", section on 'Children three years and older'.)
●
Visual fields – Visual fields can be tested by introducing objects into the peripheral field of
vision as the child focuses on an object held directly in front of them. The lateral and
superior fields of vision can be assessed more easily than can the nasal fields. (See "The
pediatric physical examination: HEENT", section on 'Vision'.)
●
Pupillary light response (direct and consensual) – A normal pupillary light reflex
requires CN II for afferent impulses and III for efferent impulses. An asymmetric,
constricted pupil in association with ptosis, enophthalmos, and anhidrosis is seen with
ipsilateral Horner syndrome as a result of sympathetic denervation of the pupil. (See
"Horner syndrome".)
●
Funduscopy – Funduscopy of children requires patience and is best accomplished in a
dimly lit room with the patient gazing straight ahead. The parent or caretaker can be
requested to keep a bright object in the hand, upon which the child is asked to focus. The
ability of the clinician to obtain an adequate funduscopic examination is often
compromised by lack of patient cooperation, nystagmus, or small pupils. In this case,
consultation should be sought with an ophthalmologist.
• A whitish opacity within the pupillary aperture is suspicious for a cataract. Etiologies
may include an inherited tendency, congenital intrauterine infections, or metabolic
disorders. Cataracts can obscure vision and require referral to an ophthalmologist.
• The optic disc is normally pink in complexion (
suggest atrophy (
picture 1). Optic disc pallor may
picture 2). (See "Congenital and acquired abnormalities of the optic
nerve", section on 'Atrophy'.)
• Hypoplasia of the optic disc (normal complexion but small size) may accompany septooptic dysplasia, which can be associated with hypothalamic insufficiency and
hypopituitarism. (See "Congenital and acquired abnormalities of the optic nerve",
section on 'Hypoplasia'.)
• Blurring of the optic disc margins along with loss of the optic disc cup and venous
pulsations are seen in papilledema (
picture 3). Approximately 30 percent of subjects
lack venous pulsations even in the absence papilledema. (See "Congenital and acquired
abnormalities of the optic nerve", section on 'Papilledema'.)
• A "cherry red" macular spot (
picture 4) is seen in lysosomal storage disorders, such
as Tay-Sachs disease and Niemann-Pick disease. (See "Preconception and prenatal
carrier screening for genetic disorders more common in people of Ashkenazi Jewish
descent and others with a family history of these disorders", section on 'Tay-Sachs
disease' and "Overview of Niemann-Pick disease".)
• Chorioretinitis, which sometimes appears like "pepper sprinkled on a red table cloth,"
can accompany congenital cytomegalovirus infections. (See "Congenital
cytomegalovirus infection: Clinical features and diagnosis".)
• Flame-shaped retinal hemorrhages (
picture 5) may accompany abusive head trauma
(nonaccidental trauma). (See "Child abuse: Epidemiology, mechanisms, and types of
abusive head trauma in infants and children", section on 'Retinal hemorrhages'.)
• Retinal degeneration may accompany mitochondrial disorders such as the syndrome of
neurologic muscle weakness, ataxia, and retinitis pigmentosa (NARP). (See
"Mitochondrial myopathies: Clinical features and diagnosis", section on 'NARP'.)
III (oculomotor), IV (trochlear), and VI (abducens) — CN III, IV, and VI are required for
extraocular movements in the horizontal, vertical, and oblique planes and can be tested by
assessing the child's ability to track a brightly colored toy or soft light.
The corneal light reflex is a helpful test to determine eye alignment (strabismus or esotropia).
When a light source is held directly in front of a patient who is staring straight ahead, normal
eye alignment will reveal a symmetric reflex in the center of each pupil (
figure 1).
Paralysis of extraocular muscles leads to eye deviation at rest [2] in the following patterns:
●
Deviation down and out – Paralysis of the inferior oblique muscle (CN III) (see "Third
cranial nerve (oculomotor nerve) palsy in children")
●
Deviation laterally – Paralysis of the medial rectus (CN III)
●
Deviation upwards – Paralysis of the inferior rectus (CN III)
●
Deviation down and inwards – Paralysis of the superior rectus (CN III)
●
Deviation upwards and out – Paralysis of the superior oblique (CN IV) (see "Fourth cranial
nerve (trochlear nerve) palsy")
●
Deviation inwards – Paralysis of the lateral rectus (CN VI) (see "Sixth cranial nerve
(abducens nerve) palsy", section on 'Clinical manifestations')
Ptosis (drooping of the upper eyelid and encroachment on the pupillary aperture) may
accompany sympathetic paralysis from lesions of the CN III, Horner syndrome, myopathies,
myasthenia gravis, and eye structural lesions (eg, neurofibroma). (See "Overview of ptosis".)
OKN is a normal gaze-stabilizing response elicited by tracking a moving stimulus across the
visual field and can be helpful as a crude assessment of the visual system. Assessment of OKN
can be performed using an OKN drum or a piece of paper or cloth with alternating black (or red)
and white stripes that is rapidly moved across the patient's visual field at reading distance. As
the stimulus is moved from left to right, normally sighted patients will show quick, jerky
movements to the left side and vice versa. Alternatively, a mirror placed in front of the patient's
eyes can be tilted in different directions to elicit ocular pursuit movements. OKN is dependent
upon the integrity of the visual system, especially visual perception, and pursuit and saccadic
eye movement [7,8]. Bilateral absence of OKN in infancy or early childhood may suggest
blindness, while unilateral absence may suggest a hemispheric lesion. Normal OKN in an
individual with a complaint of vision loss suggests hysterical blindness. (See "Vision screening
and assessment in infants and children" and "Approach to the pediatric patient with acute vision
change", section on 'Conversion disorder'.)
Abnormal eye movements may be manifestations of an underlying disease or disorder:
●
Opsoclonus is characterized by sudden chaotic bursts of eye movements in the horizontal,
vertical, oblique, or rotatory positions, often associated with myoclonus. It is a
paraneoplastic manifestation of neuroblastoma and has also been described in other
settings. (See "Clinical presentation, diagnosis, and staging evaluation of neuroblastoma",
section on 'Opsoclonus myoclonus'.)
●
Upgaze paresis may accompany Parinaud syndrome owing to pressure on the pretectal
region from a mass lesion. Impaired downgaze may be seen in children with Niemann-Pick
type C disease and can lead to difficulty going down steps. (See "Ocular gaze disorders"
and "Overview of Niemann-Pick disease".)
●
Oculomotor apraxia is characterized by a delayed initiation of the eye movement and jerky
pursuit movements that are accompanied by compensatory head thrusting. It may
accompany Joubert syndrome or ataxia with oculomotor apraxia syndrome. (See "Clinical
manifestations, diagnosis, and treatment of nephronophthisis", section on 'Joubert
syndrome' and "Overview of chorea", section on 'Ataxia with oculomotor apraxia'.)
V (trigeminal) — The sensory function of CN V can be tested by the response to light touch
over the face (use a tissue) and by sensation on the cornea and conjunctiva (see 'Superficial
reflexes' below).
Motor function of CN V is tested by assessing masseter muscle strength (asking the child to
clench their jaw while palpating for muscle contraction).
VII (facial) — The function of CN VII can be assessed by observing for symmetry of the
nasolabial folds, assessing eyelid muscle strength, and assessing the ability to wrinkle the
forehead symmetrically. In addition, CN VII mediates taste sensation over the anterior twothirds of the tongue and can be tested by applying two or three drops of a concentrated salt
solution to the lateral edge of each one-half of the tongue using a cotton applicator, while the
tongue is kept protruded.
With nuclear and infranuclear lesions of CN VII, both the upper and lower one-halves of the face
are paralyzed, whereas with supranuclear lesions, only the lower one-half of the face is affected.
(See "Facial nerve palsy in children".)
VIII (vestibulocochlear) — In infants, hearing is tested by making a soft sound close to one
ear, such as from rustling of paper. The infant should show an alerting response. By the age of
five to six months, the infant may also be able to localize the sound to a specific quadrant. The
procedure is then repeated for the opposite ear. In cooperative school-age children, speech
discrimination can be tested by softly whispering a number approximately one foot from the
ear. The traditional Rinne and Weber tests can be used as well in older children. (See "Hearing
loss in children: Screening and evaluation", section on 'Simple hearing tests'.)
Poor head control, truncal unsteadiness, gait ataxia, nausea, vomiting, and horizontal
nystagmus may indicate vestibular system dysfunction.
IX (glossopharyngeal) and X (vagus) — CN IX and CN X are responsible for swallowing
function and movement of the soft palate and are often tested by eliciting a gag reflex. Salivary
drooling or pooling of saliva also suggest dysfunction. Hoarseness of the voice can be caused
by CN X dysfunction.
XI (spinal accessory) — CN XI mediates motor function in the trapezius or sternomastoids; its
function is usually assessed by elevation of the shoulders and turning of the neck against
resistance. The pattern of weakness caused by CN IX dysfunction depends on whether the
lesion is peripheral or central.
XII (hypoglossal) — Function of CN XII in a child or adolescent is tested by asking the patient
to stick out their tongue; normally, the tongue should remain in the midline. In patients with
peripheral lesions of CN XII, the tongue points towards the paretic side. CN XII dysfunction can
also cause fasciculations (slow, ripple-like movements) in the tongue and oromotor apraxia.
Fasciculations are best observed with the mouth open and with the tongue kept immobile
within the mouth.
Motor system
Posture and involuntary movements — Abnormalities are suggested by the following
observations:
●
Asymmetry at rest in infants (may suggest hemiparesis). (See "Cerebral palsy:
Classification and clinical features", section on 'Spastic hemiplegia'.)
●
Opisthotonus (ie, persistent arching of the neck and trunk due to bilateral cerebral cortical
dysfunction). (See "Neurologic examination of the newborn", section on 'Hypertonia'.)
●
Abducted hips or "frog-legged" posture that accompanies hypotonia. (See "Neurologic
examination of the newborn", section on 'Hypotonia'.)
●
Fisting of the hand or holding the thumb adducted across the palm during quiet
wakefulness (suggests corticospinal tract involvement). However, closure of the hand
during sleep is normal.
●
Tremor (rhythmic, fine-amplitude flexion-extension movements of the distal extremity).
●
Myoclonus (quick, nonstereotyped jerks around a segment of the body). (See "Hyperkinetic
movement disorders in children", section on 'Myoclonus'.)
●
Athetosis (slow, sinuous movement of the distal extremity with pronation of the distal
extremity, generally due to a contralateral putaminal lesion). (See "Hyperkinetic movement
disorders in children", section on 'Chorea, athetosis, and ballismus'.)
●
Chorea (rapid, quasi-purposive, nonstereotyped movements of a segment of the body that
is generally proximal). (See "Hyperkinetic movement disorders in children", section on
'Chorea, athetosis, and ballismus'.)
●
Tics (highly stereotyped and repetitive movements). (See "Nonepileptic paroxysmal
disorders in children", section on 'Tics and stereotypies'.)
●
Muscle atrophy, pseudohypertrophy (bulky appearance of muscles due to fat
accumulation, with associated muscle fiber atrophy and weakness) is commonly seen in
muscular dystrophies such as Duchenne. Fasciculations (ripple-like movements of the
muscles that accompany degeneration of anterior horn cells) are commonly seen in motor
neuron diseases. (See "Duchenne and Becker muscular dystrophy: Clinical features and
diagnosis" and "Etiology and evaluation of the child with weakness", section on 'Muscle
examination'.)
●
Stereotyped hand-wringing movements and bruxism (teeth grinding) may be seen in Rett
syndrome.
●
Stereotypies are repetitive movements and/or sounds. These may include simple
movements, such as body-rocking or head-nodding, or more complex movements, such as
hand-flapping or pacing; these may be more common in children with autism spectrum
disorder. (See "Autism spectrum disorder in children and adolescents: Surveillance and
screening in primary care".)
Tone and strength — Muscle tone is the resistance felt upon passive movement of a part of
the body. In the extremities, it is assessed by placing a joint through its full range of
movement. Hypotonia is characterized by decreased resistance to passive movement and
hyperextension at the joints. Increased tone that is spastic in nature (abnormal lengtheningshortening reaction to stretch that has the feel of a "clasp knife") tends to accompany pyramidal
tract lesions. Increased tone that is characterized by muscle rigidity (has a "lead pipe" or "cog
wheel" feel during the range of motion) suggests extrapyramidal lesions. Paratonia (also known
as gegenhalten) is a form of hypertonia that is characterized by the involuntary resistance to
passive movement. Although it is more often elicited in older adults with dementia, it also can
occur in children with developmental disabilities, dyspraxia, and learning disabilities and may
be incorrectly attributed to the child not complying with the examination.
Weakness is elicited by asking the patient to move a part of the body against resistance (gravity
or gravity plus resistance imposed by the examiner). The degree of weakness is graded in a fivepoint scale:
●
Grade 0/5 – No muscle movement at all
●
Grade 1/5 – Presence of a flicker of movement
●
Grade 2/5 – Movement with gravity eliminated (eg, across the bedsheet)
●
Grade 3/5 – Movement against gravity
●
Grade 4/5 – Movement against gravity and some externally applied resistance
●
Grade 5/5 – Movement against gravity and good external resistance (normal)
Distal weakness (symmetric or asymmetric) generally accompanies peripheral neuropathy,
while proximal muscle weakness (generally symmetric) is seen in myopathies. Hereditary
neuropathies such as Charcot-Marie-Tooth disease are associated with prominent, high arches
in the feet due to atrophy of the plantar muscles. (See "Charcot-Marie-Tooth disease: Genetics,
clinical features, and diagnosis".)
Patients with proximal (hip extensor) muscle weakness may exhibit a Gower's sign (ie, they will
prop their hands against the floor or their legs for support when getting up from a sitting
position on the floor).
Assessment for the pronator drift is a useful method of detecting upper motor neuron
weakness [9]. Initially, the child is asked to extend the upper extremities with palms down. The
child is then asked to close the eyes and rotate the extended arms so that the palms are facing
upwards. During this turning maneuver with the eyes closed, a patient with upper motor
neuron weakness may pull the elbow down and in. If in the response there is an upward and
outward drift, a contralateral parietal lesion or a cerebellar process could be responsible.
Coordination — Patients with cerebellar dysfunction have difficulty in regulating the rate and
range of muscle contraction (known as dysmetria), which may manifest as nystagmus, intention
tremor, scanning speech, truncal or gait ataxia, or rebound phenomenon. To test for rebound
phenomenon, the patient flexes the arm against resistance offered by the examiner, then the
examiner abruptly releases the resistance. In rebound phenomenon, the patient is unable to
stop the muscle contraction.
Dysmetria can be assessed with the finger-to-nose test: When seated with the elbows fully
extended and the arms in a horizontal plane, the patient is asked to touch the index finger to
the nose and then return to the starting position. In a young child, use of a toy to reach for may
be a helpful surrogate. Cerebellar deficits will impair performance on this test.
Sensory system — A sensory examination in young children is often imprecise, and only gross
deficits can be detected. Information obtained from sensory testing in a child below five to six
years of age can be unreliable and may need confirmation during a second examination
session.
In children older than five to six years, sensory function is evaluated in the same manner as in
an adult, as discussed in a separate topic review. (See "The detailed neurologic examination in
adults".)
Tendon reflexes — The jaw, biceps, triceps, brachioradialis, patellar, and ankle are commonly
tested tendon reflexes, and all of these can usually be tested in infants and children. The joint
under consideration should be at approximately 90° and fully relaxed. In patients with cerebral
palsy, exhortations to "relax" may paradoxically increase contraction of the muscles and should
thus be avoided. Instead, the patient should be put at ease during reflex testing with
conversation.
To elicit the reflex, let the head of the reflex hammer drop onto the tendon at the following
locations:
●
Jaw – With the mouth held partially open and examiner's finger placed over the chin, the
finger is lightly tapped with a reflex hammer to displace the mandible downwards. This
elicits contraction of the mandible and slight closure of the mouth.
●
Biceps – Just anterior to the elbow.
●
Triceps – Just posterior to the elbow.
●
Brachioradialis – Just above the wrist, on the radial aspect of the forearm.
●
Knee (patellar) – Just below the patella.
●
Ankle (Achilles) – Just behind the ankle.
The elicitation of tendon reflexes provides information about multiple aspects of the nervous
system. Findings can be interpreted as follows:
●
Absent or diminished tendon reflexes – This generally indicates interruption of the muscle
stretch reflex arc at the level. Since the afferent impulses generated after tapping a tendon
with reflex hammer are carried via large-diameter fibers, the absence of a tendon reflex
could also signify involvement of large-diameter sensory fibers in a peripheral nerve.
●
Exaggerated tendon reflexes – This generally indicates disinhibition of the motor units,
owing to a pyramidal tract lesion. When the patellar reflex (knee jerk) is elicited, an
exaggerated (ie, abnormal) response includes spread to the opposite side in the form of a
crossed adductor response (contraction of the contralateral hip muscle) or ipsilateral
contraction of the plantar, flexures of the foot. Similarly, clonus (rhythmic muscle
contractions elicited by the stimulus) is exaggerated and abnormal.
●
Asymmetric tendon reflexes – This may indicate a cerebral hemispheric lesion. Asymmetry
is most easily detected with a gentle stimulus.
●
Differences between tendon reflexes in the upper and lower body – This may suggest a
spinal cord lesion. As an example, the jaw jerk is the only tendon reflex that is mediated
above the plane of the foramen magnum; thus, if the jaw jerk is of normal amplitude but
the biceps and other tendon reflexes are exaggerated, this might be a clue to a
craniovertebral junction lesion.
Developmental reflexes — Developmental reflexes (also known as primitive reflexes) appear at
a certain time during the course of brain development and normally disappear with progressive
maturation of cortical inhibitory functions. They are mediated at subcortical levels. Assessment
of developmental reflexes is important in the newborn period and during infancy [10,11].
Developmental reflexes are abnormal if:
●
They are absent at an age when they should normally be present
●
They are asymmetric, suggesting unilateral weakness
●
They persist beyond a time they should have normally resolved, as this suggests impaired
maturation of descending cortical inhibitory projections
Common developmental reflexes, their descriptions, and time of appearance and resolution are
listed in the following table (
table 3). (See "Neurologic examination of the newborn", section
on 'Developmental reflexes'.)
The persistence of primitive reflexes such as the asymmetric tonic neck reflex and Galant reflex
after age five months is an early clue to the development of cerebral palsy [10]. (See "Cerebral
palsy: Classification and clinical features", section on 'Early signs of cerebral palsy'.)
Superficial reflexes — Superficial reflexes can be elicited by light stimulation of the plantar,
conjunctival, abdominal, and cremaster areas.
●
The plantar reflex (S1) is elicited by stroking the plantar surface of the foot using a pointed
but not sharp object (eg, the metal end of a reflex hammer). The stroke is from a lateral to
medial direction, posterior to anterior, stopping short at the base of the great toes. The
normal response is one flexion of all toes. Patients with corticospinal tract lesions manifest
an extensor plantar response (Babinski sign), which is characterized by extension of the
great toe and fanning of other toes.
●
For the conjunctival reflex, gently touching a wisp of cotton or tissue to the surface of the
conjunctiva will elicit an eye blink. The afferent loop of the reflex is via CN V, while the
efferent loop is through the facial (VII) nerve. (See 'III (oculomotor), IV (trochlear), and VI
(abducens)' above.)
●
The superficial abdominal reflexes are elicited in the right and left upper abdominal
quadrants (T8, 9) and also in the left and right lower abdominal quadrants (T11, 12).
Stroking of a blunt metal object (eg, the metal end of a reflex hammer) in these quadrants
in a medial to lateral direction elicits contraction of the abdominal muscles. Abdominal
reflexes may be lost in the case of a pyramidal tract lesion.
●
The cremasteric reflex (L1-2) is elicited by stroking the medial aspect of the upper thigh,
which elicits contraction of the cremaster muscle and elevation of the testis.
Gait — The gait is best assessed by observing the patient walk barefooted down a long corridor
with the legs and feet exposed. Abnormalities can be brought out by having the patient walk
and run.
●
Circumduction of a lower extremity may indicate spasticity and is commonly observed in
hemiparesis
●
A broad-based, ataxic gait may accompany a cerebellar disorder
●
A high-steppage gait suggests peripheral neuropathy
●
Patients with dystonia frequently show normal posture of the feet at rest but turn their
feet inwards and walk on the outer edges of the feet
●
Myopathies, such as Duchenne muscular dystrophy, may be associated with a waddling
gait
Spine — The spine should be examined along its entire length for findings that might suggest
an underlying congenital spinal cord anomaly, such as tethered cord syndrome or spina bifida
occulta (eg, a midline tuft of hair, dermal sinus tract, or lipoma). Gross lesions (eg, meningocele
and myelomeningocele) will of course be readily visualized. (See "Myelomeningocele (spina
bifida): Anatomy, clinical manifestations, and complications".)
Patients with muscular dystrophy may display lumbar lordosis. Kyphoscoliosis may accompany
degenerative disorders, such as Friedreich ataxia and muscular dystrophies. Localized point
tenderness over the spine may suggest underlying intervertebral disc herniation, inflammation,
fracture, or neoplastic process. The range of motion of the spine should be evaluated at all
levels when indicated.
Head — Examination includes measurement of head circumference and assessment of the
fontanels and cranial sutures:
●
Head circumference – The growth in size of the head is an indirect marker for increase in
the size of the brain. The occipitofrontal head circumference (OFC) is measured by placing
the measuring tape across from just above the eyebrows to the external occipital
protuberance (
picture 6). The head circumference is compared with the standard
measurements for a given age. Serial head circumference measurements are more
reliable than a single recording. (See "Microcephaly in infants and children: Etiology and
evaluation", section on 'Monitoring head growth'.)
• Macrocephaly is defined as OFC >2 standard deviations (SD) above the mean for age,
sex, and gestation (ie, OFC ≥97th percentile). (See "Macrocephaly in infants and
children: Etiology and evaluation", section on 'Etiology'.)
• Microcephaly is usually defined as OFC ≥2 SD below the mean for age, sex, and
gestation (ie, OFC <3rd percentile), although some individuals with OFC in this range
have no clinical abnormality. Severe microcephaly is defined as OFC ≥5 SD below the
mean for age, sex, and gestation. (See "Microcephaly in infants and children: Etiology
and evaluation", section on 'Microcephaly'.)
●
Fontanels – The anterior fontanel is felt for bulging (raised intracranial pressure) or
depression (dehydration). For consistency, serial evaluations of the fontanel should always
be performed in the same position (eg, while supporting the infant who is not crying in the
semiupright position). (See "The pediatric physical examination: HEENT", section on
'Anterior and posterior fontanelles'.)
●
Sutures – The sagittal and coronal sutures are palpated for ridging (craniosynostosis) or
separation (raised intracranial pressure). Patients with raised intracranial pressure may
show frontal bossing, palpable separation of sutures, tense or bulging anterior fontanel,
and prominent veins over the scalp. Premature closure of the sagittal suture may confer
an elongated appearance of the skull in the anteroposterior plane with side-to-side
flattening (dolichocephaly). Premature closure of the coronal suture may lead to
brachycephaly, with shortening of the skull in the anteroposterior plane. Plagiocephaly or
asymmetric flattening of the skull occurs when there is premature closure of one of the
lambdoidal sutures. (See "Overview of craniosynostosis".)
ELEMENTS OF THE GENERAL PHYSICAL EXAMINATION RELEVANT TO CHILD
NEUROLOGY
Clues to the diagnosis of many childhood neurologic disorders can be obtained during a careful
general physical examination. Additional detail on these disorders is available through the topic
reviews linked below and/or in the open-access databases
Online Mendelian Inheritance in
Man or the National Center for Biotechnology Information
GeneReviews.
Dysmorphic features — The presence of an isolated unusual morphologic feature is common
(noted in approximately 15 percent of newborns in one series) and is not generally associated
with underlying abnormalities [12]. However, the presence of two or more unusual morphologic
features is much less common (0.8 percent of newborns) and is associated with an increased
likelihood of having a clinically important underlying anomaly.
The following list of dysmorphic features is by no means complete, and the reader is referred to
more comprehensive reviews on dysmorphology [13].
●
Hypotelorism may accompany the holoprosencephaly sequence and trisomy 13. (See
"Overview of craniofacial clefts and holoprosencephaly" and "Congenital cytogenetic
abnormalities", section on 'Trisomy 13 syndrome'.)
●
Hypertelorism is associated with the following:
• Cleft palate (see "Syndromes with craniofacial abnormalities")
• Sotos syndrome (cerebral gigantism) (see "Microdeletion syndromes (chromosomes 1
to 11)", section on '5q35 deletion syndrome (Sotos syndrome)')
• Apert syndrome (see "Craniosynostosis syndromes", section on 'Apert syndrome')
• Saethre-Chotzen syndrome (see "Craniosynostosis syndromes", section on 'SaethreChotzen syndrome')
• Coffin-Lowry syndrome
•
●
Aarskog syndrome
Inner epicanthal folds are associated with the following:
• Down syndrome (see "Down syndrome: Clinical features and diagnosis")
• Rubinstein-Taybi syndrome (see "Microdeletion syndromes (chromosomes 12 to 22)",
section on '16p13.3 deletion syndrome (Rubinstein-Taybi syndrome)')
•
Smith-Lemli-Opitz syndrome
• Zellweger syndrome (see "Peroxisomal disorders")
●
Slanted palpebral fissures are associated with the following:
• Down syndrome (see "Down syndrome: Clinical features and diagnosis")
• Apert syndrome (see "Craniosynostosis syndromes", section on 'Apert syndrome')
• DiGeorge (22q11.2 deletion) syndrome (see "DiGeorge (22q11.2 deletion) syndrome:
Clinical features and diagnosis")
• Miller-Dieker syndrome (see "Microdeletion syndromes (chromosomes 12 to 22)",
section on '17p13.3 deletion including PAFAH1B1 (Miller-Dieker syndrome)')
• Rhizomelic chondrodysplasia punctata (see "Peroxisomal disorders")
•
●
Aarskog syndrome
Prominent, full lips are common in Williams syndrome. (See "Microdeletion syndromes
(chromosomes 1 to 11)", section on '7q11.23 deletion syndrome (Williams syndrome)'.)
●
Low-set ears are associated with the following:
• Noonan syndrome (see "Noonan syndrome")
• Treacher Collins syndrome (see "Syndromes with craniofacial abnormalities", section on
'Treacher Collins syndrome')
• Miller-Dieker syndrome (see "Microdeletion syndromes (chromosomes 12 to 22)",
section on '17p13.3 deletion including PAFAH1B1 (Miller-Dieker syndrome)')
• Rubinstein-Taybi syndrome (see "Microdeletion syndromes (chromosomes 12 to 22)",
section on '16p13.3 deletion syndrome (Rubinstein-Taybi syndrome)')
•
Smith-Lemli-Opitz syndrome
•
Pena-Shokeir syndrome
• Trisomy 9 (see "Congenital cytogenetic abnormalities", section on 'Trisomy 9
syndrome')
• Trisomy 18 (see "Congenital cytogenetic abnormalities", section on 'Trisomy 18
syndrome')
●
A single midline incisor in the maxilla may be associated with holoprosencephaly. (See
"Overview of craniofacial clefts and holoprosencephaly".)
Skin examination — Skin findings associated with neurologic disease include the following:
●
Tuberous sclerosis may be associated with hypopigmented patches, angiofibromas over
the cheek (adenoma sebaceum), shagreen patches over the lumbar region (raised skin
lesions with an irregular surface), and a brown fibrous plaque on the forehead. (See
"Tuberous sclerosis complex: Genetics, clinical features, and diagnosis", section on
'Dermatologic features'.)
●
Neurofibromatosis type 1 is associated with six or more café-au-lait spots (>5 mm in a
prepubertal child and >15 mm in a postpubertal child), neurofibromas (soft, sessile
nodules), and axillary or inguinal freckles. (See "Neurofibromatosis type 1 (NF1):
Pathogenesis, clinical features, and diagnosis", section on 'Clinical manifestations'.)
●
A port wine stain over one-half of the face is characteristic of Sturge-Weber syndrome. The
lesion invariably involves the ophthalmic region of distribution of the trigeminal nerve.
Many patients have an associated intracranial (leptomeningeal) angioma, with hemiplegia
and focal epilepsy. (See "Sturge-Weber syndrome".)
●
Petechial hemorrhages, which confer a "blueberry muffin" appearance to the skin, may be
seen in neonates with congenital cytomegalovirus infections. (See "Congenital
cytomegalovirus infection: Clinical features and diagnosis", section on 'Clinical
manifestations'.)
●
A macular rash (located over the malar region of the face) is characteristic of systemic
lupus erythematosus, whereas drug hypersensitivity reactions tend to have a rash with a
generalized distribution. (See "Childhood-onset systemic lupus erythematosus (SLE):
Clinical manifestations and diagnosis".)
●
Erythema migrans is a reddish, target-shaped lesion that is characteristic of Lyme disease.
(See "Lyme disease: Clinical manifestations in children", section on 'Erythema migrans'.)
●
Vitiligo may be associated with autoimmune disturbances such as myasthenia gravis. (See
"Vitiligo: Pathogenesis, clinical features, and diagnosis", section on 'Autoimmune
diseases'.)
●
Lax or redundant skin may accompany Coffin-Lowry, Costello, and Ehlers-Danlos
syndromes. (See "Rhabdomyosarcoma in childhood and adolescence: Epidemiology,
pathology, and molecular pathogenesis", section on 'Inherited syndromes' and "Clinical
manifestations and diagnosis of hypermobile Ehlers-Danlos syndrome and hypermobility
spectrum disorder".)
●
Angiokeratomas, which are collections of small, reddish bumps, are seen in Fabry disease,
which is a lysosomal disorder due to absence of alpha galactosidase A. (See "Fabry
disease: Clinical features and diagnosis".)
External genitalia
●
Hypogonadism with small testicles or undescended testicles and small penile size is
common in Prader-Willi syndrome (obesity, hypogonadism, hyperphagia, and intellectual
disability). (See "Prader-Willi syndrome: Management".)
●
Ambiguous genitalia may accompany X-linked lissencephaly and the syndrome of infantile
spasms in association with hydranencephaly/lissencephaly and agenesis of the corpus
callosum due to mutations in the aristaless-related homeobox (ARX) gene. (See "Infantile
epileptic spasms syndrome: Etiology and pathogenesis".)
●
Macro-orchidism is common in fragile X syndrome. (See "Fragile X syndrome: Clinical
features and diagnosis in children and adolescents".)
●
Patients with X-linked adrenoleukodystrophy may manifest hyperpigmentation initially
over the external genitalia. (See "Clinical features, evaluation, and diagnosis of X-linked
adrenoleukodystrophy".)
Lymphadenopathy — Subacute and chronic inflammatory or neoplastic disorders (eg,
toxoplasmosis, tuberculosis, infectious mononucleosis, and lymphoma) may be associated with
enlargement of lymph nodes over multiple regions of the body. In some of these disorders,
there may be nonspecific neurologic symptoms such as lethargy or confusion.
Hepatosplenomegaly — Enlargement of the spleen and liver may be seen with the
aforementioned infectious disorders. Lysosomal storage disorders, such as
mucopolysaccharidoses and generalized GM1 gangliosidosis, and Niemann-Pick disease can
also lead to hepatosplenomegaly. (See "Mucopolysaccharidoses: Clinical features and
diagnosis" and "Inborn errors of metabolism: Classification", section on 'Lysosomal storage
disorders' and "Overview of Niemann-Pick disease".)
Abnormal hair — The following disorders have both neurologic manifestations and
abnormalities of hair. Such associations are reviewed elsewhere in more detail [14].
●
Brittle hair is common in argininosuccinic aciduria. (See "Urea cycle disorders: Clinical
features and diagnosis".)
●
The hair in Menkes disease is brittle, sparse, and tortuous. A simple clue to the diagnosis is
examining hair under low power of a light microscope. (See "Overview of dietary trace
elements", section on 'Menkes disease'.)
●
Alopecia is common in rhizomelic chondrodysplasia punctata and in Rubinstein-Taybi
syndrome. (See "Microdeletion syndromes (chromosomes 12 to 22)", section on '16p13.3
deletion syndrome (Rubinstein-Taybi syndrome)' and "Peroxisomal disorders".)
●
Hirsutism and synophrys (joined eyebrows) are common in Cornelia de Lange syndrome.
(See "Congenital anomalies: Epidemiology, types, and patterns", section on 'Syndrome'.)
●
A white forelock of hair may accompany the Waardenburg syndrome (heterochromia of
the iris, bright blue eyes, broad and prominent nasal root, midface hypoplasia, and
congenital sensorineural deafness). (See "The genodermatoses: An overview", section on
'Waardenburg syndrome'.)
Abnormal breath — The area from which abnormal smells are most easily detected is the nape
of the neck or the scalp. Infants with phenylketonuria may manifest a mousy odor. Those with
isovaleric aciduria may have an odor of sweaty feet. (See "Inborn errors of metabolism:
Epidemiology, pathogenesis, and clinical features", section on 'Abnormal odors'.)
Cardiovascular
●
High-output cardiac failure is common in newborns and infants having vein of Galen
malformations. (See "Hydrocephalus in children: Physiology, pathogenesis, and etiology",
section on 'CNS malformations'.)
●
A floppy and weak infant with cardiomegaly and poor cardiac contractility may have
Pompe disease (acid maltase deficiency or type II glycogen storage disease). (See
"Lysosomal acid alpha-glucosidase deficiency (Pompe disease, glycogen storage disease II,
acid maltase deficiency)".)
●
Duchenne and Becker muscular dystrophies are associated with cardiomyopathy. (See
"Duchenne and Becker muscular dystrophy: Clinical features and diagnosis".)
●
Patients with Friedreich ataxia frequently manifest hypertrophic subaortic cardiomyopathy
as well as progressive ataxia and diabetes mellitus. (See "Friedreich ataxia".)
●
Patients with Barth syndrome have congenital dilated cardiomyopathy as well as skeletal
myopathy and neutropenia. (See "Inherited syndromes associated with cardiac disease",
section on 'Barth syndrome'.)
Otolaryngology — Macroglossia is often noted when the tongue protrudes from between the
teeth. Macroglossia is a characteristic of Beckwith-Wiedemann syndrome and some forms of
mucopolysaccharidosis (eg, Hurler syndrome) and can also be seen in some patients with
untreated hypothyroidism. Patients with macroglossia often have obstructive sleep apnea. (See
"Beckwith-Wiedemann syndrome" and "Mucopolysaccharidoses: Clinical features and
diagnosis", section on 'Hurler syndrome'.)
DEVELOPMENTAL SCREENING TESTS
Developmental screening tests complement the history and neurologic examination, can be
conducted in the field by trained health professionals, and may facilitate early diagnosis of a
childhood neurologic disability and appropriate intervention. There are several brief and
accurate developmental screening tests that make use of information provided by the parents
or caregivers or by direct observation or elicitation of developmental skills. (See
"Developmental-behavioral surveillance and screening in primary care", section on 'Approach to
screening'.)
SUMMARY
●
History – In infants and children, the history should include information about prenatal
exposures and symptoms and assessment of developmental milestones (
table 1). (See
'Pregnancy, perinatal, and neonatal history' above and 'Developmental history' above.)
●
Observation – Observations of infants and toddlers during play (eg, while stacking blocks
or playing with an age-appropriate toy) can provide valuable information about the
patient's attention span, joint attention, babbling, speech, gross and fine motor
coordination, and problem-solving abilities. These higher cortical functions are also
assessed with a series of questions appropriate to the child's age (
table 2). (See 'Higher
cortical functions' above.)
●
Cranial nerves – Each cranial nerve (CN) is tested by performance of a specific motor or
sensory test. Testing in infants is often by observation for specific movements and
responses and is less reliable. (See 'Cranial nerves' above.)
●
Motor examination – The patient should be observed for abnormalities of posture and
movements, including asymmetry at rest, fisting of the hand, frog-legged position
suggesting hypotonia, tremor, myoclonus, or tics. (See 'Posture and involuntary
movements' above.)
Muscle tone is the resistance felt upon passive movement of a joint through its range of
motion. Hypotonia is characterized by decreased resistance to passive movement and
hyperextension at the joints. Hypertonia can be either spastic in nature or characterized by
muscle rigidity. (See 'Tone and strength' above.)
●
Sensory examination – A sensory examination in young children is often imprecise, and
only gross deficits can be detected. In children older than five to six years, sensory
function is evaluated in the same manner as in an adult. (See 'Sensory system' above and
"The detailed neurologic examination in adults".)
●
Developmental reflexes – Developmental reflexes (also known as primitive reflexes)
appear at a certain time during the course of brain development and normally disappear
with progressive maturation of cortical inhibitory functions (
table 3). Persistence of
primitive reflexes beyond the time by which they should have disappeared may be an early
clue to cerebral palsy. (See 'Developmental reflexes' above and "Cerebral palsy:
Classification and clinical features", section on 'Early signs of cerebral palsy'.)
●
General physical examination findings – Certain elements of the general physical
examination may provide clues to the diagnosis of childhood neurologic disorders.
Important features include facial dysmorphism; abnormalities of skin pigmentation, color
and texture of hair, and breath odor; hepatosplenomegaly; and evidence of cardiac
disease. (See 'Elements of the general physical examination relevant to child neurology'
above.)
Use of UpToDate is subject to the Terms of Use.
Topic 15360 Version 27.0
GRAPHICS
Common developmental milestones
Milestone
Age at acquisition
Fixes gaze briefly; habituates to stereotyped auditory, visual, and
tactile stimuli
At birth (40 weeks postconceptional age)
Smiles responsively, gurgles
2 to 3 months
Visual tracking of a bright object to 180°
3 months
Rolls over, holds head upright when pulled from supine to sitting
3 months
Reaches out for objects
4 to 5 months
Maintains sitting position independently
6 months
Grasps objects using thumb and index finger pulp
8 to 9 months
Crawls, babbles, uses nonspecific "Mama" and/or "Dada" sounds
9 to 10 months
Pulls up to stand and walks with support
10 to 11 months
Walks independently, uses 2 to 3 clear words, including specific
"Mama" and "Dada"
13 to 14 months
Can point to body parts, use simple phrases
18 to 19 months
Names body parts, states age, uses phrases
24 months
Pedals tricycle, speaks in sentences, asks questions, likely toilet
trained, can name primary colors
36 months
Masters concepts of alphabets and numbers
4 to 5 years
Able to read simple words, add, subtract
5 to 6 years
Concepts of division, multiplication, geography; general information
like cities, states, large rivers, oceans, etc
7 to 8 years
Courtesy of Suresh Kotagal, MD.
Graphic 70142 Version 3.0
Assessment of higher cortical function in children [1]
Age
6 to 12 months
Evidence of normal cortical development
Awareness of surroundings
Interaction with examiner (social smile, inquisitiveness, habituation)
Cooing and gurgling, sometimes making of nonspecific "mama" and "dada"
sounds
Looks at and pats picture to show interest
12 to 20 months
6- to 8-word vocabulary
Comprehends 1-step commands
Points to 2 or 3 body parts
Points at pictures
24 months
Names 2 or 3 body parts
Uses phrases and simple sentences
Names pictures, follows simple stories
24 to 36 months
Concept of self (referring to self as "I," knowledge of name and age)
Completes sentences and rhymes in familiar stories
36 months
Counts 3 objects
Understands prepositional concepts (eg, "over" and "under")
Asks questions
Names 3 colors
Begins to recognize letters
48 months
Copies a square and a cross
Begins to develop ability to rhyme
5 or 6 years
Spells monosyllabic words
Counts to 10
Recognizes numbers, letters, sight words
6 years
Copies a triangle
Reads and retells familiar stories
6 or 7 years
Does simple addition and subtraction
Reads polysyllabic words
7 years
Copies a diamond
Sounds out or decodes unfamiliar words
Reference:
1. DeBruin-Parecki A, Perkinson K, Ferderer L. Helping your child become a reader. US Department of Education,
Washington, DC 2000.
Graphic 78835 Version 3.0
The normal optic disc
The margins are distinct, the rim has a pinkish color, and there is a
central pale cup (arrows). This optic disc has a cup:disc ratio of 0.2.
Courtesy of Karl C Golnik, MD.
Graphic 53796 Version 1.0
Diffuse optic atrophy
Top panel: Diffuse optic atrophy.
Bottom panel: Fellow eye with normal disc color.
Courtesy of Karl C Golnik, MD.
Graphic 76278 Version 2.0
Papilledema
Papilledema, characterized by blurring of the optic disc margins,
loss of physiologic cupping, hyperemia, and fullness of the veins, in
a 5-year-old girl with intracranial hypertension due to vitamin A
intoxication.
Courtesy of Gerald Striph, MD.
Graphic 50378 Version 1.0
Macular cherry red spot
Sphingolipids accumulate in the retinal ganglion cells in the
perifoveal area of patients with sphingolipidoses causing the
perifoveal area to appear pale. The fovea, which has no ganglion
cells, retains its "cherry red" color.
Courtesy of Robert P Cruse, DO.
Graphic 65650 Version 1.0
Hemorrhagic macular cyst
Hemorrhagic cysts, such as this macular cyst, may break into the
vitreous.
Courtesy of Brian Forbes, MD, PhD.
Graphic 69754 Version 3.0
Corneal light reflex
The corneal light reflex test involves shining a light onto the child's
eyes from a distance and observing the reflection of the light on the
cornea with respect to the pupil. The location of the reflection from
both eyes should appear symmetric and generally slightly nasal to
the center of the pupil.
(A) Normal corneal reflex.
(B) Corneal light reflex in esotropia.
(C) Corneal light reflex in exotropia.
Graphic 63631 Version 3.0
Common developmental reflexes
Reflex
Moro
(startle)
Description
The examiner holds the infant supine in their arms,
then drops the infant's head slightly but suddenly.
This leads to the infant extending and abducting the
Age at
Age at
appearance
resolution
34 to 36
weeks PCA
5 to 6
months
38 to 40
weeks PCA
1 to 3
months
6 months
arms, with the palms open, and sometimes crying.
Alternatively, the examiner may lift the infant's head
off the bed by 1 to 2 inches and allow it to gently
drop back; this maneuver elicits a similar response.
Asymmetric
tonic neck
With the infant relaxed and lying supine, the
examiner rotates the head to one side. The infant
reflex
extends the leg or arm on the side towards which the
head has been turned while flexing the arm on the
contralateral side (fencing posture).
Trunk
With the infant in a prone position, the examiner
38 to 40
incurvation
(Galant)
strokes or taps along the side of the spine. The infant
twitches their hips toward the side of the stimulus.
weeks PCA
Palmar
grasp
The examiner places a finger in the infant's open
palm. The infant closes their hand around the finger,
38 to 40
weeks PCA
5 to 6
months
tightens the grip if the examiner attempts to
withdraw the finger.
Plantar
The examiner places a finger under the infant's toes.
38 to 40
9 to 10
grasp
The infant flexes the toes downwards to "grasp" the
finger.
weeks PCA
months
Rooting
The examiner strokes the infant's cheek. The infant
turns the head toward the side that is stroked and
38 to 40
weeks PCA
2 to 3
months
makes sucking motions.
Stepping
reflex
The infant is held upright and the plantar aspect of
the foot and hallux is stimulated by light placing on a
surface to reflexively produce a stepping gait.
38 to 40
weeks PCA
2 to 3
months
Parachute
The infant is held upright, back to the examiner. The
body is rotated quickly forward (as if falling). The
infant reflexively extends the upper extremities
towards the ground as if to break a fall.
8 to 9 months
of age
Persists
throughout
life
PCA: postconceptional age.
Courtesy of Suresh Kotagal, MD.
Graphic 58453 Version 7.0
Measurement of head circumference
Measuring head circumference. The measuring tape passes just
above the eyebrows and around the prominent posterior aspect of
the head.
Reproduced with permission from: Keith Cotton. Copyright ©2008 Wolters Kluwer
Health.
Graphic 70799 Version 2.0
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