Detailed Neurologic Assessment of Infants and Children

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Detailed neurologic assessment of infants and children
Author: Suresh Kotagal, MD

Section Editor: Douglas R Nordli, Jr, MD
Deputy Editor: Carrie Armsby, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2018. | This topic last updated: Aug 01, 2017.
INTRODUCTION — 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 assessment 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, to understand the nature of their health concerns regardless of whether or not they pertain to
the nervous system, and to 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 document the duration of symptoms, whether they are
constant or episodic (as in a transient ischemic attack, syncope, seizure, or migraine), and whether they are
static, progressive, or resolving. In addition, the history may suggest localization to a specific anatomical
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,
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stand, or walk.
It is important to ask questions about whether, and to what extent, the neurologic disorder has impacted
cognition, behavior, and language; the degree to which activities of daily living have been compromised; and
what rehabilitative measures have been put in place. It is a common practice to inquire about activities a
handicapped child cannot carry out. It is equally important to ask about activities the patient can do and enjoy
because these skills can be targeted for further development.
Medications — The clinician should note any current medications (and alternative medicines or nutritional
supplements), with the form of the medication (capsule, tablet, suspension), strength in milligrams/grams,
frequency, and route of administration. In addition, the medications that the child has taken in the past, as
well as the response to these medications, should be noted.
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 number of siblings, their gender and health, the age and health of the parents, and the family history of
neurologic and systemic disorders and of consanguinity. If other family members have neurologic disease, a
pedigree chart is often helpful.
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)
• 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 (because excessive maternal weight gain
may accompany preeclampsia and cause placental insufficiency; poor maternal weight gain may be
associated with fetal growth restriction) (see "Gestational weight gain")
• Exposure to systemic illnesses or infections that could affect the developing fetal brain (eg,
cytomegalovirus or Zika) (see "Congenital cytomegalovirus infection: Clinical features and
diagnosis" and "Congenital Zika virus infection: Clinical features, evaluation, and management of the
neonate")
• 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 or induced
• 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, respectively (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, particularly if the infant required therapeutic hypothermia or extracorporeal
membrane oxygenation (ECMO) (see "Clinical features, diagnosis, and treatment of neonatal
encephalopathy", section on 'Therapeutic hypothermia')
● Newborn period – Significant events in the first week of life include the need for ventilatory support,
oxygen administration, resuscitation, artificial hypothermia, exchange transfusion, status epilepticus,
metabolic derangements, feeding difficulties, and coma. Impaired sucking or swallowing and sleep-wake
difficulties in the first month of life are subtle markers of brain dysfunction.
Many 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 use of first words, phrases, and sentences (table 1) [3].
Some parents 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. 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:
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
may be helpful. 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: Clinical features and
classification", section on 'Associated conditions'.)
NEUROLOGIC EXAMINATION
General concepts — 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 funduscopy, 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. In addition, assessment of age-appropriate
milestones can help evaluate the higher cortical functions and yield clues to specific learning disabilities,
attention deficit disorder, and mild mental retardation (table 2).
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. Infant 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, 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 3 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 him or her. 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 and
III. 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.
• The optic disc is normally pink in complexion (picture 1). Optic disc pallor may suggest atrophy
(picture 2). (See "Congenital anomalies and acquired abnormalities of the optic nerve", section on
'Atrophy'.)
• Hypoplasia of the optic disc (normal complexion, but small size) may accompany septo-optic
dysplasia, which can be associated with hypothalamic insufficiency and hypopituitarism. (See
"Congenital anomalies 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 is seen
in papilledema (picture 3). Approximately 30 percent of subjects lack venous pulsations even in the
absence papilledema. (See "Congenital anomalies 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
disease in the Ashkenazi Jewish population", 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 the shaken infant syndrome. (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 in children", section on 'Clinical manifestations')
Ptosis (drooping of the upper eyelid and encroachment on the pupillary aperture) may accompany
sympathetic paralysis from lesions of the cranial nerve III, Horner syndrome, myopathies, myasthenia gravis,
and eye structural lesions (eg, neurofibroma). (See "Overview of ptosis".)
Optokinetic nystagmus (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 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 [6,7]. 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 vision change", section on 'Conversion
disorder'.)
Abnormal eye movements may be manifestations of an underlying disease or disorder:
● Opsoclonus accompanies occult neuroblastoma. It is characterized by sudden chaotic bursts of eye

movements in the horizontal, vertical, oblique, or rotatory positions, often associated with myoclonus.
Opsoclonus is a non-metastatic manifestation of malignancy.
● Up gaze paresis may accompany Parinaud syndrome owing to pressure on the pre-tectal region from a
mass lesion. Impaired down gaze may be seen in children with Niemann Pick Type C disease, and can
lead to difficulty going down steps.
● Oculomotor apraxia may accompany Joubert syndrome or oculomotor apraxia-ataxia syndrome. It is

characterized by a delayed initiation of the eye movement and jerky pursuit movements that are
accompanied by compensatory head thrusting.
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 open the jaw against
resistance).
VII (facial) — The function of CN VII can be assessed by observing for symmetry of the nasolabial folds,
assessing eye lid muscle strength, and the ability to wrinkle the forehead symmetrically. In addition, CN VII
mediates taste sensation over the anterior two thirds of the tongue, and can be tested by applying two or
three drops of a concentrated salt solution to the lateral edge of each 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 halves of the face are paralyzed,
whereas with supranuclear lesions, only the lower 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,

movement of the soft palate, and are often tested by eliciting a gag reflex. Salivary drooling or pooling of
saliva also suggests 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. (See "The
detailed neurologic examination in adults".)
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: Clinical features and
classification", 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, non-stereotyped 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, non-stereotyped 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 but with weakness), and fasciculations (ripple
like movements of the muscles that accompany degeneration of anterior horn cells). Muscle atrophy
implies decreased muscle bulk. It may be segmental or generalized, and may be due to a neuropathy,
myopathy, or disuse. (See "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.
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 lengthening-shortening 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.
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 five-point 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 bed sheet)
● 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. Patients with proximal (hip extensor) muscle
weakness may exhibit a Gower's sign: when asked to come to a standing position from sitting on the floor,
the patient will initially prop the hands against the floor or the lower extremities for support.
Assessment for the pronator drift is a useful method of detecting upper motor neuron weakness [8]. 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.
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 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 his nose and then return to the
starting position. 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, brachio-radialis, 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 degrees 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 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 is elicited, spread to the opposite side in the form of a
crossed adductor response (contraction of the contralateral hip muscle), or contraction of the plantar
flexures of the foot are considered exaggerated and abnormal. 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 cranio-vertebral 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 [9,10]. 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'.)
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 cranial nerve 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 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.
● 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 "Pathophysiology and clinical manifestations of myelomeningocele (spina bifida)".)
Patients with muscular dystrophy may display lumbar lordosis. Kyphoscoliosis may accompany degenerative
disorders, such as Friedreich's 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 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 semi-upright 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 antero-
posterior plane with side to side flattening (dolichocephaly). Premature closure of the coronal suture may
lead to brachycephaly, with shortening of the skull in the antero-posterior 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
https://www.uptodate.com/contents/detailed-neurologic-assessment-of-infants-and-children/print?search=exame%20neurol%C3%B3gico&sour… 10/25
reviews linked below, and/or in the open access databases Online Mendelian Inheritance in Man (OMIM) or
the National Center for Biotechnology information (NCBI) 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 [11]. 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 [12].
● Hypotelorism may accompany the holoprosencephaly sequence and trisomy 13. (See "Facial clefts and
holoprosencephaly" and "Congenital cytogenetic abnormalities", section on 'Trisomy 13 syndrome'.)
● Hypertelorism is commonly observed in patients with cleft palate, Sotos syndrome (cerebral gigantism)
and Apert, Saethre-Chotzen, Coffin-Lowry, and Aarskog syndromes. (See "Facial clefts and
holoprosencephaly" and "The child with tall stature and/or abnormally rapid growth", section on 'Cerebral
gigantism' and "Craniosynostosis syndromes", section on 'Apert syndrome' and "Craniosynostosis
syndromes", section on 'Saethre-Chotzen syndrome'.)
● Inner epicanthal folds accompany Down syndrome, Rubinstein-Taybi syndrome, Smith–Lemli-Opitz

syndrome, and Zellweger syndrome. (See "Down syndrome: Clinical features and diagnosis" and
"Microdeletion syndromes (chromosomes 12 to 22)", section on '16p13.3 deletion syndrome (Rubinstein-
Taybi syndrome)' and "Causes and clinical manifestations of primary adrenal insufficiency in children",
section on 'Defects in cholesterol biochemistry' and "Peroxisomal disorders", section on 'Zellweger
syndrome'.)
● Slanted palpebral fissures are common in Down syndrome, Apert syndrome, DiGeorge sequence,
Miller-Dieker syndrome, rhizomelic chondrodysplasia punctata, and Aarskog syndrome. (See "DiGeorge
(22q11.2 deletion) syndrome: Clinical features and diagnosis" and "Microdeletion syndromes
(chromosomes 12 to 22)", section on '17p13.3 deletion including PAFAH1B1 (Miller-Dieker syndrome)'
and "Peroxisomal disorders", section on 'Rhizomelic chondrodysplasia punctata type 1'.)
● 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 seen in Noonan, Treacher Collins, Miller Dieker, Rubinstein Taybi, Smith–Lemli-Opitz,
and Pena Shokier syndromes, as well as Trisomy 9 and 18. (See "Causes of short stature", section on
'Noonan syndrome' and "Syndromes with craniofacial abnormalities", section on 'Treacher Collins
syndrome' and "Congenital cytogenetic abnormalities".)
● A single midline incisor in the maxilla may be associated with holoprosencephaly. (See "Facial 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 I 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 "Systemic lupus erythematosus (SLE) in children: 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 syndrome, Costello syndrome, and the Ehlers-
Danlos syndrome. (See "Rhabdomyosarcoma in childhood and adolescence: Epidemiology, pathology,
and molecular pathogenesis", section on 'Inherited syndromes' and "Joint hypermobility syndrome".)
● 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 mental retardation). (See "Clinical features,
diagnosis, and treatment of Prader-Willi syndrome".)
● 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 "Etiology and pathogenesis of infantile spasms".)
● 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 "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 [13].
● 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 minerals", section on
'Menkes disease'.)
● Alopecia is common in rhizomelic chondrodysplasia punctata and in Rubinstein Taybi syndrome. (See
"Peroxisomal disorders", section on 'Rhizomelic chondrodysplasia punctata type 1' and "Microdeletion
syndromes (chromosomes 12 to 22)", section on '16p13.3 deletion syndrome (Rubinstein-Taybi
syndrome)'.)
● Hirsutism and synophrys (joined eyebrows) are common in Cornelia de Lange syndrome. (See "Birth
defects: 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 direct
observation or elicitation of developmental skills. (See "Developmental-behavioral surveillance and screening
in primary care", section on 'Approach to screening'.)
SUMMARY — A complete neurologic assessment consists of a focused clinical history, a detailed neurologic
examination, and a general physical examination that focuses on features that may be related to neurologic
disease.
● 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.)
● 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. 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.)
● Each cranial nerve 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.)
● 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.)
● 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.)
● 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). (See 'Developmental reflexes' above.)
● 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, breath odor, hepatosplenomegaly, and evidence of cardiac disease. (See
'Elements of the general physical examination relevant to child neurology' above.)
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REFERENCES
1. Swaiman KF. Neurologic examination of the older child. In: Neurology. Principles and Practice, 4th, Swa
iman KF, Ashwal S, Ferriero DM (Eds), Mosby Elsevier, Philadelphia 2006. p.17.
2. Caramant L, Diadori P. The neurologic examination. In: Current Management in Child Neurology, 2nd,
Maria BL (Ed), BC Dekker, Inc, 2002. p.28.
3. Glascoe FP, Marks KP. Screening for developmental and behavioral problems. In: Neurodevelopmental
Disabilities: Clinical and Scientific Foundations, Shevell M (Ed), MacKeith Press for the International Chi
ld Neurology Association, London 2009. p.85.
4. Johnson CP, Myers SM, American Academy of Pediatrics Council on Children With Disabilities.
Identification and evaluation of children with autism spectrum disorders. Pediatrics 2007; 120:1183.
5. Larsen PD and Stensaas SS. Pediatric NeuroLogic Examination videos and descriptions, 2009. Availabl
e at: http://library.med.utah.edu/pedineurologicexam/html/home_exam.html (Accessed on March 22, 20
12).
6. Papanagnu E, Brodsky MC. Is there a role for optokinetic nystagmus testing in contemporary orthoptic
practice? Old tricks and new perspectives. Am Orthopt J 2014; 64:1.
7. Brodsky MC. Pediatric Neuro-Ophthalmology, 2nd ed, Springer, New York 2010.
8. Kutscher ML. How to think like a neurologist -- Part 1: Pearls of the neurological examination.
Emergency and Office Pediatrics 1998; 11:101.
9. Zafeiriou DI. Primitive reflexes and postural reactions in the neurodevelopmental examination. Pediatr
Neurol 2004; 31:1.
10. Schott JM, Rossor MN. The grasp and other primitive reflexes. J Neurol Neurosurg Psychiatry 2003;
74:558.
11. MARDEN PM, SMITH DW, MCDONALD MJ. CONGENITAL ANOMALIES IN THE NEWBORN INFANT,
INCLUDING MINOR VARIATIONS. A STUDY OF 4,412 BABIES BY SURFACE EXAMINATION FOR
ANOMALIES AND BUCCAL SMEAR FOR SEX CHROMATIN. J Pediatr 1964; 64:357.
12. Jones KL. Smith's Recognizable Patterns of Human Malformations, Jones KL (Ed), WB Saunders, Phila
delphia 1988. p.662.
13. Michelson DJ, Shu SK. Cognitive and motor regression. In: Pediatric Neurology: Principles and Practic
e, 4th, Swaiman KF, Ashwal S, Ferriero DM (Eds), Mosby Elsevier, Philadelphia 2006. p.821.
Topic 15360 Version 18.0
GRAPHICS
Common developmental milestones
Milestone Age at acquisition
Fixes gaze briefly, habituates to stereotyped auditory, visual, and tactile stimuli At birth (40 weeks post
conceptional age)
Smiles responsively, gurgles 2-3 months
Visual tracking of a bright object to 180 degrees 3 months
Rolls over, holds head upright when pulled from supine to sitting 3 months
Reaches out for objects 4-5 months
Maintains sitting position independently 6 months
Grasps objects using thumb and index finger pulp 8-9 months
Crawls, babbles, uses non-specific "Mama", "Dada" sounds 9-10 months
Pulls up to stand and walks with support 10-11 months
Walks independently, uses 2-3 clear words, including specific "Mama" and "Dada" 13-14 months
Can point to body parts, use simple phrases 18-19 months
Names body parts, states age, uses phrases 24 months
Pedals tricycle, speaks in sentences, asks questions, likely toilet trained, can name 36 months
primary colors
Masters concepts of alphabets and numbers 4-5 years
Able to read simple words, add, subtract 5-6 years
Concepts of division, multiplication, geography, general information like cities, 7-8 years
states, large rivers, oceans, etc.
Courtesy of Suresh Kotagal.
Graphic 70142 Version 2.0
Assessment of higher cortical function in children
Age Evidence of normal cortical function
6 to 12 months Awareness of surroundings
Interaction with examiner (social smile, inquisitiveness, habituation)
Cooing and gurgling, sometimes making of nonspecific "mama" and "dada" sounds
12 to 20 months Six to eight word vocabulary
Comprehends one-step commands
Points to two or three body parts
24 months Names two or three body parts
Uses phrases and simple sentences
24 to 36 months Concept of self (referring to self as "I", knowledge of name and age)
36 months Counts three objects
Understands prepositional concepts (eg, "over" and "under")
Asks questions
Names three colors
48 months Copies a square and a cross
5 or 6 years Spells monosyllabic words
Counts to 10
6 years Copies a triangle
6 or 7 years Does simple addition and subtraction
Reads polysyllabic words
7 years Copies a diamond
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.
Diffuse optic atrophy
Top: diffuse optic atrophy. Bottom: fellow eye with normal disc color.
Courtesy of Karl C Golnik, MD.
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.
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.
Hemorrhagic macular cyst
Hemorrhagic cysts, such as this macular cyst, may break into the vitreous.
Courtesy of Brian Forbes, MD, PhD.
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.
Common developmental reflexes
Age at Age at
Reflex Description
appearance resolution
Moro (startle) The examiner holds the infant supine in his or her arms, then 34 to 36 weeks 5 to 6 months
drops the infant's head slightly but suddenly. This leads to the PCA
infant extending and abducting the 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 With the infant relaxed and lying supine, the examiner rotates 38 to 40 weeks 2 to 3 months
tonic neck the head to one side. The infant extends the leg or arm on PCA
reflex 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 strokes or 38 to 40 weeks 1 to 2 months
incurvation taps along the side of the spine. The infant twitches his or her PCA
(Galant) hips toward the side of the stimulus.
Palmar grasp The examiner places a finger in the infant's open palm. The 38 to 40 weeks 5 to 6 months
infant closes his or her hand around the finger, tightens the PCA
grip if the examiner attempts to withdraw the finger.
Plantar grasp The examiner places a finger under the infant's toes. The 38 to 40 weeks 9 to 10
infant flexes the toes downwards to "grasp" the finger. PCA months
Rooting The examiner strokes the infant's cheek. The infant turns the 38 to 40 weeks 2 to 3 months
head toward the side that is stroked, and makes sucking PCA
motions.
Parachute The infant is held upright, back to the examiner. The body is 8 to 9 months Persists
rotated quickly forward (as if falling). The infant reflexively of age throughout life
extends the upper extremities towards the ground as if to
break a fall.
PCA: post-conceptional age.
Courtesy of Suresh Kotagal, MD.
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
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Author: Suresh Kotagal, MD

● Focused clinical history

● Detailed neurologic examination

In some cases, developmental screening tests are also helpful.

Pregnancy, perinatal, and neonatal history

• Mother's age at the time of pregnancy

• Results of prenatal head ultrasound studies

• The infant's weight, length, and head circumference at birth

• Whether the infant needed resuscitation

II (optic) — The function of CN II is assessed by the following tests of visual function:

● Deviation laterally: paralysis of the medial rectus (CN III)

● Deviation upwards: paralysis of the inferior rectus (CN III)

Abnormal eye movements may be manifestations of an underlying disease or disorder:

● Opsoclonus accompanies occult neuroblastoma. It is characterized by sudden chaotic bursts of eye

● Oculomotor apraxia may accompany Joubert syndrome or oculomotor apraxia-ataxia syndrome. It is

IX (glossopharyngeal) and X (vagus) — CN IX and CN X are responsible for swallowing function,

● Tremor (rhythmic, fine amplitude flexion-extension movements of the distal extremity).

● Grade 0/5: No muscle movement at all

● Grade 1/5: Presence of a flicker of movement

● Grade 3/5: Movement against gravity

● Biceps – just anterior to the elbow.

● Triceps – just posterior to the elbow.

● Knee (patellar) – just below the patella.

● Ankle (Achilles) – just behind the ankle.

● They are absent at an age when they should normally be present.

● They are asymmetric, suggesting unilateral weakness.

● A broad-based, ataxic gait may accompany a cerebellar disorder

● A high steppage gait suggests peripheral neuropathy

ELEMENTS OF THE GENERAL PHYSICAL EXAMINATION RELEVANT TO CHILD

● Inner epicanthal folds accompany Down syndrome, Rubinstein-Taybi syndrome, Smith–Lemli-Opitz

Lymphadenopathy — Subacute and chronic inflammatory or neoplastic disorders (eg, toxoplasmosis,

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 15360 Version 18.0

Common developmental milestones

Milestone Age at acquisition

Smiles responsively, gurgles 2-3 months

Visual tracking of a bright object to 180 degrees 3 months

Reaches out for objects 4-5 months

Maintains sitting position independently 6 months

Crawls, babbles, uses non-specific "Mama", "Dada" sounds 9-10 months

Pulls up to stand and walks with support 10-11 months

Can point to body parts, use simple phrases 18-19 months

Names body parts, states age, uses phrases 24 months

Masters concepts of alphabets and numbers 4-5 years

Able to read simple words, add, subtract 5-6 years

Courtesy of Suresh Kotagal.

Graphic 70142 Version 2.0

Assessment of higher cortical function in children

Age Evidence of normal cortical function

6 to 12 months Awareness of surroundings

Interaction with examiner (social smile, inquisitiveness, habituation)

12 to 20 months Six to eight word vocabulary

Comprehends one-step commands

Points to two or three body parts

24 months Names two or three body parts

Uses phrases and simple sentences

36 months Counts three objects

Understands prepositional concepts (eg, "over" and "under")

Names three colors

48 months Copies a square and a cross

5 or 6 years Spells monosyllabic words