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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate

AuthorSuresh Kotagal, MD

Section EditorDouglas R Nordli, Jr, MD

Deputy EditorCarrie Armsby, MD, MPH

Detailed neurologic assessment of infants and children

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Apr 2015. | This topic last updated: May 01, 2015.

INTRODUCTION — Children who present with or who are found to have neurologic or neuromuscularabnormalities on a general physical examination should undergo a complete neurologic assessment [1,2]. Theelements of a complete neurological assessment are:

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 discussedseparately. (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 childand family, to understand the nature of their health concerns regardless of whether or not they pertain to thenervous system, and to anatomically localize the neurological symptoms.

In children seen in the outpatient setting, history taking is often facilitated by mailing a questionnaire to the familyin advance of the visit that includes questions pertinent to current and past illnesses, family history, and growthand development. The family is advised to complete the questionnaire in advance and bring it to the doctor visit. Askilled clinician is often able to arrive at a diagnosis by the time a complete history has been taken, and uses theexamination 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 constantor 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. Asexamples:

It is important to ask questions about whether, and to what extent, the neurological disorder has impactedcognition, behavior, and language; the degree to which activities of daily living have been compromised; and what

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Focused clinical history

Detailed neurological examination

Additional parts of the general physical examination that are relevant to child neurology

Involvement of the cerebral cortex should be suspected in patients with cognitive dysfunction and/orseizures.

Involvement of the brainstem may be accompanied by double vision, dizziness, dysphagia, hoarseness ofvoice, 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 certainaltitudinal plane, and/or bowel and bladder dysfunction.

Disorders of the motor unit (anterior horn cells, peripheral nerve, neuromuscular junction, muscle) should besuspected in patients with weakness manifested by inability to climb stairs, raise the arms, grasp, stand, orwalk.

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rehabilitative measures have been put in place. It is a common practice to inquire about activities a handicappedchild cannot carry out. It is equally important to ask about activities the patient can do and enjoy because theseskills can be targeted for further development.

Medications — The clinician should note any current medications (and alternative medicines or nutritionalsupplements), 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 asthe response to these medications, should be noted.

Allergy history — Allergies to medications and the nature of the allergic reaction should be recorded. Thisinformation may inform the choice of therapies.

Family history — Many childhood neurological disorders are inherited. Thus, the clinician should inquire about thenumber of siblings, their gender and health, the age and health of the parents, and the family history of neurologicand systemic disorders and of consanguinity. If other family members have neurologic disease, a pedigree chart isoften helpful.

Pregnancy, perinatal, and neonatal history

The prenatal history should include the following elements:

The labor and delivery history should include the following:

Low APGAR scores have some predictive value for the subsequent development of cerebral palsy. Amongnewborns weighing more than 2500 grams in a Norwegian registry study, a five­minute APGAR score of 0 to 3was associated with a 125­fold increased risk of cerebral palsy as compared with those with a score of more than8 [3]. Similar results were seen among newborns with normal birthweight in the National Collaborative PerinatalProject, in whom the risk for cerebral palsy was 4.7 percent for those with a five minute APGAR score of 0 to 3,as compared with 0.2 percent for those with scores between 7 and 10 [4].

Significant events in the first week of life include the need for ventilatory support, oxygen administration,

Mother's age at the time of pregnancy

History of mother’s previous pregnancies (gravida, para, miscarriages, and gestational age at the time ofmiscarriages)

Prenatal exposure to prescription and illicit drugs, alcohol, radiation, and infections, and the fetus’ gestationalage at the time of exposure

Amount of maternal weight gain during the pregnancy (because excessive maternal weight gain mayaccompany preeclampsia and cause placental insufficiency; poor maternal weight gain may be associatedwith fetal growth restriction) (see "Weight gain and loss in pregnancy")

Whether fetal movements were reduced (as seen in infantile spinal muscular atrophy) or exaggerated (asseen in intrauterine seizures associated with pyridoxine dependency)

Results of prenatal head ultrasound studies

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

APGAR scores at 1, 5, and 10 minutes, respectively (see "Overview of the routine management of thehealthy newborn infant", section on 'Apgar score')

Whether the infant needed resuscitation

The infant’s weight, length, and head circumference at birth.

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resuscitation, artificial hypothermia, exchange transfusion, status epilepticus, metabolic derangements, feedingdifficulties, and coma. Impaired sucking or swallowing and sleep­wake difficulties in the first month of life aresubtle markers of brain dysfunction.

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 ableto maintain a sitting position, coming to a sitting position independently, crawling, walking independently, babbling,and use of first words, phrases, and sentences (table 1) [5].

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 byasking 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 developmentalsurveillance at well­child visits, with additional developmental screening tests at specific visits, or whendevelopmental concerns are raised [6]. Clues to the presence of autism include: no babbling or gesturing by age12 months (eg, waving “bye­bye”), lack of single words by 16 months, no spontaneous two words by 24 months,and loss of previously acquired speech. (See "Autism spectrum disorder: Surveillance and screening in primarycare".)

Review of other systems — The clinician should inquire about underlying medical conditions, some of which mayhave 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 states or provinces conduct comprehensive newborn screens. An inquiry into the results of the newbornscreen may be helpful. Although screening programs are designed for high sensitivity, false­negative results mayoccur, particularly in premature or medically complicated infants. Some forms of congenital hypothyroidism are notconsistently captured by newborn screening, so testing should be repeated if there is a clinical suspicion for thisdisorder. (See "Newborn screening" and "Clinical features and detection of congenital hypothyroidism", section on'Newborn screening programs'.)

Infants and children with cerebral palsy often have a variety of problems attributable to their neurologicdysfunction, including dysphagia, gastroesophageal reflux, chronic constipation, respiratory difficulties, chronicaspiration 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 documenttheir current management, including whether they are using a feeding gastrostomy, spine instrumentation,intrathecal baclofen pump, vagus nerve stimulator, or orthotics. (See "Clinical features of cerebral palsy".)

NEUROLOGIC EXAMINATION

General concepts — When examining toddlers, the initial phase of inspection is best conducted while the child isseated in the parent's lap. This minimizes apprehension, which tends to alter the assessment of higher corticalfunctions, muscle tone and tendon reflexes. It is also advisable to defer uncomfortable and anxiety­provokingprocedures until the end of the session, such as funduscopy, otoscopy, and checking of the gag reflex.

A collection of videos depicting elements of the neurological examination in infants and children can be viewed onthe Pediatric NeuroLogic Exam website [7].

Higher cortical functions — Observations of infants and toddlers during play (eg, while stacking blocks orplaying with an age­appropriate toy) can provide valuable information about the patient's attention span, gross andfine motor coordination, and problem solving abilities. In addition, the following age­appropriate questions help toassess the higher cortical functions and yield clues to specific learning disabilities, attention deficit disorder, andmild mental retardation (table 2):

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Cranial nerves — Each cranial nerve (CN) is tested by performance of a specific motor or sensory test. Testingin infants is often by observation for specific movements and responses, and is less reliable. Multiple observationsessions 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 arhinencephaly­holoprosencephaly.

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 varyingsize. Infant older than six months of age will usually reach for scraps of paper less than 5 mm in size when theyare 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 optokineticnystagmus, with quick jerks of the eyes in a direction opposite to the movement of the drum or tape. (See "Visualdevelopment and vision assessment in infants and children", section on 'Visual acuity tests'.)

Visual fields – Visual fields can be tested by introducing objects into the peripheral field of vision as the childfocuses on an object held directly in front of him or her. The lateral and superior fields of vision can be assessedmore 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. Anasymmetric, constricted pupil in association with ptosis, enophthalmos, and anhidrosis is seen with ipsilateralHorner's syndrome as a result of sympathetic denervation of the pupil. (See "Horner's syndrome".)

Funduscopy – Funduscopy of children requires patience, and is best accomplished in a dimly lit room with thepatient gazing straight ahead. The parent or caretaker can be requested to keep a bright object in the hand, uponwhich the child is asked to focus. The ability of the clinician to obtain an adequate funduscopic examination isoften compromised by lack of patient cooperation, nystagmus, or small pupils. In this case, consultation should besought with an ophthalmologist.

In infants of 6 to 12 months age, awareness of the surroundings, interaction with the examiner (social smile,inquisitiveness, and habituation), cooing and gurgling, and making of nonspecific “mama” and “dada” soundsshould be assessed.

By 12 to 20 months, the child should have developed a six to eight word vocabulary, should be able tocomprehend simple one step commands, and point to two to three body parts.

By 24 months, the patient should be able to name two to three body parts, and use phrases and simplesentences.

The concept of self (referring to oneself as “I”, knowledge of one's own name and age) appears between 24and 30 months.

By 36 months, the child is able to count three objects, understand prepositional concepts (eg, under andover), ask questions, and name three colors.

The ability to copy a square and a cross appears by 48 months, to copy a triangle by age six years, and adiamond by age seven years.

A first grader (generally age five to six) can spell simple monosyllabic words and count to 10.

By second grade, the child should be able to do simple addition and subtraction, and read polysyllabic words.

Beyond the age of eight to nine years, the concepts of reading, spelling, calculation ability, generalknowledge, geography, logic, and reasoning evolve exponentially.

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'.)

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III (oculomotor), IV (trochlear), and VI (abducens) — CN III, IV, and VI are required for extraocularmovements in the horizontal, vertical, and oblique planes, and can be tested by assessing the child’s ability totrack 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 sourceis held directly in front of a patient who is staring straight ahead, normal eye alignment will reveal a symmetricreflex in the center of each pupil (figure 1).

Paralysis of extraocular muscles leads to eye deviation at rest [2] in the following patterns:

Ptosis (drooping of the upper eyelid and encroachment on the pupillary aperture) may accompany sympatheticparalysis from lesions of the cranial nerve III, Horner syndrome, myopathies, myasthenia gravis, and eyestructural lesions (eg, neurofibroma). (See "Overview of ptosis".)

Optokinetic nystagmus (OKN) is a normal gaze­stabilizing response elicited by tracking a moving stimulus acrossthe visual field and can be helpful as a crude assessment of the visual system. Assessment of OKN can beperformed using an OKN drum or a piece of paper or cloth with alternating black and white stripes that is rapidlymoved across the patient’s visual field at reading distance. As the stimulus is moved from left to right, normallysighted patients will show quick, jerky movements to the left side and vice versa. Alternatively, a mirror placed infront of the patient's eyes can be tilted in different directions to elicit ocular pursuit movements. OKN is dependent

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 anomaliesand 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 inpapilledema (picture 3). About 30 percent of subjects lack venous pulsations even in the absencepapilledema. (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 diseaseand Niemann Pick disease. (See "Prenatal screening for genetic disease in the Ashkenazi Jewishpopulation", section on 'Tay­Sachs disease' and "Overview of Niemann­Pick disease".)

Chorioretinitis, which sometimes appears like “pepper sprinkled on a red table cloth”, can accompanycongenital cytomegalovirus infections. (See "Congenital cytomegalovirus infection: Clinical features anddiagnosis".)

Flame shaped retinal hemorrhages (picture 5) may accompany the shaken infant syndrome. (See "Childabuse: 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 muscleweakness, ataxia, and retinitis pigmentosa (NARP). (See "Mitochondrial myopathies: Clinical features anddiagnosis", section on 'NARP'.)

Deviation down and out: paralysis of the inferior oblique muscle (CN III) (see "Third cranial nerve (oculomotornerve) 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 (trochlearnerve) palsy in children")

Deviation inwards: paralysis of the lateral rectus (CN VI) (see "Sixth cranial nerve (abducens nerve) palsy inchildren", section on 'Clinical manifestations')

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upon the integrity of the visual system, especially visual perception, and pursuit and saccadic eye movement[8,9]. Bilateral absence of OKN in infancy or early childhood may suggest blindness, while unilateral absence maysuggest a hemispheric lesion. Normal OKN in an individual with a complaint of vision loss suggests hystericalblindness. (See "Visual development and vision assessment in infants and children" and "Approach to the pediatricpatient with vision change", section on 'Conversion disorder'.)

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

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 ofCN 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 VIImediates taste sensation over the anterior two thirds of the tongue, and can be tested by applying two or threedrops of a concentrated salt solution to the lateral edge of each half of the tongue using a cotton applicator, whilethe 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 inchildren".)

VIII (vestibulocochlear) — In infants, hearing is tested by making a soft sound close to one ear, such as fromrustling of paper. The infant should show an alerting response. By the age of five to six months, the infant mayalso be able to localize the sound to a specific quadrant. The procedure is then repeated for the opposite ear. Incooperative school age children, speech discrimination can be tested by softly whispering a number about one footfrom the ear. The traditional Rinne and Weber tests can be used as well in older children. (See "Hearingimpairment in children: Evaluation", section on 'Office hearing tests'.)

Poor head control, truncal unsteadiness, gait ataxia, nausea, vomiting and horizontal nystagmus may indicatevestibular system dysfunction.

IX (glossopharyngeal) and X (vagus) — CN IX and CN X are responsible for swallowing function, movementof the soft palate, and are often tested by eliciting a gag reflex. Salivary drooling or pooling of saliva also suggestsdysfunction. 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 isusually assessed by elevation of the shoulders and turning of the neck against resistance. The pattern ofweakness caused by CN IX dysfunction depends on whether the lesion is peripheral or central. (See "The detailedneurologic examination in adults".)

XII (hypoglossal) — Function of CN XII in a child or adolescent is tested by asking the patient to stick outtheir tongue; normally the tongue should remain in the midline. In patients with peripheral lesions of CN XII, thetongue points towards the paretic side. CN XII dysfunction can also cause fasciculations (slow ripple like

Opsoclonus accompanies occult neuroblastoma. It is characterized by sudden chaotic bursts of eyemovements in the horizontal, vertical, oblique, or rotatory positions, often associated with myoclonus.Opsoclonus is a non­metastatic manifestation of malignancy.

Up gaze paresis may accompany Parinaud syndrome owing to pressure on the pre­tectal region from a masslesion. Impaired down gaze may be seen in children with Niemann Pick Type C disease, and can lead todifficulty going down steps.

Oculomotor apraxia may accompany Joubert syndrome or oculomotor apraxia­ataxia syndrome. It ischaracterized by a delayed initiation of the eye movement and jerky pursuit movements that areaccompanied by compensatory head thrusting.

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movements) in the tongue, and oromotor apraxia. Fasciculations are best observed with the mouth open and withthe tongue kept immobile within the mouth.

Motor system

Posture and movements — Abnormalities are suggested by the following observations:

Tone and strength — Muscle tone is the resistance felt upon passive movement of a part of the body. In theextremities, it is assessed by placing a joint through its full range of movement. Hypotonia is characterized bydecreased resistance to passive movement and hyperextension at the joints. Increased tone that is spastic innature (abnormal lengthening­shortening reaction to stretch that has the feel of a “clasp knife”) tends to accompanypyramidal tract lesions. Increased tone that is characterized by muscle rigidity (has a “lead pipe” or “cog­wheel”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 plusresistance imposed by the examiner). The Medical Research Council of Great Britain suggests grading weaknessaccording to the following scale:

Asymmetry at rest in infants.

Opisthotonus (a brainstem release phenomenon due to bilateral cerebral cortical dysfunction). (See"Neurologic examination of the newborn", section on 'Hypertonia'.)

Abducted hips or “frog­legged” posture that accompanies hypotonia. (See "Neurologic examination of thenewborn", section on 'Hypotonia'.)

Fisting of the hand or holding the thumb adducted across the palm during quiet wakefulness (suggestscorticospinal tract involvement). Closure of the hand during sleep is normal.

Tremor (rhythmic, fine amplitude flexion­extension movements of the distal extremity).

Myoclonus (quick, non­stereotyped jerks around a segment of the body). (See "Hyperkinetic movementdisorders in children", section on 'Myoclonus'.)

Athetosis (slow, sinuous movement of the distal extremity with pronation of the distal extremity, generallydue to a contralateral putaminal lesion). (See "Hyperkinetic movement disorders in children", section on'Chorea, athetosis, and ballismus'.)

Chorea (rapid, quasi­purposive, non­stereotyped movements of a segment of the body that is generallyproximal). (See "Hyperkinetic movement disorders in children", section on 'Chorea, athetosis, andballismus'.)

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 likemovements of the muscles that accompany degeneration of anterior horn cells). Muscle atrophy impliesdecreased muscle bulk. It may be segmental or generalized, and may be due to a neuropathy, myopathy, ordisuse. (See "Etiology and evaluation of the child with muscle weakness", section on 'Muscle examination'.)

Grade 0/5: No muscle movement at allGrade 1/5: Presence of a flicker of movementGrade 2/5: Movement with gravity eliminated (eg, across the bed sheet)Grade 3/5: Movement against gravityGrade 4/5: Movement against gravity and some externally applied resistanceGrade 5/5: Movement against gravity and good external resistance (normal)

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Distal weakness (symmetric or asymmetric) generally accompanies peripheral neuropathy, while proximal muscleweakness (generally symmetric) is seen in myopathies. Patients with proximal (hip extensor) muscle weaknessmay exhibit a Gower's sign: when asked to come to a standing position from sitting on the floor, the patient willinitially 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 [10]. Initially, thechild is asked to extend the upper extremities with palms down. The child is then asked to close the eyes, androtate the extended arms so that the palms are facing upwards. During this turning maneuver with the eyesclosed, 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 musclecontraction (known as dysmetria), which may manifest as nystagmus, intention tremor, scanning speech, truncalor gait ataxia, or rebound phenomenon. To test for rebound phenomenon, the patient flexes the arm againstresistance 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 ina 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 bedetected. Information obtained from sensory testing in a child below five to six years of age can be unreliable, andmay 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. (See "Thedetailed neurologic examination in adults".)

Vibration sense testing is performed with a 128 or 256 Hz tuning fork. After a vibrating tuning fork has beenapplied against a bony prominence in the upper or lower extremity, the vibration should be intermittentlystopped to check whether the child is responding to the actual vibration, or just to the contact of the tuningfork against the skin. Impairment of vibration sense may suggest a large fiber peripheral neuropathy or dorsalspinal column dysfunction.

Joint sense is checked by asking the patient to indicate (first with eyes open, then with eyes closed) whetherthe great toe or the thumb have been passively moved by the examiner upwards or downwards. Joint sensecan also be tested with the Romberg test: The patient is asked to stand upright, keeping both feet togetherand close the eyes, with the examiner ready to catch the patient in case of a fall. Patients with preserveddorsal column function will continue to maintain stable balance with eyes closed, while those with dorsalcolumn dysfunction will tend to stagger and fall (positive Romberg sign).

Light touch is tested by checking response to tickling or to perception of the application of a cotton wisp onto the skin. Pin prick, and cool and warm stimuli are used for checking of the small diameter peripheral nervefibers and of the spinothalamic tracts. Since pin prick testing and temperature testing give somewhat similarinformation about spinothalamic tract function, the pin prick may be omitted in younger children if temperaturesensation is normal. Some common sensory landmarks include the plane of nipple (T4 segment), umbilicus(T10 segment) and perianal region (S4­5). A useful reference for motor and sensory has been published bythe Medical Research Council of Great Britain [11].

Testing of cortical sensory function consists of two point discrimination, stereognosis (detecting the shape ofan object by touch) and graphesthesia (recognizing writing on the skin). Tactile stimuli are provided on to thevolar aspect of the fingers for two point discrimination and over the palm of the hand for stereognosis andgraphesthesia. The results may be asymmetric between the left and right sides in patients with cerebralcortical lesions, such as porencephaly or infarcts. For accurate interpretation of tests of cortical sensation,the primary, peripheral sensation needs to be preserved.

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Tendon reflexes — The jaw, biceps, triceps, brachio­radialis, patellar, and ankle are commonly tested tendonreflexes, and all of these can usually be tested in infants and children. The joint under consideration should be atabout 90 degrees and fully relaxed. In patients with cerebral palsy, exhortations to “relax” may paradoxicallyincrease contraction of the muscles, and should thus be avoided. Instead, the patient should be put at ease duringreflex testing with conversation.

To elicit the reflex, let the head of the reflex drop onto the tendon at the following locations:

The elicitation of tendon reflexes provides information about multiple aspects of the nervous system. Findings canbe interpreted as follows:

Developmental reflexes — Developmental reflexes (also known as primitive reflexes) appear at a certain timeduring the course of brain development, and normally disappear with progressive maturation of cortical inhibitoryfunctions. They are mediated at subcortical levels. Assessment of developmental reflexes is important in thenewborn period and during infancy [12,13]. Developmental reflexes are abnormal if:

Common developmental reflexes, their descriptions, and time of appearance and resolution are listed in thefollowing table (table 3). (See "Neurologic examination of the newborn", section on 'Developmental'.)

Superficial reflexes — Superficial reflexes can be elicited by light stimulation of the plantar, conjunctival,abdominal, and cremaster areas.

Jaw – with the mouth held partially open and examiner’s finger placed over the chin, the finger is lightlytapped with a reflex hammer to displace the mandible downwards. This elicits contraction of the mandibleand slight closure of the mouth.

Biceps – just anterior to the elbowTriceps – just posterior to the elbowBrachioradialis – just above the wrist, on the radial aspect of the forearmKnee (patellar) – just below the patellaAnkle (Achilles) – just behind the ankle

Absent or diminished tendon reflexes – this generally indicates interruption of the muscle stretch reflex arc atthe level. Since the afferent impulses generated after tapping a tendon with reflex hammer are carried vialarge diameter fibers, the absence of a tendon reflex could also signify involvement of large diameter sensoryfibers in a peripheral nerve.

Exaggerated tendon reflexes – this generally indicates disinhibition of the motor units owing to a pyramidaltract lesion. When the patellar reflex is elicited, spread to the opposite side in the form of a crossed adductorresponse (contraction of the contralateral hip muscle), or contraction of the plantar flexures of the foot areconsidered exaggerated and abnormal. Similarly, clonus (rhythmic muscle contractions elicited by thestimulus) is exaggerated and abnormal.

Asymmetric tendon reflexes – this may indicate a cerebral hemispheric lesion. Asymmetry is most easilydetected with a gentle stimulus.

Differences between tendon reflexes in the upper and lower body – this may suggest a spinal cord lesion. Asan 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, thismight be a clue to a cranio­vertebral junction lesion.

They are absent at an age when they should normally be presentThey are asymmetric, suggesting unilateral weaknessThey persist beyond a time they should have normally resolved, as this suggests impaired maturation ofdescending cortical inhibitory projections.

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Gait — The gait is best assessed by observing the patient walk barefooted down a long corridor with the legs andfeet exposed.

Spine — The spine should be examined along its entire length for findings that might suggest an underlyingcongenital 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 readilyvisualized. (See "Pathophysiology and clinical manifestations of myelomeningocele (spina bifida)".)

Patients with muscular dystrophy may display lumbar lordosis. Kyphoscoliosis may accompany degenerativedisorders, such as Friedreich's ataxia and muscular dystrophies. Localized point tenderness over the spine maysuggest underlying intervertebral disc herniation, inflammation, fracture, or neoplastic process. The range of motionof the spine should be evaluated at all levels when indicated.

Head — The growth in size of the head is an indirect marker for increase in size of the brain, which measuresapproximately 450 g at birth and 1200 g by three to four years of age.

The occipitofrontal head circumference (OFC) is measured using a paper or cloth tape that is placed across fromjust above the bridge of the nose to the external occipital protuberance. The head circumference is compared withthe standard measurements for a given age. Serial head circumference measurements are more reliable than asingle recording. (See "Microcephaly in infants and children: Etiology and evaluation", section on 'Measurement'.)

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

The plantar reflex (S1) is elicited by stroking the plantar surface of the foot using a pointed but not sharpobject (eg, the metal end of a reflex hammer). The stroke is from a lateral to medial direction, posterior toanterior, stopping short at the base of the great toes. The normal response is one flexion of all toes. Patientswith corticospinal tract lesions manifest an extensor plantar response (Babinski sign), which is characterizedby 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 willelicit an eye blink. The afferent loop of the reflex is via cranial nerve V, while the efferent loop is through thefacial (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 alsoin the left and right lower abdominal quadrants (T11, 12). Stroking of a blunt metal object (eg, the metal endof a reflex hammer) in these quadrants in a medial to lateral direction elicits contraction of the abdominalmuscles. Abdominal reflexes may be lost in case of a pyramidal tract lesion.

The cremasteric reflex (L1­2) is elicited by stroking the medial aspect of the upper thigh, which elicitscontraction of the cremaster muscle and elevation of the testis.

Circumduction of a lower extremity may indicate spasticity, and is commonly observed in hemiparesisA broad­based, ataxic gait may accompany a cerebellar disorderA high steppage gait suggests peripheral neuropathyPatients with dystonia frequently show normal posture of the feet at rest but turn their feet inwards and walkon the outer edges of the feet

Myopathies, such as Duchenne muscular dystrophy, may be associated with a waddling gait

Macrocephaly is defined as OFC greater than the 97th percentile for age. (See "Macrocephaly in infants andchildren: Etiology and evaluation", section on 'Etiology'.)

Microcephaly is usually defined as OFC less than the 2 or 3 percentile for age, although some individualswith OFC in this range have no clinical abnormality. (See "Microcephaly in infants and children: Etiology andevaluation", section on 'Microcephaly'.)

nd rd

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who is not crying in the semi­upright position).

The sagittal and coronal sutures are palpated for ridging (craniosynostosis) or separation (raised intracranialpressure). 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 mayconfer 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 skullin the antero­posterior plane. Plagiocephaly or asymmetric flattening of the skull occurs when there is prematureclosure of one of the lambdoidal sutures. (See "Overview of craniosynostosis".)

In young infants with enlarged heads, transillumination can be performed to detect fluid­filled intracranial lesions.This is generally possible up to about six months of age. Transillumination is carried out by placing a bright sourceof light against the scalp in a darkened room. Hydrocephalus, hydranencephaly, porencephalic cyst, and chronicsubdural hematoma can be associated an increased transillumination. Auscultation of the head during infancy mayreveal a bruit in patients with vein of Galen arterio­venous malformation. (See "Hydrocephalus", section on 'CNSmalformations'.)

ELEMENTS OF THE GENERAL PHYSICAL EXAMINATION RELEVANT TO CHILD NEUROLOGY — Cluesto the diagnosis of many childhood neurological disorders can be obtained during a careful general physicalexamination. Additional detail on these disorders is available through the topic reviews linked below, and/or in theopen access databases Online Mendelian Inheritance in Man (OMIM) or the National Center for Biotechnologyinformation (NCBI) GeneReviews.

Dysmorphic features — The presence of an isolated unusual morphologic feature is common (noted in about 15percent of newborns in one series), and is not generally associated with underlying abnormalities [14]. However,the presence of two or more unusual morphologic features is much less common (0.8 percent of newborns) and isassociated 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 morecomprehensive reviews on dysmorphology [15].

Hypotelorism may accompany the holoprosencephaly sequence and trisomy 13. (See "Facial clefts andholoprosencephaly" and "Congenital cytogenetic abnormalities", section on 'Trisomy 13 syndrome'.)

Hypertelorism is commonly observed in patients with cleft palate, Sotos syndrome (cerebral gigantism) andApert, Saethre­Chotzen, Coffin­Lowry, 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'Saethre­Chotzen syndrome'.)

Inner epicanthal folds accompany Down syndrome, Rubinstein Taybi syndrome, Smith Lemli Opitzsyndrome, and Zellweger syndrome. (See "Down syndrome: Clinical features and diagnosis" and"Microdeletion syndromes (chromosomes 12 to 22)", section on '16p13.3 deletion syndrome (Rubinstein­Taybi syndrome)' and "Causes and clinical manifestations of primary adrenal insufficiency in children",section on 'Defects in cholesterol biochemistry' and "Peroxisomal disorders", section on 'Zellwegersyndrome'.)

Slanted palpebral fissures are common in Down syndrome, Apert syndrome, DiGeorge sequence, MillerDieker syndrome, rhizomelic chondrodysplasia punctata, and Aarskog syndrome. (See "DiGeorge (22q11.2deletion) syndrome: Clinical features and diagnosis" and "Microdeletion syndromes (chromosomes 12 to 22)",section on '17p13.3 deletion including PAFAH1B1 (Miller­Dieker syndrome)' and "Peroxisomal disorders",section on 'Rhizomelic chondrodysplasia punctata type 1'.)

Prominent, full lips are common in Williams syndrome. (See "Microdeletion syndromes (chromosomes 1 to11)", section on '7q11.23 deletion syndrome (Williams syndrome)'.)

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Skin examination — Skin findings associated with neurologic disease include the following:

External genitalia

Low set ears are seen in Noonan, Treacher Collins, Miller Dieker, Rubinstein Taybi, Smith Lemli Opitz, andPena Shokier syndromes, as well as Trisomy 9 and 18. (See "Causes of short stature", section on 'Noonansyndrome' 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 andholoprosencephaly".)

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 irregularsurface), and a brown fibrous plaque on the forehead. (See "Tuberous sclerosis complex: Genetics, clinicalfeatures, and diagnosis", section on 'Dermatologic features'.)

Neurofibromatosis type I is associated with six or more café­au­lait 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 'Clinicalmanifestations'.)

A port­wine stain over one half of the face is characteristic of Sturge Weber syndrome. The lesion invariablyinvolves the ophthalmic region of distribution of the trigeminal nerve. Many patients have an associatedintracranial (leptomeningeal) angioma, with hemiplegia and focal epilepsy. (See "Sturge­Weber syndrome".)

Petechial hemorrhages, which confer a “blueberry muffin” appearance to the skin, may be seen in neonateswith congenital cytomegalovirus infections. (See "Congenital cytomegalovirus infection: Clinical features anddiagnosis", section on 'Clinical manifestations'.)

A macular rash (located over the malar region of the face) is characteristic of systemic lupuserythematosus, 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 target­shaped lesion that is characteristic of Lyme disease. (See "Lymedisease: Clinical manifestations in children", section on 'Erythema migrans'.)

Vitiligo may be associated with autoimmune disturbances such as myasthenia gravis. (See "Vitiligo",section on 'Association with autoimmune disease'.)

Lax or redundant skin may accompany Coffin Lowry syndrome, Costello syndrome, and the Ehlers Danlossyndrome. (See "Rhabdomyosarcoma in childhood and adolescence: Epidemiology, pathology, andmolecular pathogenesis", section on 'Inherited syndromes' and "Joint hypermobility syndrome".)

Angiokeratomas, which are collections of small reddish bumps, are seen in Fabry's disease, which is alysosomal disorder due to absence of alpha galactosidase A. (See "Clinical features and diagnosis of Fabrydisease".)

Hypogonadism with small testicles or undescended testicles, and small penile size is common in PraderWilli syndrome (obesity, hypogonadism, hyperphagia, and mental retardation). (See "Clinical features,diagnosis, and treatment of Prader­Willi syndrome".)

Ambiguous genitalia may accompany x­linked lissencephaly and the syndrome of infantile spasms inassociation with hydranencephaly/lissencephaly and agenesis of the corpus callosum due to mutations in thearistaless related homeobox (ARX) gene. (See "Etiology and pathogenesis of infantile spasms".)

Macro­orchidism is common in Fragile X syndrome. (See "Fragile X syndrome: Clinical features and

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Lymphadenopathy — Subacute and chronic inflammatory or neoplastic disorders (eg, toxoplasmosis,tuberculosis, infectious mononucleosis, and lymphoma) may be associated with enlargement of lymph nodes overmultiple regions of the body. In some of these disorders there may be nonspecific neurologic symptoms such aslethargy or confusion.

Hepatosplenomegaly — Enlargement of the spleen and liver may be seen with the aforementioned infectiousdisorders. Lysosomal storage disorders, such as mucopolysaccharidoses and generalized GM1 gangliosidosis,and Niemann Pick disease can also lead to hepatosplenomegaly. (See "Mucopolysaccharidoses: Clinical featuresand diagnosis" and "Inborn errors of metabolism: Classification", section on 'Lysosomal storage disorders' and"Overview of Niemann­Pick disease".)

Abnormal hair — The following disorders have both neurologic manifestations and abnormalities of hair. Suchassociations are reviewed elsewhere in more detail [16].

Abnormal breath — The area from which abnormal smells are most easily detected is the nape of the neck or thescalp. Infants with phenylketonuria may manifest a mousy odor. Those with isovaleric aciduria may have an odorof sweaty feet. (See "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features", section on'Abnormal odors'.)

Cardiovascular

diagnosis in children and adolescents".)

Patients with x­linked adrenoleukodystrophy may manifest hyperpigmentation initially over the externalgenitalia. (See "Adrenoleukodystrophy".)

Brittle hair is common in argininosuccinic aciduria. (See "Urea cycle disorders: Clinical features anddiagnosis".)

The hair in Menkes disease is brittle, sparse, and tortuous. A simple clue to the diagnosis is examining hairunder low power of a light microscope. (See "Overview of dietary trace minerals", section on 'Menkesdisease'.)

Alopecia is common in rhizomelic chondrodysplasia punctata and in Rubinstein Taybi syndrome. (See"Peroxisomal disorders", section on 'Rhizomelic chondrodysplasia punctata type 1' and "Microdeletionsyndromes (chromosomes 12 to 22)", section on '16p13.3 deletion syndrome (Rubinstein­Taybi syndrome)'.)

Hirsutism and synophrys (joined eyebrows) are common in Cornelia de Lange syndrome. (See "Approach tocongenital malformations", section on 'Syndrome'.)

A white forelock of hair may accompany the Waardenburg syndrome (heterochromia of the iris, bright blueeyes, broad and prominent nasal root, midface hypoplasia, and congenital sensorineural deafness). (See"The genodermatoses", section on 'Waardenburg syndrome'.)

High output cardiac failure is common in newborns and infants having vein of Galen malformations. (See"Hydrocephalus", section on 'CNS malformations'.)

A floppy and weak infant with cardiomegaly and poor cardiac contractility may have Pompe's disease (acidmaltase deficiency or type II glycogen storage disease). (See "Lysosomal acid maltase deficiency (glycogenstorage disease II, Pompe disease)".)

Duchenne and Becker muscular dystrophies are associated with cardiomyopathy. (See "Clinical features anddiagnosis of Duchenne and Becker muscular dystrophy".)

Patients with Friedreich's ataxia frequently manifest hypertrophic subaortic cardiomyopathy, as well asprogressive ataxia and diabetes mellitus. (See "Friedreich ataxia".)

Patients with Barth’s syndrome have congenital dilated cardiomyopathy as well as skeletal myopathy and

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Otolaryngology — Macroglossia is often noted when the tongue protrudes from between the teeth. Macroglossiais a characteristic of Beckwith­Wiedemann syndrome and some forms of mucopolysaccharidosis (eg, Hurlersyndrome), and can also be seen in some patients with untreated hypothyroidism. Patients with macroglossiaoften have obstructive sleep apnea. (See "Beckwith­Wiedemann syndrome" and "Mucopolysaccharidoses: Clinicalfeatures and diagnosis", section on 'Hurler syndrome'.)

DEVELOPMENTAL SCREENING TESTS — Developmental screening tests complement the history andneurologic examination, can be conducted in the field by trained health professionals, and may facilitate earlydiagnosis of a childhood neurological disability and appropriate intervention. There are several brief and accuratedevelopmental screening tests that make use of information provided by the parents or direct observation orelicitation of developmental skills. (See "Developmental and behavioral screening tests in primary care", sectionon 'Developmental screening tests'.)

SUMMARY — A complete neurological assessment consists of a focused clinical history, a detailed neurologicalexamination, and a general physical examination that focuses on features that may be related to neurologicdisease.

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neutropenia. (See "Inherited syndromes associated with cardiac disease", section on 'Barth syndrome'.)

In infants and children, the history should include information about prenatal exposures and symptoms andassessment of developmental milestones (table 1). (See 'Pregnancy, perinatal, and neonatal history' aboveand 'Developmental history' above.)

Observations of infants and toddlers during play (eg, while stacking blocks or playing with an age­appropriatetoy) 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 questionsappropriate 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 byobservation 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, frog­legged position suggesting hypotonia, tremor, myoclonus, or tics. (See 'Posture andmovements' above.)

Muscle tone is the resistance felt upon passive movement of a joint through its range of motion. Hypotonia ischaracterized by decreased resistance to passive movement and hyperextension at the joints. Hypertoniacan 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. Inchildren 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 braindevelopment, 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 childhoodneurological disorders. Important features include facial dysmorphism, abnormalities of skin pigmentation,color and texture of hair, breath odor, hepatosplenomegaly, and evidence of cardiac disease. (See 'Elementsof the general physical examination relevant to child neurology' above.)

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GRAPHICS

Common developmental milestones

Milestone Age at acquisition

Fixes gaze briefly, habituates to stereotyped auditory, visual, andtactile stimuli

At birth (40 weeks postconceptional age)

Smiles responsively, gurgles 2­3 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 4­5 months

Maintains sitting position independently 6 months

Grasps objects using thumb and index finger pulp 8­9 months

Crawls, babbles, uses non­specific "Mama", "Dada" sounds 9­10 months

Pulls up to stand and walks with support 10­11 months

Walks independently, uses 2­3 clear words, including specific "Mama"and "Dada"

13­14 months

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

Names body parts, states age, uses phrases 24 months

Pedals tricycle, speaks in sentences, asks questions, likely toilettrained, can name primary colors

36 months

Masters concepts of alphabets and numbers 4­5 years

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

Concepts of division, multiplication, geography, general informationlike cities, states, large rivers, oceans, etc.

7­8 years

Courtesy of Suresh Kotagal.

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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 20months

Six to eight word vocabulary

Comprehends one­step commands

Points to two or three body parts

24 months Names two or three body parts

Uses phrases and simple sentences

24 to 36months

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

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The normal optic disc

The margins are distinct, the rim has a pinkish color, and there is acentral pale cup (arrows). This optic disc has a cup:disc ratio of 0.2.

Courtesy of Karl C Golnik, MD.

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Diffuse optic atrophy

Top: diffuse optic atrophy. Bottom: fellow eye with normal disc color.

Courtesy of Karl C Golnik, MD.

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Papilledema

Papilledema, characterized by blurring of the optic disc margins, lossof physiologic cupping, hyperemia, and fullness of the veins, in a 5­year­old girl with intracranial hypertension due to vitamin Aintoxication.

Courtesy of Gerald Striph, MD.

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Macular cherry red spot

Sphingolipids accumulate in the retinal ganglion cells in the perifovealarea of patients with sphingolipidoses causing the perifoveal area toappear pale. The fovea, which has no ganglion cells, retains its"cherry red" color.

Courtesy of Robert P Cruse, DO.

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Dome­shaped retinal hemorrhage

Dome­shaped retinal hemorrhages may break into the vitreous.

Courtesy of Brian Forbes, MD, PhD.

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Corneal light reflex

The corneal light reflex test involves shining a light onto the child'seyes from a distance and observing the reflection of the light on thecornea with respect to the pupil. The location of the reflection fromboth eyes should appear symmetric and generally slightly nasal to thecenter of the pupil. A) Normal corneal reflex. B) Corneal light reflex inesotropia. C) Corneal light reflex in exotropia.

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Common developmental reflexes

Reflex DescriptionAge at

appearanceAge at

resolution

Moro(startle)

The examiner holds the infant supine in his orher arms, then drops the infant's head slightlybut suddenly. This leads to the infant extendingand abducting the arms, with the palms open,and sometimes crying. Alternatively, theexaminer may lift the infant's head off the bedby 1 to 2 inches and allow it to gently dropback; this maneuver elicits a similar response.

34 to 36 weeksPCA

5 to 6 months

Asymmetrictonic neckreflex

With the infant relaxed and lying supine, theexaminer rotates the head to one side. Theinfant extends the leg or arm on the sidetowards which the head has been turned, whileflexing the arm on the contralateral side(fencing posture).

38 to 40 weeksPCA

2 to 3 months

Trunkincurvation(Galant)

With the infant in a prone position, theexaminer strokes or taps along the side of thespine. The infant twitches his or her hips towardthe side of the stimulus.

38 to 40 weeksPCA

1 to 2 months

Palmargrasp

The examiner places a finger in the infant'sopen palm. The infant closes his or her handaround the finger, tightens the grip if theexaminer attempts to withdraw the finger.

38 to 40 weeksPCA

5 to 6 months

Plantargrasp

The examiner places a finger under the infant'stoes. The infant flexes the toes downwards to"grasp" the finger.

38 to 40 weeksPCA

9 to 10months

Rooting The examiner strokes the infant's cheek. Theinfant turns the head toward the side that isstroked, and makes sucking motions.

38 to 40 weeksPCA

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 upperextremities towards the ground as if to break afall.

8 to 9 monthsof age

Persiststhroughoutlife

PCA: post­conceptional age.

Courtesy of Suresh Kotagal, MD.

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