Neurological examination of newborns and infants    

Draft translation

Central Insitute of improving doctor’s qualification

E.A. Edelstein

Neurological examination of newborns and infants is based on the same scheme that is used for older children and adults:

1)      CN
2)      Motor function
3)      Reflexes
4)      Sensation
5)      Meningeal signs

It should be noted that neurological status of the newborns has some special features. The mainstay of investigation is the analysis of congenital reflexes which reflect the maturity if CNS, viability of the newborn and adaptation potential.

The following conditions should be fulfilled during examination: comfortable room T (25-26), and it is not recommended to examine the child immediately postprandial or before feeding because feeding determinant can change the level of his congenital reflexes.

It should be noted that congenital reflexes of newborns are very labile and are easily fatigued. One should elicit reflexes quickly and turn the child only after cranial and facial skeleton and cranial nerves have been already tested.

It is important to look for dysembryological stigmata, which can be frequently encountered: abnormal earlobes (low amount of helixes, absence of earlobes, elongated upper part – rabbit's ear, low set ears), wide nose bridge (hypertelorism), prognatism, low hair border.

Much attention should be paid to the head shape: dolicocephaly, brachiocephaly, tower-like skull, left or right inclination are all variants of normal skull. Sometimes head deformities are caused by cephalohematoma or birth swelling. Associated asymmetry of head and face bones suggests intrauterine pathology most frequently of embryonic stage of development.

HC should is measured. HC varies significantly from 33 to 37.5 cm. Analyzing HC one should take into consideration height, weight and HC to chest diameter ration. At birth HC should not exceed chest diameter by more than 1-2 cm. Average HC in a newborn whose weight=3000-3500 g; height=50-52 is 36 cm. In newborns HC may actually be less because of overriding of skull sutures.

HC should increase by 4 cm in first 3 month, i.e. HC at 3 month = 40 cm. In first month HC increases by 2 cm, in second month by 1.0-1.5 cm and in third one by 1.0 cm. During the next 3 month HC increases by 3 cm and at 6 month = 43 cm and at 1 year =46 cm (i.e. +3 cm within the next 6 month).

During the first year of life HC increases by 10 cm.

Normal head growth

Frontal fontanel should be palpated, its size should not exceed 2.5 x 3.0 cm. Coronal and saggital sutures should be palpated as well. Coronal suture is normally closed at birth. Saggital suture is sometimes open at birth but should not be wider than 0.5 cm.

When tense and bulging anterior fontanel, or opening of the saggital suture is for more than 0.5 cm is present one should suspect intracranial hypertension. Other symptoms suggestive of intracranial hypertension are:

a)      Tower-like skull with high forehead (Socrat's head)

b)      Dolichocephalic skull with prominent occipit. Child tends to hyperextend his neck (due to increased tone of extensors)

c)      Wrist tremor with tendency to finger extension

d)      Grefe's sign

e)      Setting sun sign

The latter two signs should be distinguished from each other in spite of the fact that they have similar presentation: Grefe's sign is a band of white sclera above the iris when eyeballs are not moving. In the absence of other symptoms Grefe's sign is not indicative of intracranial hypertension. It is frequently seen in premature children with exophthalmosis and hypotrophia.

Setting sun sign is elicited by repeated head nods. It presents as a down deviation of eyeballs and a white band of sclera appears above the iris. If intracranial hypertension is pronounced and when hyperbilirubinemia is present (especially in premature babies) this sign sometimes appear spontaneously without a head nod. It originates from tectum of mesencephalon and signifies local hypertension in the 3^rd ventricle and Sylvian aqeduct, irritation of the 3^rd cranial nerve nucleus and its connections to the 8^th nerve.

Cranial nerves

1^st: In response to any strong odor the child wrinkles his nose, shuts his eyes and sometimes sneezes.

2^nd: Light makes the newborn to shut his eyes. If this is not seen optic nerve damage should be suspected and ophthalmologist consultation is essential.

3, 4, 6^th: Width and symmetry of eyes should be checked. Bilateral ptosis present at birth signifies embryonic defect (underdevelopment of oculomotor nucleus) which can have genetic cause.

Posterior longitudinal fasciculus is not developed fully at birth, that is why newborns frequently do not demonstrate coordinated eyeball movements and sometimes have short periods of esotropia and nystagmic movements. Pronounced esotropia is a sign of intracranial trauma. Marked nystagmus is a sign of poor vision or blindness especially if wide pupils and absence of eye closing at light are seen.

By the end of the first month of life when cortex and its interconnections between frontal, parietal and occipital lobes are present children start to concentrate in response to a sound or a light sources following the object with their eyes. Insufficient of absent concentration reaction can be caused by abnormal psychic development secondary to intrauterine or intranatal damage of cortex or damage of visual or acoustic nerves. Exo- eso or microphthalmos can be noted (microphalmos is characteristic of infectious fetopathies: toxoplasmosis, CMV, etc). Horner's sign can be present. It is usually caused by irritation of cervical sympathetic ganglion in peripheral arm paralysis, TB infection.

Pupils react to light since birth. Examiner should note shape of the pupils. Normally pupils are round and symmetrical. Irregular form should raise suspicion of coloboma of cataract (defect of embriologic period).

Epipsoid pupils, especially if paradox reaction to light is present (Argyl-Robinson reaction) can be a sign of congenital syphilis. Characteristic atrophy seen on fundi (salt and pepper) should further increase suspicion of congenital syphilis even if VDRL is negative.

5^th: Trigeminal nerve function is important for sucking (together with 7^th and 12^th nerve).

Normally mandibule is in tight contact with maxilla and is symmetrical. Low position of mandibule, food falling out, absence of smaking sounds indicates pathology (trauma or underdevelopment) of the motor nucleus of the trigeminal nerve. Difference in sweating and color of half of the face (Harlequin’s sign) should raise the suspicion about sensitive branch involvement. Combined pathology of the motor branch of the 5^th nerve and the facial nerve is characterized by a group of congenital reflexes of oral automatisms, which will be discussed later.

7^th nerve: one should differentiate congenital face asymmetry and nerve damage. Asymmetrical face muscles are usually seen along with bone asymmetry: both facial and skull bones. Nasolabial folds are notable only in hypotrophic children, therefore, to diagnose central facial paresis (which is characterized by paresis of lower facial muscles) ipsilateral hemiparesis should be sought.

Only the presence of hemiparesis (sometimes, mild) plus facial muscle asymmetry allows to diagnose central facial nerve palsy. In central palsy the angle of the mouth is depressed and the lips are thin at the side of damage. If the damage is extensive scout reflex is weak at the ipsilateral side, when crying mouth is displaced to the undamaged side. Peripheral facial palsy is easy to diagnose. This type of palsy can be caused by intrauterine pathology (genetic or exogenous) or more frequently by birth trauma when newborn's head stays long in the birth canal, facial presentation or obstetrician-assisted delivery can be other causes. Clinical picture is similar despite multiple etiologies: eye does not close fully at sleep, sometimes lagophthalomosis is present; when crying asymmetry of palpebral fissures with more opening at the injured side, deviation of the mouth to the uninjured side are noted. At the injured side food falls out of the angle of the mouth and scout reflex is weak. Sometimes newborns have alternating Miiar-Gubler's syndrome: peripheral palsy of the facial nerve and contralateral hemiparesis. This syndrome is characteristic of the intranatal hemorrhage in the pons.

8^th. At birth the normal child reacts to sounds: loud noise cause him to shut his eyes. Eye closing is a universal reaction when checking peripheral analyzers: olfaction, vision, and acoustic. If there is now eye closing to loud sounds acoustic abnormalities due to embryologic or fetal period injury should be suspected. Sometimes loud sounds cause the child to shudder or abduct his arms (first phase of Moro's reflex). Abrupt shuddering (the so-called start reflex) can signify low seizure threshold (irritation of brain-stem structures with reflex arc closing at the level of tectum of mesenchaphalon.

Vestibular portion of the nerve can be assessed by several congenital reflexes: Moro's reflex, cervical-tonic reflex, tonic labyrinth reflex, and protective reflex. All them involve connections of vestibular nerve and reticular formation, accessory nerve and anterior horns of cervical and lumbar intumescences. 

9-10. One of the most important functions of these nerves is swallowing which is performed by the muscles of pharynx and soft palate innervated by a common motor nucleus of these nerves. Pathology of development of this nucleus makes child non-viable. As soon as feeding via NG tube stopped the child dies because of absence of swallowing reflex and swallowing itself.

When different intrauterine abnormalities of brain are present due to circulation problems intranatally, children sometimes demonstrate clinical picture of nuclear pathology (the so-called bulbar palsy) or supranuclear damage of corticonuclear pathways leading to the above mentioned nucleus (pseudobulbar palsy). It is very difficult to differentiate those conditions in newborns but the correct diagnosis is very important because of different prognosis.

Bulbar and pseudobulbar palsy are characterized by difficulty swallowing and abnormal phonation. The child cannot swallow milk, chokes and coughs, milk pours out through his nose. Voice changes are present: child’s cry is muffled, low modulated and “nasal”.

Bulbar palsy also causes shortness of breath with abnormal rhythm with no (especially at the early stages) changes in lungs. Arrhythmias are seen, periodic bradycardia is characteristic. Underlying pathologic process of bulbar syndrome is damage to caudal parts of brain (medulla oblongata) where nucleuses of vagus and hypoglossus are in vicinity of respiratory and vasomotor centers. Damage to these structures is life threatening. Pseudobulbar palsy is not.

Pseudobulbar palsy, however, may the cause of aspiration pneumonia. Dx of pseudobulbar palsy can be confirmed when central palsy of n. hypoglossus is present characterized by limited motion of the tongue. Reflexes of oral automatism are normal for newborns but pathological for adults and are included in the pseudobulbar syndrome in adults.

11^th innervates neck and shoulder muscles performing head turning and head lifting in older children. When child is lying on his abdomen this nerve is responsible for protective reflex. When this nerve is damaged torticollis occurs causing redistribution of the tone and elements of neck-tonic reflex appear. Not infrequently children demonstrate head tics (hyperkynesis caused by damage of cortico-nuclear pathways. Sometimes torticollis associated with flaccid paresis of arms as a result of spinal and brachial plexus trauma. The most frequent type of torticollis the intranatal trauma of sternocleidomatoideus with resulting intramuscular hemorrhage (the muscle is indurated and tender). This type of torticollis should be followed by orthopedist. Neurological status should be checked carefully to rule out possible damage of the accessory

12^th innervates tongue. In the normal awake child tongue is in active movement. Flaccid paresis is rarely seen and is due to underdevelopment of hypoglossal nucleus. Central paresis is much more frequent manifesting by limited motion of the tongue. It becomes tense and indurated (folded in a wad), initiation of sucking is poor.

Motor activity

The examination of the motor activity starts with noting the child’s posture. Unrestrained healthy newborn is in constant chaotic movement with predominant flexion. Arms and legs are flexed and adducted. Wrists are flexed into fist with the thumb opposed, feet are moderately extended (180 degrees to the shins). This position is called “embryo’s posture”. In contrast to intrauterine posture child extends his head because of extensors hypertonus. Limb movement should also be noted.

Pre- and intra-natal pathologies can cause changes in posture.  Open wrist (seal’ paws) are frequent in pathology of brain circulation with intracranial hypertension. If the examiner sees an extended arm with internally rotated wrist he should suspect flaccid palsy. Legs in extension with tendency to crossing, feet in varus position with plantar hyperflexion (sometimes they even reach the shins) are characteristic for spastic paresis.

Extended arms (in internal rotation) and legs (with abducted hips and sometimes with dropped feet) (frog’s posture) are frequently seen in low-neuron paresis. It is obvious that motor function in all above cases is impaired. Not infrequently motor function is abnormal even in the absence of posture changes. In this case one should suspect diffuse inhibition of motor function which often caused by pathology of brain circulation (SAH or hypertension syndrome). Asymmetric movements prompt for searching latent paresis (monoparesis, hemiparesis, etc.)

It is important to estimate muscle tone. Normally tone is greater in limb flexors and neck extensors before 1.5-2 month of life that is why it is difficult to differentiate normal tone from pathological one. Intrauterine pathology sometimes lead to hypertonicity in hip adductors. When passive abduction meets resistance the examiner should differentiate between dysplasia, congenital dyslocation and spastic muscles. This differentiation requires orthopedist consultation. Frequently newborns have muscle hypotone caused by meningeal and cerebral hemorrhages due to diashise ? . Hypotone can transform into hypertone. Diffuse hypotonia with severely limited ROM (especially in proximal limbs) suggests congenitalneuro-muscular diseases or various congenital metabolic abnormalities.

Tendon reflexes are very labile in newborns. The can be elicited only in 25-30% of children. It is advised to fix child’s knee in a kind of lock: the thumb stabilizes the shin, the index fixes the hip and the middle finger is put in the patellar fossa. Knee is bend 120 degrees (Fig. 1).

By using the light vibration the pediatrician can relax the child’s leg and find the most productive position. The stroke should be made by index or middle finger but not by a hammer.

Sensation: the newborns react to hot and cold stimulus by changing their motor activity, sometimes they show undifferentiated verbal reaction.

Meningeal signs in newborns and in several month old infants have some characteristic features.

There is no nuchal rigidity because due to open fontanels and sutures there is no tension of meninges. It is necessary to remember that nuchal rigidity checking requires stabilization of the thorax simultaneously with neck flexure to overcome physiologic hypertonicity of neck flexors. Positive Kernig and lower Brudzinsky are normal until 4-6 month old.

Involvement of meninges can be suspected with tense, pulsating fontanel, general hyperestesia, opisthotonus, hanging symptom increasing opisthotonus and leg flexion when vertically lifting the child.

Congenital reflexes

Congenital reflexes are the hallmarks of maturity of CNS, viability and adaptation resources. Arcs of these reflexes end at different levels of the spine and brain stem and reflect function of cranial nerves and motor systems. It is useful to know only those reflexes, which are the most representative since first hours of life. For maximum convenience we list reflexes not by anatomy but by child’s posture.

Reflexes elicited when child is lying on his back

1.      Oral group of reflexes (5, 7, 12^th CN):

a)      Scout reflex (Kussmaul’s reflex): touching with a finger of a pacifier of an angle of the mouth makes child to open his mouth and protrude his tongue trying to reach the stimulus.

b)      Sucking reflex: finger, pacifier or nipple put in the mouth are compressed by child’s lips and sucking begins. Pathology of cranial nerves responsible for sucking cause insufficient degree of vacuum within the oral cavity.

c)      Palm-mouth reflex of Babkin: pressing on both thenars makes child to open his mouth, slightly flex his head, sometimes protrude his tongue. Babkin’s reflex is sensitive and it disappears when CNS damage is present, especially after intranatanl circulation problems. Rapid return of this reflex is a good prognostic sign.

2.      Hugging reflex (Moro’s reflex): vestibular portion of 8^th nerve is responsible for this reflex. It is elicited by sharp blow to the table 20-30 cm from child’ head. Child should abduct his arms, extends his legs, which were previously flexed and drawn to the abdomen. Moro’s reflex consists of two phases: first phase is arm abduction, second phase is arm adduction with a tendency towards hugging himself. That is why French scientist Moro called it a “hugging reflex”.

Normally both phases are present. Sometimes initially in first weeks of life only first phase is present and the second phase appears later, this is also normal. Absence of Moro’s reflex or absence of the second phase raise suspicion of pre- or intranatal pathology involving vestibular nerve. Moro’s reflex is effected by low motor neuron at the level of cervical intumescences (arms movement) and if traumatic low motor neuron palsies are present Moro’s reflex will not be elicited in spite of the intact vestibular apparatus. Moro’s reflex is also absent in other low motor palsies. Spastic paresis cause absence of Moro’s reflex initially later it becomes exaggerated and persists.

Exaggeration of Moro’s reflex, spontaneous Moro’s reflex (to sound or with no reason) is a reflexion of tectum of mesencephalonf “start-reflex” and speaks for low seizure threshold.

3. Cervical clonic asymmetrical reflex (Magnus-Klein’s reflex) reflects maturity of 8^th and 9^th nerves and their connections to motor centers. It is elicited by passively turning the child’s head. Extremities to which the head is turned extend, arm is frequently elevated. The contralateral extremities flex. The child’s posture is called the “swordsman posture”. Extenors’ tone is increased. Not infrequently children have torticollis (the etiologies are listed above) in responce asymmetrical cervical clonic reflex develops leading to redistribution of tone in extremities which is normal. Pre- and intranatal abnormalities can cause late development of this reflex.

4.      Grasping reflex: when examiner presses on child’s palm the child grasps the examiner’s finger. Sometimes it is possible to lift the child that way. IT is important to estimate the symmetry of this reflex. Flaccid paralysis causes absent or diminished reflex of the ipsilateral side. Different types of brain circulation abnormalities causing motor insufficiency can lead to diminished reflex which can be bilaterally (suspect cerebral palsy with bilateral hemiplegia) or unilateral (often these children have hemiplegic form of cerebral palsy).

5. Plantar reflex is the analogue of the grasping reflex. Pressing at the middle of the plantar side of the foot makes child to flex his toes. Symmetricity of this reflex is also important.

6. Babinski’s reflex. It is elicited by gentle tickling of the foot. In response child extends the big toe and puts his other toes in a fan-like fashion. The examiner should note symmetricity and strength of this reflex. When motor abnormality is present Babinsky can be spontaneous and be present earlier on the involved side.

Reflexes in the vertical position

Child is supported under armpits from the back, and thumbs of the examiner support the child’s head.

1.      Support reflex is elicited when child’s feet touch the examining table. It consists of 2 stages. First stage: when child’s feet touch the table he flexes his legs. Second stage: child extends his leg against the table planting his feet. If child puts only his toes on the table one should suspect motor dysfunction. Planting of toe and crossing of legs speak for spastic paresis.

2.      Automated ambulation can be viewed as a third stage of the support reflex. When child’s body is slightly flexed (propulsion position) child begins to move his legs, making steps. If legs stuck against each other, leaning on the toes (ballet dancer’s posture) is present or if automated ambulation is absent then motor insufficiency is present with various degrees of spastic paresis.

Reflexes in a lying on the abdomen position

1.      Protective reflex: when lying on the abdomen healthy newborn immediately turns his head to the side sometimes nodding several times trying to elevate his head. When children grow 1-1.5 month old protective reflex transforms into head elevation reflex. Ante- and intranatal pathologies of CNS protective reflex appears late or even is absent. Absence of the protective reflex and later – absence of head elevation signify the poor prognosis because it speaks for impairment of 8^th and 11^th CNs with delay or absence of verticalization and motor functions.

2.      Crawling reflex (Bauer’s reflex): when child’s feet leans against examiner’s palms the child makes swimming-like movements and crawls. Sometimes child makes crawling movements spontaneously. In motor function abnormalities crawling reflex can be diminished, any palsies (low or upper neuron) cause it’s absence.

3.      Spinal reflex of Galant: light stroking parallel to the spine makes child flex his body in an arc looking away from stimulation and flex ipsilateral limbs. This reflex is diminished or absent in flaccid or spastic palsies of any etiology.

There are many other reflexes described by different authors checking the same functions and maturity of CNS. Newborn reflexes are very labile and easily fatigued that is why we decided to choose the most representative ones for each group, which allow to describe CNS condition of the infants and newborns. All the above reflexes can be elicited since first or second day of life, normally are brisk and persist until 1.5-2 month old except for sucking reflex, which persist until 1 year. With any pathology of CNS reflexes are delayed and later they can persist for years being one of the symptoms of cerebral palsy.

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