FENICHEL'S. CLINICAL. PEDIATRIC. NEUROLOGY. A Signs and Symptoms Approach. Seventh Edition. London, New York, Oxford, St Louis, Sydney, Toronto . Confidently diagnose and manage primary neurologic disorders of childhood with actionable, step-by-step assistance from Fenichel's Clinical Pediatric. The Publisher Library of Congress Cataloging-in-Publication Data Fenichel, Gerald M. Clinical pediatric neurology: a signs and symptoms approach / Gerald M.
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Fenichel GM, Clinical Pediatric Neurology, 5th Ed, , Elseiver - Download as PDF File .pdf), Text File .txt) or read online. neurologi anak. Fenichel's Clinical Pediatric Neurology 7 Ed - Ebook download as PDF File .pdf), Text File .txt) or read book online. enichel's Clinical Pediatric Neurology. Request PDF on ResearchGate | On Jan 1, , Jesus E Pina-Garza and others published Seventh edition of “Fenichel Clinical Pediatric Neurology.
Sensory Symptoms Pain, dysesthesias, and loss of sensibility are the important symptoms of disturbed sensation. Peripheral neuropathy is the most common cause of disturbed sensation at any age.
As a rule, hereditary neuropathies are more likely to cause loss of sensibility without discomfort, whereas acquired neuropathies are more likely to be painful. Discomfort is more likely than numbness to bring a patient to medical attention. Nerve root pain generally follows a dermatomal distribution. Ordinarily, it is described as deep and aching. The pain is more proximal than distal and may be constant or intermittent.
When intermittent, the pain may radiate in a dermatomal distribution. The most common cause of root pain in adults is sciatica associated with lumbar disk disease.
Disk disease also occurs in adolescents, usually because of trauma.
In children, radiculitis is a more common cause of root pain. Polyneuropathy involving small nerve fibers causes dysesthetic pain. It compares with the abnormal sensation felt when dental anesthesia is wearing off.
The discomfort is superficial, distal, and usually symmetrical. Dysesthetic pain is never a feature of hereditary neuropathies in children. Loss of sensibility is the sole initial feature in children with sensory neuropathy. Because clumsiness is the initial feature, delay in establishing a correct diagnosis is common.
Strength is normal, as are tests of cerebellar function. Tendon reflexes are absent. The combination of areflexia and clumsiness should suggest a sensory neuropathy. Table 9—1 summarizes the pattern of sensory loss as a guide to the anatomical site of abnormality. The cerebellum and its major input systems from the frontal lobes and the posterior columns of the spinal cord provide this control.
The initial and most prominent feature is usually an abnormal gait. The ataxic gait is wide- based, lurching, and staggering, and it provokes disquiet in an observer for fear that the patient is in danger of falling.
One observes a similar gait in people who are attempting to walk in a vehicle that has several directions of motion at once, such as a railroad train. When an abnormality occurs in the vermis of the cerebellum, the child cannot sit still but constantly moves the body to-and-fro and bobs the head titubation. In contrast, disturbances of the cerebellar hemispheres cause a tendency to veer in the direction of the affected hemisphere, with dysmetria and hypotonia in the ipsilateral limbs.
Bifrontal lobe disease may produce symptoms and signs that are indistinguishable from the symptoms and signs of cerebellar disease. Loss of sensory input to the cerebellum, because of peripheral nerve or posterior column disease, necessitates constant looking at the feet to know their location in space.
The gait also is wide-based, but is not so much lurching as careful. The foot raises high with each step and slaps down heavily on the ground. Station and gait are considerably worse with the eyes closed, and the patient may fall to the floor Romberg sign.
Sensory ataxia is more likely to cause difficulty with fine finger movements than with reaching for objects. Other features of cerebellar disease are a characteristic speech that varies in volume and has an increased separation of syllables scanning speech , hypotonia, limb and ocular dysmetria, and tremor.
The differential diagnosis of a child with acute ataxia or recurrent attacks of ataxia Table 10—1 is quite different from that of a child with chronic static or progressive ataxia Table 10—2. These two presentations are discussed separately. Progressive ataxia superimposes on the acute attacks.
Migraine, brainstem encephalitis, and an underlying neuroblastoma are the next considerations. Recurrent ataxia is uncommon and usually is caused by hereditary disorders; migraine is the most common cause, and disorders of pyruvate metabolism are second. Brain Tumor Primary brain tumors ordinarily cause chronic progressive ataxia see discussion later. Ataxia may be acute, however, if the brain tumor bleeds or causes hydrocephalus. In addition, early clumsiness may not become apparent until it becomes severe enough to cause an obvious gait disturbance.
Brain imaging is a recommendation for most children with acute cerebellar ataxia. The distinction between an acute and an insidious onset should be easy but can be problematic. In children with a slowly evolving hemiplegia, missing early weakness is possible until an obvious level of functional disability is attained; at this point, the hemiplegia seems new and acute. An additional presentation of hemiplegia in infants who come to medical attention because of developmental delay is slowness in meeting motor milestones and early establishment of hand preference.
Children should not establish a hand preference until the second year.
They have a static structural problem from birth hemiplegic cerebral palsy , but the clinical features are not apparent until the child is old enough to use the affected limbs. Magnetic resonance imaging MRI is the diagnostic modality of choice for investigating all forms of hemiplegia. MRI is especially informative in showing migrational defects in hemiplegic cerebral palsy associated with seizures. Magnetic resonance angiography is sufficiently informative to obviate the need for arteriography in most children.
Hemiplegic Cerebral Palsy The term hemiplegic cerebral palsy comprises several pathological entities that result in limb weakness on one side of the body. In premature infants, the most common cause is periventricular hemorrhagic infarction see Chapter 4. In term infants, the underlying causes are often cerebral malformations, cerebral infarction, and intracerebral hemorrhage.
Imaging studies of the brain are useful to provide the family with a definitive diagnosis; this often relieves guilt and prevents litigation against the obstetrician. The usual concern that brings infants with hemiplegia from birth for a neurological evaluation is delayed crawling or walking. Abnormalities of the legs are the focus of attention. An associated but seldom recognized feature is that hand dominance was established during the first year; this is never normal.
Unilateral facial weakness is never associated, probably because bilateral corticobulbar innervation of the lower face persists until birth. Epilepsy occurs in half of children with hemiplegic cerebral palsy. Infants with injury to the dominant hemisphere can develop normal speech in the nondominant hemisphere, but it is at the expense of visuoperceptual and spatial skills.
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Infants with hemiplegia and early-onset seizures are an exception; they show cognitive disturbances of verbal and nonverbal skills. Chapter 17 describes a bilateral perisylvian syndrome with speech disturbances. Seizures and mental retardation are often associated. As a rule, epilepsy is more common when congenital malformations cause infantile hemiplegia than when the cause is stroke.
The rim of gray matter around the defect in the left hemisphere indicates that the abnormity is a schizencephaly rather than an infarction. Many conditions described fully in this chapter are abnormalities of the spinal cord.
The same spinal abnormality can cause paraplegia or quadriplegia, depending on the location of the injury, so these conditions are discussed together in this chapter. Approach to Paraplegia Weakness of both legs, without any involvement of the arms, suggests an abnormality of either the spinal cord or the peripheral nerves.
Ordinarily a pattern of distal weakness and sensory loss, muscle atrophy, and absent tendon reflexes provides recognition of peripheral neuropathies see Chapters 7 and 9.
In contrast, spinal paraplegia causes spasticity, exaggerated tendon reflexes, and a dermatomal level of sensory loss. Disturbances in the conus medullaris and cauda equina, especially congenital malformation, may produce a complex of signs in which spinal cord or peripheral nerve localization is difficult; both may be involved.
Spinal paraplegia may be asymmetrical at first, then the initial feature is monoplegia see Chapter When anatomical localization between the spinal cord and peripheral nerves is difficult, electromyogram and nerve conduction studies are useful in making the distinction.
Cerebral abnormalities sometimes cause paraplegia. Leg weakness is so much greater than arm weakness, however, that paraplegia is the chief complaint. The brain and the spinal cord may be abnormal, and the abnormalities can be in continuity syringomyelia or separated Chiari malformation and myelomeningocele.
Many conditions that cause paraplegia or quadriplegia begin as monoplegia. One also must consult the differential diagnosis of spinal paraplegia provided in Table 12—1 when considering monoplegia. In addition, several cerebral disorders that cause hemiplegia may begin as a monoplegia so that tables in Chapter 11 also are applicable.
Approach to Monoplegia Either pain or weakness may cause refusal to use a limb.
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The cause of most painful limbs is injuries. Other causes are arthritis, infection, and tumor. Pain and weakness together is a feature of plexitis. Table 13—1 summarizes the differential diagnosis of acute monoplegia. Plexopathies and neuropathies are the leading causes of pure monoplegia. Stroke often affects one limb more than others, usually the arm more than the leg. The presentation may suggest monoplegia, but careful examination often reveals increased tendon reflexes and an extensor plantar response in the seemingly unaffected leg.
Any suggestion of hemiplegia rather than monoplegia or increased tendon reflexes in the paretic limb should focus attention on the brain and cervical cord as the pathological site.
When it occurs, one should suspect syringomyelia and tumors of the cervical cord or brachial plexus. Chronic progressive weakness of one leg suggests a tumor of the spinal cord or a neurofibroma of the lumbar plexus. A monomelic form of spinal muscular atrophy, affecting only one leg or one arm, should be considered when progressive weakness is unaccompanied by sensory loss.
Abnormal movements can be the main or initial features of disease, or they can occur as a late manifestation. This chapter discusses the former type. Approach to the Patient Movement disorders are not describable; they require visualization. If abnormal movements are not present at the time of examination, instruct the parents to videotape the movements at home. Some relatively common movements are recognizable by description, but the rich variety of abnormal movements and postures that may occur defies classification.
The most experienced observer, at times, mistakes one movement for another or has difficulty conceptualizing the nature of an abnormal movement. Many abnormal movements are paroxysmal or at least intermittent. Movement, startle, emotional upset, or sleep induces some movements. The physician should ask what makes the movement worse and if it is action induced.
Ask children to perform the action during the examination. Paroxysmal movements raise the question of epilepsy. The concurrent presence of seizures and involuntary movements characterizes many neurological disorders of childhood. Nocturnal paroxysmal dystonia, previously thought to be a movement disorder, is actually a frontal lobe seizure see Chapter 1. The clinical and conceptual distinction between spinal myoclonus and spinal seizures remains a gray area.
The following guidelines are useful to distinguish involuntary movements from seizures: Involuntary movements, with the exception of spinal myoclonus and periodic movements of sleep, abate or disappear during sleep; seizures persist or may worsen. Involuntary movements usually have a more stereotyped appearance and, with the exception of acute drug reactions, are more persistent than seizures. Seizures are often characterized by loss of consciousness or awareness; involuntary movements are not.
Seizures are usually accompanied by epileptiform activity on electroencephalogram EEG ; involuntary movements are not.
Low-amplitude jerking movements that move a joint or muscles may be focal seizures, chorea, myoclonus, tics, or hemifacial spasm. High-amplitude jerking movements that move a limb or limbs may be seizures, ballismus, or myoclonus. Slow, writhing movements and abnormal posturing may be due to athetosis, dystonia, continuous motor unit activity see Chapter 8 , or seizures.
The possible causes of rhythmic movements may be tremor, seizures, or myoclonus. Disorders of the visual sensory system, ocular muscles, ocular motor nerves, neuromuscular transmission, or gaze centers of the central nervous system may disturb ocular motility. This chapter discusses nonparalytic strabismus, paralytic strabismus ophthalmoplegia , gaze palsies, ptosis, and nystagmus.
Visual and pupillary disorders are discussed in Chapter Many individuals have a latent tendency for ocular misalignment, heterophoria, which becomes apparent only under stress or fatigue.
During periods of misalignment, a child may have diplopia or headache. Constant ocular misalignment is heterotropia. Children with heterotropia suppress the image from one eye to avoid diplopia. If only one eye fixates continuously, visual acuity may be lost permanently in the other developmental amblyopia. In nonparalytic strabismus, the amount of deviation in different directions of gaze is relatively constant comitant.
Each eye moves through a normal range when tested separately ductions , but the eyes are disconjugate when used together versions. Many children with chronic brain damage syndromes, such as malformations or perinatal asphyxia, have faulty fusion or faulty control of conjugate gaze mechanisms nonparalytic strabismus. In neurologically normal children, the most common cause of nonparalytic strabismus is either a genetic influence or an intraocular disorder.
Ocular alignment in the newborn is usually poor, with transitory shifts of alignment from convergence to divergence. Constant ocular alignment usually begins after 3 months of age. The eyes assume a normal position during sleep and are able to move upward reflexively. Esotropia Esotropia is an inward deviation convergence of the eyes. Early-onset or infantile esotropia is present before 1 year of age. The observation of accommodative esotropia is usually between 2 and 3 years of age and may be undetected until adolescence.
The misalignment is sufficient that family members see that a problem exists. Some children fixate almost entirely with one eye and are at risk for permanent loss of visual acuity developmental amblyopia in the other eye. Accommodative esotropia occurs when accommodation compensates for hyperopia.
Accommodation more sharply focuses the blurred image. Because convergence accompanies accommodation, one eye turns inward. Some children with accommodative esotropia cross-fixate and use each eye alternatively, while the other maintains fixation. If one eye is more hyperopic than the other eye, however, only the better eye fixates, and the unused eye has a considerable potential for amblyopia. An ophthalmologist should examine the eyes to determine whether hyperopia is present. Eyeglasses correct hyperopic errors.
The treatment of early-onset esotropia, in which only one eye fixates, consists of alternate eye patching. Early corrective surgery is required for persistent esotropia. The most common visual disorders are uncorrected refractive errors, amblyopia, strabismus, cataracts, and genetic disorders.
Two conditions that are increasing in frequency are retinopathy of prematurity and retinal hemorrhage caused by child abuse. Assessment of Visual Acuity The assessment of visual acuity in preverbal children relies mainly on assessing fixation and following and on observing the way an infant or young child interacts with the environment.
A blink response to light develops at about the same time, and the lid may remain closed for as long as light is present the dazzle reflex.
The blink response to threat may not be present until 5 months of age. These responses are integrated in the brainstem and do not provide information on the cognitive cortical aspects of vision. Observing fixation and following behavior is the principal means to assess visual function in newborns and infants. The human face, at a distance of approximately 30 cm, is the best target for fixation.
After obtaining fixation, the examiner slowly moves from side to side to test the following response. Visually directed grasping is present in normal children by 3 months of age but is difficult to test before 6 months. Absence of visually directed grasping may indicate a motor rather than a visual disturbance.
The refixation reflex evaluates the visual fields in infants and young children by moving an interesting stimulus in the peripheral field. Clues to visual impairment are structural abnormalities e. Staring at a bright light source and oculodigital stimulation indicate severe visual impairment. Many such disorders also disturb ocular motility see Chapter The basis for chapter assignment of a disorder is by the most usual initial clinical feature.
For example, the discussion of myasthenia gravis is in Chapter 15 because diplopia is a more common initial complaint than dysphagia.
Fenichel's Clinical Pediatric Neurology: A Signs and Symptoms Approach by J Eric Piña-Garza
An acute isolated cranial neuropathy, such as facial palsy, is usually a less ominous sign than multiple cranial neuropathies and is likely to have a self-limited course.
An isolated cranial neuropathy may be the first sign of progressive cranial nerve dysfunction, however. Conditions causing isolated and multiple cranial neuropathies are discussed together because they may not be separable at onset. Facial Weakness and Dysphagia Anatomical Considerations Facial Movement The motor nucleus of the facial nerve is a column of cells in the ventrolateral tegmentum of the pons.
Nerve fibers leaving the nucleus take a circuitous path in the brainstem before emerging close to the pontomedullary junction. The fibers then enter the internal auditory meatus with the acoustic nerve.
Fibers for voluntary and reflexive facial movements separate rostral to the lower pons. After bending forward and downward around the inner ear, the facial nerve traverses the temporal bone in the facial canal and exits the skull at the stylomastoid foramen.
Extracranially the facial nerve passes into the parotid gland, where it divides into several branches, which innervate all muscles of facial expression except the levator palpebrae superioris. Sucking and Swallowing The sucking reflex requires the integrity of the trigeminal, facial, and hypoglossal nerves.
Stimulation of the lips produces coordinated movements of the face, jaw, and tongue. The automatic aspect of the reflex disappears after infancy but returns in bilateral disease of the cerebral hemispheres.
Fibers of the trigeminal and glossopharyngeal nerves ending in the nucleus solitarius form the afferent arc of the swallowing reflex. The motor roots of the trigeminal nerve, the glossopharyngeal and vagus fibers from the nucleus ambiguus, and the hypoglossal nerves form the efferent arc. A swallowing center that coordinates the reflex is located in the lower pons and upper medulla.
Expansion of one compartment comes at the expense of another. In this way, intracranial volume and pressure remain constant see Chapter 4. The extracerebral spaces epidural, subdural, and subarachnoid may expand with blood and significantly affect cranial volume.
Less important factors contributing to head size are the thickness of the skull bones and the rate of their fusion. Even more important is the rate at which individual skull bones fuse.
The more recent move to have infants sleep supine instead of prone is leading to a generation of children with flat occiputs. Measuring Head Size Head circumference is determined by measuring the greatest occipitofrontal circumference. Influencing the accuracy of the measurement is fluid in and beneath the scalp and head shape.
After a prolonged and difficult delivery, edema or blood may thicken the scalp and a cephalhematoma may be present as well. Fluid that infiltrates from a scalp infusion can increase head circumference markedly. A round head has a larger intracranial volume than an oval head of equal circumference.
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Sheel Gupta. The AAP reserves the right, without prior notice, to suspend your use of the Materials if owed fees are past due. Search for books, journals or webpages This chapter discusses nonparalytic strabismus, paralytic strabismus ophthalmoplegia , gaze palsies, ptosis, and nystagmus.