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FENICHEL CLINICAL PEDIATRIC NEUROLOGY PDF

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Confidently diagnose and manage primary neurologic disorders of childhood with actionable, step-by-step assistance from Fenichel's Clinical Pediatric. FENICHEL'S. CLINICAL. PEDIATRIC. NEUROLOGY. A Signs and Symptoms Approach. Seventh Edition. London, New York, Oxford, St Louis, Sydney, Toronto . The Publisher Library of Congress Cataloging-in-Publication Data Fenichel, Gerald M. Clinical pediatric neurology: a signs and symptoms approach / Gerald M.


Fenichel Clinical Pediatric Neurology Pdf

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Editorial Reviews. Review. "This well-written, concise, and practical book has been a valuable resource for those caring for pediatric patients with neurological . Confidently diagnose and manage primary neurologic disorders of childhood with actionable, step-by-step assistance from Fenichel's Clinical. Fenichel GM, Clinical Pediatric Neurology, 5th Ed, , Elseiver - Download as PDF File .pdf), Text File .txt) or read online. neurologi anak.

Extensive coverage clearly defines age at onset, course of illness, clinical features, and treatment options. Read more Read less. Save Extra with 3 offers. Frequently bought together. Total price: Add all three to Cart. One of these items is dispatched sooner than the other.

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Page 1 of 1 Start over Page 1 of 1. Park's Pediatric Cardiology for Practitioners, 6e. Myung K. Park MD. Cloherty and Stark's Manual of Neonatal Care. Pediatric Nephrology. Practical Paediatric Neurology.

About the Author J. To get the free app, enter mobile phone number. See all free Kindle reading apps. Don't have a Kindle? In the months that follow, the infant imitates many speech sounds, babbles and coos, and finally learns the specific use of mama and dada by 1 year of age.

Fenichel's Clinical Pediatric Neurology E-Book

Receptive skills are always more highly developed than expressive skills because language must be decoded before it is encoded. By 2 years of age, children have learned to combine at least 2 words, understand more than words, and follow many simple verbal directions. Developmental disturbances in the language cortex of the left hemisphere that occur before 5 years of age displace language to the right hemisphere.

This displacement does not occur in older children. Autistic Spectrum Disorders Infantile autism is a developmental disorder of brain function defined by behavioral characteristics. The terms autistic spectrum disorders ASD and pervasive developmental disorders classify the spectrum of behavioral consequences.

Asperger disorder represents the high-functioning end of autistic spectrum disorders. The high concordance in monozygotic twins, a 4. Autism has become an increasingly popular diagnosis. An apparent increasing incidence of diagnosis suggests to some investigators an environmental factor. Data do not confirm the notion, however, of an autism epidemic or causation by any environmental factor.

Most biological studies suggest prenatal factors. Clinical Features. Major diagnostic criteria are impaired sociability, impaired verbal and nonverbal communication skills, and restricted activities and interests Rapin, Failure of language development is the feature most likely to bring autistic infants to medical attention and correlates best with the outcome; children who fail to develop language before age 5 have the worst outcome.

The IQ is less than 70 in most children with autism. Some autistic children show no affection to their parents or other care providers, whereas others are affectionate on their own terms. Nervous system—Diseases—Diagnosis. Nervous System Diseases—diagnosis—Child. Robin E. Last digit is the print number: Several people have asked how I came to use the format of a signs and symptoms approach.

The idea was not mine. The suggestion came from Dana Dreibelbis, then an editor for W. Saunders publishing company. It was probably the third edition before I finally got the organization correct.

With each new edition, the text evolved into a personal statement reflecting my approach to the practice of pediatric neurology. If I were not actively engaged in practice, I could not continue writing the text. The text is a practical approach to diagnosis and management, and it expresses my own biases in situations in which a single standard of practice is not established.

A well-taken history and directed examination remain the starting points for diagnosis. More often than not, they are the only requirements for diagnosis. Invest most of your time in listening to the history. If you have no idea what is wrong after hearing the history, it is unlikely that diagnostic tests will enlighten you. A differential diagnosis is a list that contains one correct answer and several wrong answers. There is little to commend a list of wrong answers.

Their exclusion is both time consuming and expensive. Better to think through the possibilities at the onset and zero in on the right answer. In prior editions, I have recommended two web-based resources for genetic disorders: Online Mendelian Inheritance in Man http: GeneReviews, now part of GeneClinics, contains a wealth of up-to-date information on neurological disorders. I have referenced it throughout the text and rarely go to the clinic without logging on.

The intent of this book is to provide a sensible approach to the common presenting problems of children with disorders of the nervous system. The general organization remains the same because the presenting clinical features are unchanged.

Some chapters have required more revision than others, but the reader will find new information in all. I wish to express my gratitude to Susan F.

Pioli, Publishing Director, Elsevier Health Sciences, for her friendship and assistance in developing several textbooks. Gerald M. In children, such events often clear completely. Disturbance of ion channels channelopathies is often the underlying cause. Examples of channelopathies are genetic epilepsies, migraine, periodic paralysis, and paroxysmal movement disorders. Approach to Paroxysmal Disorders The diagnosing physician almost never witnesses the paroxysmal event.

The nature of the event requires surmising what transpired by listening to the eyewitness description offered by a family member or, worse, to the secondhand description that the parent heard from a teacher. Never accept a secondhand description. The most common confusion is between seizures and syncope. Most people stiffen and tremble at the end of a faint. Spells seldom remain unexplained when viewed.

Because observation of the spell is crucial to diagnosis, ask the family to videotape the spell. Most families either own or can borrow a video camera. Even when a purchase is required, it is more cost-effective than brain imaging studies, and the family has something useful to show for the expenditure.

Always ask the following two questions: Has this ever happened before? Does anyone else in the family have similar episodes?

Often, no one offers this important information until requested. Episodic symptoms that last only seconds and cause no abnormal signs usually remain unexplained and do not warrant laboratory investigation. The differential diagnosis of paroxysmal disorders is different in neonates, infants, children, and adolescents and presented best by age groups.

With the exception of coma, these definitions are not standard. They are more precise, however, and more useful than such terms as semicomatose and semistuporous. The term encephalopathy describes a diffuse disorder of the brain in which at least two of the following symptoms are present: Encephalitis is an encephalopathy accompanied by cerebrospinal fluid CSF pleocytosis.

Fenichel's Clinical Pediatric Neurology E-Book

Lack of responsiveness is not always lack of consciousness. Infants with botulism see Chapter 6 may have such severe hypotonia and ptosis that they cannot move their limbs or eyelids in response to stimulation.

They appear to be in a coma or stupor but are actually alert. The locked-in syndrome a brainstem disorder in which the individual can process information but cannot respond and catatonia are other examples of diminished responsiveness in the alert state.

Patients with increased neuronal excitability the high road become restless and then confused; next, tremor, hallucinations, and delirium an agitated confusional state develop. Myoclonic jerks may occur. Seizures herald the end of delirium, and stupor or coma follow. Table 2—2 summarizes the differential diagnosis of the high road to coma. Tumors and other mass lesions are not expected causes.

Instead, metabolic, toxic, and inflammatory disorders are likely. Instead, awareness progressively deteriorates from lethargy to obtundation, stupor, and coma. The differential diagnosis is considerably larger than that with the high road and includes mass lesions and other causes of increased intracranial pressure Table 2—3. Table 2—4 lists conditions that cause recurrent encephalopathies. A comparison of Tables 2—2 and 3 shows considerable overlap between conditions whose initial features are agitation and confusion and conditions that begin with lethargy and coma; the disorders responsible for each are described together to prevent repetition.

The usual causes of delirium are toxic or metabolic disorders diffusely affecting both cerebral hemispheres. Schizophrenia should not be a consideration in a prepubertal child with acute delirium. Fixed beliefs, unalterable by reason, are delusions. The paranoid delusions of schizophrenia are logical to the patient and frequently part of an elaborate system of irrational thinking in which the patient feels menaced.

Delusions associated with organic encephalopathy are less logical, are not systematized, and tend to be stereotyped. A hallucination is the perception of sensory stimuli that are not present. Organic encephalopathies usually cause visual hallucinations, whereas psychiatric illness usually causes auditory hallucinations, especially if the voices are accusatory. Stereotyped auditory hallucinations that represent a recurring memory are an exception and suggest temporal lobe seizures.

History and Physical Examination Delirious children, even with stable vital function, require rapid assessment because the potential for deterioration to a state of diminished consciousness is real.

Obtain a careful history of the following: Examination of the eyes, in addition to determining the presence or absence of papilledema, provides other etiological clues. Small or large pupils that respond poorly to light, nystagmus, or impaired eye movements suggest a drug or toxic exposure.

Fixed deviation of the eyes in one lateral direction may indicate that 1 the encephalopathy has focal features, 2 seizures are a cause of the confusional state, or 3 seizures are part of the encephalopathy. The general and neurological examinations should specifically include a search for evidence of trauma, needle marks on the limbs, meningismus, and cardiac disease.

The distinction between painful and harmful headaches occurs before consultation. Nevertheless, families seek medical attention for a child with headache not only hoping to relieve pain, but also seeking assurance that the child does not have a serious intracranial disease. Not every headache is explicable, and the term psychogenic is not a synonym for idiopathic. In my practice, I see two headache patterns among most children. One is chronic low-grade headache, and the other is an intermittent disabling headache.

The cause of the former is either caffeine or analgesic abuse, and the latter is migraine. Ten percent of children 5 to 15 years old have migraine. Children with migraine average twice as many days lost from school as children without migraine.

An initial headache classification proposed by the International Headache Society in has undergone several revisions with the newest published in International Headache Society, As a rule, only poorly understood disorders require classification by a committee. Sources of Pain Table 3—1 lists pain-sensitive structures of the head and neck. The main pain-sensitive structures inside the skull are blood vessels. Mechanisms that stimulate pain from blood vessels are vasodilation, inflammation, and traction-displacement.

Increased intracranial pressure causes pain mainly by the traction and displacement of intracranial arteries see Chapter 4. The brain parenchyma, its ependymal lining, and the meninges, other than the basal dura, are insensitive to pain. The ophthalmic division of the trigeminal nerve innervates the arteries in the superficial portion of the dura and refers pain to the eye and forehead. The second and third divisions of the trigeminal nerve innervate the middle meningeal artery and refer pain to the temple.

All three divisions of the trigeminal nerve innervate the cerebral arteries and refer pain to the eye, forehead, and temple. In contrast, referred pain from all structures in the posterior fossa is to the occiput and neck.

Several extracranial structures are pain sensitive. Major scalp arteries are present around the eye, forehead, and temple and produce pain when dilating or stretched. Cranial bones are insensitive, but periosteum, especially in the sinuses and near the teeth, is painful when inflamed. The inflamed periosteum is usually tender to palpation or other forms of physical stimulation.

Muscles attached to the skull are a possible source of pain.

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The largest muscle groups are the neck extensors, which attach to the occipital ridge; the masseter muscles; and the frontalis muscle. The mechanism of muscle pain is incompletely understood but probably involves prolonged contraction. The extraocular muscles are a source of muscle contraction pain in patients with heterophoria.

When an imbalance exists, especially in convergence, long periods of close work cause difficulty in maintaining conjugate gaze, and pain localizes to the orbit and forehead.

Pain from the cervical roots and cranial nerves is generally due to mechanical traction from injury or malformation.

Pain follows this nerve distribution: Most often, headache, vomiting, personality change, and alterations in states of consciousness bring it to medical attention. Less frequently, diplopia or the observation that one or both eyes are turning in is the initial complaint. The basis of referral for some children is the diagnosis of papilledema by another physician. Some conditions causing increased intracranial pressure are discussed elsewhere in this book see Chapters 2 , 3 , 10 , and This chapter is restricted to conditions in which symptoms of increased intracranial pressure are initial and prominent features.

Pressures greater than 20 mm Hg are abnormal. When the cranial bones fuse during childhood, the skull is a rigid box enveloping its content. Intracranial pressure is then the sum of the individual pressures exerted by the brain, blood, and cerebrospinal fluid CSF.

An increase in the volume of any one component requires an equivalent decrease in the size of one or both of the other compartments if intracranial pressure is to remain constant. Because the provision of oxygen and nutrients to the brain requires relatively constant cerebral blood flow, the major adaptive mechanisms available to relieve pressure are the compressibility of the brain and the rapid reabsorption of CSF by arachnoid villi.

Infants and young children, in whom the cranial bones are still unfused, have the additional adaptive mechanism of spreading the cranial bones apart to increase cranial volume. The rate of formation is approximately 0.

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In contrast, the rate of absorption increases linearly as CSF pressure exceeds 7 mm Hg. At a pressure of 20 mm Hg, the rate of absorption is three times the rate of formation. Impaired absorption, not increased formation, is the usual mechanism of progressive hydrocephalus. Choroid plexus papilloma is the only pathological process in which formation sometimes can overwhelm absorption. When absorption is impaired, efforts to decrease the formation of CSF are not likely to have a significant effect on volume.

Slow progress in the attainment of developmental milestones may be caused by either static Table 5—1 or progressive Table 5—2 encephalopathies. In contrast, the loss of developmental milestones previously attained usually indicates a progressive disease of the nervous system, but also may result from parental misperception of attained milestones or by the development of new clinical features from an established static disorder as the brain matures Table 5—3. Two important questions require answers: In infants, the second question is often difficult to answer.

Even in static encephalopathies, new symptoms, such as involuntary movements and seizures, may occur as the child gets older, and delayed acquisition of milestones without other neurological deficits is sometimes the initial feature of progressive disorders.

When it is clear that milestones previously achieved are lost or that focal neurological deficits are evolving, however, a progressive disease of the nervous system is a consideration. It rapidly assesses four different components of development: Several psychometric tests amplify the results, but the Denver Developmental Screening Test in combination with neurological assessment provides sufficient information to initiate further diagnostic studies.

Language Delay Normal infants and children have a remarkable facility for acquiring language during the first decade of life. Children exposed to two languages concurrently learn both. Vocalization of vowels occurs in the first month, and by 5 months, laughing and squealing are established.

At 6 months, infants begin articulating consonants, usually M, D, and B. These first attempts at vowels and consonants are automatic and sometimes occur even in deaf children. Receptive skills are always more highly developed than expressive skills because language must be decoded before it is encoded.

By 2 years of age, children have learned to combine at least 2 words, understand more than words, and follow many simple verbal directions. Developmental disturbances in the language cortex of the left hemisphere that occur before 5 years of age displace language to the right hemisphere.

This displacement does not occur in older children. Autistic Spectrum Disorders Infantile autism is a developmental disorder of brain function defined by behavioral characteristics. The terms autistic spectrum disorders ASD and pervasive developmental disorders classify the spectrum of behavioral consequences. Asperger disorder represents the high-functioning end of autistic spectrum disorders.

The high concordance in monozygotic twins, a 4. Autism has become an increasingly popular diagnosis.

An apparent increasing incidence of diagnosis suggests to some investigators an environmental factor. Data do not confirm the notion, however, of an autism epidemic or causation by any environmental factor.

Most biological studies suggest prenatal factors. Clinical Features.

Major diagnostic criteria are impaired sociability, impaired verbal and nonverbal communication skills, and restricted activities and interests Rapin, Failure of language development is the feature most likely to bring autistic infants to medical attention and correlates best with the outcome; children who fail to develop language before age 5 have the worst outcome.

The IQ is less than 70 in most children with autism. Some autistic children show no affection to their parents or other care providers, whereas others are affectionate on their own terms. Autistic children do not show normal play activity; some display a morbid preoccupation with spinning objects, stereotyped behaviors such as rocking and spinning, and relative insensitivity to pain. An increased incidence of epilepsy in autistic children is probable. Infantile autism is a clinical diagnosis and not confirmable by laboratory tests.

Infants with profound hearing impairment may display autistic behavior, and tests of hearing are diagnostic. An electroencephalogram EEG is indicated when seizures are suspected.

Autism is not curable, but several drugs may be useful to control specific behavioral disturbances. Behavior modification techniques improve some aspects of the severely aberrant behavior. Despite the best program of treatment, however, these children function in a moderately to severely retarded range, although some individuals have islands of normal or extraordinary ability idiot savant. Bilateral Hippocampal Sclerosis Bilateral hippocampal sclerosis and the congenital bilateral perisylvian syndrome cause a profound impairment of language development.

The former also causes failure of cognitive capacity that mimics infantile autism, whereas the latter causes a pseudobulbar palsy see Chapter Infants with medial bilateral hippocampal sclerosis generally come to medical attention for refractory seizures.

The syndrome emphasizes, however, that the integrity of one medial hippocampal gyrus is imperative for language development. Hearing Impairment The major cause of isolated delay in speech development is hearing impairment see Chapter Hearing loss may occur concomitantly with global developmental retardation, as in rubella embryopathy, cytomegalic inclusion disease, neonatal meningitis, kernicterus, and several genetic disorders.

Hearing loss need not be profound; it can be insidious, yet delay speech development.

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The loss of high-frequency tones, inherent in telephone conversation, prevents the clear distinction of many consonants that humans learn to fill in through experience; infants do not have experience in supplying missing sounds.

The hearing of any infant with isolated delay in speech development requires audiometric testing. Crude testing in the office by slamming objects and ringing bells is inadequate. Hearing loss is suspected in children with global retardation caused by disorders ordinarily associated with hearing loss or in retarded children who fail to imitate sounds. Other clues to hearing loss in children are excessive gesturing and staring at the lips of people who are talking.

Clinicians test two kinds of tone: Phasic tone is a rapid contraction in response to a high-intensity stretch.

The tendon reflex response tests phasic tone. Striking the patellar tendon briefly stretches the quadriceps muscle. The spindle apparatus, sensing the stretch, sends an impulse through the sensory nerve to the spinal cord.

This information is transmitted to the alpha motor neuron, and the quadriceps muscle contracts monosynaptic reflex. Postural tone is the prolonged contraction of antigravity muscles in response to the low-intensity stretch of gravity. When postural tone is depressed, the trunk and limbs cannot maintain themselves against gravity, and the infant appears hypotonic. The maintenance of normal tone requires intact central and peripheral nervous systems. Hypotonia is a common symptom of neurological dysfunction and occurs in diseases of the brain, spinal cord, nerves, and muscles Table 6—1.No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher.

Data do not confirm the notion, however, of an autism epidemic or causation by any environmental factor. These first attempts at vowels and consonants are automatic and sometimes occur even in deaf children.

Prompts for neurological consultation in older children with neuromuscular disorders are failure to keep up with peers or easy fatigability. The discomfort is superficial, distal, and usually symmetrical.

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