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Book Forum: CHILD PSYCHIATRY   |    
Textbook of Pediatric Neuropsychiatry
ESTHER SOMERFELD-ZISKIND, M.D., M.A.
Am J Psychiatry 1999;156:1466-1467.
View Author and Article Information
Los Angeles, Calif.

edited by C. Edward Coffey, M.D., and Roger A. Brumback, M.D. Washington, D.C., American Psychiatric Press, 1998, 1,506 pp., $175.00.

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The editors of this book have widened the scope of necessary information in child neuropsychiatry to include anatomy, audiology, cell biology, communication, developmental medicine, endocrinology, law, neurogenetics, neurology, neuropathology, neuropsychology, neurosurgery, orthopedics, pathology, pediatrics, radiology, and rehabilitation. Consequently, this oversized book is encyclopedic, to be dipped into for quiet reading or just in emergencies. No one except a reviewer would read clear through 1,506 pages.

If a second edition is contemplated, I suggest fewer tables and more clinical case reports. Several authors have duplicated information given by others, and there is redundancy even in individual articles. Other problems I perceived included the following: In the chapter on epilepsy, phenobarbital and dilantin are given a bum rap. In the older literature there were careful studies highly recommending these medications. Creutzfeldt-Jakob disease is said to be due to a "virus"—but does not Prusiner’s 1997 Nobel prize for discovery of prions make them a more likely cause of this disease? In regard to rheumatoid arthritis, should antinecrosis factor be mentioned as a promising new treatment? Possibly the statistics on juvenile diabetes are biased toward negative outcome. In our community we see much cause for optimism in this disorder when carefully managed.

To transmit the flavor of the book, I have abbreviated the following gleanings:

Embryological development is a sequence of distinct processes with considerable spatial and temporal redundancy initially.

The outgrowth of a single axon precedes the formation of multiple dendrites and is one of the first events marking the maturation of neuroblast to neuron. Axons must be guided to their destinations, often at a great distance from the cell body. As far as we know, brain neurons do not proliferate postnatally. The glial cells responsible for myelination continue actively to proliferate and die.

The cortex of the brain finally completes its myelination cycle at 30 years of age. (I remember when Yakovlev astonished us by revealing that myelination in the brain can continue until age 70.)

Sex-specific volumetric changes, as various parts of the brain develop, have been seen in both humans and primates.

Even the simplest task eventually involves the majority of brain systems.

The frontal cortex is the last cortical region to undergo maturational rise in glucose consumption, as measured by positron emission tomography and single photon emission computed tomography methodology. At ages 4 to 10 years, the child’s brain uses twice as much glucose as does the adult’s. (This must have implications for educators, dieticians, and the mental health professions.)

Although genes control development, any organism is the result of gene action plus environment. Evidence is accumulating that biological and environmental events pose separate but synergistic risks for conduct disorder/sociopathy—the environment has less influence as adulthood progresses.

The term "extrapyramidal," introduced by Wilson in 1912, refers to the basal ganglia and brain stem nuclei to which they are connected. Dopamine has an excitatory effect on these neurons. Some or all striated neurons are lost in Huntington’s disease. The excitatory neurotransmitter of cortico­striate projections is glutamate.

Interruption of the subthalamic pathway is responsible for the violent hyperkinesia of ballismus. Remember when this was considered a psychogenic (hysterical) disorder, possibly remedial by psychoanalysis?

As a motor skill is learned, the basal ganglia take over the role of automatically executing the learned strategy. When basal ganglia are damaged, we revert to a slower, less automatic, and less accurate cortical mechanism for motor behavior.

Two neural circuits are implicated in depression. The first, excitatory, links the prefrontal cortex with the amygdala and the thalamus. The second, inhibitory, links the prefrontal cortex with the striatum, ventral pallidum, and thalamus. When children and adolescents have incapacitating headaches plus depression, treatment of depression may resolve both symptoms.

Children who are truly growth-hormone deficient have excellent final height attainments if therapy is initiated early enough in the prepubertal period. Psychosocial dwarfism, however, is a clinical malnutritive disorder in which growth failure is caused by an unloving environment or chaotic family dynamics. This can be treated by change in the situation but not by growth hormone.

The chapter titled "Normal Behavioral Development" will probably be referred to frequently. Special techniques of examination for the infant and young child are useful to physicians sophisticated enough to use the procedures recommended. (It is safer to have a psychologist nearby.) Only when an infant or young child is extremely gifted or extremely retarded can an expert predict cognitive development.

The summary tables of specific higher brain functions, syndromes in which those functions are affected, and anatomical structures involved, if authentic, could be useful to brain surgeons.

In children, brain damage not only disrupts previously acquired abilities, as in adults, but also has the potential to disrupt the normal development of abilities yet to emerge on the way to full maturity. (How important this is medicolegally!)

Neuroimaging provides unprecedented opportunity to examine in vivo brain structure and function. The choice in pediatrics is magnetic resonance imaging (MRI); it lacks ionizing radiation, allowing sequential examinations, but there is an ethical responsibility to minimize a child’s discomfort in the 10 minutes of this claustrophobic procedure. CT scanning is preferred in acute brain injury because it visualizes bone better than MRI, but 3 days later, MRI can show hemorrhage and deep white matter shearing.

Subsumed under the general term "attention" are diverse neuropsychological processes. By the time a stimulus reaches the level of awareness, it has been cataloged as to identity, orientation, memory, and significance. Children with attention deficit hyperactivity disorder (ADHD) have impaired stimulus detection and arousal. Two core features are motor restlessness and deficits in response inhibition. The behavioral and cognitive effects of stimulants on ADHD are robust and extensive.

In 1990, Weinberg and co-workers published a controversial article on what they termed "lack of vigilance." Vigilance is steady-state alertness, wakefulness, or tonic arousal. This possible syndrome overlaps with ADHD and is treated the same way, with stimulants. Weinberg and co-workers have a chapter on "disturbances of vigilance" in this book.

In regard to substance dependence, conditioned responses to drug use develop in relation to environmental cues such as certain people, places, or objects. Craving ensues as emotional, motivational, and anticipatory responses to potential reinforcement. As tolerance increases with continued drug use, reinforcing effects become difficult to obtain and abstinence becomes severe.

Dyslexia is a learning disability, language-based, of constitutional origin, characterized by difficulties in single word decoding, usually reflecting insufficient phonological processing.

There are several memory subsystems, such as episodic, semantic, location, habit, autobiographical, and short-term. Normal humans are born with preprogrammed emotional expressions universally understood: "phyletic memory."

Autistic children are said to be lacking in "theory of mind": they cannot tell from words, movements, or facial expressions what the other person is thinking or feeling. Because medical and comorbid genetic conditions are relatively common in autism, careful workup should include a family history and DNA testing for fragile X syndrome. No pharmacological intervention thus far has proven effective in autism.

New techniques have demonstrated that infants are able to extract more information from the language of their parents at an earlier age than previously imagined.

The chapters on blindness and deafness are outstandingly practical. The adjustment of deaf children is as much affected by the reactions of their parents and the community to the handicap as by the actual deafness.

An autoimmune process associated with streptococcal infections may be responsible for the majority of childhood-onset Tourette syndrome/obsessive-compulsive disorder.

Even the Los Angeles Times is calling attention to the new attitude for disabled children’s education—schools are bearing too heavy a brunt of the expense. Mentally ill children have won the right to in-home intensive mental health services in some instances.

Play therapy and child psychoanalysis receive only brief mention. The focus is on behavior therapy, didactically presented. (The difference between psychoanalysis and other current forms of psychotherapy is that psychoanalysis is an emotional experience.)

The last chapter, appropriately, deals with legal issues and is practical and helpful for mental health workers.

I recommend this book as a reference source for all libraries.

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