Evaluating the poisoned mind.

Strengthen a client's childhood lead-poisoning case by understanding the neuropsychology of these injuries.

Lead has been known to be a neurotoxin since antiquity. Two thousand years ago, Dioscorides, a Greek physician of the first century, wrote that lead "makes the mind give way."(1) However, lead is not an equal-opportunity poison. Rather, the developing brains of children, particularly those 5 years old and younger, are exquisitely sensitive to the toxic effects of this metal.

Lead poisoning, in both its prevalence and its medical effects, constitutes a more serious threat to the developing child than any other toxin. Based on numerous epidemiological and laboratory studies, the Centers for Disease Control and Prevention (CDC) has established that levels of lead equal to or greater than 100 micrograms in a liter of blood, usually stated as 10 micrograms per deciliter, are dangerous to health. The agency has reported that 1 in 11 children in the U.S. under the age of 6 has blood-lead levels that exceed this threshold. "No other health problem affects so many children in the United States," the agency has said.(2)

At first blush, it appears incongruous that plaintiff attorneys who represent lead-poisoned children might have difficulties winning cases. But some do. What is the problem? After all, the victim is young and vulnerable, and the injury is grievous--brain damage is typically permanent.

The nature of the injury is one source of the problem. Exposing a child's brain to lead at levels equal to or exceeding 10 micrograms per deciliter, and probably lower levels as well, permanently impairs cognitive functioning. Cognitive impairments--or, more simply put, thinking disorders--that result from lead poisoning are invisible or hidden injuries. Lead-poisoned children are not typically wheelchair-bound, disfigured, or distinguished in any way that is apparent on simple visual inspection. The lead-poisoned brain does not evidence discrete lesions or structural changes that would be apparent on a CT scan or an MRI scan. A child with lead-induced brain damage--whether the injury causes a devastating inability to remember simple information, pay attention for more than a few minutes, or develop and understand even the most basic concepts--typically looks perfectly normal.

A primary goal of an attorney representing a lead-poisoned child is to reveal to the jury the nature of the cognitive disability. The purpose of this article is to explain how these invisible injuries are made apparent and to explain the reasons that several different experts who evaluate the child sometimes come to opposite conclusions concerning the existence and degree of impairment.

The hidden cognitive symptoms of brain injuries can be illuminated by professionals with expertise in neuropsychology. Although neuropsychology is broadly defined as the study of the brain and behavior, much effort in this field is directed toward the clinical measurement of the cognitive and behavioral manifestations of normal and abnormal brain function.

These measurements are based on the knowledge that the brain is topographically organized so different cognitive functions are controlled by anatomically distinct areas and systems. Damage localized to one or a few areas disturbs certain cognitive functions while functions controlled by uninjured parts of the brain continue to operate normally. Standardized testing of individual functions can identify normal and impaired cognitive processes and assess the degree of impairment.

The general protocol a neuropsychologist uses to determine whether a person has suffered brain injury is first to review all pertinent medical information that might relate to a possible injury and any other factors that could influence cognitive functioning, such as illnesses, medication, and previous injuries. Following this review, the cognitive functions are tested. If impairment is detected, the nature of the problems are considered in the context of the patient's history to determine their cause.

With lead poisoning, the general protocol is shaped by three considerations specific to this particular toxin. First, the neuropsychologist must keep in mind that young children are particularly sensitive to the effects of lead.(3) Second, he or she must consider that scientists disagree on whether or not lead poisoning in children has a behavioral signature. There is no dispute that lead poisoning impairs language, attention, memory, executive functioning, fine motor processes, and sensory perception.(4) However, there is no consensus about whether lead produces the same combination of cognitive deficits in each poisoned child. Third, the neuropsychologist must account for the fact that the majority of lead-poisoned children live in deprived socioeconomic circumstances. The ways these factors influence the neuropsychological evaluation are discussed below.

Neuropsychological evaluation

The tests used to evaluate cognition --neuropsychological tests--are distinguished from psychological tests in that the former measure functions that are accepted by the neuroscientific community as basic cognitive manifestations of brain functioning--language, attention, memory, executive functioning, fine motor processes, and sensory perception. In contrast, psychological tests evaluate a variety of complex behavioral and social variables, such as emotional state, social adjustment, and scholastic achievement.

To pass legal muster, a neuropsychological test must satisfy generally accepted scientific standards of validity and reliability. A test's validity relates to its ability to measure the desired function (for instance, a valid memory test assesses memory), while its reliability corresponds to the test's capability to measure this function every time the test is given. In addition, the baseline population that is used both to standardize the test and provide the norms for comparison must be appropriate.(5)

There are many different valid and reliable tests. The choice depends on the child's age and the cognitive functions that are to be evaluated. Since lead may produce different cognitive deficits in different children, a comprehensive assessment of all the fundamental neuropsychological processes is needed so potential areas of impairment are not overlooked. Thus, language; attention; memory; executive functions like concept formation, planning, and cognitive flexibility; and sensory perception, as well as fine motor processes like speed, accuracy, and dexterity, must be evaluated.

Neuropsychological functions, such as memory and attention, are made up of a number of different processes that are controlled by different brain systems. For example, the brain processes memory for words, visual objects, and spatial locations differently in anatomically separate parts of the brain. Memory for routine movements--such as tying shoes (procedural memory), facts (semantic memory), and details of occurrences (episodic memory) --are distinct functions, as is the ability to store information for temporary uses, such as remembering a phone number only long enough to dial it (working memory).

To test global functions, such as memory and attention, it is necessary to use several different tests that tap into different neuropsychological processes and that reflect functioning of different brain systems.

In addition to neuropsychological testing, the child should take an IQ test. The only circumstance in which IQ tests should be omitted is when a child has taken one within the past several months. In this instance, familiarity with the test questions and procedures leads to an artificial inflation of the scores, a phenomenon known as the "practice effect."(6) Practice effects are particularly robust in children and, paradoxically, are often unaffected by brain damage.

The Wechsler tests; the Wechsler Intelligence Scale for Children, Third Edition (for children age 6 years to 16 years, 11 months); and the Wechsler Primary and Preschool Scale of Intelligence, Revised (for children age 3 years to 7 years, 3 months) are most often used. These tests are preferable to other intelligence tests since their psychometric properties--that is, the appropriateness of the reference population, as well as their validity and reliability--have been most thoroughly documented.

The primary purpose of IQ testing in the evaluation of a lead-poisoned child is not to identify particular brain functions that may be impaired. The exam is not a neuropsychological test battery. IQ scores are composites made up of results from individual subtests that tap multiple unrelated functions and, as such, are not particularly sensitive to the effects of brain damage. A child's IQ may decrease after serious brain injury, but the magnitude of the decrease is not commensurate with the magnitude of the damage to cognitive functioning. For example, the removal of considerable brain tissue from either the right or left temporal lobes in children causes memory impairments that negatively affect academic performance. But the removal does not significantly decrease the child's IQ.(7)

IQ testing is needed to establish a baseline against which the neuropsychologist can compare the child's performance on neuropsychological tests and determine whether impairment exists. It should be noted that, in contrast to the composite IQ score, a few of the individual subtests from the Wechsler IQ examinations are useful in assessing specific neuropsychological functions and can be administered for that purpose.

What is an impairment?

Once a patient has been tested, the results must be evaluated to determine whether any cognitive functions should be classified as impaired. In general, an injury has caused an impairment if the patient's performance on a test of a particular cognitive process is significantly below what is expected based on his or her pre-injury level of functioning. For example, if a person with an IQ of 100 (50th percentile) performed at only the first percentile in a test of visuospatial memory after a brain injury, the person would be classified as having a memory impairment.

However, it cannot be stated that under all circumstances a particular level of performance reflects an injury-induced impairment. The patient's preinjury level of functioning must be considered as the baseline.

For example, a level of performance on a concept-formation task ranking at the 30th percentile might be considered to be within normal limits for a patient with an IQ of 100, but it would indicate an impairment for a theoretical physicist with an IQ of 140 (99th percentile).

With lead poisoning, the procedure for classifying test performance as normal or impaired is affected by the facts that the injury is typically sustained in early infancy and that there is no established, stable level of premorbid functioning to serve as a baseline. Because lead disrupts the normal development of the brain, it also affects cognitive development. Thus, what is often taken as a baseline measure of intellectual functioning when evaluating an older patient--the IQ--is assumed to have been altered by the injury in a lead-poisoned child.

In neuropsychological evaluations of children with lead poisoning or with other types of brain injuries that are sustained early in development, determinations of impairment are based on comparisons between test results and reasonably certain predictions of what the child's level of intellectual functioning would have been in the absence of injury. Despite the fact that it is affected by lead, IQ is still useful in determining a baseline of functioning for purposes of comparison.

The pathological effects of a toxic substance on the developing brain depend on a number of factors including the amount (dose), age of first exposure, and duration of exposure, as well as diet and genetic makeup.(8) When brain damage is relatively localized,(9) cognitive functions controlled by damaged areas will be impaired, and those controlled by relatively healthy areas will function normally. As a result, brain damage in a young child often results in abnormal scatter in IQ subtest scores. Subtests that measure functions that have been affected by brain damage show relatively low scores, and those that measure intact functions show significantly higher scores. The higher scores indicate what the child's level of functioning would have been absent the injury.

When brain damage is diffuse, many cognitive functions will be impaired, and significant scatter may not be observed. When determining the baseline for these patients, the neuropsychologist should rely on the well-established effect of lead on overall IQ. The Environmental Protection Agency has concluded that "blood-lead levels in the range of 50-70 [micrograms per deciliter] are associated with an IQ decrease of approximately five points; blood-lead levels of 30-50 [micrograms per deciliter], with a decrement of about four points; and blood-lead levels of 15-30 [micrograms per deciliter], with a decrement of one to two points...."(10)

When using this method, due to the vagaries of blood-lead testing and the short half-life of lead in the blood, it is highly likely that the child's exposure has been underestimated. Consequently, the reference or baseline IQ is likely to be underestimated. In this situation, a deficient performance on a neuropsychological test is less likely to be classified as an impairment.

Another caveat: This method of calculating IQ based on blood-lead levels should not be used in cases where significant scatter is present since composite IQs will be lowered by the variability of subtest scores, resulting in an underestimation of the baseline.

Socioeconomic factors

In 1988, the Agency for Toxic Substances and Disease Registry reported that "lead is toxic wherever it is found, and it is found everywhere.(11) Although the statement is undeniably true, children in families with reduced economic resources who live in older urban areas are at increased risk of lead poisoning.

The Third National Health and Nutrition Examination Survey studied blood-lead levels in the U.S. population between 1988 and 1991. The survey showed that 21 percent of inner-city children had blood-lead levels equal to or greater than the CDC's maximum allowable level of 10 micrograms per deciliter. Only 5.8 percent of children who did not live in inner-city regions had blood-lead levels equal to or greater than 10 micrograms per deciliter. When classified by income level, 16.3 percent of children from low-income families had blood-lead levels equal to or greater than 10 micrograms per deciliter, compared with 5.4 percent and 4 percent of children from middle- and high-income families, respectively.(12)

Some health care professionals and defense attorneys attempt to explain away a lead-poisoned child's deficient test performance by saying it is due to poor economic status, lack of parental support, or poor education. Indeed, some research has shown that IQ scores can be affected by these environmental factors, but negative influences show up primarily on certain subtests, specifically, the tests that measure the child's vocabulary and general knowledge.(13) However, in a neuropsychological evaluation, conclusions about cognitive impairment are not based on deficient IQ composite scores.

While socioeconomic status cannot be used as an explanation for neuropsychological impairment, there is evidence that being poor increases the neurotoxic effects of low-level lead exposure. Recent research has found that poor children with blood-lead levels of less than 9 micrograms per deciliter will show cognitive deficits as they grow older, and children with similar exposure who live in more fortunate circumstances appear less affected.(14)

Prognosis

Brain injuries caused by lead are irreversible and do not lessen in impact when the patient's blood-lead levels are eventually reduced. Rather, it is highly likely that testing a child cannot describe all the neuropsychological problems that will eventually affect him or her over time.

It is now generally recognized in the field of neuroscience that the development of certain brain systems continues not only into the teenage years but also well into early adulthood. When these systems are damaged early in their development, the impact of the injury is increasingly felt as the child becomes an adult. The expected age-appropriate behavior cannot occur because it depends on neural systems that are unable to control the required cognitive functions as a result of the injury.

For example, the frontal cortex--one of the brain areas most often implicated in executive functioning (for instance, concept formation, planning, and cognitive flexibility)--continues to develop longer than other parts of the brain. Damage to this area in childhood causes a "delayed onset of defects, followed by a period of seeming progression, and, finally, an arrest of development in adolescence."(15) The frontal cortex is one of the areas most vulnerable to the effects of childhood lead exposure.(16)

In addition to the cognitive impairments lead exposure causes, secondary problems that develop over time can be as debilitating. Cognitive deficiencies adversely affect academic performance and will have a deleterious effect on social and behavioral development. Lead-poisoned children are unable to keep up with their peers in the classroom and are repeatedly reminded of their failures with every poor test result or report card. The cumulative effect of repeated failure is loss of self-esteem and social development problems. The ultimate result, particularly in teenage boys, is aggression and acting-out behavior.

It is not uncommon that a child with a well-documented history of lead poisoning will be shown to be cognitively impaired on one neuropsychological evaluation and then, when re-evaluated, be pronounced normal. Plaintiff lawyers must be prepared to defend against the defense argument that a lead-poisoned child tested normal on a neuropsychological re-evaluation and, so, has no impairments due to lead exposure. If lead is an established neurotoxin that causes cognitive deficits and neuropsychological tests are objective and standardized, how can these tests fail to confirm an already established injury?

All too often, neuropsychologists point to a lack of agreement in the published literature concerning the cognitive effects of lead poisoning as scientific support for their finding that the lead-poisoned child they tested is normal. These statements reflect either the practitioner's ignorance, gross misinterpretation of the published literature, or disingenuousness of a magnitude that borders on the unethical.

There is no disagreement in the literature concerning the fact that lead exposure associated with blood levels equal to or greater than 10 micrograms per deciliter causes brain damage that results in cognitive impairments. The only disagreement concerns whether pediatric lead poisoning causes the same pattern of impairments in each child. If this controversy is resolved with the finding that lead poisoning lacks a behavioral signature, this result would not cast doubt on the neurotoxicity of lead. Other recognized causes of brain injury--for example, ischemia, blunt-force head trauma, and penetrating brain wounds--also cause different symptoms in different patients.

Plaintiff lawyers can undermine defense tactics that rely on contradictory neuropsychological evaluations since the explanation for the conflicting results can usually be found in the re-evaluating neuropsychologist's misuse and misinterpretation of tests results. One source of inaccuracy comes from the repeated use of the same test. Often, as part of a treatment regimen, a lead-poisoned child is evaluated by practitioners who administer a few neuropsychological tests or a complete battery. Subsequently, the child is re-evaluated at the behest of the plaintiff attorney and then evaluated again at the request of the defense.

If the same neuropsychological tests are used in two or more of these evaluations and insufficient time has elapsed between successive evaluations, the influence of a practice effect is likely. As mentioned previously, practice effects will inflate performance on subsequent testing, are more pronounced in children than in adults, and are not necessarily attenuated by brain injury. It is important that these apparent "improvements" are recognized for what they are--practice effects, not recovery from brain injury.

A second source of inaccuracy is tests that are insensitive to particular cognitive impairments. For example, the California Verbal Learning Test for Children is a valid instrument for assessing certain types of rote verbal learning and verbal memory. However, this test does not measure visual memory or, for that matter, verbal memory involving semantic and syntactic information. A more extreme, and, unfortunately, more common, example is the use of an IQ test as a neuropsychological test battery. Although, as noted previously, certain subtests from the Wechsler IQ batteries can be used to assess neuropsychological processes, the majority of the subtests and the composite IQ score are suitable for psychological but not neuropsychological purposes.

A third source of inaccuracy derives from the criteria the neuropsychologist uses to classify a patient's performance as either normal or impaired. Unfortunately, many neuropsychologists describe a patient's performance only in qualitative descriptive terms, such as "normal," "impaired," and "below expectations," and omit from the report the actual quantitative data that underlie the description. In examining test results on which summary reports are based, we have discovered that some practitioners' definition of normalcy is so broad that only the comatose could be classified as impaired.

When neuropsychological tests are administered and interpreted appropriately, they are the only way to clearly demonstrate the egregious effects of lead on a developing child's brain. But when the same tests are misapplied or misinterpreted, they will portray a child with brain damage as normal. Careful consideration of the neuropsychologist's summary report in the context of the principles of testing and deficit measurement outlined in this article should help the attorney evaluate the validity of the findings.

Notes

(1.) DAVID E. HARTMAN, NEUROPSYCHOLOGICAL TOXICOLOGY 96 (2d ed. 1995).

(2.) Barbara Berney, Round and Round It Goes: The Epidemiology of Childhood Lead Poisoning, 1950-1990, MILBANK Q., Mar. 1993, at 16.

(3.) Lead absorption is greatest and brain deposition relatively highest in younger children (less than 5 years of age) compared to older children. If a young child and an older child each absorb the same amount of lead, the younger child will end up with a higher concentration of lead in the brain. However, children age 5 and older are still highly vulnerable to lead's effects since the proportion of absorbed lead that is deposited in their brains still exceeds that of teenagers or adults. Rich W. Leggett, An Age-Specific Kinetic Model of Lead Metabolism in Humans, 101 ENVTL. HEALTH PERSPS. 598-616 (1993).

(4.) See, e.g., Robert G. Feldman & Roberta F. White, Lead Neurotoxicity and Disorders of Learning, 7 J. CHILD NEUROLOGY 354-59 (1992); Lynette Stokes et al., Neurotoxicity in Young Adults 20 Years After Childhood Exposure to Lead: The Bunker Hill Experience, 55 OCCUPATIONAL ENVTL. MED. 507-16 (1998).

(5.) Theodore I. Lidsky et al., The Neuropsychologist in Brain Injury Cases, TRIAL, July 1998, at 70.

(6.) MURIEL DEUTSCH LEZAK, NEUROPSYCHOLOGICAL ASSESSMENT 711 (3d ed. 1995).

(7.) Dennis J. Dlugos et al., Language-Related Cognitive Declines After Left Temporal Lobectomy in Children, 21 PEDIATRIC NEUROLOGY 444-49 (1999).

(8.) Ava O. Onalaja & Luz Claudio, Genetic Susceptibility to Lead Poisoning, 108 ENVTL. HEALTH PERSPS. 23-28 (2000).

(9.) See Idit Trope et al., Magnetic Resonance Imaging and Spectroscopy of Regional Brain Structure in a 10- Year-Old Boy with Elevated Blood Lead Levels, 101 PEDIATRICS 1066-67 (1998); Yoram Finkelstein et al., Low-Level Lead-Induced Neurotoxicity in Children: An Update on Central Nervous System Effects, 27 BRAIN RES. REVS. 168-76 (1998).

(10.) David C. Bellinger, Learning and Behavioral Sequelae of Lead Poisoning, in LEAD POISONING IN CHILDHOOD 97 (Siegfried M. Pueschel et al. eds., 1996).

(11.) AGENCY OF TOXIC SUBSTANCES & DISEASE REGISTRY, U.S. DEP'T OF HEALTH & HUM. SERVS./PUB. HEALTH SERV., THE NATURE & EXTENT OF LEAD POISONING IN CHILDREN IN THE U.S., NO. 99-2966 (1988).

(12.) Debra J. Brody et al., Blood-Lead Levels in the U.S. Population: Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III), 1988 to 1991, 272 JAMA 277, 282 (1994).

(13.) Ingrid Wickelgren, Nurture Helps Mold Able Minds, 283 SCIENCE 1832 (1999).

(14.) David C. Bellinger, Effect Modification in Epidemiological Studies of Low-Level Neurotoxicant Exposures and Health Outcomes, 22 NEUROTOXICOLOGY & TERATOLOGY 133 (2000).

(15.) Paul J. Eslinger et al., Developmental Consequences of Childhood Frontal Lobe Damage, 49 ARCHIVES NEUROLOGY 764 (1992).

(16.) Trope et al., supra note 9; Finkelstein et al., supra note 9.

Please don't photocopy TRIAL

The Copyright Act of 1976 prohibits the reproduction by photocopy machine or any other means of any portion of TRIAL except with the written permission of the editor. ATLA members who want to reproduce one copy for personal use do not need permission.

If you would like permission to reprint a specific article, please write to TRIAL, 1050 31st St., N.W., Washington, DC 20007 or call [phone], ext. 216.

Theodore I. Lidsky is a neuroscientist at the New York State Institute for Basic Research in Developmental Disabilities in Staten Island, New York. Jay S. Schneider is a neuroscientist and a professor in the departments of neurology and pathology, anatomy, and cell biology at Thomas Jefferson Medical College in Philadelphia.