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" karen " wrote:

>I was reading in the " Files " section, and found info on thyroid and

attention deficit. Are they saying the two are linked? My son has

adhd. Please tell me more!!!

,

The article below may be of interest to you:

Ann N Y Acad Sci. 2001 Jun;931:97-112

Medical mimics. Medical and neurological conditions simulating ADHD.

Pearl PL, Weiss RE, Stein MA.

Department of Pediatrics and Neurology, Washington University

School of Medicine and Children's National Medical Center, Washington,

DC 20010, USA.

Abstract:

The medical and neurological conditions that simulate ADHD are

reviewed, as well as those disorders frequently presenting as

comorbidities with ADHD. The localization of ADHD has invoked multiple

areas, including frontal lobes, nondominant parietal lobe, and basal

ganglia, and the neural network theory of

cortical-subcortical-cortical loops has been implicated in the

pathogenesis of ADHD. The medical evaluation of patients presenting

with ADHD should be comprehensive, with an emphasis on demonstrating

chronic and permeating symptoms since early childhood without a better

medical explanation. Associated thyroid disorders are reviewed,

including the syndrome of resistance to thyroid hormone. Suggested

laboratory studies are provided, depending on the clinical circumstances.

Thyroid portion of the article:

ENDOCRINOPATHIES: THYROID DISORDERS

Thyroid hormone is responsible for normal growth and development as

well as maintenance of metabolism in the adult. Perturbations in the

hormonal milieu of the body can have profound and nonspecific effects

on behavior. The influence of thyroid hormone on the developing brain

was discovered more than 100 years ago, when cretinism and mental

retardation were recognized in children with thyroid hormone

deprivation. Thyroid hormone also influences behavior in the adult.

Abnormalities in the concentration of serum thyroid hormone can result

in behavior that is erratic and may resemble ADHD.

There are three conditions of the thyroid that have been reported to

be associated with ADHD-like symptoms: hypothyroidism,

hyperthyroidism, and the syndrome of resistance to thyroid hormone (RTH).

Hypothyroidism

Hypothyroidism is caused by insufficient production of thyroid

hormone. This is usually due to a failure of the gland to produce

thyroxine caused by an autoimmune process resulting in destruction of

the gland (Hashimoto's thyroiditis), or less commonly, to a failure of

the pituitary to appropriately stimulate the thyroid. Hypothyroidism

may result in symptoms of lethargy and inattention. Thyroid hormone

deprivation is usually accompanied by cold intolerance, weight gain,

skin and hair changes, and constipation. Elevation of serum

thyrotropin (TSH) and decreased levels of serum thyroxine (T4) and

triiodothyronine (T3) diagnose primary hypothyroidism (due to failure

of the thyroid gland to synthesize or release thyroid hormone). In a

recent study, Haddow et al. demonstrated that children from mothers

who were hypothyroid during the pregnancy had a 4.1 ± 2.1 decrease in

the WISC-III full scale IQ score (p=0.06) and a 3±2 point decrease in

the WISC-III freedom-from-distractibility score (a measure of

attention) (p=0.08). Although these are subtle differences and the

clinical significance in a larger population is unknown, it is

suggestive that the thyroid status of the mother may influence the

subsequent neurocognitive development of the child. Treatment of

hypothyroidism is usually easily achieved with T4 supplementation with

the goal to normalize the serum TSH and T4 levels. In most instances

hormone replacement results in return of behavior and psychological

profiles to baseline. It has been suggested that subjective

improvement of various behavioral parameters could be further improved

with the addition of T3. Bunevicius et al. demonstrated that in 33

patients with hypothyroidism, among 17 scores of mood, 6 were better

or closer to normal after treatment with T4 plus T3 than after

treatment with T4 only. Although this was a rather small study the

results are provocative and warrant further investigation on the use

of T3 along with T4 in the treatment of behavioral symptoms of

hypothyroidism.

Hyperthyroidism

Hyperthyroidism is caused by an overproduction of thyroid hormone.

This is usually due to an antibody directed to the TSH receptor on the

thyrocyte, stimulating release of thyroid hormone in the absence of

TSH. Less commonly, hyperthyroidism can be the result of an autonomous

production of thyroid hormone due to a nodule of the thyroid.

Hyperthyroidism is usually associated with symptoms of tremors,

palpitations with tachycardia, weight loss, fatigue, insomnia, hair

and skin changes, heat intolerance, and frequent bowel movements.

Commonly, these patients present with altered cognition, inability to

concentrate, and inattentiveness. Elevated concentrations of serum T3

and T4 and suppression of serum TSH confirm the diagnosis of

hyperthyroidism. Treatment of hyperthyroidism is aimed at decreasing

production of T4 and T3 by the thyroid gland by the use of antithyroid

medication (such as propylthiouracil or methimazole), radioactive

iodine ablation or surgery. The latter two treatments usually result

in hypothyroidism. Correction of the thyroid hormone concentration

completely reverses the symptoms of hyperthyroidism.

Resistance to Thyroid Hormone

RTH is a rare thyroid hormone disorder which is characterized by

reduced responsiveness to thyroid hormone. It is usually due to a

mutation in the thyroid hormone receptor beta gene such that the

tissues are no longer able to respond to normal concentrations of

thyroid hormone. Careful evaluation of subjects with RTH has shown

that almost one-half have some degree of learning disability with or

without ADHD. About one-quarter of subjects have intellectual

quotients (IQ) less than 85 but frank mental retardation (IQ < 60) has

been found only in 3 % of cases. IQ is on the average lower in

subjects with RTH with or without ADHD. Although, the behavioral

characteristics of children with ADHD and RTH are similar to those

with ADHD only, the former have significantly weaker ability of

perceptual organization and lower school achievement, suggesting a

more severe cognitive impairment. Impaired mental function was found

to be associated with impaired or delayed growth (below 5th

percentile) in 20% of subjects, though growth retardation alone is

rare (4%). Despite the high prevalence of ADHD in patients with RTH,

the occurrence of RTH in children with ADHD must be very rare, none

having been detected in 412 such children studied. Furthermore,

current data do not support a genetic linkage of RTH with ADHD. Rather

the association with low IQ scores may confer a higher likelihood for

subjects with RTH to exhibit ADHD symptoms, a conclusion that has been

recently contested. The reason such a rare disorder is included in

the list of thyroid diseases associated with ADHD while other more

common diseases are not, is that more than 40–60% of children with RTH

have ADHD. RTH is usually diagnosed by the presence of goiter along

with elevated serum free T4 and T3 with nonsuppressed serum TSH. These

children are usually brought to clinical attention because of the

goiter, growth disturbance, hyperactive behavior or tachycardia.

Thyroid function tests are then obtained and the classic blood tests

are obtained. Since most patients with RTH are compensated for their

defect, in the absence of concurrent thyroid disease or previous

antithyroid treatment, no treatment is necessary. Occasionally

treatment with beta-adrenergic blockers can help with symptoms related

to tachycardia. In a limited small study it was suggested that T3

treatment may be beneficial for some the inattentive symptoms in this

group.

Winona

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" karen " wrote:

>I was reading in the " Files " section, and found info on thyroid and

attention deficit. Are they saying the two are linked? My son has

adhd. Please tell me more!!!

,

The article below may be of interest to you:

Ann N Y Acad Sci. 2001 Jun;931:97-112

Medical mimics. Medical and neurological conditions simulating ADHD.

Pearl PL, Weiss RE, Stein MA.

Department of Pediatrics and Neurology, Washington University

School of Medicine and Children's National Medical Center, Washington,

DC 20010, USA.

Abstract:

The medical and neurological conditions that simulate ADHD are

reviewed, as well as those disorders frequently presenting as

comorbidities with ADHD. The localization of ADHD has invoked multiple

areas, including frontal lobes, nondominant parietal lobe, and basal

ganglia, and the neural network theory of

cortical-subcortical-cortical loops has been implicated in the

pathogenesis of ADHD. The medical evaluation of patients presenting

with ADHD should be comprehensive, with an emphasis on demonstrating

chronic and permeating symptoms since early childhood without a better

medical explanation. Associated thyroid disorders are reviewed,

including the syndrome of resistance to thyroid hormone. Suggested

laboratory studies are provided, depending on the clinical circumstances.

Thyroid portion of the article:

ENDOCRINOPATHIES: THYROID DISORDERS

Thyroid hormone is responsible for normal growth and development as

well as maintenance of metabolism in the adult. Perturbations in the

hormonal milieu of the body can have profound and nonspecific effects

on behavior. The influence of thyroid hormone on the developing brain

was discovered more than 100 years ago, when cretinism and mental

retardation were recognized in children with thyroid hormone

deprivation. Thyroid hormone also influences behavior in the adult.

Abnormalities in the concentration of serum thyroid hormone can result

in behavior that is erratic and may resemble ADHD.

There are three conditions of the thyroid that have been reported to

be associated with ADHD-like symptoms: hypothyroidism,

hyperthyroidism, and the syndrome of resistance to thyroid hormone (RTH).

Hypothyroidism

Hypothyroidism is caused by insufficient production of thyroid

hormone. This is usually due to a failure of the gland to produce

thyroxine caused by an autoimmune process resulting in destruction of

the gland (Hashimoto's thyroiditis), or less commonly, to a failure of

the pituitary to appropriately stimulate the thyroid. Hypothyroidism

may result in symptoms of lethargy and inattention. Thyroid hormone

deprivation is usually accompanied by cold intolerance, weight gain,

skin and hair changes, and constipation. Elevation of serum

thyrotropin (TSH) and decreased levels of serum thyroxine (T4) and

triiodothyronine (T3) diagnose primary hypothyroidism (due to failure

of the thyroid gland to synthesize or release thyroid hormone). In a

recent study, Haddow et al. demonstrated that children from mothers

who were hypothyroid during the pregnancy had a 4.1 ± 2.1 decrease in

the WISC-III full scale IQ score (p=0.06) and a 3±2 point decrease in

the WISC-III freedom-from-distractibility score (a measure of

attention) (p=0.08). Although these are subtle differences and the

clinical significance in a larger population is unknown, it is

suggestive that the thyroid status of the mother may influence the

subsequent neurocognitive development of the child. Treatment of

hypothyroidism is usually easily achieved with T4 supplementation with

the goal to normalize the serum TSH and T4 levels. In most instances

hormone replacement results in return of behavior and psychological

profiles to baseline. It has been suggested that subjective

improvement of various behavioral parameters could be further improved

with the addition of T3. Bunevicius et al. demonstrated that in 33

patients with hypothyroidism, among 17 scores of mood, 6 were better

or closer to normal after treatment with T4 plus T3 than after

treatment with T4 only. Although this was a rather small study the

results are provocative and warrant further investigation on the use

of T3 along with T4 in the treatment of behavioral symptoms of

hypothyroidism.

Hyperthyroidism

Hyperthyroidism is caused by an overproduction of thyroid hormone.

This is usually due to an antibody directed to the TSH receptor on the

thyrocyte, stimulating release of thyroid hormone in the absence of

TSH. Less commonly, hyperthyroidism can be the result of an autonomous

production of thyroid hormone due to a nodule of the thyroid.

Hyperthyroidism is usually associated with symptoms of tremors,

palpitations with tachycardia, weight loss, fatigue, insomnia, hair

and skin changes, heat intolerance, and frequent bowel movements.

Commonly, these patients present with altered cognition, inability to

concentrate, and inattentiveness. Elevated concentrations of serum T3

and T4 and suppression of serum TSH confirm the diagnosis of

hyperthyroidism. Treatment of hyperthyroidism is aimed at decreasing

production of T4 and T3 by the thyroid gland by the use of antithyroid

medication (such as propylthiouracil or methimazole), radioactive

iodine ablation or surgery. The latter two treatments usually result

in hypothyroidism. Correction of the thyroid hormone concentration

completely reverses the symptoms of hyperthyroidism.

Resistance to Thyroid Hormone

RTH is a rare thyroid hormone disorder which is characterized by

reduced responsiveness to thyroid hormone. It is usually due to a

mutation in the thyroid hormone receptor beta gene such that the

tissues are no longer able to respond to normal concentrations of

thyroid hormone. Careful evaluation of subjects with RTH has shown

that almost one-half have some degree of learning disability with or

without ADHD. About one-quarter of subjects have intellectual

quotients (IQ) less than 85 but frank mental retardation (IQ < 60) has

been found only in 3 % of cases. IQ is on the average lower in

subjects with RTH with or without ADHD. Although, the behavioral

characteristics of children with ADHD and RTH are similar to those

with ADHD only, the former have significantly weaker ability of

perceptual organization and lower school achievement, suggesting a

more severe cognitive impairment. Impaired mental function was found

to be associated with impaired or delayed growth (below 5th

percentile) in 20% of subjects, though growth retardation alone is

rare (4%). Despite the high prevalence of ADHD in patients with RTH,

the occurrence of RTH in children with ADHD must be very rare, none

having been detected in 412 such children studied. Furthermore,

current data do not support a genetic linkage of RTH with ADHD. Rather

the association with low IQ scores may confer a higher likelihood for

subjects with RTH to exhibit ADHD symptoms, a conclusion that has been

recently contested. The reason such a rare disorder is included in

the list of thyroid diseases associated with ADHD while other more

common diseases are not, is that more than 40–60% of children with RTH

have ADHD. RTH is usually diagnosed by the presence of goiter along

with elevated serum free T4 and T3 with nonsuppressed serum TSH. These

children are usually brought to clinical attention because of the

goiter, growth disturbance, hyperactive behavior or tachycardia.

Thyroid function tests are then obtained and the classic blood tests

are obtained. Since most patients with RTH are compensated for their

defect, in the absence of concurrent thyroid disease or previous

antithyroid treatment, no treatment is necessary. Occasionally

treatment with beta-adrenergic blockers can help with symptoms related

to tachycardia. In a limited small study it was suggested that T3

treatment may be beneficial for some the inattentive symptoms in this

group.

Winona

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Share on other sites

Yes, there " can " be a connection between ADHA and thyroid

resistance, but the way it's state, those with thyroid resistance

hava higher incidence of ADHD. Winona also provided you good info.

Janie

> >I was reading in the " Files " section, and found info on thyroid

and

> attention deficit. Are they saying the two are linked? My son has

> adhd. Please tell me more!!!

>

> ,

>

> The article below may be of interest to you:

>

> Ann N Y Acad Sci. 2001 Jun;931:97-112

> Medical mimics. Medical and neurological conditions simulating

ADHD.

>

>

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