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Neurological Manifestations of Thyroid Disease

Neurological Manifestations of Thyroid Disease

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The thyroid gland plays an important role in tissue metabolism and development. It secretes thyroxine (3,5,3’5′-tetraiodothyronine), which is abbreviated as T4, and small amounts of 3,5,3′-triiodothyronine, abbreviated T3. Both have systemic effects. Abnormal thyroid hormone levels lead to hypothyroid and hyperthyroid states. Inadequate thyroid hormone during development leads to congenital hypothyroidism (also known as cretinism) with associated irreversible brain damage.

Thyroid hormones regulate protein synthesis by affecting gene transcription and mRNA stabilization.

In hyperthyroidism (ie, thyrotoxicosis) increased thyroid function leads to increased cardiac output at rest and after exercise but to decreased muscle bulk and function.

Muscle activity shows altered electrical responses, altered energy metabolism, and increased sensitivity to beta-adrenergic stimuli. In a clinical study of experimental thyrotoxicosis, the activity of oxidative and glycolytic enzymes in skeletal muscle decreased by 21-37%. Lean body mass decreases and rate of whole body protein breakdown is enhanced. Thyroid hormones have profound effects on mitochondrial oxidative activity, synthesis and degradation of proteins, sensitivity of tissues to catecholamines, differentiation of muscle fibers, capillary growth, and levels of antioxidant enzymes and compounds. Muscles show contraction weakness and lack of normal contraction potentiation. Patients have lower levels of carnitine.

The central effects of hyperthyroidism are most pronounced in development. Cerebral circulation and oxygen consumption elevate. Studies on rat brain mitochondria show minimal effects. Measurements from rats suggest well-preserved brain iodothyronine homeostasis despite high thyroid hormone levels. Brain T4 and T3 concentrations and brain T3 production and turnover rates do not change significantly. levels of glutamate dehydrogenase and pyruvate dehydrogenase activity in the brain are reduced. Beta-adrenergic binding sites in the cerebral cortex are increased and gamma-aminobutyric acid (GABA) binding sites are decreased. Brain levels of serotonin, 5-hydroxyindoleacetic acid, and substance P are altered. Native pain sensitivity and number of opiate receptors are increased. Thyroid hormones affect myelination, therefore increased levels lead to oxidative damage to the myelin membrane and/or the oligodendroglial cells.

In hypothyroidism, muscle contraction and relaxation are slowed while duration is prolonged.

The amount of myosin ATPase decreases. Slowing of release and reaccumulation of calcium in the endoplasmic reticulum may decrease relaxation. In peripheral nerves, segmental demyelination has been observed with decreased nerve conduction velocities. Patients develop polyneuropathy with loss of reflexes and weakness. Decreases in vibration, joint-position, and touch-pressure sensations also are seen.

Thyroid deficiency can impair hippocampal neurogenesis, differentiation, and maturation in developmental and adult rat brains, suggesting a similar mechanism in humans. Hypothyroidism changes synaptic transmission and plasticity in area CA1 of the hippocampus, which, in turn, may be the mechanism that leads to impairment in learning and memory. [1]

United States

Thyroid disease is common in adults. One survey found the prevalence of hypothyroidism to be 1.4% in adult females and 0.1% in adult males. The prevalence of Graves disease, a hyperthyroid condition, is 1.9% in females and about 0.19% in males. Peak age incidence is in the range of 30-50 years. Congenital disease occurs in 1 per 4000 neonates in North America and Western Europe. This is seen more frequently in areas of iodine deficiency.

International

About 1 billion people are at risk for iodine deficiency disorders. Endemic goiter is most the common manifestation and has a varying prevalence. In communities with severe iodine deficiency, prevalence is 5-15% but can reach 100%. This situation occurs in developing countries.

No race predilection is known.

Thyroid disease is more common in women, but men also are affected.

Thyroid disease is most common in adults aged 30-50 years, but all age groups are affected. Cretinism and neonatal myxedema manifest in the intrauterine/perinatal period.

Cao L, Wang F, Yang QG, Jiang W, Wang C, Chen YP, et al. Reduced thyroid hormones with increased hippocampal SNAP-25 and Munc18-1 might involve cognitive impairment during aging. Behav Brain Res. 2012 Apr 1. 229(1):131-7. [Medline].

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Canepa C, Srinivasan R, Muhith A. Reversible and unilateral corticospinal tract disease secondary to autoimmune free-T3-thyrotoxicosis. BMJ Case Rep. 2017 Aug 7. 2017:1-6. [Medline].

Ohba S, Nakagawa T, Murakami H. Concurrent Graves’ disease and intracranial arterial stenosis/occlusion: special considerations regarding the state of thyroid function, etiology, and treatment. Neurosurg Rev. 2011 Jul. 34(3):297-304; discussion 304. [Medline].

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Gabriel Bucurescu, MD, MS Attending Neurologist, Neurology Service, Corporal Michael J Crescenz Veterans Affairs Medical Center

Gabriel Bucurescu, MD, MS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Nicholas Lorenzo, MD, MHA, CPE Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association for Physician Leadership

Disclosure: Nothing to disclose.

Thomas A Kent, MD Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center

Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, Royal Society of Medicine, Stroke Council of the American Heart Association, American Neurological Association, New York Academy of Sciences, Sigma Xi

Disclosure: Nothing to disclose.

Neurological Manifestations of Thyroid Disease

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