Chapter 48 - Thyroid disease and the nervous system

https://doi.org/10.1016/B978-0-7020-4087-0.00048-6Get rights and content

Abstract

Thyroid disorders are common in the general population and in hospitalized patients. Thyroid disease may present first with neurological complications or else may occur concurrently in patients suffering other neurological disorders, particularly those with an autoimmune etiology. For this reason neurologists will commonly encounter patients with thyroid disease. This chapter provides an overview of the neurological complications and associations of disorders of the thyroid gland. Particular emphasis is placed on conditions such as thyrotoxic periodic paralysis and myxedema coma in which the underlying thyroid disorder may be occult leading to a first, often emergency, presentation to a neurologist. Information about clinical features, diagnosis, pathogenesis, therapy, and prognosis is provided. Emphasis is placed on those aspects most likely to be relevant to the practicing neurologist and the interested reader is directed to references to good, recent review articles for further information.

Introduction

Disorders of the thyroid gland are common and frequently accompanied by neurologic complications. A recent study of unselected general medical, geriatric, and psychiatric inpatients showed that 1–2% of patients had some form of thyroid disease (Attia et al., 1999). A 2008 population-based study carried out in Tayside, Scotland, revealed a prevalence of ever having had hyperthyroidism of 1.26% in women, 0.24% in men and a prevalence of hypothyroidism of 5.14% in women and 0.88% in men (Leese et al., 2008). It is important for the neurologist to be aware of the neurologic complications of thyroid disease because thyroid disorders may present first to the neurologist but, more important still, most may be readily corrected with appropriate treatment.

The neurologic complications of thyroid disease may be the direct result of changes in the levels of thyroid hormones, may arise from immune-mediated mechanisms, or else may be the result of mechanical compression of neural structures. Alteration in the levels of circulating thyroid hormones may produce a new neurologic complication, exacerbate a pre-existing neurologic problem, or unmask a subclinical neurologic problem. Antibodies raised against targets in the thyroid gland may have effects on neural tissue with antigens in common. Autoimmune disease of the thyroid may be associated with other autoimmune diseases affecting the nervous system such as myasthenia gravis. Compression of adjacent neural structures by an enlarging thyroid gland, an enlarging pituitary gland, or infiltrated ocular muscles and fat may result in neurologic complications. Patients with thyroid carcinoma may develop intracranial metastases. Whilst research in this area continues apace, it is clear that the cellular and molecular mechanisms underlying many neurologic complications of thyroid disease remain incompletely understood.

Section snippets

The neurology of congenital hypothyroidism

Congenital hypothyroidism (CH), historically termed cretinism, is the commonest treatable cause of mental retardation, with a prevalence of 1/2000 to 1/4000 (Fisher, 1983). It is due to a deficiency in thyroid hormone present at birth. Congenital hypothyroidism may be subdivided into primary (due to agenesis of the thyroid or dyshormonogenesis), secondary (due to deficient TSH signal transduction or else as part of congenital hypopituitarism), or peripheral (due to deficits in the transport or

Myasthenia gravis

An association between myasthenia gravis and hypothyroidism has been reported, although this is less common than its association with hyperthyroidism (Sahay et al., 1965). The myasthenic symptoms may precede or present with the hypothyroidism or else develop subsequently. The severity of the myasthenia may or may not improve following treatment of the hypothyroidism.

Giant cell arteritis and polymyalgia rheumatica

In 1977, How and coworkers described a patient in whom both giant cell arteritis and hypothyroidism were present, and suggested a

Neurologic complications of hyperthyroidism and graves' disease

There are several potential underlying causes of hyperthyroidism, including (1) Graves’ disease; (2) excess release of stored hormone during subacute thyroiditis or following thyroid irradiation; (3) uncontrolled hormone formation in single or multinodular goiters (Plummer’s disease); (4) ingestion of excess thyroid hormone; (5) rare TSH-secreting pituitary tumors; (6) drug-induced disease. Graves’ disease is the commonest cause of thyrotoxicosis and occurs with a female-to-male preponderance

Myasthenia gravis

A long-recognized association exists between thyroid disease and myasthenia gravis. There is no evidence that thyroid dysfunction causes myasthenia gravis, or vice versa, and their coexistence is likely to be due to an underlying genetic predisposition to autoimmune disease. Myasthenia gravis may be associated with both hyperthyroidism and hypothyroidism (Sahay et al., 1965). Hyperthyroidism occurs in 2–17.5% of patients with myasthenia gravis (Trabelsi et al., 2006). In one study of 104

References (344)

  • A.J. Coles et al.

    Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis

    Lancet

    (1999)
  • E.L. De Schryver et al.

    Thyrotoxicosis, protein C deficiency and lupus anticoagulant in a case of cerebral sinus thrombosis

    Neth J Med

    (1999)
  • M.M. Demet et al.

    Depression and anxiety in hyperthyroidism

    Arch Med Res

    (2002)
  • A. Djemli et al.

    Congenital hypothyroidism: from paracelsus to molecular diagnosis

    Clin Biochem

    (2006)
  • O. Dohan et al.

    Advances in Na(+)/I(-) symporter (NIS) research in the thyroid and beyond

    Mol Cell Endocrinol

    (2003)
  • A.M. Dumitrescu et al.

    A novel syndrome combining thyroid and neurological abnormalities is associated with mutations in a monocarboxylate transporter gene

    Am J Hum Genet

    (2004)
  • E. Ferlazzo et al.

    Recurrent status epilepticus as the main feature of Hashimoto’s encephalopathy

    Epilepsy Behav

    (2006)
  • D.A. Fisher

    Second International Conference on Neonatal Thyroid Screening: progress report

    J Pediatr

    (1983)
  • M. Fisher et al.

    Pyramidal tract deficits and polyneuropathy in hyperthyroidism, combination clinically mimicking amyotrophic lateral sclerosis

    Am J Med

    (1985)
  • S. Aanderud et al.

    Hypothyroidism induced by anti-epileptic therapy

    Acta Neurol Scand

    (1980)
  • M.J. Abramowicz et al.

    Familial congenital hypothyroidism due to inactivating mutation of the thyrotropin receptor causing profound hypoplasia of the thyroid gland

    J Clin Invest

    (1997)
  • J. Alink et al.

    Unexplained seizures, confusion or hallucinations: think Hashimoto encephalopathy

    Acta Paediatr

    (2008)
  • V.T. Anand et al.

    Auditory investigations in hypothyroidism

    Acta Otolaryngol

    (1989)
  • S. Araki et al.

    Muscle cramps in chronic thyrotoxic myopathy Report of a case

    Arch Neurol

    (1968)
  • K. Araki et al.

    A case of polymyositis associated with chronic thyroiditis presenting as hyperthyroidism

    Jpn J Med

    (1990)
  • W. Araki et al.

    Frequent and frequently overlooked: treatment-induced endocrine dysfunction in adult long-term survivors of primary brain tumors

    Neurology

    (1997)
  • R. Asher

    Myxoedematous madness

    Br Med J

    (1949)
  • C.K. Atterwill et al.

    Effects of thyroid status on presynaptic alpha 2-adrenoceptor function and beta-adrenoceptor binding in the rat brain

    J Neural Transm

    (1984)
  • J. Attia et al.

    Diagnosis of thyroid disease in hospitalized patients: a systematic review

    Arch Intern Med

    (1999)
  • M. Baba et al.

    Persistent hemichorea associated with thyrotoxicosis

    Intern Med

    (1992)
  • R.S. Bahn

    Graves’ ophthalmopathy

    N Engl J Med

    (2010)
  • R.S. Bahn et al.

    Thyrotropin receptor expression in Graves’ orbital adipose/connective tissues: potential autoantigen in Graves’ ophthalmopathy

    J Clin Endocrinol Metab

    (1998)
  • C.C. Bailey et al.

    Magnetic resonance imaging in thyroid eye disease

    Eye (Lond)

    (1996)
  • B. Bakker et al.

    Two decades of screening for congenital hypothyroidism in the Netherlands: TPO gene mutations in total iodide organification defects (an update)

    J Clin Endocrinol Metab

    (2000)
  • S.L. Bar et al.

    Asymptomatic hypothyroidism and statin-induced myopathy

    Can Fam Physician

    (2007)
  • R. Barker et al.

    Thyrotoxic Hashimoto’s encephalopathy

    J Neurol Neurosurg Psychiatry

    (1996)
  • R.O. Barnard et al.

    Pathological findings in a case of hypothyroidism with ataxia

    J Neurol Neurosurg Psychiatry

    (1971)
  • L. Bartalena et al.

    Relation between therapy for hyperthyroidism and the course of Graves’ ophthalmopathy

    N Engl J Med

    (1998)
  • L. Bartalena et al.

    Consensus statement of the European Group On Graves’ Orbitopathy (EUGOGO) on management of Graves’ orbitopathy

    Thyroid

    (2008)
  • J.A. Bastron

    Neuropathy in disease of the thyroid

  • E. Beghi et al.

    Hypothyroidism and polyneuropathy

    J Neurol Neurosurg Psychiatry

    (1989)
  • T. Betteridge et al.

    Phenytoin toxicity and thyroid dysfunction

    N Z Med J

    (2009)
  • J. Beynon et al.

    Predictors of outcome in myxoedema coma

    Crit Care

    (2008)
  • A. Bhansali et al.

    Acute myoedema: an unusual presenting manifestation of hypothyroid myopathy

    Postgrad Med J

    (2000)
  • P. Boileau et al.

    Earlier onset of treatment or increment in LT4 dose in screened congenital hypothyroidism: which as the more important factor for IQ at 7 years?

    Horm Res

    (2004)
  • L. Brain et al.

    Hashimoto’s disease and encephalopathy

    Lancet

    (1966)
  • M.D. Brennan et al.

    Changes in skeletal muscle protein metabolism and myosin heavy chain isoform messenger ribonucleic acid abundance after treatment of hyperthyroidism

    J Clin Endocrinol Metab

    (2006)
  • M.D. Brennan et al.

    The impact of overt and subclinical hyperthyroidism on skeletal muscle

    Thyroid

    (2006)
  • D. Bronsky et al.

    An association between the Guillain–Barré syndrome and hyperthyroidism

    Am J Med Sci

    (1964)
  • B.E. Brownlie et al.

    Psychoses associated with thyrotoxicosis – “thyrotoxic psychosis” A report of 18 cases, with statistical analysis of incidence

    Eur J Endocrinol

    (2000)

    • Cited by (20)

    • Encapsulation in nervous system

      2023, Principles of Biomaterials Encapsulation: Volume 2

    • Myxoedema coma revealed by status epilepticus: A report case and review of the literature

      2017, Pratique Neurologique - FMC

    • Hypothyroidism and Thyroiditis

      2015, Williams Textbook of Endocrinology

    • Gene therapy targeting the blood-brain barrier improves neurological symptoms in a model of genetic MCT8 deficiency

      2022, Brain

    • The efforts of deep learning approaches for breast cancer detection based on x-ray images

      2022, Research Anthology on Medical Informatics in Breast and Cervical Cancer

    • Multiple cranial nerve motor deficits, resembling polyneuritis cranialis, in a cat with hyperthyroidism

      2022, Australian Veterinary Journal
    View all citing articles on Scopus
    View full text
    Copyright © 2014 Elsevier B.V. All rights reserved.