Thyroid hormone is essential for the development of the central nervous system. Deficiency in fetal life or at birth causes hypoplasia of cortical neurons with poor development of cellular processes, retarded myelination, and reduced vascularity. Deficiency of thy roid hormone beginning in adult life causes less severe manifestations that usually respond to treatment with thyroid hormone. Recent studies using 32P nuclear magnetic resonance spectroscopy of the frontal lobe of adult hypothyroid patients report reversible alterations in phosphate metabolism, suggesting impairment of mitochondrial metabolism. Cerebral blood flow is reduced in hypothyroidism, but cerebral oxygen consumption is usually normal. This finding is in accord with the observation that the oxygen consumption of isolated brain tissue in vitro, unlike that of most other tissues, is not stimulated by the administration of thy roid hormones. In severe cases, decreased cerebral blood flow may lead to cerebral hypoxia. These and other findings indicate that the adult human brain is a thyroid hormone- responsive organ. Hypothyroidism may induce neurological abnormalities at an early stage of the disease. It has been shown that peripheral and central neuropathy develops in patients of hypothyroidism at an early stage of disease and the electrophysiological investigations of such patients can help in timely detection and treatment of neuro logical disorders that occur due to thyroid hormone deficiency.

Box 1 lists the numerous symptoms suggesting either neurological or psychiatric disorders in patients with moderate to severe hypothyroidism. In adult and elderly patients, mental changes may go unrecognized because of their slow development and because they may mimic cerebral atherosclerosis. However, an unusual complacency, fatigue, and pronounced somnolence or even lethargy together with a prolonged reaction time should suggest the possibility of hypothyroidism. Special attention is required for patients who need an increasing amount of sleep (over 12– 14 h/ day). They may lapse into stupor or even coma, and develop convulsions. This may be the beginning of myxoedema coma, a rare but very serious condition, the extreme expression of severe hypothyroidism. All intellectual functions, including speech, are slowed. There is loss of initiative, and slow wittedness and memory defects are common; in a study working memory was impaired in hypothyroidism. Dementia in elderly patients may be mistaken for senile dementia. Memory is undoubtedly impaired, and attention and the desire to think are reduced. The emotional level seems definitely low, and irritability is decreased. Except in the terminal stage, reasoning power is preserved. Cognitive tests of patients with moderate to severe hypothyroidism indicate difficulties in performing calculations, recent memory loss, reduced attention span, and slow reaction time. In a metanalysis the association between subclinical hypothyroidism (sHT) and cognitive impairment has been shown only in individuals younger than 75 years of age and those with higher thyroid- stimulating hormone (TSH) concentrations.

Box1. Neurologic and psychiatric manifestations in hypothyroidism

Headaches are frequent.

In a minority of patients, nervousness and apprehension are present. Psychiatric disorders are common and are usually of the paranoid or depressive type and may induce agitation (myxoedema madness). Depression is so often associated with hypothyroidism that thyroid function tests should be performed in the evaluation of any patient presenting with this symptom. Central 5- hydroxytryptamine activity is reduced in hypothyroid patients, and T3 supplementation might increase the efficacy of antidepressant drugs. At times, this manifestation of hypothyroidism is more severe than are many of the other clinical manifestations of the dis ease. Because hypothyroidism is so readily treated, it is an especially important cause to eliminate.

In rare cases of long- standing hypothyroidism cerebellar ataxia with or without intention tremor has been found. Jellinek and Kelly described a series of myxoedematous patients with ataxia, intention tremor, nystagmus, and dysdiadochokinesia. Ataxia has been noted in 8% of a large series of hypothyroid patients. Patients may have intention tremor, nystagmus, and an inability to make rapid alternating movements. The cause of this syndrome is not apparent, but myxoedematous infiltrates of glycogen and mucinous material have been found in the cerebellum. There may be foci of degeneration and an increase in glial tissue. These symptoms show a prompt and definite decrease after replacement therapy with thyroid hormone.

Sensory phenomena are common. Numbness and tingling of the extremities are frequent. Mononeuropathies occur in hypothyroidism, as attested to by the high incidence of carpal tunnel syndrome (compression of the median nerve at the wrist). Nocturnal paraesthesia and pain in the median nerve distribution in one or both hands is a common manifestation of this condition. Paraesthesia or lancing pain in the legs are manifestations of lower extremity peripheral neuropathy. A study of 39 patients with primary hypothyroidism found complaints of polyneuropathy in 64%, findings of polyneuropathy in 33%, and a definite diagnosis by electrophysiological criteria in 72%. A metachromatic infiltrate has been found in the lateral femoral cutaneous nerve and sural nerve, together with axon cylinder degeneration.

The tendon reflexes are slow, especially during the relaxation phase, producing the characteristic ‘hung- up’ reflexes: this phenomenon is due to a decrease in the rate of muscle contraction and relaxation, rather than a delay in nerve conduction. The presence of extensor plantar responses or diminished vibration sense should alert the physician to the possibility of coexisting pernicious anaemia with combined system disease.

Electroencephalographic changes include slow α- wave activity and general loss of amplitude. The concentration of protein in the cerebrospinal fluid is often increased, but cerebrospinal pressure is normal.

Deafness is a very characteristic and troublesome symptom of hypothyroidism. It may be due to both conduction or nerve impairment and usually responds very well to treatment. Vestibular abnormalities have also been demonstrated. Serous otitis media is not uncommon. Two- thirds of patients complain of dizziness, vertigo, or occasionally tinnitus: these problems suggest damage to the eighth nerve or labyrinth, or possibly to the cerebellum. Whatever type of deafness is present, there is marked improvement after thyroid treatment. Acquired hearing loss in association with adult- onset hypothyroidism should be distinguished from the sensorineural deafness of Pendred’s syndrome. In the latter, treatment of hypothyroidism does not correct the hearing defect.

Night blindness is not uncommon. It is caused by a deficiency in the pigment retinene, which is required for the adaptation to dark.

اخر الاخبار

اخبار العتبة العباسية المقدسة

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المزيد

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المزيد

الآخبار التكنلوجية

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علماء يكتشفون انخفاض صلابة الألماس عند تحويله إلى مقياس نانوي

ثورة في علاج الصمم.. علاج جيني يحقق نتائج استثنائية في استعادة السمع

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المزيد

مواضيع ذات صلة

Organ System Manifestations of Hypothyroidism: Haematological Changes

Organ System Manifestations of Hypothyroidism: Musculoskeletal Changes

Organ System Manifestations of Hypothyroidism: Respiratory Changes

Organ System Manifestations of Hypothyroidism: Cardiovascular Changes

Organ System Manifestations of Hypothyroidism : Cutaneous Manifestations and Changes in the Connective Tissues

Thromboembolic Conditions

Conditions that Cause Excessive Bleeding in Humans

Absent Intrinsic Factor Secretion and Pernicious Anemia

Subclinical Hyperthyroidism

Thyrotoxic Periodic Paralysis: Clinical Features

Nutritional Causes of Folate Deficiency

Neurologic Dysfunction with Cobalamin Deficiency