INTRODUCTION — Hypothyroidism is a common medical condition in the general population. Common systemic manifestations include fatigue, constipation, cold intolerance, weight gain, hair loss, dry skin, and hoarseness. A variety of central and peripheral nervous system manifestations are common in patients with hypothyroidism (table 1). In many cases, the neurologic manifestations occur in conjunction with the systemic features of the disease and may be noted only incidentally. However, symptoms and signs of neurologic dysfunction may be the presenting feature in some patients and can contribute significant disability. Most of these complications are partially or fully responsive to thyroid replacement.
This topic reviews the common neurologic manifestations of hypothyroidism. Other clinical manifestations of hypothyroidism are discussed separately. (See "Clinical manifestations of hypothyroidism".)
SEQUELAE OF FETAL AND NEONATAL HYPOTHYROIDISM — Fetal and/or neonatal hypothyroidism causes neurologic sequelae, including impaired intellectual and motor development. The severity of the impairment depends upon the severity and duration of fetal/neonatal hypothyroidism. Although the effects of postnatal hypothyroidism can be ameliorated by prompt treatment, the sequelae of gestational hypothyroidism, particularly in the first trimester, persist throughout life. One cause of hypothyroidism in neonates is maternal and infant iodine deficiency, which is still endemic in some parts of Europe and elsewhere in the world.
Neurologic sequelae include:
●Intellectual disability – The severity of cognitive impairments is associated with both the degree and duration of thyroid (or iodine) deficiency in utero and early life [1]. Severe deficiency in the first trimester of pregnancy in particular is associated with severe irreversible intellectual as well as motor impairment [2,3].
Even children exposed to mild degrees of iodine deficiency in gestation and those with postnatal congenital hypothyroidism that is promptly recognized at birth are likely to have mild, often subclinical, neuropsychiatric deficits when compared with siblings and other control groups [4]. Studies suggest that in postnatal hypothyroidism, earlier administration of higher-dose thyroxine (T4) treatment is associated with less severe deficits [5]. (See "Treatment and prognosis of congenital hypothyroidism".)
●Impaired motor development – Severe gestational and postnatal hypothyroidism are associated with dysfunction of pyramidal and extrapyramidal motor systems. Typical deficits include rigidity and spasticity of the trunk and proximal extremities, with relative sparing of the distal arms and legs [6]. Neuroimaging studies have revealed calcification in the basal ganglia and subcortical areas on computed tomography (CT), as well as magnetic resonance imaging (MRI) signal abnormalities in the globus pallidus and substantia nigra [6,7].
Up to 40 percent of children and adolescents with congenital hypothyroidism have been shown to demonstrate mild findings of cerebellar dysfunction, such as intention tremor, difficulty with tandem gait, clumsy running, fine motor dysfunction, and unsteady stance [8,9]. The findings were more prominent in those diagnosed with hypothyroidism during the first few months of life compared with those diagnosed after the first year of life. A delay to treatment also influences the severity of findings in these children [10]. Animal studies have shown that hypothyroidism interferes with cerebellar development [11,12].
●Other deficits – These can include strabismus and sensorineural hearing loss.
Iodine deficiency and congenital hypothyroidism are discussed in detail separately. (See "Iodine deficiency disorders" and "Clinical features and detection of congenital hypothyroidism" and "Treatment and prognosis of congenital hypothyroidism".)
MYXEDEMA COMA — Myxedema coma is a rare manifestation of severe hypothyroidism. Patients present with altered consciousness ranging in severity from confusion and lethargy to coma, usually in conjunction with hypothermia and other symptoms and signs of hypothyroidism (hypotension, bradycardia, hyponatremia, hypoglycemia, and hypoventilation). Seizures are common.
Myxedema coma is a medical emergency with a high mortality rate. This topic is discussed separately. (See "Myxedema coma".)
COGNITIVE IMPAIRMENT AND DEMENTIA — The pathogenesis of cognitive dysfunction in hypothyroidism is unknown. Decreased cerebral blood flow and decreased cerebral oxygen and glucose metabolism as seen on single-photon emission computed tomography (SPECT) and positron-emission tomography (PET) studies have been implicated in some patients, but not in others [13-16]. Animal studies suggest that hypothyroidism can produce alterations in the synaptic plasticity of neural pathways mediated by the dorsal hippocampus, which are important for many higher cognitive functions [17].
Mild cognitive impairment in hypothyroidism may be mediated by anxiety and depression, both of which have been linked to hypothyroidism. Depression and anxiety can impair attention and executive function, the same cognitive spheres that are most often and earliest affected in hypothyroidism. Studies of post-thyroidectomy patients who undergo induced hypothyroidism (for the purpose of thyroid cancer assessment) find that patients exhibit symptoms of anxiety and depression with proportionate disturbances in attention and executive function [18].
Clinical features and associations
Overt hypothyroidism — Cognitive dysfunction is a common feature of overt hypothyroidism (low serum free thyroxine [T4], elevated serum thyroid-stimulating hormone [TSH]), occurring in 66 to 90 percent of patients [19].
Cognitive impairment in hypothyroidism is most often manifest by slowed mentation, poor concentration, and decreased short-term memory [13,20]. Also common are social withdrawal, psychomotor retardation, depressed mood, and apathy. Cortical features (aphasia, apraxia) are generally absent. Less commonly, hypothyroidism presents with other neuropsychologic symptoms including psychosis, confusion, and disorientation; this syndrome has been called "myxedema madness."
When neuropsychologic testing is performed, deficits may be most pronounced in tests of attention and executive function [13,20-23]. Memory retrieval, learning, verbal fluency, and motor speed are also often particularly impaired. Electroencephalography (EEG) may show generalized background slowing [13].
Cognitive change in overt hypothyroidism is commonly accompanied by other clinical features associated with this condition, including lethargy, fatigue, cold intolerance, dry skin, constipation, and decreased exercise tolerance. These symptoms may occur concurrently with or precede cognitive decline. (See "Clinical manifestations of hypothyroidism".)
Subclinical hypothyroidism — Subclinical hypothyroidism is defined biochemically as a normal serum free T4 concentration in the presence of an elevated serum TSH concentration. This is in contrast with overt hypothyroidism, which is characterized by a low free T4 concentration. Despite its name, subclinical hypothyroidism may occur with mild symptoms of hypothyroidism; however, these are typically vague and nonspecific in this setting.
Subclinical hypothyroidism is common in the adult population, occurring in 4 to 15 percent; the prevalence rises with age and is higher in females than males. (See "Subclinical hypothyroidism in nonpregnant adults".)
Investigations of the association between subclinical hypothyroidism and dementia or cognitive impairment have had somewhat conflicting results, due in part to whether the study was cross-sectional or followed patients over time and the types of cognitive testing employed [21,23-35]. In the aggregate, as summarized by a 2016 systematic review and meta-analysis, and confirmed in a subsequent cohort study, there is no convincing evidence that cognitive impairment or dementia is associated with subclinical hypothyroidism [36-38].
Despite this, there may be a rationale for treating patients with subclinical hypothyroidism and significant cognitive impairment as discussed below.
Alzheimer disease — Some studies have suggested that thyroid disease may be a risk factor for Alzheimer disease (AD) [39-41], but the bulk of evidence does not support an etiologic relationship [39,41-47].
Hashimoto encephalopathy — Autoimmune or Hashimoto thyroiditis is the most common cause of hypothyroidism in iodine-sufficient areas of the world. Hashimoto encephalopathy describes a syndrome of altered mental status and seizures that occurs in individuals with serologic manifestations of Hashimoto thyroiditis. Unlike the syndromes described above, the clinical manifestations are believed to result from autoimmunity, not from hypothyroidism. This topic is discussed separately. (See "Hashimoto encephalopathy".)
Treatment and prognosis — While hypothyroidism is generally understood to be a "treatable" dementia, studies of the efficacy of thyroid replacement on cognitive function are somewhat limited [48,49]. Nonetheless, thyroid replacement is recommended for patients with overt hypothyroidism and is also suggested for subclinical hypothyroidism with TSH >7 mU/L regardless of cognitive status. (See "Treatment of primary hypothyroidism in adults" and "Subclinical hypothyroidism in nonpregnant adults", section on 'Management'.)
●Overt hypothyroidism – In patients with overt hypothyroidism, thyroid hormone replacement can improve cognition [22,50]. However, the degree of recovery is variable and may be incomplete in patients with more severe and longer duration of hypothyroidism. Cognitive recovery may also be delayed for several months following a return to a euthyroid state [13]. Studies that report either no or limited improvement often had short follow-up times [20,51]. The treatment of hypothyroidism is discussed separately. (See "Treatment of primary hypothyroidism in adults".)
●Subclinical hypothyroidism – Few randomized, placebo-controlled studies have assessed the effect of thyroid replacement on cognitive performance in patients with subclinical hypothyroidism. A randomized, placebo-controlled trial in 94 patients, aged 65 years and older with subclinical hypothyroidism, demonstrated no significant improvement in Mini-Mental State Examinations and other tests of cognition following six months of thyroid replacement; however, only one subject was cognitively impaired at baseline, and there was a high dropout rate [52]. In smaller studies, replacement with T4 led to objective and/or subjective improvements in memory [53-56]. Several uncontrolled trials have also indicated that a significant improvement in attention, memory, verbal fluency, and executive functions occurs with thyroid replacement [21,35,53]. Most of these patients did not have dementia.
While these studies are not conclusive, we suggest a treatment trial with thyroid replacement for most patients with subclinical hypothyroidism and measured cognitive impairment. Arguments against treatment include the risks of overtreatment as well as possibly inducing cardiac symptoms in susceptible patients. Treatment should be stopped in patients who don't appear to have a clinical benefit. Other aspects of management including other indications for the treatment of subclinical hypothyroidism are discussed separately. (See "Subclinical hypothyroidism in nonpregnant adults", section on 'Management'.)
Screening for hypothyroidism in cognitive impairment — Given the high prevalence of hypothyroidism in the older adult population and the potential for treatment benefit, we suggest screening for hypothyroidism with a serum TSH in patients with cognitive impairment and dementia as recommended by the Quality Standards Subcommittee of the American Academy of Neurology [57,58]. (See "Evaluation of cognitive impairment and dementia".)
The yield of screening for hypothyroidism in unselected patients with dementia is very low. In a community-based series of the 560 patients with dementia, no cases were felt to be attributable to hypothyroidism [50].
For most patients, a screening TSH assay level is sufficient, as assays are very sensitive for detecting primary hypothyroidism in ambulatory patients. Settings in which it may be appropriate to also obtain a free T4 level include suspicion for central hypothyroidism; this is discussed in detail separately. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Screening tests'.)
MOVEMENT DISORDERS
Parkinson disease — An association between hypothyroidism and Parkinson disease (PD) has not been conclusively defined; some studies suggest an association [59-61] while others do not [62,63]. One meta-analysis of three cohort studies and six case-control studies reported an increased likelihood of PD in patients with hypothyroidism (pooled odds ratio [OR] 1.56, 95% CI 1.38-1.77), although moderate heterogeneity among the studies precluded firm conclusions [61].
However, many clinical features are common to both hypothyroidism and PD, including general slowness (bradykinesia), rigidity, decreased facial expression, monotonous voice, apathy, and depression. Because identification of hypothyroidism may be masked by PD, some suggest that thyroid function studies be performed in patients with PD who do not respond to treatment [64,65].
Testing for hypothyroidism may be complicated in the setting of PD. L-dopa suppresses the thyrotropin-releasing hormone response. A small reduction in serum thyroid-stimulating hormone (TSH) levels has been shown to occur two hours after carbidopa-levodopa administration [66]. Serum TSH screening may produce false-negative results if the serum is drawn during the first few hours following administration of a dopaminergic medication [59]. This is discussed in detail separately. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Screening tests'.)
Cerebellar ataxia — In early case series of patients with adult-onset hypothyroidism, a wide-based gait ataxia was a prominent feature in a significant number (10 to 30 percent) [67,68]. In some cases, this was the presenting feature, and variably included limb ataxia (clumsiness, intention tremor, dysmetria) and dysarthria [69-71]. Treatment of the hypothyroid state led to improvement or resolution of the cerebellar features [8,69,71-73]. These cases are compelling, even though other reports have challenged the association of cerebellar dysfunction and hypothyroidism [74,75].
Cerebellar dysfunction is also a feature of congenital hypothyroidism. (See 'Sequelae of fetal and neonatal hypothyroidism' above.)
Hemichorea — A single case of reversible hemichorea has been reported in association with other features of hypothyroidism. The chorea resolved after several weeks of thyroid replacement [76].
PERIPHERAL NEUROPATHY
Carpal tunnel syndrome — Carpal tunnel syndrome (CTS) refers to compression of the median nerve within the carpal tunnel or bony canal in the wrist. CTS is a common symptom in the general population, with a reported prevalence of 3.0 to 5.8 percent in women and 0.6 to 2.1 percent in men [77]. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)
CTS is common in patients with hypothyroidism. In small case series of patients with newly diagnosed hypothyroidism, clinical signs of CTS were present in 25 to 38 percent [78,79]; an even higher proportion may have electrodiagnostic signs [80]. In the majority of these patients, the findings were bilateral. No correlation between the severity of hypothyroidism and the presence of CTS has been reported. In one study, increased body mass index (BMI) was an important risk factor for CTS in hypothyroid patients [81]; obesity is also a risk factor for CTS in the general population. However, according to one meta-analysis, the association between thyroid disease and CTS is modest and potentially explained by confounding factors [82].
The reported prevalence of hypothyroidism in patients with CTS varies widely in the literature [77,83-86]. A systematic review of the literature found that reported prevalence of hypothyroidism in CTS patients ranged from 1.3 percent to 10.3 percent [77]. The highest associations between CTS and hypothyroidism were in studies of patients undergoing surgical therapy, suggesting that hypothyroidism may be associated with more severe CTS [84,85].
●Pathology – The pathogenesis of CTS in hypothyroidism is believed to be due to mucinous infiltration of the perineurium and endoneurium of the median nerve within the carpal tunnel [87,88]. Mucopolysaccharide protein complexes with synovial thickening have been identified in tendons and synovial sheaths. The deposition of mucin material leads to increased compartmental pressure within the carpal tunnel, producing direct pressure on the median nerve and causing focal demyelination. The pathologic findings improve or resolve with treatment of the hypothyroidism.
●Clinical manifestations and diagnosis – The symptoms and signs of CTS in hypothyroidism do not differ from CTS in other patients. Patients classically present with numbness, tingling, or pain in the hand, which is particularly bothersome at night. Sensory loss is demonstrable in the first three fingers and half of the fourth finger. Weakness and atrophy of the thenar muscles occur in severe cases. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)
CTS symptoms may precede other clinical features of hypothyroidism.
One report describes three patients with hypothyroidism and CTS who experienced unilateral tingling on the medial sole and heel of the foot, suggesting a clinical diagnosis of tarsal tunnel syndrome which was subsequently confirmed by nerve conduction studies (NCS) [89]. It seems plausible that hypothyroidism might be associated with entrapment neuropathies other than or in addition to CTS.
The diagnosis of CTS in hypothyroid patients is similar to other settings. NCS are a useful diagnostic tool and can guide treatment decisions. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)
●Screening for hypothyroidism in CTS – Given the potential health risk of undiagnosed hypothyroidism, its relatively high prevalence in CTS, the relative ease of screening for the disease, and the altered treatment approach to CTS in the setting of hypothyroidism, we suggest screening for hypothyroidism with a serum thyroid-stimulating hormone (TSH) level in patients with CTS [90]. Settings in which it may be appropriate to also obtain a free T4 level include suspicion for central hypothyroidism; this is discussed in detail separately. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Screening tests'.)
The efficacy of screening for hypothyroidism in patients presenting with CTS has not been well studied, and it does not appear to be broadly recommended [77]. Most studies associating hypothyroidism in CTS do not indicate whether the diagnosis of hypothyroid disease was made before or after the diagnosis of CTS. One study that did so reported that 13 of 18 hypothyroid diagnoses were made after presentation with CTS [83].
●Treatment – A number of clinical observations report clinical and electrodiagnostic improvement or resolution of the CTS following thyroid replacement and return to a euthyroid state [79,91,92]. With thyroid replacement, symptoms may improve within weeks to months. However, one study found that among 21 treated patients with hypothyroidism, symptoms and electrophysiologic signs of CTS were common (73 and 29 percent, respectively) [80]. Unsystematic observations suggest that a longer duration of CTS prior to treatment is associated with poorer response to hormone replacement [79].
Other treatments used in CTS, such as wrist splinting, corticosteroid injection, and surgical carpal tunnel release, are also options in these patients, although they have not been well studied in hypothyroid-related CTS [93]. Since improvement with return to the euthyroid state is common, surgical intervention is often unnecessary and should probably await a treatment trial of hormone replacement. (See "Carpal tunnel syndrome: Treatment and prognosis".)
Polyneuropathy — The incidence of polyneuropathy in hypothyroid patients is not precisely known. In various studies of mostly newly diagnosed hypothyroidism, distal sensory complaints occur in 29 to 64 percent, clinical signs of polyneuropathy are seen in 25 to 42 percent, and electrophysiologic evidence of polyneuropathy is reported in 17 to 72 percent [78,79,94-96].
●Pathogenesis – The pathogenesis of the hypothyroid neuropathy is incompletely understood. Pathologic descriptions have varied and include:
•Mucopolysaccharide-protein complexes within the endoneurium and perineurium
•Reduction in the number of large, myelinated fibers with segmental demyelination and remyelination [88]
•Aggregates of glycogen granules, mitochondria, lipid droplets, and lamellar bodies [88,97]
•Axonal degeneration with shrinkage of axons, and disruption of neurotubules and neurofilaments [97,98]
Some believe that the primary pathology in hypothyroid neuropathy is demyelination, perhaps as a result of metabolic abnormalities of the Schwann cells, with secondary axonal degeneration [88,99]. Others propose a primary axonal pathology with secondary demyelination [97,100]. Hypothyroidism may affect slow axonal transport due to a disturbance in microtubule assembly, thereby contributing to nerve damage.
●Clinical features – The most common clinical manifestation of hypothyroid neuropathy is a sensory disturbance in a symmetric, distal-predominant distribution, affecting the feet earlier and more severely than the hands. Sensory loss, tingling, and painful dysesthesias are common complaints. Findings on neurologic examination include loss or reduction of deep tendon reflexes and a symmetric "stocking-glove" distribution of sensory loss. Delayed relaxation of the reflexes is a characteristic feature of hypothyroidism. Rarely, in more severe cases, distal weakness and atrophy may be present [94].
The onset and duration of neuropathic symptoms is generally correlated to the onset and duration of hypothyroidism [98]. However, symptoms of neuropathy may be present for years before the diagnosis of hypothyroidism is made. The severity of neuropathic symptoms does not directly correlate with the degree of thyroid deficiency, but may be associated with the duration of hypothyroidism.
●Electrophysiology and other testing – Various findings on NCS have been reported, including low-amplitude or absent sensory nerve action potentials, mild slowing of motor and sensory conduction velocities, and mild prolongation of distal motor latencies [88,97,98]. These findings suggest a combination of axonal and demyelinating features (see "Overview of nerve conduction studies"). These abnormalities can be seen in patients with subclinical as well as overt hypothyroidism and in patients without symptoms of neuropathy [101].
A subset of patients with hypothyroidism complains of typical neuropathic pain, but have normal NCS [102]. This suggests that some patients may have an isolated small fiber polyneuropathy. Other studies using skin biopsy and noninvasive measures of small fiber function, including laser Doppler imager flare technique and corneal confocal microscopy, have also provided evidence of a small fiber polyneuropathy in hypothyroidism [103,104].
●Diagnosis – The presence of distal sensory loss and reduced or absent deep tendon reflexes suggests a sensory polyneuropathy in a patient with known hypothyroidism. Electrophysiologic tests help to confirm as well as characterize the polyneuropathy. There are no specific clinical or electrophysiologic features that distinguish hypothyroid polyneuropathy from neuropathy due to other causes.
●Treatment and prognosis – Hormone replacement is effective in the treatment of hypothyroid polyneuropathy. With a return to euthyroid state, clinical and electrophysiologic improvement occurs [79,88,105]. In one case series, NCS normalized in four of seven patients examined three months after initiation of treatment [79]. The nonresponders had a longer duration of symptoms and more axonal features on NCS.
Autoimmune demyelinating neuropathies — Cases of Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy of autoimmune origin have been reported in patients with Hashimoto thyroiditis [106-108]. These likely reflect an underlying predisposition to autoimmune disease. The presence of progressive weakness and prominent demyelinating features (conduction block) on NCS should suggest these diagnoses. It is important to consider and recognize these syndromes, as the appropriate treatment is immunosuppressive or immunomodulatory therapy, rather than thyroid replacement alone. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis".)
MYOPATHY — Muscle involvement in a variety of forms is a frequent problem in both congenital and adult-onset hypothyroidism, as well as in hypothyroidism resulting from rapid reduction of thyroid hormone [109]. Typically, patients complain of myalgias and muscle stiffness and have mild proximal muscle weakness and elevated serum muscle enzymes. The myopathy resolves with thyroid replacement. This topic is discussed in detail separately. (See "Hypothyroid myopathy".)
OTHERS
Visual loss — While visual fields restriction and other visual field defects are common on formal visual field testing in patients with hypothyroidism, these are rarely, if ever, a presenting complaint [110-112]. These occur as a result of pituitary hyperplasia, itself a consequence of decreased negative feedback from thyroid hormone [111,113]. These deficits are usually subtle and subclinical, and improve with thyroid replacement.
Hearing loss — Hearing loss, which may be subclinical, and tinnitus are also common in hypothyroid patients and improve with treatment [114]. The hearing loss is usually sensorineural rather than conductive. The pathogenesis is unknown; in some studies, a cochlear pathology or an endolymphatic hydrops have been implicated [115,116]. Some patients have been initially diagnosed with Meniere disease, which has overlapping symptoms and signs [117]; in some reports, an etiologic association of hypothyroidism in some cases of Meniere disease has been suggested [116]. (See "Meniere disease: Evaluation, diagnosis, and management".)
Pendred syndrome is an autosomal recessive disorder that is characterized by the combination of sensorineural hearing loss, goiter, and an abnormal organification of iodide with or without hypothyroidism [118]. (See "Approach to congenital goiter in newborns and infants", section on 'Inborn errors of thyroid hormone production'.)
Dysphonia — The typical hoarseness of hypothyroidism is believed to result from myxedematous changes in the larynx rather than from neurologic involvement [119]. (See "Clinical manifestations of hypothyroidism", section on 'Clinical manifestations'.)
Myasthenia gravis — The incidence of myasthenia gravis (MG) is somewhat higher in patients with hypothyroidism than in patients without thyroid disease [120]. This likely reflects a shared autoimmune pathogenesis between MG and Hashimoto thyroiditis, a common cause of hypothyroidism. MG is also associated with Graves' disease [121]. (See "Neurologic manifestations of hyperthyroidism and Graves' disease".)
Headache — A relationship between headache and hypothyroidism is not established; both are common conditions and therefore may co-occur. Uncontrolled case series suggest that thyroid replacement treatment sometimes, but not always, improves headaches in individuals with both conditions [122,123].
Some studies have suggested a modest association between hypothyroidism and headache [124-126], but others have not found an association [127-129]. (See "Clinical manifestations of hypothyroidism", section on 'Respiratory system'.)
SUMMARY AND RECOMMENDATIONS
●Spectrum of disease – Neurologic manifestations of hypothyroidism (table 1) are both common and protean, affecting both the central and peripheral nervous system. Although usually occurring in the setting of other clinical manifestations of hypothyroidism, they may be the presenting feature, and can cause significant disability. (See 'Introduction' above.)
●Sequelae of fetal and neonatal hypothyroidism – Neurologic sequelae of fetal and neonatal hypothyroidism may include intellectual disability, impaired motor development, strabismus, and sensorineural hearing loss. The severity of the neurologic sequelae depends on the degree and duration of hypothyroidism. (See 'Sequelae of fetal and neonatal hypothyroidism' above.)
●Myxedema coma – Coma is a rare manifestation of severe hypothyroidism and a medical emergency that usually occurs in conjunction with hypothermia and other symptoms and signs (hypotension, bradycardia, hyponatremia, hypoglycemia, and hypoventilation). Seizures are common. (See "Myxedema coma".)
●Cognitive impairment – Cognitive dysfunction is a common feature of clinical hypothyroidism, occurring in more than two-thirds of patients. The degree of improvement with thyroid replacement is variable and may be incomplete. (See 'Cognitive impairment and dementia' above.)
●Other manifestations – Cerebellar ataxia, carpal tunnel syndrome, peripheral neuropathy, and myopathy are additional common neurologic manifestations of untreated hypothyroidism (table 1). Most are partially or fully responsive to thyroid replacement. (See 'Movement disorders' above and 'Peripheral neuropathy' above and 'Myopathy' above.)
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