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Hashimoto encephalopathy

Hashimoto encephalopathy
Literature review current through: Jan 2024.
This topic last updated: Aug 23, 2022.

INTRODUCTION — Hashimoto encephalopathy (HE) is an uncommon syndrome associated with Hashimoto thyroiditis (HT). "Steroid-responsive encephalopathy associated with autoimmune thyroiditis" (SREAT) and a more general term, "nonvasculitic autoimmune meningoencephalitis," are also used to describe this condition.

Originally described in 1966, it remains a somewhat controversial disorder [1]. HE is most often characterized by a subacute onset of confusion with altered level of consciousness, seizures, and myoclonus. In contrast with the cognitive dysfunction associated with hypothyroidism or hyperthyroidism, HE is believed to be an immune-mediated disorder rather than representing the direct effect of an altered thyroid state on the central nervous system.

HE will be reviewed here. HT and other neurologic complications of thyroid disease are discussed separately. (See "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)" and "Myxedema coma" and "Neurologic manifestations of hypothyroidism" and "Neurologic manifestations of hyperthyroidism and Graves' disease".)

PATHOPHYSIOLOGY — The mechanism of HE is unknown. It does not appear to be directly related to hypothyroidism or hyperthyroidism, as the majority of reported patients are euthyroid at the time of presentation. A toxic effect of increased thyrotropin-releasing hormone on the central nervous system has been proposed, as some patients appear to improve with thyroid supplementation despite being euthyroid [2-4]. However, these cases appear to be the exception rather than the rule.

The bulk of evidence points to an autoimmune vasculitis or other inflammatory process, perhaps associated with immune complex deposition, and possibly disrupting the cerebral microvasculature [2,5]:

Pathologic examination at autopsy or brain biopsy in a few patients has identified lymphocytic infiltration around small arterioles and venules [3,6].

Most patients with HE appear to respond to glucocorticoid therapy or other immunosuppressive therapies.

The disorder is more common in women, as is true of most autoimmune disorders [2-4].

Elevated antithyroid antibodies, an essential feature of this disorder, are consistent with an active autoimmune process.

In one series, seven of eight patients had HLA B8 DRw3 haplotypes compared with 30 percent of a control population [7]. This profile is common to other patients with autoimmune diseases.

The nature of the relationship between Hashimoto thyroiditis (HT) and HE is unclear. Some argue that the association is entirely spurious [8]. Elevated antithyroid antibodies in the serum correlate well with pathologic thyroiditis. However, elevated titers are prevalent in the general healthy population, occurring in 2 to 10 percent of young adults and 5 to 20 percent of older adults. It is possible, therefore, that elevated titers are a coincidental finding.

Others argue that the relationship between HT and HE is just that seen among autoimmune disorders in general [3]. HT itself is associated with neurologic and systemic autoimmune diseases including myasthenia gravis, systemic lupus erythematosus, and type 1 diabetes mellitus [7]. Support for this argument includes the observation that the symptoms of HE are not paralleled by symptoms of thyroiditis. In addition, changes in antithyroid autoantibody levels do not consistently correspond with neurologic symptoms or improvement with treatment. These findings lead some to propose that steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) is a more appropriate designation for this disorder [9-11].

The nature of the putative autoimmune response in HE is speculative. A number of observations and investigations in small numbers of patients have elicited different theories:

HE may result from a direct antibody-mediated neuronal injury. Immunohistochemical analysis in one patient with HE detected an antineuronal antibody that reacted with human cerebral cortex [12].

HE may represent a vasculitis that results from either endothelial inflammation or immune complex deposition. Findings of perfusion deficits on single-photon emission computed tomography (SPECT) suggest vascular involvement [3,7,13].

A potentially specific marker for HE has been identified in an autoantibody expressed against the amino terminal end of the enzyme alpha enolase. In one study, reactivity was found in five of six HE patients compared with 2 of 17 patients with HT [14]. No reactivity was found either in 25 healthy controls or in 25 patients with other autoimmune or encephalopathic neurologic disorders. A pathogenic role for this antibody is not understood; however, as alpha enolase is expressed on endothelial cells, it may mediate a vasculitis.

HE may be a primary demyelinating process akin to acute disseminated encephalomyelitis (ADEM). This is corroborated by pathologic and magnetic resonance imaging (MRI) findings in a few patients with HE, which appear similar to those seen in ADEM [3,15]. However, MRI findings of white matter disease are not typical of most reported patients with HE. These ADEM-like cases may represent anomalous cases of acute demyelinating disease in patients with incidentally elevated antithyroid antibody levels.

HE may represent an immune complex disease, since immune complexes were found in the cerebrospinal fluid (CSF) in a series of six patients with HE [16]. However, CSF immunoglobulin G (IgG) indices are inconsistently elevated in HE. Also, the degree of inflammation on CSF analysis and neuroimaging appears mild in HE and therefore at odds with this pathogenesis.

It seems unlikely that the antithyroid antibodies play a pathogenic role in HE. There is no evidence of a central nervous system antigen recognized by these antibodies. On the other hand, antithyroid antibodies were identified in the CSF of all six of the patients with HE in one report and in none of the controls [16]. This, in the absence of blood-brain barrier disruption, suggests possible intrathecal synthesis of these antibodies. However, others have not found these antibodies to be reliably present in the CSF in patients with HE [5].

RELATED DISORDERS

Nonvasculitic autoimmune inflammatory meningoencephalitis — Less frequently reported than HE are similar syndromes in other autoimmune disorders (eg, Sjögren's disease) that have been labeled nonvasculitic autoimmune inflammatory meningoencephalitis (NAIM) [17-19]. HE and NAIM are clinically similar and have similar diagnostic findings, suggesting that HE may be a subset of NAIM. A lymphocytic pleocytosis in the cerebrospinal fluid (CSF) is not, as one might expect from its name, a cardinal feature of NAIM and is also relatively uncommon among reported cases of HE. A steroid-responsive encephalopathy has been reported in one patient with Graves' disease, an autoimmune disorder that causes hyperthyroidism [20].

Acute disseminated encephalomyelitis — Acute disseminated encephalomyelitis (ADEM) is an inflammatory, presumably autoimmune, demyelinating disease of the central nervous system. (See "Acute disseminated encephalomyelitis (ADEM) in children: Pathogenesis, clinical features, and diagnosis".)

Some propose that HE is a form of ADEM. One series identified a high rate of possible provoking factors for HE, such as infection and surgery, which are also noted in ADEM [7]. Although a few reported cases of HE have similar MRI and pathologic findings to ADEM, most do not. It seems possible that these exceptional cases are in fact cases of ADEM with incidental elevations of antithyroid antibodies. Unlike HE, ADEM is a monophasic disorder and is not generally associated with other autoimmune diseases.

EPIDEMIOLOGY — A systematic review published in 2016 identified 251 published cases of HE [21]. The syndrome may be underrecognized [2]. A hospital-based epidemiologic study aggressively screened for HE in patients with unexplained neurologic symptoms consistent with HE and estimated the prevalence of HE to be 2.1 per 100,000 [22].

Among reported cases, the mean age of onset of initial symptoms is 51 years (range 9 to 86) [2-4,21,23,24]. Women are more commonly affected than men, at a ratio of approximately four to one.

CLINICAL FEATURES — Clinical manifestations of HE most often include an acute to subacute onset of confusion with alteration of consciousness [2,5]. Two patterns of presentation have been described:

A stroke-like pattern of multiple, recurrent, acute to subacute episodes of focal neurologic deficits with a variable degree of cognitive dysfunction and alteration of consciousness. Approximately 25 percent of patients follow this course [3].

A diffuse, progressive pattern, characterized by slowly progressive cognitive impairment with dementia, confusion, hallucinations, or somnolence [2,25]. Some cases have a more fulminant presentation in which rapid deterioration to coma occurs [2,7]. In one systematic review, 15 percent of patients presented in coma [21].

These clinical patterns can overlap. In addition to confusion and mental status changes, other neurologic signs are common in both groups:

Approximately two-thirds to one-half of patients experience focal or generalized tonic-clonic seizures [3,21,23,26,27]. Seizures are reported to be a presenting symptom in 47 percent of patients [21]. Status epilepticus has been reported in 25 percent [28].

Myoclonus or tremor is seen in up to 38 percent of patients [3,23]. Myoclonus may be focal or multifocal.

Diffuse hyperreflexia and other pyramidal tract signs are present in 85 percent of patients [2].

Psychosis, particularly visual hallucinations, but also paranoid delusions, have been reported in 25 to 36 percent of patients [3,21,23]. Approximately 10 to 25 percent of patients present with isolated psychiatric symptoms [21,28].

The long-term course of illness may be self-limited, relapsing-remitting, or progressive [29,30].

Rare syndromes associated with HE include a cerebellopathy with or without encephalopathy, isolated myelopathy, and chorea [24,31-35]. Peripheral nervous system involvement with electrophysiological evidence of a sensory ganglionopathy, demyelinating polyneuropathy, and/or amyotrophy has been described in individual cases of HE [36-38].

There are no systemic symptoms, including fever, with rare exceptions [7]. Neurologic symptoms can occur in patients with a known diagnosis of Hashimoto thyroiditis (HT) or in patients without a previous diagnosis. The development of clinical HT may occur up to three years after presentation with HE [4].

LABORATORY FEATURES

Antithyroid antibodies — An elevated serum level of antithyroid peroxidase antibody (TPOAb) and/or antithyroglobulin antibody (TgAb) is an essential laboratory feature of HE. The median anti-TPOAb level at diagnosis was 900 international units/mL according to one review [21]. However, there is no clear relationship between the severity of neurologic symptoms and the type or serum concentration of antibodies; in addition, antibody levels may or may not decrease following treatment [3,7,11,22,23]. Given the prevalence of these antibodies in the general healthy population of 2 to 20 percent, this cannot be considered to be a specific finding for HE.

Antithyroid antibodies are infrequently measured in the cerebrospinal fluid (CSF). One case series found that 9 of 12 patients with encephalopathy and elevated serum antithyroid antibodies had elevated CSF autoantibody titers [22]. The authors suggested that serum antibody titers were overly sensitive. However, other investigators did not find antithyroid antibodies in the CSF of patients with HE [5]. The specificity and sensitivity of antithyroid antibodies in the CSF are unclear.

Thyroid hormone levels — Thyroid status varies among patients with reported HE, ranging from overt hypothyroidism to overt hyperthyroidism. In systematic reviews, 23 to 35 percent of patients with HE have subclinical hypothyroidism and 17 to 25 percent have overt hypothyroidism [3,23]. Approximately 7 percent are hyperthyroid; the remainder are euthyroid [21].

Cerebrospinal fluid — CSF analysis is abnormal in approximately 80 percent of patients [2]. The following findings have been noted [2,21]:

The most common abnormality is an elevated protein concentration (reported range 48 to 298 mg/dL), which occurs in approximately 82 percent of patients. Levels greater than 100 mg/dL are uncommon, occurring in approximately 20 percent.

A lymphocytic pleocytosis (8 to 169 cells) is present in 10 to 25 percent of patients [2,21,23].

The glucose concentration is normal.

Both the presence and absence of oligoclonal bands are reported [2].

Elevated 14-3-3 protein, a finding associated with Creutzfeldt-Jakob disease, has been reported in HE but is not a universal finding [23,30,39].

Electroencephalography — Nonspecific electroencephalographic (EEG) abnormalities are seen in 90 to 98 percent of patients, usually demonstrating nonspecific slowing of background activity [2,7,9,40]. Focal spikes or sharp waves and transient epileptic activity are less common. Triphasic waves and frontal intermittent rhythmic delta activity (FIRDA) have also been described.

Some report that EEG abnormalities recover rapidly with steroid administration [9], whereas others note that EEG improvement lags behind clinical improvement [7,41].

Neuroimaging — MRI in patients with HE is usually normal, but approximately half of patients may demonstrate cerebral atrophy or nonspecific T2 signal abnormalities in the subcortical white matter [3,21]. The latter have been described in approximately one-half of patients and do not enhance with gadolinium [2,3,7]. This may be an incidental finding, although a few reports have described regression or resolution of these findings with treatment [3].

In exceptional cases of HE, MRI findings of diffuse or focal white matter changes suggesting primary demyelination have been described [3,15,42,43]. Other findings noted in individual case reports include meningeal enhancement [43] and T2 signal abnormalities in both hippocampi [42].

Follow-up imaging is not often described. In some cases, the findings appear to regress or resolve with treatment [3].

Other tests also reveal nonspecific findings. Cerebral angiography, when performed, is normal [2]. Single-photon emission computed tomography (SPECT) may show focal, multifocal, or global hypoperfusion [3,7,13].

Other — C-reactive protein and the erythrocyte sedimentation rate are elevated in some patients [43]. In one series, mild elevations of liver enzymes were found in 12 of 20 patients [43].

DIFFERENTIAL DIAGNOSIS — Any disease associated with a syndrome of delirium or rapidly progressive dementia may be confused with HE. These include:

Creutzfeldt-Jakob disease

Acute disseminated encephalomyelitis (ADEM)

Toxic metabolic encephalopathies (table 1)

Meningoencephalitis

Psychiatric disease (depression, anxiety, psychosis)

Carcinomatous meningitis

Paraneoplastic or autoimmune encephalitis

Degenerative dementia (Alzheimer disease, dementia with Lewy bodies, frontotemporal dementia)

Stroke or transient ischemic attack

Basilar or hemiplegic migraine

Cerebral vasculitis

The essential testing required to exclude these conditions is discussed in the subsequent section. (See 'Diagnosis' below.)

One study examined the clinical features of 32 patients presenting with progressive encephalopathy associated with elevated antithyroid antibody titers [43]. Of the 12 patients who did not respond to steroids, four with autopsy data were later proven to have alternative diagnoses: Creutzfeldt-Jakob disease, frontotemporal dementia, and dementia with Lewy bodies. Notably, these are all untreatable conditions.

DIAGNOSIS — The finding of elevated antithyroid peroxidase antibody (TPOAb) or antithyroglobulin antibody (TgAb) in patients with a compatible clinical presentation is required for the diagnosis of HE. These findings and a response to glucocorticoids generally define this syndrome. Thyroid hormone levels should be measured but, as noted above, thyroid status is variable in HE. (See 'Thyroid hormone levels' above.)

Essential testing to exclude other diagnoses includes:

Lumbar puncture to include cultures for bacteria, viruses, fungi, and mycobacterium

EEG

MRI with gadolinium administration

Laboratory testing for usual causes of delirium (see "Diagnosis of delirium and confusional states", section on 'Diagnostic tests')

Because the treatment of HE consists of immunosuppressive therapy, it is especially important to thoroughly exclude infection. Other, less routine diagnostic test considerations should include cerebrospinal fluid (CSF) analysis for 14-3-3 protein (for possible Creutzfeldt-Jakob disease), CSF cytology, antibody testing for possible paraneoplastic or autoimmune encephalopathy, and screening for underlying neoplasm. (See "Clinical features and diagnosis of leptomeningeal disease from solid tumors", section on 'Diagnostic evaluation' and "Creutzfeldt-Jakob disease", section on 'Diagnosis' and "Autoimmune (including paraneoplastic) encephalitis: Clinical features and diagnosis".)

TREATMENT — HE is usually treated with glucocorticoids and treatment of a dysthyroid state, if present. An optimal glucocorticoid dose has not been defined. Oral prednisone doses ranging from 50 to 150 mg daily have been used [2,21]. According to one review, high-dose intravenous methylprednisolone was administered initially in 65 percent of reported patients (approximately one-third receiving 1 gram intravenous for three days) prior to oral prednisone, but a benefit compared with oral glucocorticoids is unknown. Spontaneous recovery is also reported, but most patients are treated if the syndrome is recognized [21,22,40].

Symptoms typically improve or resolve over a few months. The duration of treatment and the rate of taper are generally titrated to the clinical response. In some patients, this is as long as two years.

While most patients (90 to 98 percent) respond to glucocorticoid therapy, recovery may be incomplete. In one series of 24 patients, only 32 percent obtained a complete response to steroids [28]. Response to glucocorticoids was not predicted by clinical features or antibody levels.

A small number (5 percent) of reported patients have been treated with other immunosuppressive medications, including azathioprine, cyclophosphamide, methotrexate, rituximab, and hydroxychloroquine [5,7,21,44,45]. These are generally reserved for patients who cannot tolerate glucocorticoids, or those who do not respond to or relapse after or during tapering of glucocorticoid therapy. Clinical improvement with intravenous immune globulin [46,47] and plasmapheresis [48-51] has been reported in individual cases.

Treatment of seizures with an antiseizure medication may be necessary as a temporary measure. In some patients, seizures do not respond to antiseizure medications but may respond to steroid therapy [7]. The management of acute symptomatic seizures is discussed separately. (See "Evaluation and management of the first seizure in adults", section on 'Management'.)

PROGNOSIS — The prognosis of HE is generally but not universally good; a complete or partial neurologic response has been reported in 93 percent of cases three months after the initial diagnosis [21]. While a delay to diagnosis and therefore treatment might be expected to be associated with less complete recovery, case series and reports suggest that patients can improve with treatment even after a few years of symptoms. However, residual cognitive impairment occurs in approximately 25 percent of patients with long-standing untreated disease [7,40,43].

Many patients remain in remission after discontinuation of steroids over several years of follow-up. However, relapses are reported in 16 percent of patients followed over a median follow-up time of 12 months (range 0.2 to 110 months) [21], and some patients require long-term immunosuppressive therapy [7,43].

SUMMARY AND RECOMMENDATIONS

Epidemiology and definition – Hashimoto encephalopathy (HE) is a syndrome of acute or subacute encephalopathy that is associated with elevated antithyroid antibody titers. HE appears to be rare but may be underrecognized. As with Hashimoto thyroiditis (HT), women are more commonly affected than men. (See 'Epidemiology' above.)

Pathophysiology – The bulk of evidence suggests that HE is an autoimmune disorder and is not due to thyroid disease. (See 'Pathophysiology' above.)

Clinical presentation – The presentation is heterogeneous with a fulminant, subacute, or more chronic course of declining mental status that is frequently accompanied by seizures and myoclonus. Some patients present with coma and others with isolated psychiatric features. (See 'Clinical features' above.)

Evaluation and diagnosis – The presence of elevated antithyroid antibody titers and the exclusion of other causes of encephalopathy support the diagnosis of HE. While the entity of HE is disputed, there appears to be enough evidence to support checking antithyroid antibody levels as a second- or third-tier diagnostic test in patients presenting with unexplained encephalopathy and considering the diagnosis of HE if levels are elevated.

Other test findings are nonspecific. Nonetheless, MRI, EEG, cerebrospinal fluid (CSF) analysis, and other laboratory studies are essential in these patients to exclude other causes of encephalopathy. (See 'Differential diagnosis' above and 'Diagnosis' above.)

Management – In a patient with encephalopathy and elevated antithyroid antibody levels in whom other causes of encephalopathy are rigorously excluded, we suggest an initial trial of glucocorticoid therapy rather than other immunosuppressive therapies (Grade 2C). Other immunosuppressive treatments have also been used in patients who cannot take glucocorticoids, who are refractory to glucocorticoids, or who relapse after initial treatment. (See 'Treatment' above.)

Prognosis – Most patients have a good outcome, but a significant minority have persistent cognitive deficits, particularly those with long-standing untreated disease. Relapses may require prolonged immunosuppressive therapy. (See 'Prognosis' above.)

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Topic 4821 Version 21.0

References

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