Psychiatric Manifestations Of Hashimoto's Encephalopathy Essay

1. Introduction
Hashimoto’s encephalopathy (HE) is a rare and underdiagnosed autoimmune condition caused by the formation of antithyroid antibodies. HE can occur independently or in association with Hashimoto thyroiditis (HT), which is also an autoimmune disease of the thyroid cells (Pavlovic, Pavlovic and Lackovic 2009, p. 383). Autoimmunity can be defined as an inflammatory immune response that is characterized by the formation of self-reactive cytotoxic T-cells or antibodies against the body’s own cells because of a maladaptive immune system. The autoantigen could be either tissue-specific (β-cells or thyroid) or systemic in origin. Usually, all the cells of the body are recognized as their own owing to cell receptors. Currently, the early phase and onset of autoimmune disorder have not yet been clearly understood; however, researchers believe that the process of autoimmunity begins much earlier when compared to the manifestation of the autoimmune disorder (Rich et al. 2013, p. 593). Due to the diverse clinical presentations of HE and lack of evidence between thyroid autoimmunity and encephalitis, scientists are unsure about the classification of HE as a separate symptomatic entity. HE was first described in 1966 in a patient who presented symptoms of HT along with hypothyroidism. In current practice, patients with unexplained encephalopathy along with the presence of thyroid antibodies in the brain are termed as HE patients (Payer, Petrovic, Lisy and Langer 2012, p. 506).
2. Formation of autoantibodies in HE
HE characterized by the formation of anti-thyroperoxidase (TPOab) antibodies but some cases have reported the formation of antibodies against thyroglobulin (TGab) and/or the thyrotropin receptor (TRab). The patients usually present low to normal thyroid functioning. In addition to antithyroid antibodies, amino terminal of alpha-enolase (NAE) antibodies are found in 68 to 83% of the patients with HE, making it a specific diagnostic tool for HE, along with TPOab. The apparent lack of knowledge regarding the etiology of HE has resulted in studying HE as an autoimmune disorder of the thyroid associated with encephalopathy. Therefore, HE is often described in tandem with symptoms and the etiology of HT (Payer et al. 2012, p. 507). Anti-thyroid antibodies are found not only in HE and HT patients, but also in healthy individuals, especially women. These naturally occurring antibodies are poly-reactive, which recognized both self-cells and antigens. In case of autoimmune disorders, the anti-thyroid antibodies are specifically directed against the epitopes present on the thyroid cells. The immunogenic activity associated with autoimmunity predominantly involves IgG (more than 99%) and minimally the IgM form while the reverse is true in case of natural antibodies with the additional involvement of IgA. Studies have indicated that serum of HT patients containing TG promotes the B cell capture of IgG and proliferation of CD4+ T cells, establishing the relationship between reactive T cell proliferation and autoantibodies (Nielsen, Hegedüs and Leslie 2004, p. 268).
3. Diffuse gliosis as a clinical feature of HE
HE is diagnosed by the prominent occurrence of stroke-like episodes, mimicking of Creutzfeldt-Jakob disease (CJD), cognitive dysfunction, behavioral changes and epileptic seizures (Mocellin, Walterfang and Velakoulis 2007, p. 801). Changes to the brain tissues have been established through limited post mortem brain biopsies that have indicated that HE results in perivascular lymphocytic cuffing, nonspecific lesions, perivascular inflammation and diffuse gliosis of the grey matter in the cortex, thalamus, hippocampus or basal ganglia. The grey matter is abundant in astrocytes, a form of glial cell, which makes diffuse astrogliosis a common outcome of HE (Sofroniew and Vinters 2010, p. 8). Gliosis is characterized by an increase in cell size or growth and often occurs because of a brain injury. The immediate pathophysiological impact of gliosis is thought to be seizure, which is often a symptom of HE. Gliosis is believed to be a precautionary mechanism where the damaged brain tissue is effectively isolated from the healthy tissue through the subsequent formation of the glial scar surrounding the gliosis tissue. Diffuse gliosis, which is reversible in nature, occurs as a nonspecific proliferation over a wide area in the grey matter and does not lead to scar formation (Sofroniew and Vinters 2010, p. 18). Evidences from mice studies suggest that astrocytes might play an essential role in behavioral disorders, where disruption of the Na+, K+-ATPase specific to the astrocytes might lead to anxiety and impaired learning. Gliosis is also thought to be implicated in the disruption of the reward circuit leading to depression and drug addiction (Sofroniew and Vinters 2010, p. 18).
4. Psychiatric manifestations of HE
Psychiatric symptoms along with neurological symptoms, normal MRI and nonspecific EEG are some of the earliest signs of HE. A study emphasizes that psychiatric manifestation of HE is similar to schizophrenia and could go underdiagnosed (Payer et al. 2012, p. 511). 80% of the people diagnosed with HE exhibit cognitive dysfunction such as loss of memory, social isolation, agitation or language disabilities while 30% exhibit psychosis that is marked by hallucinations of the visual type and delusions of the persecutory type. 90 to 100% show behavioral changes and mood disturbances. 60 to 70% of the patients exhibit seizures while a fourth of the HE patients suffer stroke-like symptoms (Mocellin et al. 2007, p. 801). Other psychiatric symptoms include depression or mood elevation, psychosis, dementia, sleep disturbances. Therapy for HE involves the use of corticosteroids, which revert the psychiatric deterioration very quickly (Pavlovic et al. 2009, p. 384).
5. Conclusion
The disorder is poorly understood but manageable if treated at the right time. HE could prove fatal if untreated, possibly owing to the psychiatric deterioration associated with HE.

Reference

Mocellin, R., Walterfang, M., & Velakoulis, D. (2007). Hashimoto’s encephalopathy. CNS drugs. Vol. 21, no. 10, pp. 799-811.
Nielsen, C. H., Hegedüs, L., & Leslie, R. G. Q. (2004). Autoantibodies in autoimmune thyroid disease promote immune complex formation with self antigens and increase B cell and CD4+ T cell proliferation in response to self antigens. European journal of immunology. Vol. 34, no. 1, pp. 263-272.
Pavlović, D. M., Pavlović, A. M., & Lačković, M. (2009). Hashimoto encephalopathy: Neurological and psychiatric perspective. Archives of Biological Sciences. Vol. 61, no. 3, pp. 383-394.
Payer, J., Petrovic, T., Lisy, L., & Langer, P. (2012). Hashimoto encephalopathy: a rare intricate syndrome. International Journal of Endocrinology and Metabolism. Vol. 10, no. 2, pp. 506.
Rich, R. (Ed.). (2013). Clinical immunology principles and practice (4th ed.). London: Elsevier Saunders. Pp. 593.
Sofroniew, M. V., & Vinters, H. V. (2010). Astrocytes: biology and pathology. Acta neuropathological. Vol. 119, no. 1, pp. 7-35.