|Year : 2017 | Volume
| Issue : 2 | Page : 118-119
Neurocognition and hypothyroidism: Critical points
Avinash De Sousa1, Amresh Shrivastava2
1 Department of Psychiatry, Lokmanya Tilak Municipal Medical College, Mumbai, Maharashtra, India
2 Department of Psychiatry, Lawson Health Research Institute, Western Ontario, Canada
|Date of Web Publication||8-Dec-2017|
Avinash De Sousa
Carmel, 18, St. Francis Road, Off S.V. Road, Santacruz West, Mumbai - 400 054, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
De Sousa A, Shrivastava A. Neurocognition and hypothyroidism: Critical points. Ann Indian Psychiatry 2017;1:118-9
Hypothyroidism is a common medical condition associated with low thyroid hormone levels and has a large number of physical and neurocognitive symptoms that may manifest across life based on when' the disorder sets in. The important point is that many of these neurocognitive deficits may, in fact, be reversible with the correction of thyroid abnormalities. The present editorial shall focus on neurocognitive aspects of hypothyroidism that are seen in adults and the diagnostic and confounding factors that surround the same. Clinically patients with neurocognitive deficits may be diagnosed and treated as either age-associated cognitive impairment, dementia, and depression without a proper assessment of thyroid function and hypothyroidism may thus carry on undiagnosed for a number of years. It is of equal interest that symptoms of depression and neurocognitive deficits associated with hypothyroidism may show a mixed response to thyroid pharmacotherapy, and hence, it is all the more essential to clinically dissect and decipher the cause of such symptoms.
Most of the published studies on neuropsychological functioning in adults with hypothyroidism have evaluated specific cognitive domains based on the battery of tests used, and many aspects of cognition remain unassessed. Complex problem-solving abilities, executive functions, reasoning – both simple and abstract, visual attention, visual information processing, agnosia, and problems in praxis have been relatively under assessed in studies of neurocognition in hypothyroidism. Visuospatial deficits and memory deficits have often been documented in these studies. Whenever we unearth neurocognitive deficits in hypothyroidism, it is essential to analyze whether these deficits were existent before the start of the disorder and showed a worsening thereafter or whether they are a consequence of hypothyroidism. Studies assessing the same are sparse, and it is difficult to elucidate the facts. Every patient with neurocognitive deficits in hypothyroidism must also undergo a psychiatric assessment to rule out existing or previous depression and impending dementia that has just started or already set in. This shall help ascertain the cause of neurocognitive deficits and facilitate the right treatment. Not all cases of neurocognitive dysfunction in hypothyroidism show a positive response to thyroid treatment, and hence, other causes must be ruled out. There is also no clinical correlation between the level of impairment in neurocognition and decline in serum thyroid hormone levels. This is essential as patients with major abnormalities in thyroid hormones may show minimal neurocognitive deficits while patients with major neurocognitive deficits may show minimal thyroid abnormalities.
Dementia has been linked to hypothyroidism with myxedema being posited as one of the reversible causes of dementia. This is however not the case and not all cases of dementia in the context of myxedema reverse with medical treatment and thyroid correction. This is more common in the elderly where dementia may be in process with aging and due to Alzheimer's or a vascular etiology and the emergence of myxedema may worsen or cause further decline in dementia. Multiple medical comorbidities and multiple medications may also hamper total cognitive recovery in dementia associated with myxedema and hypothyroidism. In the geriatric population, there is greater chance of age-associated hypothyroidism developing and there is also a greater chance of neglect of the condition due to improper use of health-care facilities. Many of the symptoms of hypothyroidism seen for the first time in late life may be attributed to aging itself, and the disorder may be clinically missed.
Another clinical dilemma in neurocognitive deficits seen in hypothyroidism is that unlike full-blown dementia isolated deficits are common, i.e., forgetfulness, reasoning deficits, and specific area dysfunction that may be reversible with treatment and yet not enough to be diagnosed dementia as per clinical criteria thus hampering treatment in many settings. We need studies which show decline on neurocognitive tests correlated with thyroid hormone levels that indicate decline and later improvement with treatment. It is only then that we could uphold the reversibility of neurocognitive deficits in hypothyroidism. Cognitive retesting may impair testing due to the relearning effect seen in these tests. Thus, studies that claim the complete reversibility of dementia and neurocognitive aspects of hypothyroidism are strewed with multiple confounding and methodological difficulties. Further systematic longitudinal studies that assess neurocognition serially in hypothyroid patients are warranted.
One thing that has however been proven across studies that cognitive decline occurs whenever thyroid replacement therapy is delayed. Neurocognitive screening tests are not enough to determine improvement or decline in hypothyroidism. Intense batteries that test multiple domains of cognition and which are culture free are important in the assessment. There is also a need to reduce the costs of these assessments as repeated evaluations may be needed. These assessments would help determine whether the patients shall need aggressive or restrictive lines of management and treatment. The confounding influence of test-retest effect needs to be considered in reevaluation of cases after treatment. Reduction in cognitive decline must be considered as a clinically plausible goal with thyroid replacement therapy though total reversal may not be possible in all cases due to various factors as cited above. Early cognition evaluation in adults with hypothyroidism even at baseline in the absence of cognitive decline shall provide useful data for showcasing decline whenever it ensues and later showing a return to normalcy after treatment. Neuroimaging with its recent advances may help document the physical aspect of cognitive decline seen. There is a need for an integrated framework of treatment in this domain with the treatment team being made up of an endocrinologist, a physician, psychiatrist, neuropsychologist, and neurologist so that various factors in every case are evaluated, and the best possible treatment is administered.
The brain is a very important target organ for thyroid hormones and alterations in mood and cognition are known to occur with thyroid dysfunction. Recent advances in the field of cognitive neurosciences have led to focused testing of cognitive domains in patients with altered thyroid function. Based on recent population-based studies, there do not appear to be major deficits in cognitive functioning in overt or subclinical thyroid disease. The most commonly affected domains are working memory and executive function. In addition, present are alterations in mood, manifested by increased rates of depressive and anxiety symptoms. The key factor is that all these deficits are reversible and improve when hypothyroidism is treated.,
Dementia can be a manifestation in patients with clinically low or high thyroid stimulating hormone (TSH). Dementia in this group of patients is reversible when treated with thyroid replacement therapy. On the other hand, when looking into individuals with normal TSH levels and otherwise normal thyroid function, researchers have found a relationship between the TSH levels and risk of developing Alzheimer's disease.
One of the key factors in clinical populations is the need for endocrinologists, psychiatrists and psychologists to be on the same page when examining patients with hypothyroidism and giving every patient a thorough evaluation. Although every patient with hypothyroidism may not manifest with cognitive symptoms, there is a high likelihood that subtle cognitive deficits which are easily amenable to therapy may hamper the quality of life of these cases. One must be vigilant and detect these cases early before permanent damage to the brain sets in. There is also a need for cognitive evaluation and home-based cognitive rehabilitation techniques being used in adults with hypothyroidism when the need arises. Sometimes, cognitive symptoms may be the first manifestation of anxiety or depression which may be subclinical or subthreshold in nature and that shall need treatment as well.
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