Interpretation of this information
is best left to medical professionals trained to do so, as there may be factors
the layman is unaware of that make any conclusions we draw from reading these
abstracts misleading or erroneous. Please talk to your doctor if you have any
questions.
Psychoneuroendocrinology 2000
Feb;25(2):201-11
Long-term residual complaints and psychosocial sequelae after remission of
hyperthyroidism.
Fahrenfort JJ, Wilterdink AM, van der Veen EA
Bureau Fahrenfort, Epidemiologic Research, Leiden, The Netherlands.
The issue of residual complaints after treatment for hyperthyroidism in current
euthyroid patients was investigated by means of a survey. Patients treated for
hyperthyroidism were selected from medical records of the previous 6 years in
two Dutch University Clinics. After the exclusion of patients with comorbidity,
303 one-time hyperthyroid respondents were included in the analysis. A total of
77% of these patients had been diagnosed with Graves' Disease. The newly
developed Hyperthyroidism Complaint Questionnaire (HCQ), was used to quantify
problems of somatic and mental functioning. The SymptomsCheckList-90 (SCL-90)
was used to assess self-reported psychopathological symptoms, the Nottingham
Health Profile was used to measure perceived health/quality of life. Dysthyroid
patients (n = 20) had a mean HCQ-score of 14.5 (+/- 8.1) complaints; patients
who reported euthyroidism for less than 12 months (n = 171) had a mean of 9.3
(+/- 7.6) residual complaints; patients who reported euthyroidism for more than
12 months (n = 54) a mean of 6.6 (+/- 6.8) residual complaints. On each
dimension of psychopathology covered by the SCL-90, including depression and
anxiety, approximately one third of the total sample had a score exceeding 80%
of adult females. According to the NHP lack of energy was evident in 53% of all
respondents. Over one third of patients with a full-time job were unable to
resume the same work after treatment. It appears that many of these patients
are in need of psychological support.
A survey study of neuropsychiatric complaints in patients with Graves'
disease.
Stern RA, Robinson B, Thorner AR, Arruda JE, Prohaska ML, Prange AJ Jr.
Neurobehavioral Research, Department of Psychiatry, Rhode Island Hospital,
Providence 02903, USA.
One hundred thirty-seven patients with treated Graves' disease completed a
questionnaire pertaining to neuropsychiatric complaints. Psychiatric symptoms,
especially anxiety and irritability, were common prior to treatment of
hyperthyroidism. These complaints appeared to result in delays in seeking
treatment as well as delays in receiving appropriate diagnosis. Subjects
reported significantly worse memory, attention, planning, and productivity while
hyperthyroid than prior to becoming hyperthyroid, and, although somewhat
improved once euthyroid, they reported residual cognitive deficits. These
results suggest that neuropsychiatric impairments are highly prevalent in
Graves' disease, may lead to initial misdiagnosis or delays in diagnosis of the
endocrine disorder, and may continue even once patients are believed to be
euthyroid.
A psychiatric and neuropsychological study of patients with untreated Graves'
disease.
Trzepacz PT, McCue M, Klein I, Levey GS, Greenhouse J.
Department of Psychiatry, University of Pittsburgh, Pennsylvania.
We studied 13 untreated Graves' disease subjects in a clinical research unit
using endocrine, psychiatric, and neuropsychological assessments. We used SADS
interviews, RDC, standardized symptom rating scales, and motor activity
monitoring to update earlier studies and quantified psychiatric symptoms to
elucidate any correlations between endocrine and psychiatric status. Nine of 13
subjects had major depression, 8/13 had generalized anxiety disorder, and 3/13
were hypomanic. Anxiety levels were much higher than in other hospitalized
medical patients. Using a broad battery of neuropsychological testing, we found
mild deficits in attention, memory, and complex problem solving that were
consistent with previous studies of hyperthyroid patients. The severity of
psychiatric symptoms could easily result in an inappropriate referral to a
psychiatrist prior to the diagnosis of hyperthyroidism. The relationship between
psychiatric symptoms and possible CNS effects of excess levels of thyroid
hormone is discussed.
Hyperthyroidism is often confused with psychiatric illnesses. Undiagnosed
hyperthyroidism sometimes results in inappropriate use of psychotropic
medications. Delay in therapy markedly worsens the prognosis for recovery, but
complications can be prevented by early treatment. Prompt recognition of
hyperthyroidism through thyroid function screening is good medical practice in
the evaluation of patients with psychiatric symptoms.
Perrild H, Hansen JM, Arnung K, Olsen PZ, Danielsen U.
Electroencephalography (EEG) and neuropsychological tests empirically shown to
be sensitive to diffuse cerebral damage were performed in 26 patients 10 years
after successful treatment of hyperthyroidism and in a control group with
non-toxic goitre. In the hyperthyroid state 81% had abnormal EEG before
treatment, and 10 years after treatment 68% still had abnormal EEG compared with
41% in the control group (P less than 0.05). In 7 out of 11 neuropsychological
tests the previously hyperthyroid patients showed significant impairment
compared with the control group. Twenty-three per cent of the patients displayed
marked to severe intellectual impairment, 31% moderate and 41% slight or no
impairment compared with 0%, 31% and 69%, respectively, in the control group (P
less than 0.05). Four patients had been granted disability pension on the basis
of the intellectual dysfunction. Signs of intellectual impairment indicating
irreversible brain dysfunction after thyrotoxicosis thus seem to be a frequent,
although hitherto not generally recognized, finding.
Hyperthyroidism
Induces Apoptosis in the Adult Cerebral Cortex: Direct Action of T3 on
Mitochondria
R. Singh1, G. Upadhyay2, A. Kapoor3, S. Kumar3, A. Kumar4, M. Tiwari4, M.M.
Godbole4 1Cell Biology Section, National Institute of Environment and Health
Sciences, Research Triangle Park, North Carolina, USA; 2Department of Internal
Medicine 1, University of Ulm, Ulm, Germany; and Departments of 3 Microbiology
and 4Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences,
Lucknow, India
Differential thyroidal status is known to cause decrease in cell number and
induces irreversible morphometric changes in adult brain resulting in different
neuronal abnormalities. Whether the decrease in cell number is mediated by
apoptosis is not known. We studied the effect of differential thyroidal status
on adult rat cerebral cortex and cerebellum and direct action of T3 on cerebral
cortex mitochondria to induce apoptosis. Altered thyroidal status induces DNA
fragmentation in cerebral cortex and not in cerebellum. Enhanced caspase-3 and
caspase-9 activity was observed in cerebral cortex whereas only basal level in
cerebellum. The expression of Bcl-2, Bcl-xl and Bax proteins remained unaltered
under differential thyroidal status in both cerebral cortex and cerebellum.
Cytochrome c was localized in cytosol only in the hyperthyroid state both in
cerebral cortex and cerebellum, but not under hypothyroid conditions. SMAC was
absent in the adult cerebral cortex and cerebellum whereas altered thyroidal
status not only induced expression but also its translocation to cytosol. In
vitro experiments demonstrate that mitochondria from cerebral cortex treated
with triiodothyronine (T3) do not induce PT. However, T3-induced released
proteins cause nuclear condensation, protruding bodies and DNA fragmentation.
Treatment with increasing concentration of T3 results in elevated levels of
cytochrome c in supernatant. To our knowledge these results for the first time
demonstrate that differential thyroidal status induces apoptosis in adult
cerebral cortex. Triiodothyronine acts directly on cerebral cortex mitochondria
and induces release of cytochrome c to induce apoptosis. Adult cerebellum seems
to be less responsive to changes in thyroidal status.
Back to top
* The information
in this web site is for educational purposes only and is not providing
medical or professional advice. It should not be used for diagnosing or
treating a health problem or disease. It is not a substitute for
professional medical care. If you have or suspect you might have any
health problems, you should consult a physician.
