Biomedical subjects

A Ozkardes

Publications and source records attributed to A Ozkardes.

5 recordsLinked to original sources

PubMed1997

Auditory even-related brain potentials in hyperthyroidism.

Several studies based on psychometric tests have demonstrated an impairment of cognitive functions in hyperthyroid patients. Long-latency auditory event related potentials (ERPs) allow the measurement of a kind of cerebral reaction time that is unavailable to psychometric tests. However, ERPs alterations in hyperthyroidism have been investigated only in experimentally induced hyperthyroidism in healthy subjects, but no study has reported on thyrotoxic patients so far. Therefore, we investigated alterations of P300 wave latency in hyperthyroid patients before and after antithyroid treatment. ERPs were elicited in 20 untreated patients with hyperthyroidism (mean age: 27.40 +/- 2.10 years) and in 30 sex-, age- and education-matched controls. ERPs recordings were repeated 4 months after attainment of euthyroidism. Untreated patients had longer mean P300 latencies when compared to those in controls (338.3 +/- 26.6) vs 320.7 +/- 16.2 msec, P = 0.020). Slowing of P300 latency was marked in 4 of 20 patients and its normalization was observed after treatment. The mean P300 latencies also returned to normal (320.5 +/- 15.5 msec) 4 months after achievement of euthyroidism. Our study shows that P300 is normal in most cases, while we have found in a subgroup of patients a small but statistically significant slowing. However, these alterations are reversed 4 months after attainment of euthyroidism.

Adult↗

PubMed1996

Evaluation of central motor conduction in hypothyroid and hyperthyroid patients.

Deficiency or excess of thyroid hormones is associated with central nervous system (CNS) disturbances. Although the CNS involvement either in hypothyroidism or in hyperthyroidism have previously been shown on the basis of visual, auditory and somatosensory evoked potentials studies, less is known about the function of central motor pathways in both disorders. We studied the motor evoked potentials (MEPs) following the magnetic stimulation of the motor cortex and spinal roots in 20 patients with hypothyroidism and in 19 patients with hyperthyroidism both before treatment and after they became euthyroid and compared with findings in 20 age-, sex- and height-matched control subjects. Disease duration (expressed as time from diagnosis of diseases to the time of neurological testing) is less than one month in both disorders. Central motor conduction time (CMCT) was determined as the differences between MEPs latencies after cortical and spinal stimulation. The mean CMCTs before treatment in hypothyroid patients (8.31 +/- 1.52 msec.) and in hyperthyroid patients (7.92 +/- 1.06 msec.) were significantly prolonged as compared to those in normal controls (6.82 +/- 0.83 msec. p = 0.002 and p = 0.004, respectively). Four of the 20 (20.0%) hypothyroid patients and 2 of 19 (10.5%) hyperthyroid patients had abnormal CMCT (values exceeding mean +2.5 SD of normal control). The mean CMCT values in both groups were not significantly decreased after euthyroidism was achieved, although a tendency of the decrease in CMCT was observed. Improvement of CMCT abnormalities was observed in 1 of 4 hypothyroid patients and in one of 2 patients with hyperthyroidism, who had CMCT abnormalities before treatments, after they became euthyroid. No correlation was found between CMCT and free T3, free T4, or TSH levels as well as the onset age, the severity of the diseases or the disease duration in both disorders. We conclude that abnormal CMCT could be documented in few patients in both disorders. However, these alterations could not be improved completely after restoration of euthyrodism. Thus, it remains to be determined if long-term treatment would completely improve CMCT abnormalities in both disorders. Since abnormal CMCT values in both disorders were observed only in few patients, our results also suggest that CMCT measurement does not have, at present time, a clinical usefulness to assess the peripheral action of thyroid hormones. Thus, the data obtained need a more extensive evaluation.

Adult↗

PubMed1996

Acute hypothyroidism leads to reversible alterations in central nervous system as revealed by somatosensory evoked potentials.

Although functional alterations in the central nervous system (CNS) and peripheral nerves are well documented in overt hypothyroidism, little is known about alterations of CNS in acute hypothyroidism. Sixteen patients with differentiated thyroid carcinoma were studied when prepared for radioiodine scanning after stopping levothyroxine (L-T4) therapy for 6 weeks to determine whether acute hypothyroidism leads to alteration in somatosensory evoked potentials (SSEPs). Repeat SSEPs were performed on the same patients at 6 months following L-T4 therapy when patients were euthyroid. Neurophysiological findings were compared with a group of 20 normal controls with no history of thyroid disease. Peripheral and central conduction in the median and tibial nerve stimulated SSEPs studied. A significant prolongation of central conduction time in SSEPs was found in patients with acute hypothyroidism when compared to those in control subjects. Abnormal latencies were not correlated with thyroid hormone levels. These neurophysiologic abnormalities were completely restored to normal at 6 months after L-T4 therapy. We conclude that acute hypothyroidism leads to reversible alterations in CNS as determined by SSEP recordings. Our results also suggest that SSEPs could be useful tests to monitor functional alteration of the CNS in acute hypothyroidism.

Acute Disease↗

PubMed1995

Subclinical hypothyroidism does not lead to alterations either in peripheral nerves or in brainstem auditory evoked potentials (BAEPs).

Functional alterations in the central nervous system and peripheral nerves are well documented in overt hypothyroidism, but not in subclinical hypothyroidism. Twenty-seven patients with subclinical hypothyroidism were compared with a control group of 20 age- and sex-matched subjects to determine whether subclinical hypothyroidism can lead to alterations in peripheral nerves or in the brainstem auditory evoked potentials (BAEPs). None of the patients had carpal tunnel syndrome or any other neurological or metabolic disturbances. Disease duration (expressed as the time from diagnosis of subclinical hypothyroidism to the time of neurological testing) ranged from less than 1 month to 6 months (median 2.5 months). We studied the distal motor latency, nerve conduction velocity (NCV), compound muscle action potentials, and F response in the median and peroneal nerves whereas the sensory nerve conduction velocity and sensory potential amplitude were measured in the sural and median nerves. Electrophysiological parameters and interpeak latencies yielded no significant difference between patient and control groups. The present study indicates that subclinical hypothyroidism of short duration does not lead to abnormalities of peripheral nerves or brainstem auditory evoked potentials.

Action Potentials↗

PubMedDate not supplied

Central and peripheral neural responses in males with idiopathic hypogonadotropic hypogonadism.

It has previously been shown that abnormal neurophysiologic responses are associated with Kallmann's syndrome. However, little is known about neurophysiologic responses in idiopathic hypogonadotropic hypogonadism (IHH). Fifty-six untreated male patients with IHH (mean age: 20 +/- 0.7 years) were compared with a control group of 20 age-matched male subjects to determine whether IHH can lead to alterations in somatosensory evoked potentials (SSEPs) and brainstem auditory evoked potentials (BAEPs). We have also investigated the effect of gonadotropin replacement (hCG/hMG) therapy on these tests in 20 randomly selected patients. Significant cervical 7 (N13), Erb (N9) and thoracic 12 (N22) latency prolongation was observed in median and tibial nerve SSEPs in patients with IHH as compared with a matched control group. Other components of SSEPs and interpeak latencies of BAEPs yielded no significant difference between untreated patients and control group. Abnormal components of SSEPs did not correlate with basal hormone levels and did not improve with gonadotropin therapy. We conclude that IHH results abnormalities in peripheral but not central nervous system components of SSEPs and that short term gonadotropin treatment cannot correct these abnormalities.

Adolescent↗