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Biomedical subjects

Hung-Yi Hsu

Publications and source records attributed to Hung-Yi Hsu.

11 recordsLinked to original sources
PubMed2006

Isolated hand weakness in cortical infarctions.

Isolated hand weakness due to stroke is infrequently observed, and often misdiagnosed as peripheral lesions. This study investigated the clinical and radiologic profiles in such patients. Five men and one woman were studied. All patients underwent cranial magnetic resonance imaging (MRI) to confirm the diagnosis. Four patients had uniform weakness and the other two had either differential radial or ulnar weakness, respectively. MRI showed acute infarctions involving the hand knob area of the primary motor cortex (M1) in five patients and the postcentral gyrus sparing the precentral gyrus in one patient. Two patients with uniform digit weakness had additional involvement of the inferior parietal lobule. These findings suggest that isolated or predominant hand weakness in patients with cerebral infarctions is not necessarily caused by lesions in the M1 knob area, and that the control center of hand movement is not limited to the knob area alone.

Adult↗
PubMed2006

Effects of atenolol and losartan on baroreflex sensitivity and heart rate variability in uncomplicated essential hypertension.

Baroreflex sensitivity (BRS) and heart rate variability (HRV) are potential therapeutic targets. The present study was conducted to assess changes in BRS and HRV after monotherapy with losartan versus that of atenolol in uncomplicated essential hypertension. Thirty subjects with uncomplicated essential hypertension were randomized to receive atenolol 50 mg to 100 mg (n = 15) or losartan 50 mg to 100 mg (N = 15) daily for 6 months. Instantaneous systolic blood pressure (SBP) and heart rate were assessed using servo-controlled infrared finger plethysmography before treatment and at the end of 3 months and 6 months after treatment. The fluctuation in SBP and interpulse interval (IPI) was divided into three specific frequency ranges by fast Fourier transform as high frequency (HF; 0.15 Hz-0.4 Hz), low frequency (LF; 0.04 Hz-0.15 Hz), and very low frequency (VLF; 0.004 Hz-0.04 Hz). The BRS was expressed as (1) SBP-IPI transfer function with its magnitude in the HF and LF ranges and (2) BRS index alpha. The HRV was expressed as total power and power in the LF and HF ranges of interpulse interval. Blood pressure was reduced to a similar extent in both groups. Compared with the baseline, BRS did not improve in both groups at month 3. However, BRS was significantly improved in the losartan group (P < 0.05) but not in the atenolol group at month 6. In addition, BRS was significantly higher in the losartan group than the atenolol group at month 3 and month 6 (P < 0.05). Moreover, heart rate variability was significantly reduced in the atenolol group at month 6 (P < 0.05), but not in the losartan group. The HRV in the losartan group was significantly higher than that in the atenolol group at month 6 (P < 0.05). These findings suggest superior effects of losartan on BRS and HRV than atenolol in uncomplicated essential hypertension, which may be beyond blood pressure reduction/resetting.

Adult↗
PubMed2005

Distribution of carotid arterial lesions in Chinese patients with transient monocular blindness.

BACKGROUND AND PURPOSE: Asian patients with cerebrovascular diseases have more intracranial atherosclerosis and less extracranial carotid artery stenosis compared with white patients. We systemically evaluated the distribution of carotid arterial lesions in Chinese patients with transient monocular blindness (TMB), which was rarely reported. METHODS: We prospectively evaluated 105 consecutive patients with TMB. All of the patients received ocular and physical examinations, blood tests for coagulation function and autoimmune diseases, and ultrasonography of cervical and intracranial arteries. All of the carotid lesions were confirmed by magnetic resonance angiography or cerebral angiography. RESULTS: Of the 36 (34.3%) patients with significant carotid stenosis (> or =50%), 16 (15.2%) had extracranial carotid stenosis; 17 (16.2%) had carotid siphon stenosis; and 3 (2.9%) had both. The duration, onset, and patterns of visual loss were not different between patients with and without carotid arterial lesion. CONCLUSIONS: This study signified the importance of carotid siphon stenosis as a probable underlying etiology for TMB in Chinese patients.

Aged↗
PubMed2005

Comparison of critical closing pressures extracted from carotid tonometry and finger plethysmography.

BACKGROUND: The reliability of critical closing pressure (CrCP) estimates derived from peripheral blood pressure (BP) measurements is unclear. We attempted to evaluate the influences of peripheral circulation on determining CrCP. METHODS: Twenty-five young healthy volunteers were studied. BP waves were obtained with plethysmography (Portapres) and carotid applanatory tonometry, respectively, for analysis. Transcranial Doppler was used to monitor cerebral flow velocity. Using linear regression analysis, beat-to-beat CrCP was calculated at rest, during voluntary hyperventilation and during 5% CO2 inhalation. RESULTS: Twenty of 25 participants demonstrating satisfactory tonometric tracings for both tests were included in the analysis. The systolic BP measured using plethysmography was higher than that derived from tonometry (139.4 +/- 24.7 vs. 105.5 +/- 29.6, p < 0.001). CrCP values derived from tonometry were all positive and higher than CrCP values derived from plethysmography (62.9 +/- 19.9 vs. 11.1 +/- 17.8, p < 0.001). The changes in CrCP induced by 5% CO2 inhalation and hyperventilation had a correlation between two BP monitoring methods (r = 0.52, p = 0.001). CONCLUSIONS: Pressure waveform is an important determinant in calculating CrCP by linear regression analysis. The relative changes in CrCP induced by hemodynamic challenges remained a relevant indicator of cerebrovascular regulation regardless of the methods used for non-invasive BP recording.

Adolescent↗
PubMed2005

Changes in flow-mediated dilatation, cytokines and carotid arterial stenosis during aggressive atorvastatin treatment in normocholesterolemic patients.

BACKGROUND: Aggressive statin therapy to reduce low-density lipoprotein (LDL) cholesterol in patients with normal LDL-cholesterol levels reduces the incidence of future cardiovascular events and enhances atherosclerotic regression in the common carotid artery. We tried to quantify changes in flow-mediated dilatation (FMD), inflammatory cytokines, and the severity of carotid arterial stenosis, after aggressive statin administration to patients with normal LDL-cholesterol levels, and stroke or transient ischemic attack ipsilateral to carotid arterial stenosis. METHODS: Twenty patients with at least a 50% reduction in the diameter of the carotid artery were studied. Atorvastatin 10 mg daily was prescribed for 4 months. Serial changes in the severity of carotid arterial stenosis, and brachial-artery FMD were evaluated by high-resolution ultrasound. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), soluble endothelin-1 (ET-1), and high-sensitivity C-reactive protein (hs-CRP), were measured before, and after 2 and 4 months of, atorvastatin treatment. RESULTS: Atorvastatin significantly decreased plasma levels of total cholesterol and LDL-cholesterol after 1, 2 and 4 months of treatment (p < 0.01). FMD showed significant improvement after only 4 months (10.0% vs 6.8% at baseline; p = 0.019). The overall severity of carotid arterial lesions was not significantly reduced by atorvastatin. Changes in TNF-alpha, IL-1beta, IL-6 and ET-1 showed trends towards a progressive decline after atorvastatin, but none of the cytokines was reduced significantly. FMD did not correlate with the severity of carotid arterial stenosis, lipid profile, or cytokine levels. CONCLUSION: Atorvastatin effectively reduced plasma concentrations of total cholesterol and LDL-cholesterol, and had beneficial effects on endothelial function, in Chinese patients with carotid arterial stenosis and normal LDL-cholesterol levels.

Aged↗
PubMed2005

Reversible electroencephalographic and single photon emission computed tomography abnormalities in Hashimoto's encephalopathy.

Hashimoto's encephalopathy (HE) is a well-established disease that occurs most commonly in patients with euthyroidism. We report 3 patients diagnosed with HE. Cases 1 and 2 were young females who had experienced intractable seizures and presented with cognitive impairment. Reversible slow waves on the electroencephalogram (EEG), and nearly complete recovery of cognition, were noted after steroid treatment. Case 3 was an elderly male who presented with a sudden onset of vertigo, diplopia, and recurrent gait ataxia. Reversible hypoperfusion in the upper portion of the left cerebellum, on (99m)Tc hexamethylpropyleneamine oxime (HMPAO) single photon emission computed tomography (SPECT), was noted after steroid treatment. We also review 25 cases from the literature of patients diagnosed with HE. All patients had antithyroid antibodies. A reversible inflammatory process is supported by brain magnetic resonance imaging, SPECT, EEG and cerebrospinal fluid studies. Vasculitis is the most probable pathogenesis according to laboratory findings. Steroids are the treatment of choice, and result in a favorable outcome when administered early in the disease course.

Adult↗
PubMed2004

Correlations among critical closing pressure, pulsatility index and cerebrovascular resistance.

We attempted to explore the relationships among critical closing pressure (CrCP), resistance-area product (RAP) and traditional resistance indices of cerebral hemodynamics. Twenty healthy volunteers were studied. Blood pressure was obtained with servo-controlled plethysmography. Cerebral blood flow velocity (CBFV) was monitored by transcranial Doppler. Hemodynamic changes were induced by hyperventilation and by 5% CO(2) inhalation. Beat-to-beat CrCP and RAP values were extracted by linear regression analysis of instantaneous arterial blood pressure (ABP) and CBFV tracings. Gosling's pulsatility index (PI) and cerebrovascular resistance (CVR) were calculated. RAP correlated well with CVR at rest and during provocative tests (p = 0.006 approximately <0.001). There was no correlation among CrCP, CVR and PI. The changes in CVR correlated with those in RAP (p = 0.008 for the 5% CO(2) test and p = 0.014 for the hyperventilation test). The changes in PI and CrCP showed significant correlation (p = 0.004 for the 5% CO(2) test and p = 0.003 for the hyperventilation test). RAP reliably reflected cerebrovascular resistance. The changes in CrCP were valuable in assessing cerebrovascular regulation. Estimating changes in CrCP and RAP provided better understanding of the nature of cerebrovascular regulation.

Adolescent↗
PubMed2003

Mechanisms underlying phase lag between systemic arterial blood pressure and cerebral blood flow velocity.

To explore the mechanisms underlying the phase lag between oscillations in arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV), ABP and CBFV signals were recorded noninvasively from normal volunteers who lay quietly in a supine position. Mean ABP (MAP) and CBFV (MFV) were calculated beat-to-beat by means of integration. Cerebral vascular resistance (CVR) was calculated by dividing MAP with MFV. Frequency domain analysis of MAP, MFV and CVR signals revealed very-low frequency (VLF, 0.016-0.04 Hz), low-frequency (LF, 0.04-0.15 Hz), and high-frequency (HF, 0.15-0.4 Hz) components. The transfer phase of MAP-CVR coupling in the LF and HF range was frequency-dependent, which is equivalent to a time delay of 2 s. However, the transfer phase differed in the CVR-MFV coupling in that the phase was distributed around 180 degrees across the LF and HF ranges. Cross-correlation analysis revealed a positive relationship between MAP-CVR coupling, with MAP leading by 2 s, and a negative relationship between CVR-MFV coupling, with CVR leading by 0.3 s. We concluded that the phase lag between oscillations in ABP and CBFV was chiefly contributed to by the starting latency of cerebral autoregulation (i.e. cerebral vasomotion, revealed by MAP-CVR coupling). Moreover, the negative correlation of the CVR-MFV coupling could offer a different explanation for the physiologic significance of the phase lead of CBFV-ABP oscillations.

Adult↗