Biomedical subjects
Publications and source records attributed to K K Liao.
A genetic analysis identified 2 patients, approximately one-tenth of our patients with familial parkinsonism, who had expanded trinucleotide repeats in SCA2 genes. The reduction of 18F-dopa distribution in both the putamen and caudate nuclei confirmed that the nigrostriatal dopaminergic system was involved in parkinsonian patients with SCA2 mutation.
PURPOSE: To present a case of bilateral neurotrophic keratopathy with miosis after bilateral Vidian neurectomy for vasomotor rhinitis. METHODS: Observational case report. RESULTS: A 68 year-old man presented with irritation and blurred vision in both eyes 2 weeks after bilateral Vidian neurectomy. Slit-lamp examination revealed a large epithelial defect, typical of neurotrophic keratopathy, in the inferior two-thirds of cornea in both eyes. Corneal sensitivity test with a Cochet-Bonnet anesthesiometer and electrical study of the blink reflex indicated bilateral trigeminal dysfunction. Both pupils were miotic, and tests with hydroxyamphetamine 1% and epinephrine 0.1% showed postganglionic sympathetic nerve damage. The corneal epithelial defects healed after 2 months of treatment with systemic prednisolone, vitamin B(12) and tarsorrhaphy. CONCLUSION: Neurotrophic keratopathy associated with dry eye syndrome may be a serious complication of Vidian neurectomy.
OBJECTIVES: We can assess brain function by measuring the cortical relay time (CRT) of long latency reflex (LLR) of hand muscle. We would study if measurement of CRT of LLR can explore the brain involvement of adrenomyeloneuropathy (AMN). METHODS: Two AMN patients were included in the study. Both of them had spastic gait and mild sensory deficits but normal mental function. The LLRs were provoked at the first dorsal interosseous muscle by electrical stimulation of the middle finger. We measured the latency of LLR and its CRT. RESULTS: Delayed LLR and prolonged CRT were noted in AMN patients, even though the magnetic resonance imaging of brain did not show any significant abnormalities. CONCLUSIONS: Measuring CRT of LLR reveals brain involvement of AMN patients, and it is an adjunct in the assessment of brain function though without specific anatomic diagnosis.
BACKGROUND: Human oscillator is observed in and outside the nervous system. Cardiac rhythm is generated by heart itself but can be modulated by brain. Using the technique of transcranial magnetic stimulation (TMS) and resetting index, we studied if single-pulse TMS could reset the cardiac rhythm and help differentiate oscillator of neurogenic or non-neurogenic origin. METHODS: In addition to the study of 4 patients with essential tremor, cardiac rhythm was studied in 6 normal subjects. The magnetic intensity was initiated from motor threshold of hand muscle, and then with an increment of 10% up to the maximal output of magnetic stimulator. We used the resetting index (RI) to quantify the influence of the TMS. RESULTS: The resetting phenomenon was observed in essential tremor (RI = 0.92) but not in cardiac rhythm (RI = 0.02). CONCLUSIONS: Single-pulse TMS is able to reset the rhythm of essential tremor but not heart beat. The pacing mechanism is different between essential tremor and heart beat. The cardiac rhythm is regulated and modulated chiefly by heart itself. Essential tremor should not share the same mechanism with heart beat.
A 50-year-old woman taking carbamazepine (CBZ) 1200 mg daily for her partial epilepsy developed acute confusion after valproate (VPA) add-on treatment for 10 days. The administration of VPA started from 1000 mg daily and, 3 days later, increased to 1500 mg daily. Beside a mildly elevated serum ammonia level (81 microg/dL), her electroencephalogram showed diffuse background slowing intermixed with 2-2.5 Hz of high-amplitude slow waves, which indicated a diffuse encephalopathy. The serum levels of VPA and CBZ were 49.1 mg/L and 8.6 mg/L, both being non-toxic. The liver functions appeared normal. She recovered rapidly after discontinuation of VPA. In this patient, a safe previous administration of VPA did not preclude the occurrence of encephalopathy. A relatively large initial VPA dosage could possibly be the culprit.
OBJECTIVES: Magnetic stimulation of the motor cortex can be used to determine the involvement of the cortex in rhythmic movement disorders. Symptomatic palatal tremor (SPT) is thought to come from a pacemaker that is relatively resistant to internal and external stimulation. In this study, we investigated the effect of magnetic stimulation of motor cortex on SPT. METHODS: Five male patients, aged 67-79 years, with SPT after brain stem infarction or hemorrhage, all had a synchronous mouth angle twitch with the palatal movement. Electromyographic activity was recorded with a monopolar needle electrode from orbicularis oris. In experiment 1, transcranial magnetic stimulation (TMS) was delivered at 200% motor threshold (MT) to reset SPT. In experiment 2, the effect of TMS intensities was studied at 80-240% MT in two SPT patients. To determine the influence of the TMS, we used the resetting index (RI). RESULTS: TMS reset the tremor in all 5 SPT patients at 200% MT with RIs of 0.86-0.96. The latency of the tremor reappearance after TMS was longer than the pre-stimulus tremor interval, and the intervals between the subsequent tremor bursts were also prolonged. The degree of tremor resetting was closely correlated with the magnetic stimulus intensity and the latency of the tremor reappearance after TMS. CONCLUSIONS: Stimulation of the motor cortex may modulate the generator of SPT.
BACKGROUND: Mardin-Darby canine kidney (MDCK) cells cultured in hydrated collagen gels develop simple epithelial cysts or branching tubules, depending on the presence of hepatocyte growth factor (HGF). Constituents of extracellular matrix can modulate the morphogenesis of MDCK cells. Collagen is one of the few well-defined structural entities that display gross structural changes with aging. This study was conducted to delineate the effects of age-induced changes of collagen on the morphogenesis of MDCK cells cultured in collagen gel. METHODS: We employed Y224 and MDCK clone II 3B5 cells to study cystogenesis and branching tubulogenesis, respectively. Cells were cultured in three-dimensional collagen gels prepared from 1-, 4-, 8-, and 16-month-old rat tail tendons, and their capacity to develop cysts or branching tubules was assessed. We also analyzed the compositions and physical structures of collagen of various ages. RESULTS: Y224 cells developed generally larger spherical cysts in collagen gels prepared from rats that were more than four months old. The ratio of apoptosis of cells cultured in one-month-old collagen gel was markedly higher than in the gel of older ages. The results were consistent with the observations that collagen gel overlay-induced apoptosis of Y224 cells in one-month-old collagen was higher than that in older collagen. On the other hand, 3B5 cells exhibited a remarkable scattering morphology when cultured in one- or four-month-old collagen gel with HGF. In contrast, 3B5 cells exhibited more intercellular adhesion and were organized into branching tubule structures only in the collagen gel that was more than eight months old. The differences in morphogenesis could be explained by the observations that collagen of younger ages exerted markedly higher HGF-triggered migration capability than collagen of older ages. CONCLUSIONS: Age-related alterations in collagen influence epithelial cell morphogenesis via regulation of cell apoptosis, proliferation, and/or motility.
BACKGROUND: Problem-based learning (PBL) in small-group tutorials has been a trend in medical education. Chinese students are known to be reserved and passive; thus, they may not be adaptable to PBL. Neuroanatomy, important to clinical neurology, is difficult to learn. We incorporated clinical neurology with PBL, complementary to the traditional neuroanatomy curriculum, to evaluate the feasibility of PBL for Chinese students in Taiwan. METHODS: Forty-two second-year medical students and seven tutors participated in the clinical neurology PBL small-group tutorials. Twelve case reports were discussed weekly beginning in February, 1999. Each case was designed to meet the progressive curriculum of the neuroanatomy course. The tutors evaluated the students by the degree of their preparation, participation, key-point comprehension and interaction. All tutors and students filled out questionnaires at the end of each session. RESULTS: The majority of the students and tutors agreed that the case materials were clearly written. Ninety percent of the students agreed that the case materials matched the traditional content of neuroanatomy. Eighty-five percent of students and 71% of tutors were satisfied and found the class rewarding. Ninety-one percent of students and 74% of tutors were in favor of PBL being continued. CONCLUSIONS: This preliminary PBL, small-group tutorial learning in clinical neurology showed satisfactory results and was, indeed, complementary to a traditional neuroanatomy course. The students, as early as during the second year of their medical school education, were able to learn through the PBL. More integration of basic and clinical sciences by PBL may be considered in future curricula designs.
OBJECTIVE: In this study, 2 updated brain-imaging modalities, technetium-99m hexamethylpropylene amine oxime-single-photon-emission computed tomography (HMPAO-SPECT) and fluorine-18 2-fluoro-2-deoxy-D-glucose-positron emission tomography (FDG-PET), were used to simultaneously detect regional cerebral blood flow (rCBF) and glucose metabolism of the brain in patients with systemic lupus erythematosus (SLE). METHODS: Twenty-five female SLE patients, ages 25-40 years, were enrolled in this study and assigned to 1 of 2 groups. Group 1 consisted of 13 patients with neuropsychiatric manifestations (7 had major and 6 had minor manifestations). Group 2 consisted of 12 patients without neuropsychiatric manifestations. Serum levels of anticardiolipin antibodies (aCL) and anti-ribosomal P antibodies (anti-P) were measured. All patients had normal brain magnetic resonance imaging (MRI) findings. Ten healthy female volunteers also underwent brain MRI, HMPAO-SPECT, and FDG-PET for comparison. RESULTS: 99mTc-HMPAO-SPECT revealed hypoperfusion lesions in 11 (44%) of 25 SLE patients, including 9 (69%) of the 13 patients in group 1, 7 (100%) of the 7 patients with major manifestations, 2 (33%) of the 6 patients with minor manifestations, and 2 (17%) of the 12 patients in group 2. Parietal lobes were the areas most commonly involved. FDG-PET revealed hypometabolism in 7 (54%) of the group 1 patients, 6 (86%) of the 7 patients with major manifestations, and 1 (17%) of the 6 patients with minor manifestations. Temporal lobes were the most commonly involved areas. However, no significant hypometabolism brain lesions were found in group 2 patients. All of the 4 patients with headaches and dizziness or headaches alone had normal findings on HMPAO-SPECT and FDG-PET. Nine (36%) of the 25 patients were positive for aCL. However, the presence of aCL was not related to neuropsychiatric manifestations or to HMPAO-SPECT or FDG-PET findings. Five (20%) of the 25 patients had anti-P antibodies and psychosis/depression. CONCLUSION: In patients with normal brain MRI findings, decreases in glucose metabolism coupled with decreases in rCBF are associated with serious neuropsychiatric SLE (NPSLE) presentations, while normal glucose metabolism with decreases in rCBF may be found in SLE patients with or without NPSLE.
Involvement of the brain is one of the most important complications of systemic lupus erythematosus (SLE); however, its diagnosis is difficult due to the lack of effective imaging methods. We combined three brain imaging modalities - positron emission tomography with fluorine-18 2-fluoro-2-deoxy-d-glucose (FDG-PET), single-photon emission computed tomography with technetium-99m hexamethylpropylene amine oxime (HMPAO-SPET) and magnetic resonance imaging (MRI) - in order to detect brain involvement in SLE. Thirty-seven SLE patients, aged 22-45 years, were divided into three groups. Group 1 (G1) consisted of ten patients with major neuropsychiatric manifestations; group 2 (G2) consisted of 15 patients with minor manifestations; and group 3 (G3) consisted of 12 patients without manifestations. FDG-PET findings were abnormal in 51% of patients: 90% of G1, 67% of G2 and 0% of G3 patients respectively. HMPAO-SPET findings were abnormal in 62% of patients: 100% of G1, 73% of G2 and 17% of G3 patients respectively. MRI findings were abnormal in 35% of patients: 70% of G1, 40% of G2 and 0% of G3 patients respectively. Grey matter was more commonly involved than white matter; 62% of patients presented with lesions in the cerebral cortex, 27% with lesions in the basal ganglion, 5% with lesions in the cerebellum, and 19% with lesions in white matter. No white matter lesions were found on FDG-PET or HMPAO-SPET. However, in 19% of patients, MRI demonstrated abnormally high signal lesions in white matter. Forty-three percent of cases had positive serum anticardiolipin antibodies (ACA). However, ACA was not related to FDG-PET, HMPAO-SPET or MRI findings. It may be concluding that HMPAO-SPET is a more sensitive tool for detecting brain involvement in SLE patients when compared with FDG-PET or MRI. However, MRI is necessary for detecting lesions in white matter.
UNLABELLED: We attempted to label leukocytes with stabilized Tc-99m D,L-HMPAO by methylene blue and sodium phosphate buffer (S-HMPAO). METHODS: The results were compared with unstabilized Tc-99m D,L-HMPAO (U-HMPAO). U-HMPAO was obtained by reconstituting a commercial vial of D,L-HMPAO. Stabilization of the kit was performed by the addition of methylene blue. The leukocytes were labeled using a modified published method. The test samples of S-HMPAO and U-HMPAO were prepared immediately, and stood for 0.5, 1, 2, 4, and 6 h, respectively, at room temperature before analysis. RESULTS: In comparison with U-HMPAO: (1) the radiochemical purity of S-HMPAO was higher; (2) the labeling efficiencies of S-HMPAO labeled leukocytes were higher and consistent; (3) the viability of S-HMPAO labeled leukocytes was as high as the viability of U-HMPAO labeled leukocytes at any time; and (4) the percentages of disintegrated from S-HMPAO labeled leukocytes in plasma were lower. CONCLUSION: S-HMPAO is more stable than U-HMPAO and can provide higher leukocyte labeling efficiency. S-HMPAO, therefore, has the potential to replace U-HMPAO as a leukocyte-labeling agent.
The effects of conditioning stimulation of an upper limb on motor evoked potentials (MEPs) of relaxed muscles in both lower limbs were studied in 7 normal subjects and two patients with left thalamic infarction. A possible mechanism for the Jendrassik maneuver (JM) is that induced proprioceptive input ascends supraspinally to facilitate the descending volleys. In order to mimic the JM with a more controlled influence, we used an electrical conditioning (C) stimulation (4 times sensory threshold) delivered to the left index finger preceding the transcranial (T) magnetic stimulation at C-T intervals of 0-200 ms. The MEP facilitation of bilateral tibialis anterior (TA) and gastrocnemius medialis (GC) was within C-T 70-110 ms. The peak facilitation was at C-T 80 ms for ipsilateral TA (309%) and GC (405%) and at C-T 90 ms for contralateral TA (207%) and GC (283%). In the two thalamic infarction patients with right-sided sensory loss, the facilitation did not occur when the conditioning stimulation was delivered to the affected index finger. Therefore, it is likely that the peripheral volley must be transmitted supraspinally to facilitate MEPs of the lower limbs. This method for studying sensory facilitation is more quantitative and reproducible than the JM and technically better than other previously described methods for somatosensory conditioning.
It has been speculated that impaired salivary flow contributes to abnormal acid clearance of the esophagus in gastroesophageal reflux and results in reflux esophagitis (RE). To test this hypothesis, salivary functions were measured by quantitative salivary scintigraphies in patients with RE and in age- and sex-matched controls for comparison. Nineteen patients with RE and 36 healthy volunteers were enrolled in the study. After an intravenous injection of 5 mCi Tc-99m pertechnetate, sequential images of 1 min/frame were acquired for 30 min. The 1- and 15-min uptake ratios (UR) of the tracer in the four major salivary glands over the backgrounds were calculated. Saliva excretion was stimulated by 1 tablet of 200 mg ascorbic acid given orally 15 min after injection of the tracer, then the maximal excretion ratios (ER) of the four major salivary glands were calculated for the sialagogue stimulation. RE patients had lower values of 1st and 15th min UR and maximal ER than controls in the 4 major salivary glands. Poor salivary functions which represented a decrease in both UR and ER for patients with RE have been confirmed by quantitative salivary scintigraphy in this study.
BACKGROUND: Hemifacial spasm and blepharospasm are both dystonic disorders. They may seriously affect individuals' lifestyle and social activities. In 1990, the Food and Drug Administration of the USA approved botulinum toxin A as a therapeutic agent in the treatment of hemifacial spasm and blepharospasm. We present a therapeutic review of botulinum toxin A in 80 patients in Taiwan. METHODS: Fifty-eight patients with hemifacial spasm and 22 with blepharospasm. Botulinum toxin A was prepared and injected into the facial and eyelid muscles. Patients were monitored every two weeks and classified into four groups (excellent, moderate, mild and no improvement) according to the clinical improvement scale. Complications were also recorded. RESULTS: A total of 86.2% of hemifacial spasm patients and 81.8% of blepharospasm patients had excellent improvement on the spasm intensity scale, while 6.8% of hemifacial spasm and 9.0% of blepharospasm patients had moderate improvement. The complication rate was low and included transient mild facial weakness (5%), ptosis (3.8%), eyelid swelling and/or ecchymosis (3.8%), nausea/vomiting (2.5%) and transient severe facial weakness (1.3%). CONCLUSION: Botulinum toxin A is an excellent therapeutic agent to improve spasm intensity and has a low complication rate.
BACKGROUND: Botulism may involve the autonomic nervous system. METHODS: We assessed the autonomic function of 6 botulism patients with heart rate variations, sympathetic skin responses, and plasma norepinephrine. RESULTS: Two weeks after onset, all the patients had absent sympathetic skin response in the palm and sole. Compared with controls, the heart rate variation of botulism patients was significantly decreased at rest (3.1 +/- 1.2% vs. 20.9 +/- 2.0%, p = 0.0018) and during deep breathing (4.3 +/- 2.3% vs. 29.7 +/- 2.6%, p = 0.0018). The botulism patients had significantly lower plasma norepinephrine levels (supine 29.2 +/- 10.1 pg/ml vs. 257.5 +/- 65.8 pg/ml, p = 0.0018; standing 40.3 +/- 13.1 pg/ml vs. 498.5 +/- 85.6 pg/ml, p = 0.0018). The heart rate variation and sympathetic skin response was greatly improved 6 months after onset. CONCLUSIONS: Heart rate variation, absence of sympathetic skin response, and low plasma norepinephrine are all manifestations of autonomic dysfunction in botulism patients.
Cutaneous reflex (CR) was measured in 15 patients with acute lacunar stroke and in 15 age- and sex-matched normal subjects. EMG activities were recorded from the first dorsal interosseous muscle with surface electrodes, rectified and averaged. Intensity of the stimulation on the index finger was four times the sensory threshold. Aided by audio- and visual-feedback monitoring, the subjects abducted the index finger. Side-to-side comparison was made on all the subjects. CR abnormalities were found in all of our patients. The early inhibitory (I1) and second excitatory (E2) components were attenuated in 11 of 15 patients. The I1-E2 interpeak amplitude (A2) was significantly reduced in all the patients. Prolonged latency of I1-E2 components was found to be pronounced in six of eight patients with sensory symptoms. Eight patients were followed up 1 month later. By that time, the abnormal CR had reversed to some degree in all of them. CR alternation was still present in two fully recovered patients. Our results implied a thalamic relay in the afferent limb of the CR. CR could be a valuable adjunct for assessing long tract dysfunction and monitoring functional recovery.
OBJECTIVES: We used an electrical conditioning stimulation followed by transcranial magnetic stimulation (TMS) to facilitate the occurrence of long latency potentials (LLPs) in order to study the relationship between primary motor evoked potentials (MEPs) and LLPs in the lower limbs. MATERIALS AND METHODS: The study group included 6 healthy subjects, 1 patient with right thalamic infarction, and 3 patients with spinal cord injuries. The subjects were subjected to electrical conditioning (C) stimulation delivered to the left big toe at 250 Hz in a train of pulses of 20 ms duration prior to TMS (T) from 0 to 150 ms at an increment of 10 ms. The surface electromyographic signals were recorded at the tibialis anterior and gastrocnemius medialis for 400 ms. RESULTS: The C-T test facilitated both primary MEPs and LLPs with a pattern similar to the primary MEPs of its antagonist. There was no facilitation of the primary MEPs or LLPs in the affected limb of patients with thalamic or spinal cord lesions. CONCLUSION: At appropriate C-T interval, LLPs could be consistently provoked by TMS. The LLPs were absent in the patients with thalamic infarction and spinal cord injuries. It suggests that LLPs might be provoked through a supraspinal control.
OBJECTIVES: Our study was designed to clarify the role of the thalamus in the generation of the electrically elicited long-latency reflexes (LLR) in voluntarily activated hand muscles. MATERIALS AND METHODS: EMG responses of the thenar muscles were evoked by electrical stimulation of the median nerve at the wrist at motor threshold intensity in 10 patients with acute pure sensory stroke due to thalamic infarction. Concomitant recording of somatosensory evoked potentials (SEPs) was performed. The subjects were asked to steadily abduct the thumb at 20-30% of maximal force against a force transducer. Rectified and averaged EMG activities were recorded. RESULTS: The LLR II was missing completely or significantly attenuated in the majority of the patients (9 of 10), of whom 3 also had delayed latency. Abnormal SEPs were documented in 7 patients (7 of 10). In the follow-up, 5 patients had partial reversal of LLR II. LLR II was still pathological in 1 fully recovered patient. CONCLUSION: Our results further confirm the transcortical generation of LLR II and imply that a thalamic relay is present in the afferent limb of the LLR.