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Biomedical subjects

K P Kao

Publications and source records attributed to K P Kao.

At least 19 recordsLinked to original sources
PubMed2001

Brain dysfunction explored by long latency reflex: a study of adrenomyeloneuropathy.

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.

Adrenoleukodystrophy↗
PubMed2000

Modulation of symptomatic palatal tremor by magnetic stimulation of the motor cortex.

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.

Aged↗
PubMed1999

Effect of stimulation of an upper limb on motor evoked potentials in lower limb muscles to transcranial magnetic stimulation in normal subjects and patients with thalamic infarction.

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.

Adult↗
PubMed1999

Use of botulinum toxin A in the treatment of hemifacial spasm and blepharospasm.

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.

Adult↗
PubMed1999

Molecular epidemiologic study of mitochondrial DNA mutations in patients with mitochondrial diseases in Taiwan.

We report an 8-year molecular study of mitochondrial DNA (mtDNA) mutations in patients with mitochondrial diseases in Taiwan. One hundred and seventy-seven patients met the diagnostic criteria of mitochondrial disease and were recruited into the study. The results showed that 32 patients, including 25 with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome, one with Kearns-Sayre syndrome (KSS), one with diabetes mellitus and deafness, and five with chronic progressive external ophthalmoplegia (CPEO), harbored the A3243G mtDNA mutation. The A8344G mutation was found in nine patients, all of whom suffered from myoclonic epilepsy and ragged-red fibers (MERRF) syndrome. The G11778A mtDNA mutation was found in 18 of 22 patients with Leber's hereditary optic neuropathy. The T8993C and T8993G mutations were found, respectively, in one and two patients with Leigh syndrome. Large-scale deletions of mtDNA were found in 17 patients with CPEO, one with KSS, one with MELAS, and two with MERRF syndrome. The mtDNA mutations in patients with each of the mitochondrial diseases found in Taiwan were restricted mainly to a single site, while those reported for the same diseases in other ethnic groups occurred in many sites. Furthermore, significant levels of additional mtDNA mutations occurred in some patients with mitochondrial encephalomyopathies. We suggest that these additional (or secondary) mtDNA mutations are generated as a consequence of the preexisting primary mtDNA mutations and may contribute to the age-dependent progressive deterioration characteristic of mitochondrial diseases.

Adolescent↗
PubMed1999

Chronic hepatitis B exacerbated by Guillain-Barré syndrome: a report of two cases.

Several neurologic complications involving both the central and peripheral nervous systems due to acute viral hepatitis have been described, but Guillain-Barré (G-B) syndrome occurring as a complication of chronic viral hepatitis is extremely rare. Although it is generally agreed that G-B syndrome develops as an immune-mediated reaction, its exact pathogenesis remains obscure. We report the cases of two patients with chronic hepatitis B virus (HBV) infection acutely exacerbated by the development of G-B syndrome. G-B syndrome was diagnosed by nerve conduction velocity studies, electromyographic studies and a rise in acellular total protein in the cerebrospinal fluid (albumino-cytologic dissociation). In these two patients, we were able to accurately define the relationship between the onset of acute exacerbation of chronic HBV infection and G-B syndrome. The neurologic symptoms of G-B syndrome resolved with the return of liver enzymes to normal. Interferon therapy may be beneficial in relieving neurologic symptoms in patients with HB infection-related G-B syndrome.

Adult↗
PubMed1998

Cutaneous reflexes in patients with acute lacunar infarctions.

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.

Aged↗
PubMed1998

Genetic polymorphism and Parkinson's disease in Taiwan: study of debrisoquine 4-hydroxylase (CYP2D6).

Debrisoquine 4-hydroxylase (CYP2D6) is one of the cytochrome P450 enzyme families that catalyze the breakdown of a variety of exogenous and endogenous compounds. Previous reports have suggested that genetic polymorphisms of debrisoquine 4-hydroxylase are associated with susceptibility to Parkinson's disease (PD) in Caucasians. To determine if CYP2D6 also confers susceptibility to PD in Chinese patients, we carried out a study of genetic association using three polymorphic markers of the CYP2D6 gene, 188C/T, 1934G/A (mutant B), and 4268G/C. No differences of allele or genotype frequencies of these three polymorphisms were detected upon comparison of primary PD patients (n=53) with normal controls (n=94). The 1934A allele (mutant B), which accounts for the majority of poor metabolizers in Caucasians, is extremely rare in Chinese. Our data do not support the suggestion that the CYP2D6 gene is related to PD susceptibility in Chinese.

Adult↗
PubMed1998

Conditioning effect on the long latency potentials in the lower limb to transcranial magnetic stimulation.

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.

Adult↗
PubMed1998

Long latency responses in pure sensory stroke due to thalamic infarction.

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.

Adult↗
PubMed1996

Systemic amyloidosis with initial polyneuropathy.

We report a case of systemic amyloidosis with the initial sign of polyneuropathy. The patient eventually developed heart failure, macroglossia, and ecchymoses 6 years later. Biopsies from the sural nerve and normal-looking skin both proved the existence of amyloid.

Aged↗
PubMed1996

Human foamy virus genome in the thymus of myasthenia gravis patients.

The etiological relationship of human foamy virus (HFV), which is a spumaretrovirus, with human diseases is not clear. We analyzed thymus specimens from four patients with myasthenia gravis for the presence of HFV proviral genome by polymerase chain reaction (PCR). The results showed the presence of both 257 base pair (bp) and 299 bp DNA fragments representing a part of gag and bel-2 sequences, respectively, in all four thymuses. Their specificity was confirmed by Southern blot hybridization with the corresponding probes. This was also confirmed by sequence analysis, although there were some point mutations. We confirmed the presence of gag related sequence, a 1353 bp Xba I-cleaved DNA fragment in all four thymus samples, a 693 bp fragment in two (#3 and #4) and a 4300 bp Hind III-cleaved DNA fragment in another two (#1 and #4), indicating possible chromosomal integration of the HFV partial genome. To our knowledge, this is the first report on the presence of HFV genome in thymus tissues of myasthenia gravis patients. Our efforts to isolate the infectious HFV by cultivation of the tissues were not successful. Low titers of neutralizing antibody were detected in all four patients' serum samples. The possible role of the HFV in this autoimmune disease needs further investigation.

Adult↗
PubMed1996

Myasthenia gravis complicated with hyperthyroidism, thymoma and serological evidence of systemic lupus erythematosus: a case report.

A 55-year-old woman with a several-decade history of thyroid goiter is presented here as a case of myasthenia gravis complicated with hyperthyroidism and thymoma with serological evidence of systemic lupus erythematous (SLE). She had had right eyelid ptosis since July 1992, with a positive tensilon test. The acetylcholine receptor antibody titer was 4.01 nmol/L. A thyroid function test revealed T3: 162 ngidl, T4: 14.98 micrograms/dl, TSH:0.09 microIU/ml and positive anti-microsomal antibody (1:400). An MRI of the chest showed a thymoma in the left thymus. Other autoantibody screenings include ANA (1:320, speckled pattern) and anti-ds DNA (+) suggesting a serological association with SLE. After three courses of plasmapheresis, she received an extended maximal thymomectomy and a subtotal thyroidectomy. She was then treated with prednisolone, Mestinon, Eltroxin and discharged without complications. The coexistence of myasthenia gravis, hyperthyroidism, thymoma and a serological evidence of SLE have not previously been documented in the literature.

Female↗
PubMed1996

Polyneuropathy associated with acute monoblastic leukemia: a case report.

Polyneuropathy associated with acute myelocytic leukemia is rare. We report a woman aged 34 years with acute monoblastic leukemia and polyneuropathy in hematology remission. The clinical, electrophysiological and pathological findings revealed acute symmetrical sensorimotor axonal polyneuropathy that differs from previous reports of three cases.

Adult↗
PubMed1995

Correlation between NGF levels in wound chamber fluid and cytological localization of NGF and NGF receptor in axotomized rat sciatic nerve.

When a silicone tube is implanted in transected rat sciatic nerve, there is plasma accumulation and formation of a fibrin cable followed by proliferation and migration of neural and nonneural cells from the nerve stumps into the cable. The wound fluid exhibited neurotrophic activity of unknown origin and nature. In this study, we analyzed the NGF level in wound fluid by a sensitive enzyme immunoassay and correlated the NGF level with the cytological localization of NGF, low affinity NGF receptor (p75NGFR), and Trk receptor in the axotomized nerve by immunohistochemistry. We demonstrated a rising NGF level in wound fluid from 490 pg/ml on Day 1 to 950 pg/ml on Day 7; the serum NGF level was 1/20 of that in the wound fluid. The infiltrating leukocytes expressed strong NGF but no p75NGFR. The proliferative fibroblasts and vascular cells exhibited a short period of NGF but no p75NGFR staining. Schwann cells in the distal segment showed a prolonged period of NGF and p75NGFR expression. No Trk receptor was demonstrated on leukocytes or non-neural cells. These findings suggest that locally synthesized NGF is mainly responsible for the neurotrophic activity in the wound chamber fluid. The NGF produced by the nonneural cells may be bound and stored in the p75NGFR in Schwann cells in the distal segment prior to the arrival of the regenerating axons.

Animals↗