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To determine whether heart rate recovery (HRR) following an exercise tolerance test (ETT) is correlated with a changing ratio of peak oxygen consumption (VO2) and maximal metabolic equivalents (METmax).
A total of 60 acute myocardial infarction (AMI) patients who underwent ETT at both assessment points - 3 weeks (T0) after the AMI attack and 3 months after T0 (T1) were included. After achieving a peak workload, the treadmill was stopped with a 5-minute cooldown period, and the patients recovered in a comfortable and relaxed seated position. HRR was defined as the difference between the maximal heart rate (HRmax) and the HR measured at specific time intervals - immediately after the cool down period (HRR-0) and 3 minutes after the completion of the ETT (HRR-3).
HRR-0 and HRR-3 increased over time, whereas VO2max and METmax did not show significant changes. There was a positive correlation between HRR at T0 and the exercise capacity at T0. HRR at T0 also showed a positive correlation with the exercise capacity at T1. There was no significant correlation between HRR measured at T0 and the change in the ratio of VO2max and METmax, as calculated by subtracting VO2max and METmax obtained at T0 from those obtained at T1, divided by VO2max at T0 and multiplied by 100.
Post-exercise HRR measured at 3 weeks after the AMI onset can reflect the exercise capacity 3 months after the first ETT. However, it may be difficult to correlate post-exercise HRR at T0 with the degree of increase in cardiopulmonary exercise capacity in patients with AMI.
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To quantify changes in cardiopulmonary function using a lower body positive pressure supported (LBPPS) treadmill during the exercise tolerance test (ETT) in healthy subjects before applying the LBPPS treadmill in patients with gait problems.
We evaluated 30 healthy subjects who were able to walk independently. The ETT was performed using the Modified Bruce Protocol (stages 1–5) at four levels (0%, 40%, 60%, and 80%) of LBPPS. The time interval at each level of the LBPPS treadmill test was 20 minutes to recover to baseline status. We measured systolic blood pressure, diastolic blood pressure, peak heart rate (PHR), rating of perceived exertion (RPE), metabolic equivalents (METs), and oxygen consumption rate (VO2) during each LBPPS condition.
Systolic blood pressure increased as the LBPPS level was increased (40% to 80%). PHR, RPE, METs, and VO2 were negatively associated with the LBPPS condition, although they were not always significant different among the LBPPS levels. The equation from a random effect linear regression model was as follows: VO2 (mL/kg/min)=(2.75×stage)+(–0.14×LBPPS level)+11.9 (r2=0.69).
Detection of the changes in physiological parameters during a submaximal ETT using the LBPPS system may be helpful for applying the LBPPS treadmill in patients who cannot perform the ETT due to gait problems, even at submaximal intensity.
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To investigate the effect of pulsed radiofrequency (PRF) applied proximal to the injured peripheral nerve on the expression of tumor necrosis factor-α (TNF-α) in a neuropathic pain rat model.
Nineteen male Sprague-Dawley rats were used in the study. All rats underwent chronic constriction injury (CCI) procedure. After 7 days of CCI, withdrawal frequency of affected hind paw to mechanical stimuli and withdrawal latency of affected hind paw to heat stimulus were measured. They were randomly divided into two groups: group A, CCI group (n=9) and group B, CCI treated with PRF group (n=10). Rats of group B underwent PRF procedure on the sciatic nerve. Withdrawal frequency and withdrawal latency were measured at 12 hours, and 7 days after PRF. Immunohistochemistry and Western blot analysis were performed using a TNF-α antibody.
Before PRF, withdrawal frequency and withdrawal latency were not different in both groups. After PRF, withdrawal frequency decreased and withdrawal latency prolonged over time in group B. There was significant interaction between time and group for each withdrawal frequency and withdrawal latency. Group B showed decreased TNF-α immunoreactivity of the spinal cord and sciatic nerve at 7 days.
PRF applied proximal to the peripheral nerve injury is potentially helpful for the reduction of neuropathic pain by neuromodulation of inflammatory markers.
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A 37-year-old man with a right transfemoral amputation suffered from severe phantom limb pain (PLP). After targeting the affected supplementary motor complex (SMC) or primary motor cortex (PMC) using a neuro-navigation system with 800 stimuli of 1 Hz repetitive transcranial magnetic stimulation (rTMS) at 85% of resting motor threshold, the 1 Hz rTMS over SMC dramatically reduced his visual analog scale (VAS) of PLP from 7 to 0. However, the 1 Hz rTMS over PMC failed to reduce pain. To our knowledge, this is the first case report of a successfully treated severe PLP with a low frequency rTMS over SMC in affected hemisphere.
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To investigate the effects of aerobic exercise on neuropathic pain and verify whether regular treadmill exercise alters opioid receptor expression in the rostral ventral medulla (RVM) in a neuropathic pain rat model.
Thirty-two male Sprague-Dawley rats were used in the study. All rats were divided into 3 groups, i.e., group A, sham group (n=10); group B, chronic constriction injury (CCI) group (n=11); and group C, CCI+exercise group (n=11). Regular treadmill exercise was performed for 30 minutes a day, 5 days a week, for 4 weeks at the speed of 8 m/min for 5 minutes, 11 m/min for 5 minutes, and 22 m/min for 20 minutes. Withdrawal threshold and withdrawal latency were measured before and after the regular exercise program. Immunohistochemistry and Western blots analyses were performed using antibodies against µ-opioid receptor (MOR).
Body weight of group C was the lowest among all groups. Withdrawal thresholds and withdrawal latencies were increased with time in groups B and C. There were significant differences of withdrawal thresholds between group B and group C at 1st, 2nd, 3rd, and 4th weeks after exercise. There were significant differences of withdrawal latencies between group B and group C at 3rd and 4th weeks after exercise. MOR expression of group C was significantly decreased, as compared to that of group B in the RVM and spinal cord.
In neuropathic pain, exercise induced analgesia could be mediated by desensitization of central MOR by endogenous opioids, leading to the shift of RVM circuitry balance to pain inhibition.
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Churg-Strauss syndrome (CSS) is a rare systemic necrotizing vasculitis. Cranial nerve involvement is very rare in CSS. A 59-year-old woman had complained of both hearing impairments for eight months and left facial palsy for three months. Left facial and cochlear neuropathies were detected in electrodiagnostic studies. Paranasal sinus computed tomography (CT) showed chronic pansinusitis. Chest CT revealed eosinophilic infiltration in the right upper lobe. Tissue biopsy of the right inferior turbinate displayed necrotizing vasculitis with eosinophilic infiltration. She was diagnosed as CSS, based on the presence of eosinophilia, pulmonary infiltration, paranasal sinusitis, and biopsy containing blood vessels with extravascular eosinophils. She was treated with intravenous and oral steroids and azathioprine, showing relatively good prognosis on facial palsy and hearing impairment. We report a very rare case of CSS presented with hearing impairment and facial palsy.
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Cerebral venous sinus thrombosis (CVST) is an uncommon cause of cerebral infarction, compared to arterial diseases. It is often unrecognized at initial presentation due to the diversity of causes and clinical manifestations. A 29-year-old female patient complained of severe headache and presented at the emergency room with altered consciousness. Brain computed tomography and brain magnetic resonance image revealed the left sigmoid sinus thrombosis with venous hemorrhagic infarction (VHI) in the left temporal lobe. The patient had no past medical and family history of bleeding diathesis. The laboratory finding at the admission showed severe iron-deficiency anemia (IDA), and protein C and S activities were decreased. After the neurosurgery, iron replacement, and neurorehabilitation, the patient had a good recovery. There has been no known recurrence. We report our therapeutic intervention on a very rare case of CVST and VHI, with IDA as a probable cause of cerebral thrombosis.
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Spontaneous cervical epidural hematoma (SCEH) is an uncommon cause of acute nontraumatic myelopathy. SCEH presenting as Brown-Sequard syndrome is extremely rare. A 65-year-old man had motor weakness in the left extremities right after his mother's funeral. He received thrombolytic therapy under the impression of acute cerebral infarction at a local hospital. However, motor weakness of the left extremities became aggravated without mental change. After being transferred to our hospital, he showed motor weakness in the left extremities with diminished pain sensation in the right extremities. Diagnosis of SCEH was made by cervical magnetic resonance imaging. He underwent left C3 to C5 hemilaminectomy with hematoma removal. It is important for physicians to be aware that SCEH can be considered as one of the differential diagnoses of hemiplegia, since early diagnosis and management can influence the neurological outcome. We think that increased venous pressure owing to repetitive Korean traditional deep bows may be the cause of SCEH in this case.
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To investigate the effect of combined therapy of exercise and nootropic agent on cognitive function in a focal cerebral infarction rat model.
Forty 10-week old male Sprague-Dawley rats were subjected to photothrombotic cerebral infarction of the left parietal lobe. All rats were randomly divided into 4 groups: group A was photothrombotic cerebral infarction rats without any treatment (n=10); group B was photothrombotic cerebral infarction rats with swimming exercise (n=10); group C was photothrombotic cerebral infarction rats with oral administration of acetyl-L-carnitine (n=10); group D was photothrombotic cerebral infarction rats with swimming exercise and oral administration of acetyl-L-carnitine (n=10). Cognitive function was evaluated using the Morris water maze test on the 1st day, and the 1st, 2nd, and 4th week after the induction of cerebral infarction. The activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in the hippocampus were measured. The neuronal cells of the hippocampus were histopathologically evaluated.
The escape latency was shorter in groups B, C, and D than in group A. However, the differences were not statistically significant at the 1st, 2nd and 4th week. The activity of SOD was the highest in group D. The level of MDA was the lowest in group D. We observed more normal neuronal cells in groups B, C, and D.
The combined therapy of exercise and nootropic agent was helpful in ameliorating oxidative stress in the focal cerebral infarction rat model. However, the effect did not translate into improvement of cognitive function.
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A 53-year-old man abruptly developed headache and unconsciousness. Brain computed tomography (CT) and CT angiography showed subarachnoid hemorrhage, intraventricular hemorrhage, and multiple tortuous vascular structures on the brain stem and upper cervical spinal cord. Four-vessel angiography displayed intradural ventral arteriovenous fistula, supplied by the left vertebral and occipital arteries. Drainage was via both sigmoid sinus and cervical venous plexus. He had been treated with transarterial coil embolization of the left vertebral artery. Subsequently, he suffered from left hemiplegia and cognitive problem. Brain magnetic resonance (MR) and MR angiography performed 4 weeks later revealed multiple infarctions on the left cerebellum, left upper cervical spinal cord, and both medial thalamus, as well as occlusion of the left vertebral artery with reduction in varix size. After rehabilitative management, his muscle strength and cognitive function improved. We report a very rare case of dural arteriovenous fistula on the brain stem and upper cervical spinal cord.
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A 49-year-old man received prolotherapy in the upper cervical region at a local medical clinic. Immediately after the procedure, he felt a sensation resembling an electric shock in his right upper and lower extremities, and continuously complained of numbness and discomfort in the right hemibody. He visited our clinic a week later. Upon physical examination, there were no significant abnormal findings. The visual analog scale was 60 points. T2-weight magnetic resonance images of the cervical spine showed a 0.7 cm sized bright oval spot on the right side of the spinal cord at the level of C4-C5 disc, suggesting spinal cord injury. There were no definite electrodiagnostic abnormalities. Digital infrared thermal images showed moderately decreased surface temperature on lateral aspect of the right forearm and dorsum of the right hand compared with the other side. Considering that very rare complications like spinal cord injury may develop after prolotherapy, we suggest that special interventions such as prolotherapy be performed by professional experts.
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