• Perspectives in Nursing Science
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• v.2 no.1
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• pp.19-36
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• 2005

Muscle atrophy is defined as a decrease in muscle mass, cross-sectional area, and myofibrillar protein content. Causes inducing muscle atrophy may be inactivity, denervation, undernutrition and steroid. Inactivity may decrease protein synthesis and increase protein breakdown of skeletal muscle. The muscle atrophy due to inactivity was induced by bed rest, hindlimb suspension, cast, total hip replacement arthroplasty, anterior cruciate ligament reconstruction. Denervated atrophy may be induced by the loss of innervation from lower motor neuron. The atrophy was apparent in the lower limb of hemiplegic patients following ischemic stroke and in the hindlimb of ischemic stroke rats. Protein breakdown of skeletal muscle in the undernourished state results in muscle atrophy. The atrophy due to undernutrition was evident in cancer and leukemia patients and in the undernourished rats. Steroids have been used to treat allergies, inflammatory diseases, autoimmune diseases and to inhibit immune function following transplantation. Steroids may induce muscle atrophy by protein breakdown of skeletal muscle. Muscle Physiology Laboratoryat College of Nursing, Seoul National University proved that dexamethasone may induce hindlimb muscle atrophy in rats and exercise and DHEA may attenuate hindlimb muscle atrophy induced by the steroid in rats. Nurses working with patients undergoing steroid treatment need to be cognizant of steroid induced muscle atrophy. They need to assess whether muscle atrophy is being occurred during and after the steroid treatment. Moreover, they need to apply exercise and DHEA to the patients undergoing steroid treatment in order to attenuate the steroid induced muscle atrophy.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.17 no.2
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• pp.146-148
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• 2006

Spasmodic dysphonia is a voice disorder characterized by involuntary voice breaks during speech. Adductor spasmodic dysphonia is most common and characterized by strained and strangled voice breaks. The current standard of treatment of therapy for adductor spasmodic dysphonia is chemodenervation of thyroarytenoid muscle with botulinum toxin(Botox). However, Botox is a temporary treatment with each injection lasting approximately 3 months on average and require repeated injections. In this study, we report our experience with surgical treatment for adductor spasmodic dysphonia. In this procedure, the thyroarytenoid branch and lateral cricoarytenoid branch of recurrent laryngeal nerve is selectively denervated unilaterally, and its distal nerve stump of thyroarytenoid branch is reinnervated with branch of the usa cervicalis nerve. And lateral cricoarytenoid muscle partial myotomy was done unilaterally. After 6 months of treatment, voice fluency had improved and no period of breathiness or dysphagia was noted.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.21 no.1
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• pp.27-31
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• 2010

Mild vocal fold hypomobility is a common finding of which clinical significance is incompletely understood. Recently, electrophysiologic investigations have shown that vocal fold hypomobility is a continuum of neurogenic dysfunction ; partial denervation (paresis), complete denervation (paralysis), and variable degrees and patterns of reinnervation. Despite a sound pathophysiological basis for its existence, interest in and acceptance of the diagnosis of vocal fold paresis is relatively recent. Vocal fold paresis may be a relatively common and often overlooked condition that can be difficult to diagnose since laryngoscopy does not reliably distinguish innocent laryngeal asymmetry from hypomobility caused by paresis. Although not entirely free from error, laryngeal electromyography seems to hold more promise as a means of reliable diagnosis than laryngoscopy, and should be employed systematically in the evaluation of suspected paresis. The means to help most patients with paresis already exists in the repertoire of interventions developed to treat paralysis. However, since the vocal fold retains substantial movement, more conservative treatment strategy is recommended as a first line of treatment. The authors reviewed the representative reports of vocal fold paresis and summarized the controversies and consensus regarding the vocal fold paresis.

• International Journal of Oral Biology
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• v.40 no.3
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• pp.127-133
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• 2015

The salivary gland undergoes complex process of growth and differentiation of the branching morphogenesis of ductal system during the prenatal and early postnatal periods which are regulated by various elements in the extracellular matrix. Extracellular matrix metalloproteinase inducer (EMMPRIN) is a cell adhesion molecule. In the present study, localization and expression of EMMPRIN in development and effects of chorda-lingual denervation and cyclosporine A (CsA) treatment on the EMMPRIN expression were investigated. Immunohistochemistry, RT-PCR and Western blot were used to determine expression level. Immunohistochemistry revealed that EMMPRIN was localized specifically in the cytoplasm of ductal cells, not acini of the submandibular gland all the postnatal periods. At prenatal day 18, when the formation of ducts was not definite, no immunoreactivity was observed. Both Western blot and RT-PCR analyses revealed that EMMPRIN expression was maintained up to postnatal day 7, decreased after postnatal day 10. The EMMPRIN expression was upregulated by the surgical denervation of the chorda-lingual nerve in the gland as well as by the CsA treatment. The present study suggests that EMMPRIN is a crucial molecule for maintaining physiological functions of the salivary gland.

• Annals of Clinical Neurophysiology
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• v.2 no.2
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• pp.125-129
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• 2000

Benign monomelic amyotrophy(BMA) is an uncommon cause of progressive mildly disabling atrophy and weakness of a limb. It predominantly affects the distal upper limb of young men. I present two men with BMA of the lower extremities. Although the disorder seemed clinically confined to a arm or leg, I confirmed by electromyography evidence of denervation in the other extremities. I reviewed the literatures and discuss the differential diagnosis. BMA is a diagnosis of exclusion that requires consideration in men with unilateral arm or leg atrophy and weakness.

• The Korean Journal of Pain
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• v.29 no.2
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• pp.78-85
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• 2016

Loin pain haematuria syndrome (LPHS) is an uncommon clinical entity that has divided renal physicians, pain practitioners, and even psychiatrists since its initial description. A relative paucity of data exists regarding the condition, with best practice guidelines lacking amid the existing threads of anecdotal experiences and variable follow-up observations. The aim of this article was to review the cumulative published experience of pain relief strategies for LPHS.

• Journal of Chest Surgery
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• v.9 no.1
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• pp.20-26
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• 1976

Author has performed experimental study on hemodynamic changes of lung following radical hilar stripping and contralateral pulmonary artery ligation. In view of hemodynamic changes in group 1 (right pulmonary artery ligation only) and group 2(left hilar stripping+right pulmonary artery ligation). group 2 showed remarkable decrease rate in oxygen uptake (P<0.001) and total pulmonary blood flow(P<0.001), and the more increase rate in mean pulmonary artery pressure(P<0.02) and total pulmonary vascular resistance (P<0.001). Meanwhile, the decrease percent of left lung vascular resistance was lower than group 1(P<0.001). The hemodynamic changes in group 1 returned to control range two weeks later. In the group 2, two dogs were expired as a result of atelectasis and pulmonary hypertension. Among allying 8 dogs, five months after operation, follow up studies performed in two dogs, which showed normal pulmonary hemodynamics similar to preoperative data. The altered blood gas values and decreased oxygen uptake are more remarkable in denervated lung, which may due to pulmonary hypertension and partly retained more secretion in bronchial trees than usual. Important factors of raising pulmonary vascular resistance and pulmonary artery pressure are considered as the increased blood flow to remaining left lung and dysfunction of pulmonary vascular bed to accept the increased blood flow after denervation. Loss of nerve innervation had a influence, to some extent, to the decrease of oxygen uptake and the increase of pulmonary vascular resistance and pulmonary artery pressure. There can be little question that denervation does impair the pulmonary hemodynamics, however, intact pulmonary nerve innervation is not absolutely essential for survival of the animal.

• Archives of Plastic Surgery
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• v.32 no.4
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• pp.403-407
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• 2005

Following a transverse rectus abdominis musculocutaneous(TRAM) flap breast reconstruction, denervated state of the flap causes the flap skin prone to thermal injury, calling for special attention. During the last 5 years, 69 breast reconstruction with 72 free TRAM flaps, were performed. Four out of thesse 69 patients sustained burn injury. Heat sources were a warm bag(n=2), heating pad(n=1) and warming light (n=1). The thermal injuries occured from 2 days to 3 months following the reconstruction. Three patients healed with conservative treatment, but one patient required debridement and skin graft. Initially 3 out of 4 patients with the burn had shown superficial 2nd degree burn with small blebs or bullae. However all 4 patients healed with scars. Mechanism of burn injuries of the denervated flap are known to be resulting from; 1) loss of behavioral protection due to denervation of flap with flap elevation and transfer, 2) loss of autonomic thermoregulatory control with heat dissipation on skin flap vasculature contributing to susceptibility of burn injury. 3) changes of immunologic and normal inflammatory response increasing thromboxane, and a fall in substance P & NGF (nerve growth factor). Including the abdominal flap donor site, sensory recovery of the reconstructed breast varies individually from 6 month even to 5 years postoperatively. During this period, wound healing is delayed, resulting in easier scarring compared to that observed in the sensate skin. Patients should be carefully informed and warned of possible burn injuries and taught to avoid exposure to heat source at least until 3 years postoperatively.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.683-693
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• 2001

This study was attempted to investigate the effect of raclopride, a dopamine $D_2$ receptor antagonist, on renal function in dog. Raclopride (70-220$\mu\textrm{g}$/kg), when given intravenously, Produced antidiuresis along with the decrease in free water clearance ( $C_{H_2O}$), urinary excretion of sodium and potassium ( $E_{Na}$ , $E_{K}$), partially decreased osmolar clearance ( $C_{osm}$) and increased reabsorption rates of sodium and potassium in renal tubules ( $R_{Na}$ , $R_{K}$). Raclopride administered into a renal artery did not influence on renal function in small doses (10 and 30$\mu\textrm{g}$/kg), whereas exhibited the decrease of urine volume (Vol) and $C_{H_2O}$ both in experimental and control kidney in much dose (100$\mu\textrm{g}$/kg), at this time, the decreased rates of both Vol. and $C_{H_2O}$) were more prominent in control kidney rather than that elicited in experimental kidney, and then only via was decreased in control kidney but increased in experimental kidney. Raclopride administered via carotid artery (30-200$\mu\textrm{g}$/kg) did not influence at all on renal function. Antidiuretic action induced by raclopride given intravenously was not affected by renal denervation. Raclopride given into carotid artery was little effect on renal function without relation to renal denervation. Above results suggest that raclopride produces antidiuresis by potentiation of antidiuretic hormone (ADH) action in blood without increase of ADH secretion in posterior pituitary gland, it is not related to renal nerve function in dogs.ogs.s.

• Clinical Pain
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• v.18 no.2
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• pp.88-91
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• 2019

Unexplained pain and weakness, i.e., without obvious predisposing factors, are often encountered by physiatrists and efforts should be made to determine the cause. A 63-year-old male presented with radiating pain in his right arm and mild weakness of the right hand. An electrodiagnostic examination revealed distal symmetric sensory polyneuropathy in the upper and lower extremities, and denervation potentials in the forearm muscles, which were inconsistent with the cervical spine MRI images and symptoms. A predisposing undiscovered disease was revealed, i.e., squamous cell carcinoma in the lung; brain metastasis affecting the left primary motor cortex was also detected. Therefore, we concluded that the pain and weakness were related to paraneoplastic syndrome and brain metastases of the hand knob. The observed denervation potentials were characterized as trans-synaptic changes in the brain metastasis. This case highlights the importance of unexplainable focal pain and weakness in the increasing prevalence of cancer.