• Clinics in Shoulder and Elbow
• /
• v.6 no.2
• /
• pp.108-114
• /
• 2003

The shoulder is a complex area which makes it vulnerable to painful pathologic processes. Chronic shoulder pain has become more common recently due to increased use of computers and a ,generally more sedentary life style among most people . Trigger point injection and neural blockade are useful for the management of chronic shoulder pain which has not improved with conservative treatment. Published articles concerning trigger point injection or neural blockade for chronic shoulder pain were reviewed to evaluate promising methods. If we are careful to remain aware of the details and complications in addition to adhering to effective treatments, these should be good armamentarium for doctors enthusiastic about the management of chronic shoulder pain.

• The Korean Journal of Pain
• /
• v.9 no.1
• /
• pp.271-274
• /
• 1996

Epidural hematoma during anticoagulant therapy is a rare complication of central neural blockade, but it may result in serious neurologic sequelae. A 61-year-old male receiving warfarin due to heart failure was referred to the pain clinic for control of severe herpetic neuralgia. Epidural catheterization was done at $T_{8-9}$ interspace. At that time, PT and aPTT were extremely prolonged. The next morning, severe back pain, motor paralysis and urinary difficulty developed. On spine MRI, epidural hematoma was detected at $T_{8-9}$ interspace. Four days later, he died due to underlying diseases. Central neural blockade in patient with anticoagulant therapy is contraindicated in most cases. If is undertaken, close observation of patients's neurologic functions and monitoring of coagulation profiles(PT, aPTT, etc) are necessary. If epidural hematoma develops, early surgical decompression is mandatory.

• The Korean Journal of Physiology
• /
• v.29 no.1
• /
• pp.91-102
• /
• 1995

The role of neurohumoral mechanisms in the regulation of cardiovascular functions and the effects of ethanol (EOH) on these mechanisms were examined in hemorrhaged conscious Wistar rats. The rats were bled at a constant rate (2 ml/kg/min) through the femoral artery until mean arterial pressure (MAP) was reduced by 30 mmHg. We studied the responses to hemorrhage 1) under normal conditions (Normal), and after pretreatments with 2) neural blockade (NB), pentolinium, 3) arginine vasopressin V1-receptor antagonist (AVPX) + NB, 4) angiotensin II ATI-receptor antagonist (AngIIX) + NB, 5) combined humoral blockade (HB), and 6) neurohumoral blockade. Intravenous administration of 30% EOH (6.3 ml/kg) attenuated the baroreceptor reflex sensitivity, and enhanced the depressor action of AngIIX. During hemorrhage, NB produced a faster fall ill MAP than Normal both in the saline and EOH groups. However, HB accelerated the rate of fall in MAP only in the EOH group. The recovery from hemorrhagic hypotension was not different between NB and Normal rats, but was attenuated in HB rats in the saline group. Under NB, AngIIX, but not AVPX, retarded the recovery rate compared with NB alone. EOH attenuated the recovery of MAP after hemorrhage in Normal rats, but completely abolished the recovery in HB rats. We conclude that 1) the maintenance of MAP during hemorrhage is mediated almost entirely by the autonomic functions, 2) angiotensin II plays an important role in the recovery from hemorrhagic hypotension, but AVP assumes little importance, 3) AVP release largely depends on the changes in blood volume, whereas renin release depends on the changes in blood pressure rather than blood volume, and 4) EOH increases the dependence of cardiovascular regulation on angiotensin II and impairs the recovery from hemorrhagic hypotension through the attenuation of autonomic functions.

• Biomolecules & Therapeutics
• /
• v.28 no.5
• /
• pp.389-396
• /
• 2020

Valproic acid is a clinically used mood stabilizer and antiepileptic drug. Valproic acid has been suggested as a teratogen associated with the manifestation of neurodevelopmental disorders, such as fetal valproate syndrome and autism spectrum disorders, when taken during specific time window of pregnancy. Previous studies proposed that prenatal exposure to valproic acid induces abnormal proliferation and differentiation of neural progenitor cells, presumably by inhibiting histone deacetylase and releasing the condensed chromatin structure. Here, we found valproic acid up-regulates the transcription of T-type calcium channels by inhibiting histone deacetylase in neural progenitor cells. The pharmacological blockade of T-type calcium channels prevented the increased proliferation of neural progenitor cells induced by valproic acid. Differentiated neural cells from neural progenitor cells treated with valproic acid displayed increased levels of calcium influx in response to potassium chloride-induced depolarization. These results suggest that prenatal exposure to valproic acid up-regulates T-type calcium channels, which may contribute to increased proliferation of neural progenitor cells by inducing an abnormal calcium response and underlie the pathogenesis of neurodevelopmental disorders.

• Journal of The Korean Dental Society of Anesthesiology
• /
• v.13 no.3
• /
• pp.71-79
• /
• 2013

Local pain management is the most critical aspect of patient care in dentistry. Local anesthesia is a reversible blockade of nerve conduction in an applied area that produces loss of sensation. The chemical agents used to produce local anesthesia stabilize neuronal membranes by inhibiting the ionic fluxes required for the propagation of neural impulses. Proper local anesthesia permits the dental surgeon to perform the necessary surgical procedure in a careful, gentle fashion that will be less stressful for both the operator and the patient. The improvements in agents for local anesthesia are probably the most significant advances that have occurred in dental science. Today's anesthetics are safe, effective, and can be administered with insignificant soft tissue damage and minimal concerns for allergic reactions. This article reviews the widely used local anesthetic agents for obtaining local anesthesia, and also discusses some frequently seen complications.

• The Korean Journal of Pain
• /
• v.29 no.3
• /
• pp.158-163
• /
• 2016

Background: Phenol and alcohol have been used to ablate nerves to treat pain but are not specific for nerves and can damage surrounding soft tissue. Lidocaine at concentrations > 8% injected intrathecal in the animal model has been shown to be neurotoxic. Tests the hypothesis that 10% lidocaine is neurolytic after a peri-neural blockade in an ex vivo experiment on the canine sciatic nerve. Methods: Under ultrasound, one canine sciatic nerve was injected peri-neurally with 10 cc saline and another with 10 cc of 10% lidocaine. After 20 minutes, the sciatic nerve was dissected with gross inspection. A 3 cm segment was excised and preserved in 10% buffered formalin fixative solution. Both samples underwent progressive dehydration and infusion of paraffin after which they were placed on paraffin blocks. The sections were cut at $4{\mu}m$ and stained with hemoxylin and eosin. Microscopic review was performed by a pathologist from Henry Ford Hospital who was blinded to which experimental group each sample was in. Results: The lidocaine injected nerve demonstrated loss of gross architecture on visual inspection while the saline injected nerve did not. No gross changes were seen in the surrounding soft tissue seen in either group. The lidocaine injected sample showed basophilic degeneration with marked cytoplasmic vacuolation in the nerve fibers with separation of individual fibers and endoneurial edema. The saline injected sample showed normal neural tissue. Conclusions: Ten percent lidocaine causes rapid neurolytic changes with ultrasound guided peri-neural injection. The study was limited by only a single nerve being tested with acute exposure.

• Biomolecules & Therapeutics
• /
• v.26 no.5
• /
• pp.439-445
• /
• 2018

T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and $GSK3{\beta}$-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.

• The Korean Journal of Pain
• /
• v.9 no.2
• /
• pp.415-418
• /
• 1996

The first reported the neural blockade of ganglion impar for pain control of perineal pain in 1990 by Plancarte and his fellows. they used 6ml of 10 percent phenol. but the point of issues, same as other neurolytics, are that it is impossible to check and control its spreading, so it might be possible to destruct the coccygeal plexus and sacral nerve, and also it has only short action time. Because of these problems, it could be very dangerous to attempt this procedure especially not for relieving the pain on cancer terminal patient, but for the sympathectomy of ganglion impar on the other purpose. We used the RF generator which had the control ability to point out the destructive lesion accurately. inserted We made the small burr hole on the sacrum near the sacrococcygeal junction directly, through the hole, and performed thermocoagulation to the ganglion impar.

• The Korean Journal of Pain
• /
• v.13 no.2
• /
• pp.247-250
• /
• 2000

Recently, some authors reported that discogenic low back pain should be regarded as a referred pain in respect of neural pathway. The afferent pathways of discogenic low back pain is transmitted mainly by sympathetic afferent fibres from the sinuvertebral nerves in the second lumbar nerve root. This pain arises from the lumbar intervertebral discs, and it had been transmitted mainly through the sympathetic afferent fibres contained in the second lumbar spinal nerve root. Second lumbar dermatome corresponds to the low back area. We experienced a case of low back pain which could not be controlled by conventional therapy and progressed wax and wane. The CT finding showed bulging disc between $L_4$ and $L_5$ and spinal stenosis in $L_4$ area. And epiduroscopic feature showed severe adhesion in $L_4$, $L_5$ and $S_1$. After we blocked $L_2$ root, pain score decreased 10 to 2. Therefore, the $L_2$ root block may be a useful diagnostic procedure as well as provide therapeutic value.

• The Korean Journal of Physiology and Pharmacology
• /
• v.13 no.6
• /
• pp.461-467
• /
• 2009

The auditory cortex (A1) encodes the acquired significance of sound for the perception and interpretation of sound. Nitric oxide (NO) is a gas molecule with free radical properties that functions as a transmitter molecule and can alter neural activity without direct synaptic connections. We used whole-cell recordings under voltage clamp to investigate the effect of NO on spontaneous GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons preserving functional presynaptic nerve terminals. GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) in the A1 were completely blocked by bicuculline. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reduced the GABAergic sIPSC frequency without affecting the mean current amplitude. The SNAP-induced inhibition of sIPSC frequency was mimicked by 8-bromoguanosine cyclic 3',5'-monophosphate, a membrane permeable cyclic-GMP analogue, and blocked by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger. Blockade of presynaptic $K^+$ channels by 4-aminopyridine, a $K^+$ channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic $Ca^{2+}$ channels by $Cd^{2+}$, a general voltage-dependent $Ca^{2+}$ channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. These findings suggest that NO inhibits spontaneous GABA release by activation of cGMP-dependent signaling and inhibition of presynaptic $Ca^{2+}$ channels in the presynaptic nerve terminals of A1 neurons.