OBJECTIVE: We investigated the useful electrodiagnostic indicators and the extent of retrograde degeneration (RD) in carpal tunnel syndrome (CTS). METHOD: We measured median mixed nerve action potentials (MMNAP) in 26 CTS and 37 normal hands by recording at the elbow and stimulating 0, 3, 6 and 9 cm proximal to the distal wrist crease. The 3 MMNAP parameters such as amplitude, latency and conduction velocity were compared between CTS and control group. The most useful indicator was compared between subgroups of CTS (mild and severe) and control group. RESULTS: The amplitudes of all MMNAPs in CTS group, except stimulating 9 cm proximal to the wrist (MA9), were significantly smaller than those in control group (p<0.05). MA9 in severe CTS subgroup, not mild subgroup, was significantly smaller than that in control group (p<0.05). CTS and control group were not significantly different in the MMNAP latencies, except stimulating 9 cm proximal to the wrist (p<0.05), and in the MMNAP conduction velocity, except stimulating in 0 cm to 3 cm segment proximal to the wrist. CONCLUSION: The amplitude of MMNAP in forearm can be the most useful indicator of RD in CTS, and the conduction velocity, a less useful indicator. We believe that RD progresses as the severity of CTS increases, and dose beyond 9 cm proximal to the distal wrist crease.
Action Potentials ; Carpal Tunnel Syndrome* ; Elbow ; Forearm ; Hand ; Retrograde Degeneration* ; Wrist

OBJECTIVE: To find out the incidence of reduced median conduction velocity of forearm (MNCV-F) in carpal tunnel syndrome (CTS) and to compare clinical and electrophysiologic characteristics of CTS with reduced MNCV-F and to observe the changes of reduced MNCV-F after carpal tunnel release. METHOD: One hundred and fifty nine hands with CTS are divided into two groups; MNCV-F of 50 m/sec and above as group I and that of below 50 m/sec as group II. For the electrophysiologic comparison, median sensorimotor distal latency, peak-to-peak amplitudes and abnormal spontaneous activity of abductor pollicis brevis were observed and for clinical comparison, sensorimotor symptoms, Phalen and Tinel sign were observed. Twenty four hands which had successful carpal tunnel release were examined for the changes of MNCV-F. RESULTS: The hands with reduced MNCV-F were 29 among 159 hands. Sensorimotor distal latency were significantly prolonged and sensorimotor amplitudes also significantly reduced in group II. Sensory change and Phalen signs were more frequently observed in group II. MNCV-F in group I had not changed after carpal tunnel release, but MNCV-F in group II was improved significantly. The changes MNCV-F in group II were much delayed than the improvement of parameters of distal conduction studies. CONCLUSION: The incidence of reduced MNCV-F in CTS was 18.24%. Patients with reduced MNCV-F had more severe CTS both electrophysiologically and clinically. Reduced MNCV-F had improved significantly, but there was significant time gap between the electrophysiologic improvements of distal and proximal portions of nerve. This findings may suggest that retrograde degeneration may play a partial role in reduced forearm motor nerve conduction velocity of the median nerve in CTS.
Carpal Tunnel Syndrome* ; Forearm* ; Hand ; Humans ; Incidence ; Median Nerve* ; Neural Conduction ; Retrograde Degeneration

BACKGROUND: To understand the fundamentals of neural tissue injury, experiments on the nano-structured nerve system of animals are essential. This study was designed to reveal the nanostructure changes of an isolated ligatured rat sciatic nerve using the synchrotron small-angle X-ray scattering (SAXS) technique. METHODS: Male Sprague-Dawley rats (weighing approximately 250 grams) were used in this study. The SAXS patterns of 1 week after ligatured nerves (N = 5) and the normal sciatic nerves (N = 5) for the control were acquired after extracted approximately 15 mm before the experiment. Experiments were conducted at the 4C1 beam line at the Pohang Accelerator Laboratory in Korea. The exposure time was 60 sec, and 8 to 12 images per sample were acquired in 0.5 mm intervals, including the regions above, around and below the ligatured position. RESULTS: The periodic peaks of the myelin sheath and the interfibrillar space of collagen completely disappeared at the ligatured position. Farther from the ligatured point, weak and quite different SAXS patterns were observed for the myelin sheath and interfibrillar space. However, the collagen fiber peaks appeared at all positions, although they were weaker near the ligatured position. CONCLUSIONS: The ligature treatment totally destroyed the myelin sheath and interfibrillar space of collagen. In addition, retrograde degeneration developed 2 mm above the ligatured site. The myelin sheath and interfibrillar space of collagen were damaged 6 mm below the ligatured site. However, the collagen fiber structure was not significantly affected by the ligature, indicating a much different structural organization.
Animals ; Collagen ; Gyeongsangbuk-do ; Humans ; Korea ; Ligation ; Male ; Myelin Sheath ; Nanostructures ; Rats* ; Rats, Sprague-Dawley ; Retrograde Degeneration ; Sciatic Nerve* ; Synchrotrons*

Slowing in forearm median nerve conduction in patients with carpal tunnel syndrome(CTS) has been described. But the cause of slowing is still unclear whether it is related to a technical artifact on electrodiagnostic appr oach or pathophysiologic changes in the proximal segment of median nerve. To investigate the possible retrograde degeneration of median nerve in the forearm segment(wrist to elbow) in patients with known carpal tunnel syndrome, the median nerve conduction studies were performed in 23 normal persons as control and 25 patients with carpal tunnel syndrome. To evaluate the median nerve conductions in the forearm, the recording bar-electrode were placed at the volar aspect of the wrist and stimulating electrodes were applied at the elbow area. The mixed nerve action potentials and conduction velocities were measured. The median mixed nerve action potential(FNAP) amplitudes recorded at the wrist and motor nerve conduction velocity(MMCV) in patients with carpal tunnel syndrome patients were significantly reduced compared to those of control group(p<0.05). However, the median mixed nerve conduction velocity(FNCV) was not reduced significantly. The median mixed nerve action potential amplitudes demonstrated positive correlation with the decrease of motor and sensory action potential amplitudes and velocities. This result suggests that the retrograde degeneration progresses as the carpal tunnel syndrome progresses and the retrograde degeneration may play a major role in reduced motor nerve conduction velocity of the median nerve in the forearm. We propose that FNAP amplitude and MMCV might be used to evaluate the severity of retrograde degeneration in patients with carpal tunnel syndrome.
Action Potentials ; Artifacts ; Carpal Tunnel Syndrome* ; Elbow ; Electrodes ; Forearm ; Humans ; Median Nerve ; Neural Conduction ; Retrograde Degeneration ; Wrist

BACKGROUND: The terminal destruction of the striatal dopaminergic axon can produce the retrograde degeneration of nigral dopaminergic neurons. An analyses of the postsynaptic dopamine D1 & D2 receptors and the DOPAC/DA level, revealed that this model mimics the early course of Parkinson's disease in humans. We evaluated the time course of the retrograde dopaminergic neuronal degeneration and the pattern of dopaminergic neuronal loss in the substantia nigra after various doses of 6-hydroxydopamine (6-OHDA) injections in the striatum of rats. METHODS: Different doses of 6- OHDA (0.0, 1.25, 2.5, 5, 10 ug/ul in 3.5 ul of saline) were unilaterally injected into the right striatum of rats using a stereotaxic frame. Structural and functional deficits were quantified and compared using apomorphine-induced rotations and tyrosine hydroxylase-immunoreactive (TH-IR) cell numbers in the substantia nigra pars compacta (SNpc) at 3, 6, 9 weeks after lesioning. RESULTS: Striatal 6-OHDA lesions produced dose-dependent decreases in TH-IR cell numbers in SNpc at 3 weeks (-3.8%, 17.9%, 41.2%, 58.5%, 69.9% cell loss compared with the contralesional side respectively), where the ventrolateral portion of the SNpc were more affected. As time progressed, nigral cell loss was significantly increased in all dosage groups and the lesion extended to the medial side of the SNpc and the ventral tegmental area. Apomorphine-induced rotations did not correlate well with nigral TH-IR cell loss. CONCLUSIONS: Intrastriatal injections of 6-OHDA, results in time-dependent and dose-dependent progressive degeneration of nigral dopaminergic neurons. We conclude that this rat model can be useful for the evaluation of further neuroprotective and neurotrophic therapies.
Animals ; Apoptosis ; Axons ; Cell Count ; Cell Death ; Dopamine* ; Dopaminergic Neurons ; Humans ; Models, Animal ; Oxidopamine* ; Parkinson Disease ; Rats* ; Retrograde Degeneration ; Substantia Nigra ; Tyrosine ; Ventral Tegmental Area

After general anesthesia with intra-venous pentothal sodium, half of the optic nerve was sectioned on both sides with special care to preserve vessels of the optic nerve. To observe retrograde degeneration of the optic nerve, the animals were sacrifised 1, 2, 3, 4, and 5 weeks after nene section. Eye ball and optic nerve was removed and fixed in 10% formalin solution. Eye baIl and optic nerve was cut and stained with Hematoxylin Eosin and Luxol Fast Blue stain for light microscopic examination. Until 2 weeks. no significant pathologic changes were observed. Specimens 3 weeks after optic nerve section showed decreased retinal ganglion cell numbers and gliosis and myelin loss in optic nerve and these changes were intensified on 4th and 5th weeks specimens. So, I observed the followings: 1. Retrograde degeneration of the optic nerve occurred simultaneously through out the length of the nerve fibers instead progressively from the cut end toward the ganglion cell. 2. The retrograde degeneration of the optic nerve started 3 weeks after section.
Anesthesia, General ; Animals ; Atrophy* ; Eosine Yellowish-(YS) ; Formaldehyde ; Ganglion Cysts ; Gliosis ; Hematoxylin ; Myelin Sheath ; Nerve Fibers ; Optic Nerve* ; Rabbits* ; Retinal Ganglion Cells ; Retrograde Degeneration ; Sodium ; Thiopental

The ultrastructural changes of sciatic nerve and immunohistochemical changes of beta-catenin, PCNA, substance P were studied at the proximal segment of rat sciatic nerve after compression injury. We used 90 Sprague Dawley rats and the sciatic nerve compressed using silicon tube. We divided experimental groups which were the compression group for 1 hour (1C), for 2 hours (2C), and for 3 hours (3C), the release group for 1 day (1C1R) and 3 days (1C3R) after the compression for 1 hour, the release group for 1 day (2C1R) and 3 days (2C3R) after the compression for 2 hours, the release group for 1 day (3C1R) and 3 days (3C3R) after the compression for 3 hours. The rats were sacrified and took the sciatic nerve specimen. The specimens were investigated under the light microscope after hematoxylin & eosin, toluidin blue, and immunohistochemical stainings. In the H & E finding, the axon of the 1C disappeared, but recovered at the 1C3R. The part of nerve fibers at the 2C were swollen, but began to be partially recovered at 2C3R. Most nerve fibers were enlarged at the 3C, but markedly decreased at the 3C1R. The beta-catenin reaction disappeared at the 1C, but almost recovered at the 1C3R. This reaction of the 2C disappeared in the large fibers, but began to be recovered in the small fibers at the 2C1R. This reaction of the 3C disappeared in the large fibers, but began to be recovered at the 3C1R and 3C3R. The PCNA reaction prominently appeared at the 1C3R and 2C3R, the more prominent reaction at the 3C1R, and markedly increased reaction at the 3C3R. The substance P reaction of the 1C1R was mild positive, and the 2C1R and 3C1R were strong positive. In the toluidin blue staining, the myelin sheaths near the perineurium began to be thickened at the 1C, but almost recovered at the 1C3R. Many myelin sheaths became to be very thickened at the 2C and 3C, but almost recovered at the 2C3R and 3C3R. In the electron microscopic findings, the myelin sheaths of the 1C underwent the demyelination with the separated lamellae and the increase microtubules. At the 1C3R, the axolemma was attached on the myelin sheath and the axon was recovered. the myelin sheaths of the 2C underwent the demyelination with the separated axolemma. At the 2C1R, the myelin sheath was recovered by the developing Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. At the 2C3R, the myelin sheath tended to be recovered by the increased rough endoplasmic reticulum and mitochondria of Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. The myelin sheaths of the 3C began to be underwent severe demyelination from the middle portion of the sheath and the vacuolization of intraaxonal mitochondria. At the 3C1R, the myelin sheaths were recovered and contained many extended microtubules, mitochondria, and small granules. At the 3C3R, severe demyelinated nerve fibers were recovered by increasing microtubules. The proximal retrograde degeneration of sciatic nerve by the acute compression appeared the loss of the axons and the swelling of nerve fibers. The beta-catenin reaction was disappeared by the compression, but recovered by releasing. This reaction may be played a important role of the recover of demyelination. The PCNA reaction of Schwann cells was increased by the nerve compression. In the substance P finding, the pain after the compression appeared at the 1 day after releasing. Electron microscopic changes after sciatic nerve compression were the demyelination, the separated lamellae and the increase of intraaxonal microtubules. After releasing, the nerve fibers were recovered by developing Schwann cell, the intraaxonal mitochondria, and the transported granules through extending microtubules.
Animals ; Axons ; beta Catenin* ; Demyelinating Diseases ; Endoplasmic Reticulum, Rough ; Eosine Yellowish-(YS) ; Hematoxylin ; Microtubules ; Mitochondria ; Myelin Sheath ; Nerve Fibers ; Peripheral Nerves* ; Proliferating Cell Nuclear Antigen* ; Rats* ; Rats, Sprague-Dawley ; Retrograde Degeneration ; Schwann Cells ; Sciatic Nerve ; Silicones ; Substance P*

Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.
Animals ; *Apoptosis ; Axonal Transport ; Disease Models, Animal ; In Situ Nick-End Labeling ; *Intraocular Pressure ; Male ; Ocular Hypertension/*complications ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*pathology ; Retrograde Degeneration/etiology ; Sclera/blood supply

OBJECTIVE: To investigate the role of neuropeptide Y(NPY) positive interneurons in the generation and compensation of temporal lobe epilepsy. METHODS: Pilocarpine-induced rat model was founded. Immunohistochemistry was used to observe the number changes and axonal sprouting of NPY interneurons at different time points in the hippocampus of rats. RESULTS: After lithium-chloride and pilocarpine administration, 92.9% rats were induced status epilepticus (SE) successfully, and the mortality rate was 19.2%. In the experimental group, the number of NPY positive neurons decreased in the hilus of the hippocampus, and was least on 7 d after the SE (P<0.01). In the chronic phase, the number of hilus NPY neurons partially recovered, but was still less than the number in the control group on 60 d after the SE (P<0.05). No evident changes of the number of NPY neurons existed in CA domains (P>0.05) except the loss of them in CA3 area on 7 d after the SE (P>0.05). Increased NPY positive fibers could be seen in the molecular layer of the dentate gyrus on 30 d after the SE. CONCLUSION NPY interneurons have different sensitivities to the injuries induced by seizures at different time points and domains. Loss of NPY interneurons plays an important role in the generation of temporal lobe epilepsy, while axonal sprouting of them may play a significant role in the compensation of temporal lobe epilepsy.
Animals ; Epilepsy, Temporal Lobe ; chemically induced ; pathology ; Hippocampus ; metabolism ; pathology ; Interneurons ; metabolism ; pathology ; Male ; Neuropeptide Y ; metabolism ; Pilocarpine ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Retrograde Degeneration ; pathology ; Status Epilepticus ; chemically induced ; pathology