Hand size affects branching of the deep ulnar nerve and deep palmar arch.

PURPOSE: Understanding the anatomy of the deep neurovascular structures of the hand is essential in surgical planning. There is a lack of literature regarding hand size and its influence in branching variation and the distances between branches of various neurovascular structures. Our study quantifies the variation in branching distances of the deep ulnar nerve and deep palmar arch branches. METHODS: Twenty-five fresh-frozen cadaveric hands were dissected. Each branch of the deep ulnar nerve and deep palmar arch was identified. The distance from the most distal portion of the pisiform to the proximal aspect of the branch was measured. The relationship between the length of the third metacarpal and the distance of each branch from the pisiform was examined. RESULTS: There was no relationship between branching differences in the deep ulnar nerve and the length of the third metacarpal. There was a significant association between the length of the third metacarpal and the second, third, and fourth branches of the deep palmar arch (p < 0.05). CONCLUSIONS: Our study found a significant association between the branching distances of the second, third, and fourth branches of the deep palmar arch and hand size as measured by the length of the third metacarpal.

Histological Assessment of Wallerian Degeneration of the Rat Tibial Nerve Following Crush and Transection Injuries.

BACKGROUND: Wallerian degeneration (WD) following peripheral nerve injury (PNI) is an area of growing focus for pharmacological developments. Clinically, WD presents challenges in achieving full functional recovery following PNI, as prolonged denervation of distal tissues for an extended period of time can irreversibly destabilize sensory and motor targets with secondary tissue atrophy. Our objective is to improve upon histological assessments of WD. METHODS: Conventional methods utilize a qualitative system simply describing the presence or absence of WD in nerve fibers. We propose a three-category assessment that allows more quantification: A fibers appear normal, B fibers have moderate WD (altered axoplasm), and C fibers have extensive WD (myelin figures). Analysis was by light microscopy (LM) on semithin sections stained with toluidine blue in three rat tibial nerve lesion models (crush, partial transection, and complete transection) at 5 days postop and 5 mm distal to the injury site. The LM criteria were verified at the ultrastructural level. This early outcome measure was compared with the loss of extensor postural thrust and the absence of muscle atrophy. RESULTS: The results showed good to excellent internal consistency among counters, demonstrating a significant difference between the crush and transection lesion models. A significant decrease in fiber density in the injured nerves due to inflammation/edema was observed. The growth cones of regenerating axons were evident in the crush lesion group. CONCLUSION: The ABC method of histological assessment is a consistent and reliable method that will be useful to quantify the effects of different interventions on the WD process.

Pudendal nerve stretch reduces external urethral sphincter activity in rats.

PURPOSE: Most animal models of stress urinary incontinence simulate maternal injuries of childbirth since delivery is a major risk factor but they do not reproduce the nerve stretch known to occur during human childbirth. We hypothesized that pudendal nerve stretch produces reversible dysfunction of the external urethral sphincter. MATERIALS AND METHODS: Female virgin Sprague-Dawley® rats were anesthetized with urethane. Bilateral pudendal nerve stretch or sham injury was performed for 5 minutes. External urethral sphincter electromyography and leak point pressure were recorded immediately before and after, and 10, 30, 60 and 120 minutes after pudendal nerve stretch. Post-pudendal nerve stretch results were compared to prestretch values and to values in sham injured animals. The pudendal nerves underwent qualitative histological assessment. The nucleus of Onuf was evaluated by immunohistochemistry and polymerase chain reaction for ß-APP and c-Fos expression as markers of neuronal activity and injury. RESULTS: A total of 14 rats underwent bilateral pudendal nerve stretch (9) or sham injury (5). Each nerve was stretched a mean ± SEM of 74% ± 18% on the left side and 63% ± 13% on the right side. Electromyography amplitude decreased significantly immediately after stretch compared to before stretch and after sham injury (p = 0.003) but it recovered by 30 minutes after stretch. There was no significant change in leak point pressure at any time. Two hours after injury histology showed occasional neuronal degeneration. ß-APP and c-Fos expression was similar in the 2 groups. CONCLUSIONS: Acute pudendal nerve stretch produces reversible electrophysiological dysfunction but without leak point pressure impairment. Pudendal nerve stretch shows promise in modeling injury. It should be tested as part of a multi-injury, chronic, physiological model of human childbirth injury.

Safety of local anesthetics administered intrathecally in diabetic rats.

OBJECTIVES: Although retrospective studies show the risk of neurological complications after spinal anesthesia with local anesthetics is small in diabetic patients, there is still concern about the safety of different local anesthetics in diabetics undergoing neuroaxial anesthesia. We examined block duration and histology of spinal cord and roots with intrathecal local anesthetics in diabetic rats. METHODS: Rats were made diabetic with streptozotocin injection. Blood glucose levels confirmed diabetes, and diabetic neuropathy was verified by tactile hypersensitivity. Diabetic and nondiabetic rats received four intrathecal injections at 3-4-day intervals of 0.75% bupivacaine, with/without 100 µg/mL epinephrine; and 2% lidocaine, with/without 100 µg/mL epinephrine, and duration of sensory (pinprick) and motor (toe-spreading reflex) response inhibition recorded. Four days after the last drug injection, histology of spinal cord and roots was performed. RESULTS: All streptozotocin rats became diabetic and had pronounced tactile allodynia. Intrathecal injection of local anesthetics showed longer duration of sensory and motor block in diabetic rats vs nondiabetics. Histology of caudal spinal cord showed no difference in neuropathology between diabetic and nondiabetic rats. Necrotic neurons were not seen in either group, and white-matter pathology involved less than 0.1% of fibers. Histology of the spinal roots also showed no difference in pathology between groups, and pathology involved less than 0.1% of fibers. Neuron somas in the dorsal root ganglia were normal. CONCLUSIONS: Duration of local anesthetic spinal block is longer in diabetic animals than in nondiabetics. However, there was no increased pathology of spinal cord, roots, or dorsal root ganglia.

Compound Motor Action Potentials During a Modest Nerve Crush.

Nerve crush injury results in axonotmesis, characterized by disruption of axons and their myelin sheaths with relative sparing of the nerve's connective tissue. Despite the widespread use of crush injury models, no standardized method for producing these lesions has been established. We characterize a crush model in which a narrow forceps is used to induce a modest and controlled compressive injury. The instantaneous compound motor action potential (CMAP) is monitored in situ and in real-time, allowing the characterization of neuromuscular response during and after injury. The tibial nerves of 11 anesthetized rats were surgically isolated. After the placement of electrodes, CMAPs were elicited and registered using a modular-data-acquisition system. Dumont-#5 micro-forceps were instrumented with a force transducer allowing force measurement via a digital sensor. Baseline CMAPs were recorded prior to crush and continued for the duration of the experiment. Nerve crushing commenced by gradually increasing the force applied to the forceps. At a target decrease in CMAP amplitude of 70%-90%, crushing was halted. CMAPs were continually recorded for 5-20 min after the termination of the crushing event. Nerves were then fixed for histological assessment. The following post-crush mean values from 19 trials were reported: peak CMAP amplitude decreased by 81.6% from baseline, duration of crush was 17 sec, rate of applied force was 0.03 N/sec, and maximal applied force was 0.5 N. A variety of agonal phenomena were evident post-lesion. Following the initial decrease in CMAP, 8 of 19 trials demonstrated a partial and transient recovery, followed by a further decline. Thirteen trials exhibited a CMAP amplitude near zero at the end of the recording. Twelve trials demonstrated a superimposed EMG background response during and after the crush event, with disappearance occurring within 4-8 min. Qualitative histology assessment at the lesion site demonstrated a correspondence between CMAP response and partial sparing of nerve fibers. By using a targeted decline in CMAP amplitude as the endpoint, researchers may be able to produce controlled, brief, and reproducible crush injuries. This model can also be used to test interventions aimed at enhancing subsequent regeneration and behavioral recovery.

Optimizing public health strategies for stroke education: need for a controlled trial.

This brief review examines certain strategies for increasing community awareness and recognition of the warning signs and symptoms of stroke. Attention should be given to the intended audience, especially at-risk groups. To enhance stroke literacy, a complete message should include the following 4 aspects: (1) a stroke is a serious medical problem that involves the blood supply to the brain, (2) all 5 approved warning signs and symptoms, (3) the many risk factors involved in stroke, and (4) the need to promptly call 911 for emergency services and treatment. Such knowledge could lead to improvement in the rapid arrival to an emergency room and promote optimal and timely medical treatment. With several educational paradigms and strategies in existence, we propose that more rigorous study of their comparative performance and utility is needed. In a preliminary survey, our own program, called "KNOW FIVE - STAY ALIVE," provided greater posttest knowledge compared with the "FAST" program and a National Institutes of Health brochure called "Know Stroke. Know the signs, Act in time."

Early behavioral and histological outcomes following a novel traumatic partial nerve lesion.

A new partial nerve lesion (PNL) model is needed to better simulate traumatic lesions seen clinically that result in both dysfunction and neuropathic pain. We assessed surgical variability and several outcome measures including histology during the acute postoperative period. A surgical lesion was created in the rat tibial nerve by removing a segment, later confirmed by myelinated axon counts. Variability in the model was assessed with four different outcome measures during the first postoperative week (n=24), with additional histological outcomes at 7 days (n=13) and pain testing at 21 days (n=9). At 7 days postoperative, the PNL resulted in a tibial functional index (TFI) of -41.3% distinct from a percent motor deficit (PMD) of -76.3%. However, the respective deficits from 2 to 7 days were similar. Either test could detect outliers, but PMD measurements had a lower coefficient of variation and were easier to perform and analyze. The deleted segment contained 26% of the myelinated axons and resulted in distal degeneration that was either 46% based on axon counts or 54% based on area. Replicated experiments confirmed the PMD, muscle atrophy, and formation of neuropathic pain. In conclusion, our partial lesion histologically progresses twofold during the first postoperative week with profound behavioral deficits involving both motor and sensory loss. These results based on sensitive and correlative outcome measures support the application of this novel model in experimental nerve lesion studies.

Gross anatomy of the brachial plexus sheath in human cadavers.

BACKGROUND AND OBJECTIVES: Major nerves and vessels run alongside each other in a "neurovascular bundle" kept together by connective tissue that is often referred to by anatomists, surgeons, and anesthesiologists as the "sheath." Our goal was to macroscopically demonstrate the brachial plexus sheath in embalmed and fresh cadaver dissections. METHODS: Systematic dissections were performed on 11 embalmed cadavers (6 females and 5 males), plus one fresh, unembalmed male cadaver. Dissections were started in the arm, and progressed proximally to the axilla and the supraclavicular area. Notes and photographic documentation were obtained. RESULTS: A sheath around the neurovascular bundle of the brachial plexus was visible to the naked eye in every dissection. The sheath had a fibrous external appearance, and was filled with loose connective tissue. No evidence of septa was found. CONCLUSIONS: We observed a macroscopic fibrous structure surrounding the plexus, which was filled with loose connective tissue lacking any apparent organization.

What Protects Certain Nerves from Stretch Injury?

The human tibial nerves is less prone to injury following joint arthroplasty compared with the peroneal nerves. Besides the anatomical distribution, other features may confer protection from stretch injury. We therefore examined the size, shape and connective tissue distribution for the two nerves. The tibial and peroneal nerves from each side of nine fresh human cadavers we reharvested mid-thigh. Proximal segments manually stretched 20%-25% were fixed in aldehyde, while the adjacent distal segments were fixed in their natural length. Paraffin sections stained by Masson's trichrome method for connective tissue were examined by light microscopy. Tibial nerves had 2X more fascicles compared with the peroneal, but the axonal content appeared similar. Analysis showed that neither nerve had a significant reduction in cross sectional area of the fascicles following stretch. However, fascicles from stretched tibial nerves become significantly more oval compared with those from unstretched controls and peroneal nerves. Tibial nerves had a greater proportion that was extrafascicular tissue (50-55%) compared with peroneal nerves (38%-42%). This epineurium was typically adipose tissue. Perineurial thickness in both nerves was directly related to fascicular size. Tibial nerves have several unique histological features associated with size, shape and tissue composition compared with the peroneal nerve. We suggest that more fascicles with their tightly bound perineurium and more robust epineurium afford protection against stretch injury. Mechanical studies should clarify how size and shape contribute to nerve protection and/or neurapraxia.

A comparison of cryoprobe and crush lesions in the rat sciatic nerve.

This study examines the behavioral, sensory, motor and structural recovery during the first 2 months following a freeze (cryoprobe) lesion compared to a nerve crush (forceps). There is a complete loss of sensory and motor function following either type of lesion during the first 2 weeks of recovery. The toe spreading reflex and the sciatic functional index of locomotion behavior returned to normal without significant group differences. Latency times for the pain withdrawal reflex were slightly shorter in the cryoprobe group, but both groups returned to baseline during the second month. An improved regenerative pattern was suggested for the motor recovery in the cryoprobe group as expressed by the amplitude of the digital twitch tension curves. However, the respective curve areas were not different. Morphometric analysis indicated a significant reduction in the distal nerve cross-sectional area, an increase in the mean myelinated fiber density and an increase in the estimated total number of myelinated nerve fibers in both experimental groups. Mean fiber diameter and myelin sheath thickness had not fully returned to normal in either experimental group. Both the fiber size and myelin sheath thickness were significantly reduced in the cryoprobe group. In conclusion, the two lesion types have remarkably similar patterns of recovery. Functional data suggest that motor recovery precedes sensory recovery following a cryoprobe lesion.

A comparison of peripheral nerve regeneration in acellular muscle and nerve autografts.

Regeneration of the rat sciatic nerve through acellular muscle and nerve autografts was evaluated 6-28 days postoperatively by the sensory pinch test, immunocytochemical staining for neurofilaments, and light and electron microscopy. Data points generated by the pinch test were plotted against postoperative time periods and by the use of regression analysis the initial delay period for muscle grafts was determined to 10.3 days. This value was similar to that previously published for acellular nerve grafts (9.5 days), but significantly longer than that for fresh nerve grafts (3.6 days). The calculated regeneration rate (slope of the regression line) for muscle grafts (1.8 mm/day) did not differ significantly (p > 0.05) from that calculated for acellular nerve grafts (2.1 mm/day) or for fresh nerve grafts (1.5 mm/day). The front of regenerating axons shown by axonal neurofilament staining confirmed the pinch test results. Both types of acellular grafts were repopulated with host non-neuronal cells and the muscle graft contained occasional ectopic muscle fibres. Remnants of graft basal laminae were evident at the ultrastructural level. These results indicate the suitability of either acellular muscle or nerve grafts for nerve repair despite their prolonged initial delay periods compared with conventional fresh nerve grafts.

Effect of acute versus continuous glycemic control on duration of local anesthetic sciatic nerve block in diabetic rats.

BACKGROUND AND OBJECTIVES: The duration of nerve block is longer in streptozotocin (STZ)-induced diabetic rats for all local anesthetics (with and without adjuvants) compared with normal rats. Perioperative glycemic control is currently practiced to reduce adverse events in many at-risk patients, especially in diabetic patients, to prevent neuropathy, poor wound healing, and greater incidence of infection. The aim of this study was to investigate in diabetic rats the importance of glycemic control before peripheral nerve block. METHODS: To induce diabetes, rats were intravenously injected with a single dose of 50 mg/kg STZ to destroy pancreatic beta cells. Tactile allodynia in response to von Frey filament stimulation of the plantar hind paws was used as the criterion for diabetic neuropathy. Diabetic rats were randomly divided into experimental treatment groups. The continuous glycemic control experiment compared: 3 U/d insulin implant for 14 days, 1.5 U/d insulin implant for 14 days, and placebo treatment. The acute glycemic control experiment compared a single 6U Human Insulin Isophane Suspension (NPH) injection and placebo treatment. Nondiabetic rats received placebo implants or injections. Following treatment, 0.1 mL of 1% lidocaine hydrochloride with 5 µg/mL epinephrine hydrochloride was injected into the left sciatic notch. Animals were then reevaluated at 10-minute intervals for the absence or presence of sensory and motor response. RESULTS: All STZ-injected rats had blood glucose levels greater than 350 mg/dL and tactile allodynia. After insulin implants or injections, diabetic rats had much lower blood glucose levels than diabetic rats with placebo treatment. With both 3 and 1.5 U/d continuous glycemic control, the local anesthetic solution produced a shorter duration of sensory and motor nerve block in insulin-treated diabetic rats compared with placebo-treated diabetic rats, and shorter duration was similar to nondiabetic rats. With 6 U acute glycemic control in diabetic rats, there was no reduction in nerve block duration compared with placebo-treated diabetic rats. CONCLUSIONS: With continuous glycemic control in diabetic rats, the duration of sensory and motor nerve block was about 40 minutes shorter than that in the untreated diabetic rats and similar to that of normal rats. However, acute glycemic control did not affect nerve block duration, suggesting that this neuropathy cannot be rapidly reversed.

Local anesthetic sciatic nerve block and nerve fiber damage in diabetic rats.

BACKGROUND AND OBJECTIVES: A concern for anesthesiologists is whether local anesthetics are more toxic to peripheral nerves in diabetic patients. A previous study in streptozotocin-induced diabetic rats showed that larger doses of lidocaine produce moderate nerve injury after nerve block in normal rats and worse injury in diabetic rats. However, it is not clear whether a smaller local anesthetic dose that produces negligible nerve fiber damage in normal rats will produce significant nerve damage in diabetic rats and if adding adjuvant drugs modulates this effect. METHODS: Rats were intravenously injected with 50 mg/kg streptozotocin to induce diabetes (blood glucose levels 9250 mg/dL) and diabetic neuropathy. After waiting 35 days, an injection (0.1 mL) of 1% lidocaine alone, or with 5 kg/mL epinephrine or 7.5 kg/mL clonidine added, or 0.5% ropivacaine alone was performed at the left sciatic notch in both diabetic and nondiabetic rats. The duration of sensory (pin prick) and motor (toe spreading reflex) nerve block in the hind paws was determined.For histologic controls, all rats also received saline vehicle injection into the right sciatic notch. Another group of uninjected rats was used as naive controls. Left and right nerves were removed 2 days after injection and fixed in situ with a 4% glutaraldehyde solution. Myelinated axon profiles suggestive of neuropathy (myelin figures, pale and swollen,or dark-staining axoplasm) were counted and expressed as a percentage of the total number of fibers in each rat sciatic nerve. RESULTS: All streptozotocin-injected rats became diabetic and had pronounced tactile allodynia. All rats had sensory and motor nerve blocks lasting for at least 50 mins after injection of local anesthetic. The duration of sensory and motor nerve block was longer in diabetic rats than in nondiabetic rats for all drug groups tested. None of the sciatic nerves examined showed greater than 3% nerve fiber degeneration. Although lidocaine in diabetic rats did not produce nerve fiber damage,diabetic rats receiving lidocaine/clonidine or ropivacaine had more abnormal myelinated axon profiles than did nondiabetic rats receiving the same drug. CONCLUSIONS: The duration of sciatic nerve block with local anesthetics is longer in diabetic compared with nondiabetic rats. A small, but statistically significant, increase in nerve damage occurred in diabetic rats after nerve block with ropivacaine alone or when duration of lidocaine block was extended with clonidine. These findings may have implications for dosing of local anesthetics in diabetic patients undergoing regional analgesia with nerve blocks.

The behavioral and immunological effect of GM-1 ganglioside on nerve root regeneration following C5 nerve root avulsion in a rat model.

Preganglionic nerve root avulsion precludes sensory return, but motor regeneration is possible with sparing of motoneurons. The effect of GM-1 ganglioside treatment was studied with parallel evaluation of the autoimmune response. Rats (N=64) received injections of either GM-1 ganglioside or saline for 30 days following either C5 root avulsion or a hemilaminectomy control. The Bertelli grooming test assessed functional return. Before sacrifice at 5 months, serum was collected for enzyme-linked immunoabsorbent assay testing. Only 44% of the rats treated with ganglioside had a good functional outcome compared with 50% for controls. Although 17% of the rats developed anti GM-1 antibodies, there was no functional or histological evidence of neuropathy in any of the rats. We conclude that ganglioside treatment did not enhance recovery from peripheral nerve injury. Although an immune response was present in some rats, no overt signs of neuropathy were observed.

Dual simulated childbirth injury delays anatomic recovery.

A dual childbirth injury model, including vaginal distension (VD) and pudendal nerve crush (PNC), may best represent the injuries seen clinically. The objective of this study was to investigate urethral function, anatomy, and neurotrophin expression after several simulated childbirth injuries. Groups of 140 rats underwent PNC, VD, PNC+VD, or neither (C). Four days after injury, all injury groups had significantly decreased leak-point pressure (LPP) compared with C rats. Ten days after injury, LPP in PNC and PNC+VD rats remained significantly lower than C rats. Three weeks after injury, LPP in all injury groups had recovered to C values. Histological evidence of injury was still evident in the external urethral sphincter (EUS) after VD and PNC+VD 10 days after injury. Three weeks after injury, the EUS of PNC+VD rats remained disrupted. One day after VD, brain-derived neurotrophic factor (BDNF) expression in the EUS was reduced, while neurotrophin-4 (NT-4) and nerve growth factor (NGF) expression was unchanged. BDNF, NT-4, and NGF expression was dramatically upregulated in the EUS after PNC. After PNC+VD, NGF expression was upregulated, and BDNF and NT-4 expression was upregulated somewhat but not to the same extent as after PNC. Ten days after injury, PNC+VD had the least number of normal nerve fascicles near the EUS, followed by PNC and VD. Twenty-one days after injury, all injury groups had fewer normal nerve fascicles, but without significant differences compared with C rats. PNC+VD therefore provides a more severe injury than PNC or VD alone.

Assessment of axonal growth into collagen nerve guides containing VEGF-transfected stem cells in matrigel.

The early events associated with axonal growth into 10-mm nerve gaps were studied histologically in the rat sciatic nerve model to determine if the outgrowth of blood vessels, Schwann cells, and axons could be enhanced. In the first two experimental groups, collagen nerve guides were filled with either saline or Matrigel. Marrow-derived mesenchymal stem cells (MSCs) were added to Matrigel in two other groups, one of which contained cells transfected with VEGF (MSC/VEGF). After 21 days, the injury site was exposed, fixed, sectioned, and volume fractions of the conduit contents were determined by point counting. The bioresorbable collagen conduits appropriately guided the axons and vessels in a longitudinal direction. The volume fraction of axons was significantly greater in the group with saline when compared with all three groups with Matrigel. This measure had a significant positive correlation with actual counts of myelinated axons. The blood vessel volume fraction in the Matrigel group decreased compared with the saline group, but was restored in the MSC/VEGF group. All Matrigel groups had comparable cellularity and showed a distribution of residual Matrigel in acellular zones. The saline group, by contrast, sustained a network of delicate fibroblastic processes that compartmentalized the nerve and its natural matrix as it became infiltrated by axons as minifascicles. In conclusion, the reduction of axonal outgrowth in the Matrigel groups, when compared with the saline group, suggests that Matrigel may impede the early regenerative process even when enriched by the addition of MSCs or VEGF-transfected cells.

Time course of neuroanatomical and functional recovery after bilateral pudendal nerve injury in female rats.

The pudendal nerve innervates the external urethral sphincter (EUS) and is among the tissues injured during childbirth, which may lead to symptoms of stress urinary incontinence (SUI). To understand the mechanisms of injury and repair, urethral leak-point pressure (LPP) was measured 4 days, 2 wk, or 6 wk after bilateral pudendal nerve crush. Morphometric changes in the distal nerve and EUS were examined by light and electron microscopy. To determine whether recovery resulted from pudendal neuroregeneration, LPP was measured before and after pudendal nerve transection 2 wk after nerve crush. LPP was significantly decreased 4 days after pudendal nerve crush compared with sham-injured animals as well as 2 or 6 wk after nerve crush. LPP was not significantly different 2 or 6 wk after nerve crush compared with sham-injured animals, suggesting that urethral function had returned to normal. Four days after pudendal nerve crush, the EUS branch of the pudendal nerve distal to the injury site showed evidence of nerve degeneration and the EUS appeared disrupted. Two weeks after nerve crush, the distal nerve and EUS both showed evidence of both nerve degeneration and recovery. Two weeks after nerve crush, LPP was significantly decreased after nerve transection. Six weeks after nerve injury, evidence of neuroregeneration was observed in the pudendal nerve and the EUS. This study has demonstrated that functional recovery and neuroregeneration are significant 2 wk after nerve crush, although by anatomical assessment, recovery appears incomplete, suggesting that 2 wk represents an early time point of initial neuroregeneration.

Striated muscle and nerve fascicle distribution in the female rat urethral sphincter.

The anatomical basis for urinary continence depends on a thorough understanding of the tissues in the urethra. The objective of this study was to evaluate the morphology and neuroanatomy of urethral striated muscle, called the rhabdosphincter or external urethral sphincter, in normal female rats. Urethras from 12 female rats were dissected from the bladder, fixed, embedded in paraffin or epon, and sectioned every 1 mm. Striated muscle content was taken as the ratio of the striated muscle area to net urethral area. Nerve fascicles containing myelinated axons near the rhabdosphincter were counted and mapped. Both striated muscle content and number of nerve fascicles peak in the proximal third of the urethra, with a secondary peak at the distal end of the urethra. This secondary peak may correspond to an analog of the combined compressor urethrae/urethrovaginal sphincter located in the distal urethra in human. The rhabdosphincter has a variable distribution along the length of the urethra. In the middle and distal thirds of the urethra, the dorsal striated muscle fibers between the urethra and vagina become more sparse. The majority of nerve fascicles are contained in the lateral quadrants of the urethra, similar to the lateral distribution of somatic nerves in humans. In conclusion, this study demonstrates the normal distribution of the striated musculature and neuroanatomy in the urethra, with similarities to the human. It thus supports and extends the usefulness of the rat as an experimental model for studying urinary incontinence.

Sensory neurons and fibers from multiple spinal cord levels innervate the rabbit lumbar disc.

OBJECTIVE: To establish the neurotransmission pathway from the lumbar L5/6 intervertebral disc (IVD) to the spinal cord in the rabbit. DESIGN: Fluorogold particles injected into the posterior portion of the rabbit L5/6 IVD were traced by examining gold-positive neurons and fibers in the dorsal root ganglion (DRG) and spinal cord at various root levels. RESULTS: Fluorogold-labeled neurons were observed bilaterally in primary afferent DRG neurons from the L3 through L5 segments; a small number of gold-labeled neurons were found at the L1 level. Fluorogold-labeled neurons were predominantly present in the ipsilateral DRG (the side of the injection) at the L5 level, but they were more equally distributed (on both sides) at the L4 and L3 levels. In the posterior horn of the spinal cord, Fluorogold particles were found in nerve fibers as rostral as the T12 level. CONCLUSIONS: Our study has shown that Fluorogold particles injected into the rabbit L5/6 IVD are taken up by primary sensory neurons in the DRGs and primary sensory fibers in the posterior horn of the spinal cord at multiple levels. This diffuse innervation pattern of the lumbar disc may help explain why discogenic back pain in humans is often poorly localized.

Repair of partial lesions with nerve grafting methods in the rat tibial nerve.

A partial nerve lesion and associated neuroma can be either left alone or repaired with a graft. A by-pass graft around the undisturbed lesion with end-to-side attachments might be a good alternative. This study in rats examines these strategies using walking-track analysis, muscle weights, and histology. After a tibial nerve partial lesion (3 mm) and a 21-day delay, the reexposed lesion was either not repaired, repaired with an interposed allograft, or a by-pass allograft. Functional results showed that all three groups had a steady improvement over the 8-week period, but without significant group differences. Gastrocnemius muscle ratios reflected intermediate atrophy. Axons regenerating through the lesion were more advanced than those which regenerated through the grafts and a neuroma was absent. The partial lesion can regenerate to an intermediate level without any intervention, including a by-pass graft, although the delayed repair strategy may have counteracted any potential benefits.