The ansa cervicalis is a neural loop in the neck formed by connecting the superior root from the cervical spinal nerves (C1–2) and the inferior root descending from C2–C3. It has various anatomical variations and can be an important acknowledgment in specific operations of the neck region. This is a review the anatomy, variations, pathology and clinical applications of the ansa cervicalis.
Hypoglossal Nerve ; Neck ; Pathology ; Spinal Nerves

The approach we suggest was developed for cases in which the fourth and fifth lumbar and first sacral spinal nerves were affected in lumbar degenerative disc disease. Retrodiscal transforaminal epidural injection is known to be very effective for lumbar radiculopathy because of excellent access to primary pathology; however, access below L5 is often restricted by the anatomic characteristics of the L5–S1. In the translateral recess approach (TLR), proper final needle placement (i.e., in the axillary portion between the exiting and traversing nerve roots) can be achieved by setting the direction of the needle laterally and superiorly from the distal tip of the infra-adjacent spinous process toward the medial wall of the pedicle and neural foramen of the given level without neural injury. This approach is possible because of the wide interlaminar space in the L5–S1. Preganglionic epidural injection through TLR is an effective and safe spinal intervention for lumbosacral radiculopathy.
Injections, Epidural ; Needles ; Pathology ; Radiculopathy ; Spinal Nerves

In recent years, the sural nerve biopsy has become a commonly performed procedure in the diagnostic work-up of patients with peripheral neuropathy. This paper reviews the diagnostic usefulness and limitations of this procedure. Based on 385 sural nerve biopsies, we found clinically helpful or relevant information in 45% of cases. In 24% of cases, specific diagnoses were obtained, among which vasculitic neuropathy was most common.
Biopsy/methods/standards ; Evaluation Studies ; Histological Techniques ; Human ; Peripheral Nervous System Diseases/classification/*diagnosis ; Spinal Nerves/*pathology ; Sural Nerve/*pathology

Described here is a case of accidental intrathecal administration of vincristine with pathologic findings in the central nervous system. A 3-year-old boy with acute lymphoblastic leukemia, was given his ninth course chemotherapy. Vincristine was accidentally injected intrathecally. The clinical course was rapidly progressive (6-day course) and resulted in death. An autopsy was done. The brain and spinal cord was grossly edematous and congested without any specific feature. Histologically, profound loss of neuron was noted in the spinal cord. Remaining neurons in the spinal cord, particularly anterior horn cells were markedly swollen. The spinal nerves show diffuse axonal degeneration and myelin loss. The upstream portion of the spinal cord (brain stem, cerebellum, cerebrum) showed patchy loss of neurons, especially Purkinje cells and granular cells of the cerebellar cortex. Many neurons showed axonal reaction (chromatolysis) with swelling. Several neurons show intracytoplasmic eosinophilic inclusion body. Myelin loss, axonal swelling and enlargement of perivascular spaces were seen throughout the white matter of central nervous system.
Antineoplastic Agents/therapeutic use* ; Brain/pathology ; Brain/drug effects ; Case Report ; Central Nervous System/pathology ; Central Nervous System/drug effects* ; Child, Preschool ; Fatal Outcome ; Histocytochemistry ; Human ; Injections, Spinal ; Leukemia, Lymphocytic, Acute/drug therapy* ; Male ; Medication Errors* ; Spinal Cord/pathology ; Spinal Cord/drug effects ; Spinal Nerves/pathology ; Spinal Nerves/drug effects ; Vincristine/therapeutic use* ; Vincristine/administration & dosage

OBJECTIVETo explore the possibility of peripheral nerve damage induced by antiepileptic drugs (AEDs) in different age rats and its pathogenesis.

METHODSAdult (2-month-old) and infant (7-day-old) rats were divided into 8 groups (n = 16 in each) and treated with the following 7 AEDs respectively: phenytoin [PHT, 62.5 mg/(kgxd)], phenobarbital [PB, 30.0 mg/(kgxd)], sodium valproate [VPA, 312.5 mg/(kgxd)], clonazepam [CZP, 1.25 mg /(kgxd)], carbamazepine [CBZ, 187.5 mg/(kgxd)], topiramate [TPM, 40 mg/(kgxd)], oxcarbazepine [OXC, 312.5 mg/(kgxd)], remaining one group was used as control. Four weeks later, 8 rats were sacrificed randomly from each group and serum, sciatic nerves and spinal cord samples were collected. The rest half rats were sacrificed 4 week after AEDs withdrawal. Histological observations were performed on the sciatic nerves samples, including teased fibers, semi-thin sections and electron microscopy. The activity of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in serum and sciatic nerves were detected respectively. Expression of apoptosis-related proteins Bcl-2 and Bax was detected by immunohistochemistry. Neurons apoptosis in the anterior horns of spinal cord were detected by TUNEL.

RESULTS(1) Except for TPM group, various incidence (7.2% - 20.2%) of teased fibers abnormalities were observed in all the other different age groups. PHT group showed the most serious changes followed by PB (adult) or VPA (infant), CBZ, CZP and OXC groups. The predominant abnormality of teased fibers was demyelination. (2) There was no significant difference in the incidence of pathologic changes in teased fibers between adult and infant groups. Four weeks after AEDs withdrawal, recovery of pathologic changes in teased fibers in infant groups was much better than adult. (3) Significantly increased expression of Bax protein and ratio of Bax/Bcl-2 was only found in infant rats treated with PB, CNP or VPA compared with control (P < 0.05), the results of TUNEL was in accordance with immunohistochemistry. (4) Compared with control, the activity of T-AOC and SOD decreased in both infant and adult rats treated with PHT, CZP, CBZ and OXC, and the reduction of SOD activity in serum and sciatic nerves samples was also found in PB groups. Serum activity of GSH-PX was decreased in both age groups treated with PHT, PB, VPA, CZP, CBZ and OXC. The reduction of GSH-PX activity in sciatic nerves samples was remarkably in both adult and infant rats treated with PHT, PB, CBZ, OXC as well as the infant rats treated with CZP.

CONCLUSIONSSix AEDs (PHT, PB, CBZ, VPA, CZP, OXC) showed the potential to cause peripheral nerves damage. Demyelination was the predominant pathologic change. Both adult and infant rats had the same susceptibility. Recovery of pathologic changes in teased fibers in both age groups was slow, but infant rats were prone to revive more quickly. There was no significant correlation between spinal cord neuron apoptosis and peripheral nerves damages in rats treated with AEDs. Breakdown of oxidation-antioxidation balance was closely related to development of peripheral nerves damages caused by most AEDs.

Animals ; Anticonvulsants ; adverse effects ; Demyelinating Diseases ; chemically induced ; pathology ; Oxidative Stress ; Peripheral Nerves ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sciatic Nerve ; pathology ; Spinal Cord ; pathology

Dorsal root ganglion (DRG) neurons have peripheral terminals in skin, muscle, and other peripheral tissues, and central terminals in the spinal cord dorsal horn. Hyperpolarization-activated current (I(h)) of the hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels are present in the DRG. The genes encoding HCN channels have four subtypes named HCN1 to HCN4. HCN channels are permeable to both K(+) and Na(+). They underlie the depolarization that modulates the rhythmic generations of action potentials (APs), contribute to the resting membrane potential, and modify the waveform of propagated synaptic and generator potentials. Neuropathic pain is characterized by spontaneous pain, hyperalgesia and allodynia. After spinal nerve injury, the cell bodies of the primary sensory neurons in segmental DRG become hyperexcitable, characterized for some neurons by the presence of spontaneous firing (or ectopic discharge). In the following, we summarize our observations on the role of HCN channels in DRG neurons in neuropathic pain. 1 HCN subtypes and I(h) in DRG neurons Immunohistochemical staining revealed a subgroup of neurons in the DRG that were stained with rabbit polyclonal antibodies specific for HCN1, 2, 3 and 4. The most prominently expressed HCN subtype was HCN1. HCN1-positive cells in DRG were medium to large in size and doubly labeled with neurofilament-200 (NF-200), and were not labeled with isolectin B4 (IB4), a C fiber marker. In contrast, HCN2, 3 or 4 was expressed in all DRG neurons at a lower level. HCN4 was confined to small neurons. DRG neurons expressed I(h). When membrane was hyperpolarized, the channel was activated, mediating a slowly activated, inward current. I(h) was distributed mainly in large and medium-sized DRG neurons. 2 Changes in expression of HCN in DRG after spinal nerve ligation Western blotting was used to detect the changes in the expression of HCN subtypes in the DRG after spinal nerve ligation. HCN1 mRNA and protein were reduced in the DRG whose spinal nerve had been ligated. HCN1 expression was decreased to the lowest level at day 14 and restored at day 28 after spinal nerve ligation. HCN2 mRNA and medium molecular weight protein was also decreased in spinal-nerve ligated DRG. HCN3 and 4 in the same ganglion remained unchanged as evidenced by immunohistochemical staining, until day 28 when they became significantly decreased. HCN4 mRNA in DRG did not change, and protein expression slightly increased. Interestingly, abundant axonal accumulation of HCN channel protein at the injured sites in chronic constriction injury (CCI) rats. Electron immunomicroscopy showed strong positive immunolabeling on the axolemma of myelinated thick axons. 3 Role of I(h) in neuronal excitability and ectopic discharges after spinal nerve ligation ZD7288, a specific I(h) blocker, inhibited I(h) in a time- and concentration-dependent manner. With patch-clamp recording on acutely isolated DRG neurons, it was found that ZD7288 perfusion resulted in a decrease of both I(h) activity and the activation time constant. ZD7288 decreased the number of repetitive APs and caused an increase in AP rise time, accompanied by a small hyperpolarization of the membrane resting potential. The results demonstrated that I(h) was involved in AP firing, and possessed the physiological functions to facilitate neuronal excitability and ectopic firing. Extracellular electrophysiological recording from dorsal root fibers associated with the spinal nerve-ligated ganglion revealed three different firing patterns of ectopic discharges: tonic or regular, bursting and irregular. The average frequency of ectopic discharges and the proportions of active filaments also changed rapidly, both parameters reaching a peak within 24 h then declining gradually in the following days. It was also found that proportions of three different firing patterns changed dynamically over time. The tonic and bursting types were dominant patterns in the first 24 h, while the irregular became the only pattern at day 14. We found that all three firing patterns (tonic, bursting and irregular) were dose- and time-dependently inhibited by local application of ZD7288 to DRG. The rate of suppression was negatively related to the frequency of firing prior to the application of ZD7288. We also found that, while the tonic firing pattern was gradually transformed to bursting type by application of 100 mumol/L ZD7288, it could be transformed to integer multiples firing by 1000 mumol/L ZD7288. 4 Effects of administration of ZD7288 on mechanical allodynia after spinal nerve ligation or CCI After spinal nerve ligation, i.t. injection of 30 mug ZD7288 significantly increased the 50% paw withdrawal threshold, ipsilateral to the ligated nerve. ZD7288 had no effect if the dose was lower than 15 mug, but resulted in motor deficits if the dose was higher than 60 mug. ZD7288 produced much better effects in the early stage (5 or 14 days after spinal nerve ligation) than that in the late stage (28 days after spinal nerve ligation). In CCI rats, ZD7288 application to the injured sited also significantly suppressed the ectopic discharges from injured nerve fibers with no effect on impulse conduction. Moreover, mechanical allodynia was inhibited. In conclusion, these results demonstrated that I(h) participated in the development and maintenance of peripheral sensitivity associated with neuropathic pain and that it is a potential target for the design of novel analgesics in the future.
Action Potentials ; Animals ; Cyclic Nucleotide-Gated Cation Channels ; metabolism ; Ganglia, Spinal ; physiopathology ; Hyperalgesia ; physiopathology ; Membrane Potentials ; Nerve Fibers ; pathology ; Neuralgia ; physiopathology ; Neurons, Afferent ; pathology ; Rats ; Rats, Sprague-Dawley ; Spinal Nerves ; pathology

Adolescent ; Adult ; Aged ; Female ; Follow-Up Studies ; Fracture Fixation ; instrumentation ; Humans ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures ; instrumentation ; Postoperative Period ; Radiography ; Spinal Fractures ; diagnostic imaging ; pathology ; physiopathology ; surgery ; Spinal Nerves ; physiopathology ; Spine ; surgery

OBJECTIVETo investigate whether analgesic effect of electroacupuncture (EA) is affected by p38 mitogen-activated protein kinase (p38 MAPK) on microglia.

METHODSThere were two experiments. The experiment 1: 40 male Sprague-Dawley (SD) rats were randomly divided into the normal, surgery, EA and sham EA groups, and the L5 spinal nerve ligation (SNL) on the right side was used to establish neuropathic pain model. EA was applied to bilateral Zusanli (ST36) and Kunlun (BL60) at 24, 48 and 72 h after SNL for 30 min, once per day. The paw withdrawal thresholds (PWTs) were measured before surgery (as base) and at 24, 25, 49 and 73 h after surgery. Phospho-p38 MAPK (p-p38 MAPK), oxycocin-42 (OX-42, marker of microglia), and glial fibrillary acidic protein (GFAP, marker of astrocyte) in bilateral spinal cord dorsal horn (SCDH) were detected by immunofluorescence, respectively. The experiment 2: 40 male SD rats were cannulated for SNL-induced neuropathic pain, and then were randomly divided into the dimethyl sulfoxide (DMSO), EA plus DMSO, 4-(4-fluorophenyl)-2-(4-methylsulfonylpheny)-5-(4-pyridyl)-1H-imidazole (SB203580) and EA plus SB203580 groups. SB203580 (30 nmol/L) was administered 5 min prior to EA treatment. The PWTs and OX-42 in bilateral SCDH were measured as mentioned above.

RESULTSSNL-induced neuropathic pain reduced PWTs and increased the expression of p-p38 MAPK and OX-42 in bilateral lumbar SCDH of rats (P<0.01). Spinal p-p38 MAPK was only co-localized with OX-42 in our study. EA treatment significantly alleviated SNL-mediated mechanical hyperalgesia, and suppressed the expression of p-p38 MAPK and OX-42 in lumbar SCDH (P<0.05 or P<0.01). Intrathecal injection of low dose SB203580 had no influence on PWTs (P>0.05), but significantly inhibited the expression of OX-42 positive cells in bilateral SCDH (P<0.01 or P<0.05). EA plus SB203580 synergistically increased PWTs, and reduced the expression of bilateral spinal OX-42 (P<0.01 or P<0.05).

CONCLUSIONSThe central mechanism of EA-induced anti-hyperalgesia may be partially associated with the reduced expression of p-p38 MAPK, and subsequently reducing the activation of OX-42 in neuropathic pain. Therefore, EA may be a new complementary and alternative therapy for neuropathic pain.

Animals ; Biomarkers ; metabolism ; CD11b Antigen ; metabolism ; Electroacupuncture ; Fluorescent Antibody Technique ; Hyperalgesia ; pathology ; therapy ; Imidazoles ; pharmacology ; Ligation ; Male ; Microglia ; drug effects ; enzymology ; pathology ; Neuroglia ; drug effects ; metabolism ; Phosphorylation ; drug effects ; Posterior Horn Cells ; drug effects ; enzymology ; pathology ; Pyridines ; pharmacology ; Rats, Sprague-Dawley ; Spinal Nerves ; drug effects ; pathology ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo study the ability of aqueous extract of Hericium erinaceus mushroom in the treatment of nerve injury following peroneal nerve crush in Sprague-Dawley rats.

METHODSAqueous extract of Hericium erinaceus was given by daily oral administration following peroneal nerve crush injury in Sprague-Dawley rats. The expression of protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways; and c-Jun and c-Fos genes were studied in dorsal root ganglia (DRG) whereas the activity of protein synthesis was assessed in peroneal nerves by immunohistochemical method.

RESULTSPeripheral nerve injury leads to changes at the axonal site of injury and remotely located DRG containing cell bodies of sensory afferent neurons. Immunofluorescence studies showed that DRG neurons ipsilateral to the crush injury in rats of treated groups expressed higher immunoreactivities for Akt, MAPK, c-Jun and c-Fos as compared with negative control group (P <0.05). The intensity of nuclear ribonucleoprotein in the distal segments of crushed nerves of treated groups was significantly higher than in the negative control group (P <0.05).

CONCLUSIONH. erinaceus is capable of promoting peripheral nerve regeneration after injury. Potential signaling pathways include Akt, MAPK, c-Jun, and c-Fos, and protein synthesis have been shown to be involved in its action.

Agaricales ; chemistry ; Animals ; Axons ; pathology ; Female ; Ganglia, Spinal ; metabolism ; Glucans ; analysis ; MAP Kinase Signaling System ; Nerve Crush ; Nerve Regeneration ; physiology ; Peripheral Nerves ; enzymology ; physiology ; Peroneal Nerve ; physiology ; Protein Biosynthesis ; Proto-Oncogene Proteins c-akt ; metabolism ; Proto-Oncogene Proteins c-fos ; genetics ; metabolism ; Proto-Oncogene Proteins c-jun ; genetics ; metabolism ; Rats, Sprague-Dawley