An animal experimental model of auditory neuropathy induced in rats by auditory nerve compression.

Several animal models of auditory neuropathy (AN) have been produced by employing pharmacological agents to damage auditory neurons or hair cells selectively. The specificity of pharmacological lesions is generally assessed by observation of visible structural damage but it is difficult to localize the delivery, which could lead to functional side effects in other anatomical structures. Although genetic analyses of human AN patients have provided important information on the pathophysiology of AN, specific genetic defects have not been fully correlated with functional deficits in the auditory nervous system. To address this problem, we compressed rat auditory nerves to assess neural degeneration for up to 35 weeks. The method produced a good model of auditory neuropathy, including profound deterioration of the auditory brainstem response and preservation of both cochlear microphonics and distortion product otoacoustic emissions. Histological examination revealed that in spite of profound degeneration of the auditory nerve, the hair cells remained intact. The model provides a complementary alternative to those based on pharmacological lesions and genetic analyses of AN patients and should allow analysis of the pathophysiology of auditory neuropathy with less risk of the results being confounded by unknown deficits in other cell types.

[Structural and functional response of lymph node to sciatic nerve compression in combination with lymphotropic correction and without it].

Morpho-functional state of lymph node (LN) after the sciatic nerve compression was studied experimentally in rats and the application of lymphotropic drugs was substantiated. Sciatic nerve compression resulted in the changes of the relative area, occupied by structures of LN and in formation of definite cortico-medullary ratio. With the increase of duration of postcompression period, the stable augmentation of the dimensions of a thymus-dependent zone was found in combination with the prevalence of a thymus-independent zone, which is indicative of the mixed variant of immune response to sciatic nerve compression. Application of lymphotropic drugs (lymphotropic injections, "Phytopan" biologically active additive) was shown to change LN structural response to sciatic nerve compression. The degree of response of various structures of a denervated LN, found in rats receiving the drugs, was different as compared with that one in untreated animals, and was characterized by an inverse mode of reaction of LN T- and B-dependent zones. The results obtained emphasize the necessity of taking into account the state of LN in pathology of peripheral nervous system.

Caudal spinal cord ischemia after lumbar vertebral manipulation.

Neurological complications after lumbar spine manipulation are uncommon. The cause is usually a herniated disk or displaced bony structure. We report a case of paraplegia that developed a few hours after manipulation of the lumbar spine. Magnetic resonance imaging was consistent with ischemia of the caudal spinal cord. No disk fragment or bony structure impinging on the spinal cord was seen. Spinal cord ischemia may deserve to be added to the list of possible adverse events after lumbar spine manipulation.

[Effect of Yiqi Huayu Recipe on regeneration process after L5 nerve root compression in rats].

OBJECTIVE: To study the effect of Yiqi Huayu Recipe on neurons in neuromuscular junction after L5 nerve root compression in rats. METHODS: By using immunohistochemistry, confocal laser scanning techniques and protein gene product 9.5 as a neuronal marker, the motor endplates were visualized with fluorescein-conjugated alpha-BTX. The effect of Yiqi Huayu Recipe on nerve terminals of neuromuscular junction at 10, 20, 30, 60 days after L5 nerve root compression was observed in rat soleus muscles during regeneration. The overlap areas of terminals and endplates were measured with NIH image technique. RESULTS: As for the aggregates, sprouts, extension of nerve terminal during regeneration, the connecting speed and range of nerve terminal with endplates, as well as the reformation of neuromuscular junctions during regeneration, Yiqi Huayu Recipe group was better than that of the control group. CONCLUSION: Yiqi Huayu Recipe can promote the hyperplasia of neurons and enhance the regeneration function. It also can accelerate the neuromuscular junction reformation and shorten the process of regeneration.

Medial superior cluneal nerve entrapment neuropathy in teenagers: a report of two cases.

Medial superior cluneal nerve entrapment neuropathy causes pain radiating from the low back down to the posterior thigh. It tends to be misdiagnosed as a lumbar spine disorder. Patients in previous reports were in the middle or old age at the onset. Proposing simultaneous full flexion of the ipsilateral hip and knee joints as a provocation test, we present two cases of teenager females who spent long before diagnosis of their condition. Both of them had engaged in vigorous sports activities and completely recovered from the disability following local anaesthetic and corticosteroid injection at the trigger point.

Hyperalgesia due to nerve injury-role of peroxynitrite.

We carried out a partial ligation of the sciatic nerve in rats to induce nerve injury and neuropathic hyperalgesia. We showed that nitrotyrosine, a marker of peroxynitrite activity, was formed after partial nerve injury. Double-labelling immunohistochemistry showed that nitrotyrosine-immunoreactive cells were mainly macrophages and Schwann cells. Daily treatment with uric acid, a scavenger of peroxynitrite, decreased nitrotyrosine formation in the injured sciatic nerve, and produced concomitant alleviation of thermal hyperalgesia and Wallerian degeneration. These results provide the first evidence that peroxynitrite is formed after partial nerve injury, and contributes to the initiation of thermal hyperalgesia and Wallerian degeneration. We hypothesize that uric acid alleviates hyperalgesia and Wallerian degeneration by inhibiting oxidative damage caused by peroxynitrite and possibly also by decreasing the production of other inflammatory mediators such as prostaglandins.

Mechanisms of neurovascular compression within the spinal and intervertebral canals.

OBJECTIVE: To describe some possible causes of encroachment on human spinal and intervertebral canal (foramen) neurovascular II structures. DATA SELECTION AND SYNTHESIS: A review of some imaging films of patients aged 38 to 52 years and some human autopsy histopathologic sections from 40- to 60-year-old cadavers to determine what structures may be responsible for neurovascular compression in individuals in this relatively young-to-middle-age group and to illustrate some examples. RESULTS: Stenosis of the spinal and intervertebral canal neurovascular structures can be caused by various bony and soft-tissue structures. Stenosis can be related to osteophytosis of the vertebral body, uncoverte-intervertebral disc protrusion, ossification of the posterior longitudinal ligament, and ligamentum flavum hypertrophy or buckling. DISCUSSION: Various forms of spinal and intervertebral canal stenosis can cause compression of neurovascular structures that may, in turn, be responsible for symptomatology. Of course, autopsy findings cannot be equated with painful syndromes in patients.

Vascular complication involving the conus medullaris or cauda equina after vertebral manipulation for an L4-L5 disk herniation.

A case of injury to the cauda equina or conus medullaris after lumbar vertebral manipulation is reported. In contrast to all other previously reported cases, no migrated disk fragment was demonstrated. Similar to experience at the cervical spine, lumbar vertebral manipulation may carry a risk of vascular injury. The neurological manifestations in our patient were consistent with compression of the Desproges-Gotteron artery by a small L4-L5 disk herniation.

Quantitative analysis of optic disc cupping in compressive optic neuropathy.

PURPOSE: Cupping of the optic disc, a characteristic sign of glaucoma, has been anecdotally described in association with compressive optic neuropathy. The aim of this study is to perform a masked, controlled, and quantitative measurement of the optic disc cup to determine if compressive lesions of the afferent visual pathway were associated with increased cupping. METHODS: The ratio of cup area:disc area of 29 patients with intracranial lesions impinging on the optic nerves and the chiasm (14 with pituitary adenomas, 7 with meningiomas, 6 with craniopharyngiomas, and 2 with aneurysms) was compared with those of 20 age-matched control subjects. The areal ratios were derived planimetrically from hand-drawn images of magnified stereophotographs. Patients were divided into three groups based on the degree of laterality of visual compromise. Uninvolved eyes served as an internal control for patients with unilateral disease. RESULTS: The median ratio of cup area:disc area was 0.37 for all eyes with visual compromise (n = 51) and 0.10 for control eyes, which was statistically significant (P = 0.0001). The median intereye difference in the ratio of cup area:disc area was 0.13 for patients with unilateral lesions and 0.04 for control subjects. This difference also was statistically significant (P = 0.0001). CONCLUSIONS: The finding of intereye asymmetry in patients with unilateral optic nerve compression is convincing evidence that the enlarged cup is an acquired feature. Several types of compressive lesions of the anterior visual pathway can be associated with increased cupping of the optic disc in the absence of increased intraocular pressure.

[A case of osteopoikilosis combined with dermal changes and compression syndromes of peripheral nerves]. / Ein Fall von Osteopoikilie kombiniert mit dermalen Veränderungen und Kompressionssyndromen peripherer Nerven.

In the case of combination of osteopoikilosis with dermal alterations we wanted to know if the hereby discussed general mesenchymal lesions are the cause of the additional entrapment syndromes of peripheral nerves present in our case. For this purpose we recorded the pressure at the distal median and ulnar nerves within and out of the entrapment location. The results of the pressure recording of not point to a primary nerve lesion by a elevated pressure susceptibility or a pressure elevation at the peripheral nerve out of a defined entrapment location e.g. by an increase of connective tissue. Because of a hypertrophic scar formation in this case it should be paid attention to the wound healing of all patients with osteopoikilosis. The histologically verified nevoid mesenchymal alterations of the connective tissue found in this case, are to be delineated from the disseminated lenticular dermatofibrosis of the Buschke-Ollendorff syndrome.

Cupping of the optic disc with compressive lesions of the anterior visual pathway.

Cupping of the optic nerve, classically a sign of glaucoma, was demonstrated in 16 patients with lesions compressing the anterior visual pathway. Color contrast determinations of the cup/disc ratio demonstrated a ratio greater than 0.49 in 31 eyes. Further evaluation by stereobiomicroscopy showed cavernous degeneration by contour changes in 25 of the optic nerves. None of the patients had intraocular pressures greater than 22, and seven had normal tonography. Visual fields demonstrated bitemporal field defects in most patients and none were typical of glaucoma. Snellen acuity loss, out of proportion to the extent of optic disc cupping was found in 12 patients. This study indicates that diseases other than glaucoma can cause significant cupping of the optic nerves. Detailed evaluation of the disc changes and the visual fields will prevent confusion between compressive lesions of the optic nerves or chiasm and glaucoma.

Optic cupping caused by an intracranial aneurysm.

A 51-year-old woman had optic disk cupping from optic nerve compression by an intracranial aneurysm. Slit-lamp stereoscopic examination of the living eye immediately post mortem revealed an optic cup vertically oral, elongated superiorly, and indistinguishable from disk changes seen early in glaucoma. The histopathological changes differed from those in glaucoma by showing no glial atrophy. Instead, the cupping was caused by loss of axons in the prelaminar region of the nerve head and collapse of glial columns.