Improved regeneration after femoral nerve injury in mice lacking functional T- and B-lymphocytes.

The immune system plays important functional roles in regeneration after injury to the mammalian central and peripheral nervous systems. After damage to the peripheral nerve several types of immune cells, invade the nerve within hours after the injury. To gain insights into the contribution of T- and B-lymphocytes to recovery from injury we used the mouse femoral nerve injury paradigm. RAG2-/- mice lacking mature T- and B-lymphocytes due to deletion of the recombination activating gene 2 were subjected to resection and surgical reconstruction of the femoral nerve, with the wild-type mice of the same inbred genetic background serving as controls. According to single frame motion analyses, RAG2-/- mice showed better motor recovery in comparison to control mice at four and eight weeks after injury. Retrograde tracing of regrown/sprouted axons of spinal motoneurons showed increased numbers of correctly projecting motoneurons in the lumbar spinal cord of RAG2-/- mice compared with controls. Whereas there was no difference in the motoneuron soma size between genotypes, RAG2-/- mice displayed fewer cholinergic and inhibitory synaptic terminals around somata of spinal motoneurons both prior to and after injury, compared with wild-type mice. Extent of myelination of regrown axons in the motor branch of the femoral nerve measured as g-ratio was more extensive in RAG2-/- than in control mice eight weeks after injury. We conclude that activated T- and B-lymphocytes restrict motor recovery after femoral nerve injury, associated with the increased survival of motoneurons and improved remyelination.

Impacts of lesion severity and tyrosine kinase receptor B deficiency on functional outcome of femoral nerve injury assessed by a novel single-frame motion analysis in mice.

Functional recovery after peripheral nerve injury is often poor. Comprehension of cellular and molecular mechanisms limiting or promoting restoration of function and design of efficient therapeutic approaches remain serious challenges for neuroscience and medicine. Progress has been restricted by the lack of reliable methods for evaluation of motor functions in laboratory animals. We describe a novel approach for assessment of muscle function in mice after femoral nerve damage, an injury causing impairment of knee extension. The functional deficit can be precisely estimated by angle and distance measurements on single video frames recorded during movements of the animals with or without body weight support. Using this method we describe here the precise time-course and degree of functional recovery after femoral nerve crush and transection. In addition, we show that restoration of function is considerably impaired in mice with a reduced expression level of the tyrosine kinase receptor B, a cognate receptor for the neurotrophin brain-derived neurotrophic factor. This finding is consistent with known functions of brain-derived neurotrophic factor and tyrosine kinase receptor B and demonstrates the potential of the method. The principles of the approach are highly relevant for the development of novel functional assays in other peripheral and, in particular, central nervous system injury paradigms.

[Delayed paresis of the femoral nerve after total hip arthroplasty associated with hereditary neuropathy with liability to pressure palsies (HNPP)]. / Tomakulöse Neuropathie (HNPP) als Ursache einer verzögerten Parese des N. femoralis nach Hüfttotalendoprothesenimplantation.

Delayed lesions of the femoral or sciatic nerve are a rare complication after total hip arthroplasty. Several cases in association with cement edges, scar tissue, broken cerclages, deep hematoma, or reinforcement rings have been published. We report about a 62-year-old female who developed a pure motor paresis of the quadriceps muscle 2 weeks after total hip arthroplasty. After electrophysiological evaluation had revealed an isolated femoral nerve lesion, revision of the femoral nerve was performed. During operative revision no pathologic findings could be seen. One week later the patient developed paralysis of the left wrist and finger extensors after using crutches. Electrophysiological evaluation revealed several nerve conduction blocks in physiological entrapments and the diagnosis of hereditary neuropathy with liability to pressure palsies (HNPP) was established. Hereditary neuropathy with liability to pressure palsies (HNPP) is a rare disease with increased vulnerability of the peripheral nerve system with mostly reversible sensorimotor deficits. It should be taken into consideration in cases of atypical findings of compression syndromes of peripheral nerves or delayed neuropathy, e. g., after total hip arthroplasty.

Valoración geriátrica / Geriatric assessment

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