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< Back Dr. Krishna A. Reddy Consultant Orthopaedic Oncologist, M.S., FRCS (Trauma & Orthopaedics) Current Institution: Vanderbilt University Medical Center (USA) / Formerly Royal Orthopaedic Hospital, Birmingham (UK) Location: Nashville, Tennessee, USA Professional Summary Dr. Krishna Reddy is an orthopaedic surgeon with extensive international experience in musculoskeletal oncology, sports medicine, and reconstructive orthopaedics . He completed his orthopaedic residency in India and moved to the United Kingdom in 2002, where he became a Fellow of the Royal College of Surgeons (Trauma & Orthopaedics) . He received advanced Orthopaedic Oncology training at the renowned Royal Orthopaedic Hospital in Birmingham and later pursued fellowships at Vanderbilt University (Orthopaedic Oncology) and the University of Cincinnati (Sports Medicine) . Dr. Reddy has contributed to numerous peer-reviewed publications and international presentations , focusing on limb-salvage surgery, sarcoma reconstruction, and long-term functional outcomes. Oncologic Orthopaedics reddykh@ucmail.uc.edu Previous Next

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< Back Dr. Sefa Giray BATIBAY University of Health Sciences, Istanbul, Umraniye Research and Education Hospital Oncologic Orthopaedics sefabatibay@hotmail.com Previous Next

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< Back Peripheral Nerve Structure and Function Peripheral Nerves Function: Connect CNS ↔ muscles, joints, tendons, skin; carry motor, sensory, autonomic fibers Neuron structure: Soma (nucleus), dendrites (input), axon (signal), synapse (communication) Axon: Diameter 0.2–20 μm; conduction ↑ with larger diameter & myelin Myelin: Lipid-protein sheath by Schwann cells → faster conduction, less energy Connective layers: Endoneurium (axon), perineurium (fascicle, barrier), epineurium (whole nerve + vessels) General Features Peripheral nerves connect the central nervous system with muscles, bones, joints, tendons, and skin. They play a role in both motor and sensory transmission. Voluntary movement, reflex activity, and sensory perception rely on the integrity of these structures. Basic Structure of the Neuron Cell body (soma): The metabolic center, containing the nucleus and organelles. Dendrites: Short extensions that receive inputs from other neurons. Axon: A single, long extension that propagates electrical signals to distant targets. The axon hillock is the site where the action potential is generated. Synapse: Specialized junction enabling communication between neurons. Axonal Structure Axon diameter ranges from 0.2–20 µm. The cytoplasm contains mitochondria and microtubules. Conduction velocity is determined by axonal diameter and myelination. Axon terminals form synaptic contacts with target cells. Myelin and Its Function Myelin is a multilayered lipid- and protein-rich sheath that insulates axons, increasing conduction velocity and reducing energy expenditure. In the peripheral nervous system, Schwann cells are responsible for myelin formation. Unmyelinated axons conduct impulses more slowly. Connective Tissue Layers Endoneurium: Surrounds individual axons. Perineurium: Encloses fascicles; contributes to the blood–nerve barrier. Epineurium: Envelops the entire nerve, containing blood vessels and lymphatics. Functional Properties Peripheral nerves contain both afferent (sensory) and efferent (motor) fibers. Afferent fibers: Transmit mechanical, thermal, and nociceptive stimuli. Efferent fibers: Control muscle contraction and glandular secretion. Autonomic fibers are also carried within peripheral nerves. Clinical Relevance Peripheral nerve injuries result in motor and sensory deficits. Their regenerative capacity is limited, although axonal elongation is possible. Demyelination decreases conduction velocity and represents a fundamental pathophysiological mechanism in neuropathies. Peripheral Nerve System Injury: Diagnosis and Management Mechanisms of Injury Peripheral nerve injuries may result from trauma, surgical interventions, tumors, metabolic disorders, or inflammatory processes. Following injury, endoneurial and epineurial permeability increases, leading to edema. Distal to the lesion, Wallerian degeneration occurs: macrophages clear myelin debris while Schwann cells support regeneration. Classifications Seddon classification: Neurapraxia: Conduction block with intact axons; recovery occurs within weeks. Axonotmesis: Axonal disruption with preserved connective tissue sheaths; regeneration is possible. Neurotmesis: Complete transection of both axons and connective sheaths; spontaneous recovery is poor, requiring surgical repair. Sunderland classification: Five grades, ranging from Grade I (neurapraxia) to Grade V (complete transection), offering more detailed prognostic information. Clinical Presentation Motor deficits, sensory loss, and diminished reflexes are typical. Muscle atrophy and trophic skin changes may develop. Autonomic involvement can result in abnormal sweating and circulatory disturbances. Pain may be acute or chronic. Diagnostic Methods Clinical examination is the first step, assessing motor strength, sensory distribution, and reflexes. Nerve conduction studies (NCS): Assess conduction velocity and amplitude. Electromyography (EMG): Detects denervation and reinnervation. Imaging: Ultrasound and MR neurography visualize nerve continuity and compression sites. Treatment Approaches Conservative management: Indicated in neurapraxia and mild axonotmesis; includes rest, anti-inflammatory therapy, physiotherapy, and splinting. Regeneration is monitored over time. Surgical repair: Required for neurotmesis and high-grade Sunderland injuries. Techniques include epineural or perineural suturing. For large defects, nerve grafting or nerve transfers are performed; microsurgical techniques improve outcomes. Rehabilitation: Aims to preserve muscle strength, maintain joint mobility, and support functional recovery. Regeneration and Recovery Axonal regrowth occurs at a rate of ~1–3 mm/day. Schwann cells enhance conduction by remyelination. Recovery depends on injury severity, timing of repair, and rehabilitation. Children generally exhibit faster recovery than adults. Complications Aberrant axonal sprouting may lead to neuroma formation. Persistent sensory and motor deficits can result in long-term disability. Chronic pain syndromes and muscle atrophy negatively impact quality of life. Conclusion Early diagnosis and appropriate treatment are critical for functional outcomes in peripheral nerve injuries. Classification systems, diagnostic tools, and surgical techniques guide clinical decision-making, while comprehensive rehabilitation is essential for long-term success. 1. Zhang K, Guo J, Zhang Y, Chen B, Du X. Innovations in peripheral nerve regeneration: biomaterials, growth factors, and cell therapy. Front Neurosci . 2024;18:1594435. doi:10.3389/fnins.2025.1594435 2. Liu X, Li X, Zhang T, Xu W, Guan Y, Li X, et al. Electrical stimulation accelerates Wallerian degeneration and promotes nerve regeneration after sciatic nerve injury. Glia . 2023;71(3):758–774. doi:10.1002/glia.24309 Previous Next

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