Physiological Changes After Peripheral Nerve Injury PDF

PHYSIOLOGICAL CHANGES AFTER PERIPHERAL NERVE INJURY ELECTRICAL STIMULATION PTY 214 Lect 9 fchs.ac.ae OBJECTIVES When you have completed this lecture, you Should be able to describe: ◼ Describe the dynamic processes of degeneration and reinnervation ◼ Understand concep...

PHYSIOLOGICAL CHANGES AFTER PERIPHERAL NERVE INJURY ELECTRICAL STIMULATION PTY 214 Lect 9 fchs.ac.ae OBJECTIVES When you have completed this lecture, you Should be able to describe: ◼ Describe the dynamic processes of degeneration and reinnervation ◼ Understand concept of electrical stimulation for peripheral nerve injury- NMES and FES  Peripheral nerve injury ◼ MOI : Nerves can be injured by stretch (traction), laceration ,compression, or burning. ◼ Disease of PNS ◼ Damage varies in severity from transient to complete interruption. ◼ Damage of cell body, axon, myelin sheath, connective tissue, blood supply. ◼ Symptoms of PNI: sensory symptoms- numbness and pain, motor symptoms- weakness. ◼ Long-term (chronic) pain can be a major problem for some people ! Peripheral nerve Anatomy Peripheral nerves are made up of axon endoneurium Connective tissue perineurium epineurium Nerve trunks myelinated fibre unmyelinated fibre Myelin- protein-lipid complex function insulating layer  Seddon Sunderlan Pathophysiological Basis d Local myelin damage. Axons Neuropraxia I preserved. No degeneration. Endoneural tube preserved. Axon II degeneration. Loss of endoneural tube continuity. III Perineurium intact. Axon Axonotmesis degeneration. Endoneural tube and perineurium IV disrupted. Epineurium intact. Axon degeneration. Neurotmesis V Complete loss of neural continuity Modified from Lundborg G (1987): Nerve regeneration and repair. Acta Orthop Scand 58:p. 150, 1987. PROGNOSIS OF PNIs Tissue damage Recovery Epineurium None Perineurium Endoneurium Incomplete Axon Myelin Full Sunderland grade 1 2 3 4 5 Seddon grade Neuropraxia Axonotmesis Neurotmesis Pathological changes ◼ Three basic processes: ◼ Wallerian degeneration ◼ Axon degeneration ◼ Demyelination  Cause: the degeneration of axons that take place distal to an injury 1.Wallerian degeneration ◼ The process occurs within 7-10 days of injury and this portion of the nerve is not responsive to stimulation (inexcitable) ◼ Nerve fibers distal to the injury site undergo Wallerian degeneration. The denervated Schwann cells (SCs) proliferate, elongate and line the endoneurial tubes to guide and support regenerating axons. ◼ No degeneration process in Neuropraxia. 2. Axon degeneration ◼ Distal degenerated nerve is inexcitable electrically. ◼ Seen in generalized neuropaty. ◼ Regeneration can occur since the basement membrane of the Schwann cell survives and act as a skeleton along which tha axon regrows up to a rate of about 1mm per day. 3. Demyelination ◼ Segmental destruction of the myelin sheath occurs without axonal damage. ◼ The primary lesion affects the Schwann cell and causes marked slowing of conduction or conduction block. ◼ Local demyelination is caused by inflammation, eg: Guillain-Barre syndrome. Regeneration and reinnervation ◼ Injured peripheral nerves but not central nerves have the capacity to regenerate and reinnervate their target organs. ◼ Regeneration- the formation of axonal sprouts, their outgrowth as regenerating axons and the reinnervation of original targets. ◼ Reinnervation- Restoration of nerve function after it has been lost. ◼ Reinnervation may occur spontaneously or be achieved by nerve grafting. PERIPHERAL NEUROPATHY Neuropathy is damage or dysfunction of one or more nerves. This high blood sugar can by time will start damaging vessels and nerve (usually nerve damage happens in feet so pt with diabetes sufferers from problem with sensation this is called :diabetic nuropathy if it progress it leads to amputation Caused either by diseases of the nerve or from the side-effects of systemic illness. Classification 1. Mononeuropathy 2. Mononeuritis multiplex 3. Polyneuropathy 4. Autonomic neuropathy  MONONEUROPATHY ◼ Is a type of neuropathy that only affects a single nerve. ◼ Carpal tunnel syndrome is one example of this. ◼ Diagnostically useful to distinguish them from polyneuropathies. ◼ Cause is a localized trauma or infection. ◼ The most common cause of mononeuropathy is by physical compression of the nerve, known as compression neuropathy. MONONEUROPATHY MULTIPLEX ◼ is the clinical result of damage to several different nerves, either serially or concurrently. ◼ The pattern of involvement is asymmetric. ◼ It is caused by or associated with medical conditions such as diabetes mellitus and vasculitis. ◼ Symptoms include: ◼ loss of sensation, weakness, or paralysis in one or more parts of the body; loss of bladder or bowel control; and tingling, burning, or pain in one or more parts of the body.  POLYNEUROPATHY ◼ Is a pattern of nerve damage which is quite different from mononeuropathy. ◼ In a polyneuropathy,many nerve cells in different parts of the body are affected, without regard to the nerve through which they pass. ◼ Medical condition can lead to polyneuropathy as diabetes, autoimmune disease, hereditary condition, bacterial or viral infection. ◼ Guillain–Barré syndrome? AUTONOMIC NEUROPATHY ◼ Is a form of polyneuropathy which affects the autonomic nervous system. ◼ Affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. ◼ Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. ◼ In most but not all cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.  Most importantly for paralysis muscle grade (0,1,2) to prevent atrophy Electrical stimulation ◼ Start early –acute stage ◼ Frequency of 20Hz for one hour accelerates the outgrowth of axons across the site of surgical repair of transected nerve stumps to result in accelerated target reinnervation. What is the difference between functional electrical stimulation and electrical stimulation ? FES : important for functional movement :walking , standing, grap  STRENGTH DURATION CURVE (SDC) To stimulate a nerve, the stimulus has to be both of sufficient strength (intensity) and of sufficient duration to depolarize the nerve membrane. Duration = Pulse width Strength = Amplitude The strength relationship can be determined by applying single rectangular pulses of differing pulse widths to a peripheral nerve. The intensity of current required to produce a single muscle contraction (often called a twitch contraction) is recorded along with the time (pulse width) for which it is applied. STRENGTH DURATION CURVE (SDC) Rheobase is the minimum, current (stimulus strength) that will produce a minimal visible response. “rheo” means current “base” means foundation Chronaxie is a duration that gives a minimal visible response when the nerve is stimulated at twice the rheobase strength  STRENGTH DURATION CURVE (SDC) 150 Nerve No stimulation 120 Denervated muscle even in much intensity (mA) higher intensities Stimulus 90 60 30 0 0.01 0.03 0.1 0.3 1 3 10 30 100 300 1000 Pulse duration Time (ms) TYPES OF ELECTRICAL STIMULATION Neuromuscular Electrical Stimulation (NMES) ⚫ Used to produce muscular contraction Functional Electrical Stimulation (FES) ⚫ Used when the aim of treatment is to enhance or produce functional movement. EMG-triggered ES ⚫ Stimulator will be triggered by muscle contraction Transcranial Direct Current Stimulation (tDCS) ⚫ Direct stimulation of the brain using direct current. Changes brain excitability ELECTRODE PLACEMENT WRIST AND FINGER EXTENSION Monopolar method: Indifferent (passive) electrode (Should be bigger in size) on origin of muscle group ⚫ Active electrode (smaller in size) on the motor point of muscle group Active electrode should be moved to find the best spot Bipolar method: Two same size electrode on target muscle ELECTRODE PLACEMENT FOR KNEE EXTENSION Bipolar method: ⚫ Both electrodes are active and usually in same size Electrodes 2 1 ELECTRODE PLACEMENT Quadripolar method: ⚫ all electrodes are active and usually in same size 1. Neuromuscular electrical stimulation (NMES) ⚫ Aims: restore function and strength, prevent muscle atrophy, and reduce muscle spasms and swelling. ⚫ Side effect: skin irritation or rash. ⚫ https://www.youtube.com/watch?v=_eBU skzKaPI – How to prepare for NMES NMES ⚫ The most important is prevention of atrophy when grade is 0 or 1 ⚫ Can be apply 1 hour after the injury. ⚫ Applied 2X daily, at the maximum tolerable intensity for 15 contractions. Dosage? Quality of contraction ! Other benefit of ES ⚫ Increase circulation ⚫ Increase ROM ⚫ Reduce spasticity if we apply ES for CNS conditions. THERAPEUTIC USE OF ES OF INNERVATED OR PARTLY INNERVATED MUSCLES 1. Strengthening 2. Increasing endurance 3. Muscle re-education 4. Maintaining contractibility  MUSCLE PUMP CONTRACTIONS A MECHANISM FOR BLOOD RETURN ⚫ Regular muscle contractions normally help to stimulate circulation by pumping fluid and blood through venous and lymphatic channels back into the heart ⚫ This mechanism fails after paresis or paralysis of skeletal muscles ⚫ ES of muscles in the affected extremity can help in reestablishing the proper circulatory pattern One-way valves ⚫ Using elastic bandage on the limb increase the effects of ES.  ENHANCEMENT OF CIRCULATION MUSCLE PUMP CONTRACTIONS ⚫ The part to be treated should be elevated ⚫ The patient should be instructed to allow the electricity to make the muscles contractions Active ROM should be encouraged if it is not contraindicated ⚫ Total treatment time 20-30 minutes, two to five times daily  INCREASING RANGE OF MOTION IN PATIENT WITH HEMIPLEGIA ⚫ Limiting structure is spastic muscle group ⚫ To maintain the normal ROM Regular passive movements and splinting are recommended ⚫ An alternative therapeutic method Electrical stimulation of antagonistic muscles ⚫ Example Hemiplegic patient with wrist and finger flexor spasticity Target muscle for ES: Wrist and finger extensor muscles RECIPROCAL INHIBITION MECHANISM TO REDUCE SPASTICITY Antagonist - Muscle inhibited + Agonist Muscle Facilitated MUSCLE REEDUCATION ⚫ The patient should be instructed to allow the electricity to make the muscles contractions Allowing the patient to see and feel the response The patient should alternate voluntary muscle contraction with current-induced contractions ⚫ Total treatment time 15 minutes, several times daily RETARDATION OF ATROPHY Muscle injury, and ES of skeletal pain muscle Prevents muscular Help to maintain activity muscular activity Decrease Increase physical and chemical events physical and chemical events associated with muscle function associated with muscle function Muscular atrophy Maintain muscle bulk FES ⚫ is a technique that uses electrical currents to activate nerves innervating extremities affected by paralysis resulting from head injury, stroke, MS, CP. 2. Functional electrical stimulation (FES) FES bicycle FES and Treadmill training FES- ankle DF Motor reeducation Tibialis anterior Walking – functional activity FES Parametars Evidenced Based for LL ⚫ FES can replace AFO ( important for teenager) ⚫ Increase self-esteem, walking easier and faster, less pain in CP (Pool, 2015). ⚫ FES improve QOL when is drop foot ( Lee, 2019). ⚫ The kids who are not focus on exercises are good candidate for FES( Chiu, 2014). FES- UL REFERENCE Gordon T. (2009) The role of neurotrophic factors in nerve regeneration. Neurosurg Focus.;26(2):E3