Week 2 Neuro Summary PDF

2.6 GMS Intro Clinical Presentation GBS: n damage bc own body defenses, autoimmune disorder targeting peripheral n (myelin sheath mainly) Physiology/Presentation impair n. signal propagation for M & S LMN - weakness, poor muscle activation DEMYELINATION M&S - loss of reflexes - numbness, poor sensor...

2.6 GMS Intro Clinical Presentation GBS: n damage bc own body defenses, autoimmune disorder targeting peripheral n (myelin sheath mainly) Physiology/Presentation impair n. signal propagation for M & S LMN - weakness, poor muscle activation DEMYELINATION M&S - loss of reflexes - numbness, poor sensory feedback AIDP (acute inflammatory demyelinating polyneuropathy) most common myelin membrane on both motor & sensory peripheral n. attacked CN, Autonomic n., pain signals also involved AMAN (acute motor axonal neuropathy) axonal membranes of motor n. only AMSAN both motor & sensory peripheral n axons miller fisher cross reactive antibodies attack CN or BS paralysis of eye muscles muscle incoordination areflexia facial weakness dysphasia dysarthria respiratory failure CIDP (chronic inflammatory demyelinating polyneuropathy) slower disease course than AIDP motor impairments sensory dysfxn paresthesia kinda like MS but with peripheral nervous system in comparison of single acute attack in AIDP in GBS cauda equina & conus medullaris more apparent where peripheral n concentrated Clinical Presentation pathogenesis: progression of demyelination to axon damage tingling of feet/hands problems getting up from chair days later areflexia weakness distal sensory loss weakness to LE then UE sensory motor pattern ascends body in hours/days involve trunk intercostals neck muscles CN respiration problems b&b fxn areflexia, hyporeflexia, muscle flaccidity not initially atrophy history of GI virus more presentations fatigue - physiological: change in CNS or PNS by looking at loss of muscle force - CNS: change in neurotransmitter activity, mental or physical activity (hard to focus), loss of voluntary control - PNS: change in neuromuscular jxn, muscle activation by activity/mvmt - experienced fatigue: person’s perception/psychosocial impacts GBS thought to have high level of central fatigue minimize neural activations bc thought to damage muscle due to demyelination muscle perceives higher exertion -> central fatigue Summary GBS non progressive neuromuscular disease unclear etiology LMN impaired strength, sensation, ANS, participation when working w/ GBS watch out for peripheral fatigue bc can cause them to regress 2.7 GBS Medical Management Differential Diagnosis look at pattern of impairments - focal, multifocal, generalized subjective history to narrow down or use diagnostic tests - blood lab, CSF exam main presentations weakness in more than one limb symptoms progress in days/4 weeks helps identify what type progression is distal to prox can move to respiratory/CN involvement RULE OUT dont fall under GBS on a child w/ AIDP vs AMAN Nerve Conduction Velocity Tests increased conduction of velocity/ latency as time goes on CMAP = compounded muscle action potential - decrease w/ progression in both AIDP: less SNAP (sensory nerve axonal potential) SNAP not found in AMAN AIDP: 2 mV vs AMAN: 1 mV CMAP in AMAN way lower = more motor axon involvement Management of GBS PLEX plasma exchange removes cross reactive antibodies from BS to limit attack process - take blood, separate platelets, red cells, lymphocytes, granulocytes by centrifuge/filter - trash bad ones - red cells combined w/ fake plasma (colloid replacement) - put back takes hours 2-5 sessions over days decreases time on ventilator, improve disability/motor scores complications: drop in BP, arrhythmias, relapse started before 7 days better outcome Intravenous Immunoglobulin (IVIg) less invasive, less side effects, cheaper targets immune cells attacking myelin adding healthy antibodies improves recovery, clinical outcomes but not mortality best within 2 weeks symptom onset DONT DO BEFORE PLEX bc then just remove good stuff not great for mild cases read general medical management Disease Course viral infection (GI 2 weeks before) cross reactive antibodies build up attacking myelin & PNS symptoms plateau w/in 4 weeks of onset months recover post plateau - better fxnal status rehab/compensatory schwann cells remyelinate which helps motor fxn partial recovery (2-4wks post plateau) - weakness, fatigue Prognosis & Outcomes fatality - 3-10% bc respiratory problems - 20-30% need mechanical vent disability - 75% - fatigue, paresthesias, pain/weakness ambulatory - 15% - cant walk indep Erasmus GBS Outcome SCore potential to walk again age, diarrhea, GBS disability score higher = higher chance of not walking indep at 6 months Poor prognostic indicators GI illness severeity of muscle weakness respiratory/mechanical vent CN involvement older age severity of nadir, prolonged time to reach nadir (higher chance of relapse) Summary GBS diagnosed based on progressive LE to UE weakness & areflexia high potential for survival & recovery of fxn & participation w/ residual impairments nadir = point of greatest disease severity 2.8 GBS REHAB PLAN OF CARE Evaluation: Relevant tests. MMT, CN Testing, Sensory, Functional Mobility Depending on function and goals BERG, Functional gait , Activities Specific balance, ten meter walk test, Six Meter Minute walk test, five times Sit to Stand Depending on Severity Presence and extent of the common impairments and functional limitations People recovering from GBS have a high chance of recovering strength and function, so outcome measures should allow for recovery and not have too much a ceiling effect Due to demyelination, do not test patients to fatigue or overwork weakness Quick notes: Someone with a grade 4, over the age of 60, has a 70% chance of walking in 6 months Someone who is over 60 and require ventilation has 50% chance of walking in 6 months Assessment of fatigue: Need to assess physiological and experienced fatigue Subjective and Objective outcome measures Objective: Check for muscle belly tenderness Gentle pressure with the palmar surface of hand and fingers to a relaxed muscle belly of a major muscle group. Patient rates 0-10 pain intensity For Physiological Fatigue: measuring force generated by muscle from electrical stimulation. Voluntary and involuntary contraction. Record decline of force which represents the fatigue Subjective: Patient reports perceived fatigue and impact on daily function and participation. Fatigue severity scale and modified impact scale are the two used measures. Rate level of agreement with various read statements ACUTE REHAB Individual is likely in hospital and need close monitoring and may require assistance. Assess vital capacity or other pulmonary measures Physical Therapy intervention is dependent on the severity. When able to increase endurance, patients should assume upright positions Educate and teach respiratory exercises Ensure range of motion. Range of motion commonly affected areas. Hip Flexors, ankle plantarflexors, knee flexors, shoulder and elbows Order of subacute rehabilitation Strength Training Often patients will be at a 1-2 grading scale in MMTs Training should be done with gravity eliminated positions with full ROM in mind Strength training can eventually be moved towards multi joint and multiplanar movements against gravity. Focus on submax strength for both fast twitch muscle fibers and eccentric muscle contractions. Durable Medical Equipment Ankle foot Orthosis. AFO For foot drop, and propulsion during gait 2/3 participants continue to use AFO at discharge 1/3 continue use 1 year after discharge