Neuro Test 2 Review Questions PDF

Neuro Test 2 Review Questions Tone lecture What is tone? - Property of muscle's contractile and fascial structures True or false: Tone is the amount of tension in contracted muscles - False it is in relaxed muscles How is tone regulated? - Spinal reflexes and multiple descending suprasp...

Neuro Test 2 Review Questions Tone lecture What is tone? - Property of muscle's contractile and fascial structures True or false: Tone is the amount of tension in contracted muscles - False it is in relaxed muscles How is tone regulated? - Spinal reflexes and multiple descending supraspinal (brainstem/cerebellum/cortex) mechanisms Which muscles of postural control and stability is tone necessary for? - Neck - Shoulder/ pelvic girdle - Trunk (core) True or false: Tone is necessary for active voluntary movement and movement control - True! What is the definition of normal tone - Right amount of tension inside the muscle at rest - Allows the muscle the inherently contract on command and be ready for voluntary movement What is hypotonia? - Flaccidity in muscles - Low tone = not enough tension in the muscle - Feels slightly mushy or floppy - Limb easily moved What problems are seen with hypotonia - Problems of motor control/coordination, postural instability; joint laxity; weakness; decreased endurance What conditions are often associated with hypotonia - Lower motor neuron conditions - Neuropathies (Guillain barré) - Cerebellar lesions - Early stages of acquired brain (TBI) or spinal cord lesions (SCI) What is hypertonia - High tone: too much tension in the muscle, tight and tense even when relaxed/not active causing movement to be difficult, awkward, stiff, and/or painful What conditions are often associated with hypertonia? - Upper motor neuro conditions and extra pyramidal conditions - Congenital conditions CP What are the 2 types of hypertonicity and associated conditions 1. Spasticity MS, stroke, TBI 2. Rigidity Parkinson What is spasticity? - **velocity dependent** resistance to stretch --amount of "stiffness" felt is related to speed of the passive stretch movement; specific patterns of involvement ie flexors in UE, extensors in LE. Upper motor neuron (pyramidal). What is rigidity - **non velocity-dependent** resistance -- **uniform increased** tone whether the joint is passively moved quickly or slowly, affects both flexors and extensors (agonists & antagonists) Extra-pyramidal. How Do you perform an assessment of tone? - Move limb segments through passive lengthening range of motion (limb relaxed) and feel the amount of resistance during the movement resistance is qualified or graded - Tonic response to (relatively) slow stretch) - Low tone - Feel no or little resistance - Can be overly flexible and could be soft on palpation - Qualitative assessment only no objective grading of low tone - High tone - Objectively graded (0-4) using the standardized test called modified Ashworth scale Explain how to use the modified Ashworth scale - Patient in supine - For a muscle that primarily flexes a joint (ie. biceps): place the joint in a maximally flexed position (**shortened position**) & passively move to a position of maximal extension (**lengthened position)-**full ROM over 1 second *(ie. count \"one thousand one" while lengthening)* - Feel for **amount of resistance** while moving limb & **where in range** resistance is felt.  What are the impacts of no tone? - Total flaccid paralysis What are the impacts of low tone? - Postural control issues - Joint instability - Decreased endurance - Weakness - Movement and coordination problems What are the impacts of high tone - Mild stiffness to difficulty moving to complete immobility - Weakness - Spastic paresis - Mild discomfort to severe pain What are the PT treatments of low tone - Muscle activation/facilitation/strengthening (with manual and proprioceptive input or resistance) - Stabilizing and endurance exercises for postural and anti-gravity muscles - Core muscle stimulation - Weight bearing activities - E-stim - Rhythmic stabilization exercises What are medical managements of spasticity - Pharmacological agents - Oral medications such as baclofen - Baclofen pump into spinal fluid - Cannabis - Botox injections - Paralyses the spastic muscle - Small amounts injected into selected sites - Surgery - Dorsal rhizotomy selective spinal nerve roots are severed - Neurectomy removal or peripheral nerve What are was the medical team managed spasticity - Reduction/ avoidance of noxious stimulation or discomfort - **Decrease pain or effects** from triggers such as pressure ulcer, ingrown toenail, contracture, kinked catheter, urinary tract infection, DVT, fecal impaction, sepsis, fracture, other sources - Positioning - **Avoid:** *poor positioning & postures associated with patterns* ie hip extension, adduction, internal rotation), ankle plantarflexion; sh adduction, internal rotation, elbow & wrist flexion - **In bed or chair:** place the patient in *"out of pattern" positions* for U & LE with good trunk What are the PT management strategies for spasticity - Stretching/exercises in PROM - start pROM & stretches early in the treatment of any neurologic condition; - esp important after botox and or surgery - Splinting or casting - to maintain or lengthen muscle length, prevent tissue shortening - Physical modalities - cooling or icing ie quick icing to affect antagonist or prolonged cooling for direct agonist effect - heat ie superficial or deep - E Stim - TENS (Transcutaneous electrical nerve stimulation) - NMES (Neuro-muscular electrical stimulation (agonist or antagonist) What are the medical management strategies for rigidity - Pharmacology - Oral medications - Surgery - Deep brain stimulation - Precise brain area ablations What are the PT Interventions for Rigidity - Stretching/exercises - Daily movement & flexibility routine and general exercise program - Rhythmic exercises and trunk rotation - Physical modalities - Heat or hot baths - Cooling or ice only sometimes - Relaxation activities and exercises A screenshot of a computer screen Description automatically generated Can Spasticity be beneficial? - Yes! - In some patients spasticity can allow them to have the muscle activity to facilitate standing an walking due to an increased tone response. - When the spasticity is decreased, they are unable to do these tasks What are the Superficial reflexes and what are they associated with? - Babinski/ plantar reflex - Sensory stim on the lateral aspect of the sole of the foot from the heel to the toes - Normal toes flex - Abnormal toes flare out an up, great toe goes up - Hoffmans reflex - Tapping or flicking the nail of the terminal phalanx of the middle finger - Abnormal flexion of the terminal phalanx of the thumb - Associated with upper neuron conditions What kind of response is associate with the deep tendon reflex? - Phasic response to a quick brief stretch What are the different DTRs and their associated spinal nerve roots? - Biceps = **C5**/C6 - Brachioradialis = C5C8 - Patellar = L2-**L4** - Achilles = **S1**/S2  What lesion is associated with a pendular reflex? What is a Pendular reflex? - Cerebellar lesions - reflexes are not brisk but actually involve poor agonist-antagonist movement control; loosely swings forwards and backwards several times, slows down & stops. What is clonus? - An abnormal and involuntary rhythmical series of contractions (oscillations) - Upper motor neuron sign When is clonus tested - Only when DTR's are increases/hyperactive How is clonus tested - Muscle in relaxed state; tested most often **in ankle & wrist** but may also be present elsewhere - Briskly **stretch** and **hold** - No clonus = no movement = normal - Clonus = abnormal response - unsustained -- stops by itself (note \# beats) - sustained (constant) -- does not stop What is motor coordination? - The ability to execute smooth, accurate, and controlled motor responses - Described as selection of the right muscle at the right time with the proper intensity to achieve desired action - Characterized by appropriate speed, distance, direction, timing, and muscular tension (force) - Typified by optimal interaction of muscle function Coordination required integration/involvement of what systems - Motor - Sensory - Vestibular - The cerebellum What is Ataxia? - Abnormal coordination but not due to muscle weakness; associated with cerebellar dysfunction What movement qualities are important to observe and evaluate? - Speed and timing - Accuracy and precision (range, direction, and force) - Fluidity and smoothness (multi-joint) What are two assessments of coordination and explain them 1. Rapid alternating movements (RAM) a. Quick succession of agonist-antagonist movements = diadochokinesia b. UE finger/hand tapping; forearm pronation/supination c. LE foot tapping d. Abnormal = dysdiadochokinesia (not rhythmic; slow) 2. Point to point movements e. Evaluates accuracy, precision and fluidity of multi jointed movements f. UE finger opposition; finger to nose g. LE heel to shin h. Abnormal i. Dysmetria under/overshooting target ii. Dyssynergia jerky multijointed movement What are the recommendations for a Tone assessment? - **Explain, demo** or **passively guide test movement** - Ask patient to perform movements **as quickly** and **as accurately** as able; eyes **remain open** - **Observe movement** for any abnormalities or irregularities in - speed/timing, accuracy/precision, fluidity; compares sides (tests must be **performed on both sides for comparison (even in unilat problem)** - Time (s) to perform 5 or 10 reps **(objective outcome)** What standardize tests are used to evaluate Ataxia - Scale to assess ad rate Ataxia SARA - International cooperative ataxia rating scale ICARS What is sensory ataxia - A form of dyscoordination caused by loss of sensory input and NOT by cerebellar dysfunction Adult NMC Lecture What is a neuromuscular condition - A condition/disease that affects the peripheral nervous system, the neuromuscular junctions, or skeletal muscles, all of which are components of the motor unit What is Guillain Barré syndrome? - Acute inflammatory demyelinating polyneuropathy (AIDPN) - Body's immune system attacks part of PNS What are the signs and symptoms of GBS - Bilateral and rapid onset - Mild, intermittent tingling in hands and feet paresthesia - Progressive weakness UE, LE, trunk, and face distal to proximal - Respiratory muscle paralysis may require mechanical ventilation - Bulbar involvement - Difficulty swallowing - Low volume speech - Nasal tones - 1-4 days of constant, painful muscular aching and tenderness - Loss of stretch reflex - Autonomic involvement - Tachycardia - Change in BP - Urine retention What is the cause of GBS? - Unknown syndrome vs disease - Autoimmune disease - Few days to 4 weeks post viral or bacterial infection - Respiratory or GI - 5-10% following a surgery - Flu vaccine 1976-1977 What is the incidence and prevalence of GBS - Incidence 3500/year in usa and Canada - Prevalence 1-2/100,000 How is GBS diagnosed - Clinical and medical history - Lumbar puncture increase protein in CSF - Nerve conduction velocity tests are slowed What are the stages of GBS - Acute decline - Stable period - Recovery What is the treatment for GBS? - No cure - Plasmapheresis - High dose Immunoglobulin theraoy - Corticosteroids not recommended - Supportive treatment What is Miller Fisher Syndrome? - Variant of GBS - Ataxia, ophthalmoplegia, areflexia - Severe weakness less common What are the PT assessment guidelines for GBS for body function and structure (impairments) - Motor weakness - Trunk and extremities: use manual muscle testing or hand-held dynamometer - Note the Pulmonary Function Test values as breathing may be completely diaphragmatic - Observe for any swallowing difficulties and facial weakness - Pain - Tenderness to palpation, pain on mobilization of joints - Pain intensity - Visual analog scale - Sensory - Usually not a complete sensory loss - Presents as stocking -- glove distribution - i.e., distal to proximal with fading borders - Decreased light touch, vibration and joint position sense - Autonomic - Sudden hypotension or hypertension - Cardiac arrhythmias - Postural hypotension - Loss of bowel & bladder control - rare What are the PT assessment guidelines for GBS for Activity limitations - Endurance - Two 6 min walk tests - Functional status - Gait speed - Functional mobility, bed mobility, transfers, TUG, stairs - ADL scales - Barthel index What is the expected participation restrictions with GBS - Within 3 weeks of dx 80% of cases have reached their lowest point for weakness; some cases 1-2 months. - Recovery of muscle strength usually begins 2-4 weeks after the plateau phase. - 80% become ambulatory within 6 months of onset. - 50% may show minor neurological deficits - 15% may show persistent residual deficits in function - 5% mortality rate - 3% may suffer a relapse many years after the initial attack - Health-related quality of life measures such as: - Medical Outcomes Trust Short Form 36 (SF-36) - Sickness Impact Profile (SIP) - best used for out-patients. What are the PT interventions in Acute phase GBS - +/- intubated; trach'ed, usually in ICU - Get involved ASAP - DO NOT **FATIGUE** PATIENT - Goals - Skin protection - Special mattress - Positioning to prevent sores - Prevention of contractures and DTV - Passive ROM - positioning so that groups of muscles are in a lengthened position for a minimum of ½ an hour every other day is enough to prevent loss of range. PROM for each muscle group takes an inordinate amount of time - Splints for hands and feet - More at risk for contractures if patient is respirator dependent, quadriplegic or if pain is present - Role of Continuous Passive Motion machines -- unclear benefit - Pain relief - TENS - Medication - PROM - Maintain pulmonary function - Prevent chest infection - Chest physio secretion clearance and improve ventilation - Monitor physical status - Mostly motor function with regular strength assessments - Useful in deciding further medical treatments What are the PT Interventions in Plateau phase of GBS - Continue as acute phase but mobilize as tolerated - Phase can last a few days or as long as 4-6 weeks - May be off ventilator, trach'ed, Percutaneous Endoscopic Gastrostomy (PEG) - Continue ROM: - Positioning at end range with low tension or load for a minimum of 2 hours per day, 5 days per week for 4 weeks is necessary to make gains in ROM - Monitor changes in end feel - Minimize postural hypotension: - e.g., tilt table, dangle, elastic stockings, abdominal binders - danger signs include: - diastolic BP drop \>20mm Hg - HR \>120 - Sweating, nausea, blurred vision - No fatiguing What are the PT interventions in recovery phase of GBS - Returning muscle strength - Improvement in sensory deficits - Autonomic stability - Return of stretch reflexes - Duration varies with age, severity of disease, and comorbidity - Maintain patient's musculoskeletal system in optimal state - Pace recovery to obtain maximal function as re-innervation occurs - Guidelines for an active exercise program: (exercise prescription) - Short periods of **non-fatiguing** exercise - Increase activity or exercises if [no deterioration] occurs after one week - Return to previous activity if deterioration occurs - Use functional exercises as well as specific muscle strengthening exercises, e.g., sit to stand - Limit fatiguing exercises for one year - Exercises will not hasten or improve nerve regeneration - Signs of deterioration - Recurring muscle tenderness - Loss of reflexes - Resumption of paresthesia - Loss of function - PNF - Endurance training - Cardiovascular fitness What is Post-Polio Syndrome? - progressive clinical syndrome consisting of [new] weakness, fatigue and pain in those individuals who have recovered from past paralytic polio What is Poliomyelitis (Polio) - poliomyelitis (polio), a contagious viral illness that in its most severe form causes paralysis, difficulty breathing and sometimes death - fewer than 1% of polio infections ever result in paralysis (paralytic polio) - poliovirus can spread widely before cases of paralysis are seen - a person may have been infected, not present any signs of illness, yet be contagious as the virus is shed intermittently in feces. - infection leads to inflammation of nerve cells in the ventral horns of the spinal cord -- damages motor neurons (anterior horn cells) How is PPS diagnosed? - Exclusion - Clinically based - Criteria - [previous acute paralytic pol]io which is [confirmed] by history, physical exam and EMG studies. - a [period of recovery] followed by a [period of neurological and functional stability] usually \> 15 years duration [before the onset of new difficulties.] - [gradual or abrupt onset of new muscle weakness] which may or may not be accompanied by other difficulties such as: - excessive fatigue - [ muscle pain] - decreased endurance - [joint pain] - decreased function - atrophy - the **[exclusion]** of medical, orthopaedic or neurological disorders which could be producing the new problems. - symptoms persist for at least one year What is the etiology (cause) of PPS? - Unclear - likely possibility -- peripheral disintegration of enlarged post-polio motor units - possible contributing factors: - normal ageing process - growth hormone and insulin-like growth factor deficiency - overuse - may produce weakness in partially denervated muscles - muscle disuse - limited activity from joint pain, illness - uncertain factors - significance of poliovirus genome fragments detected in CSF of PPS patients - **role of immune mechanisms -- active inflammation in spinal cord** What are the risk factors for PPS - greater severity of acute paralytic polio - iron lungs - greater recovery after acute episode - quadriparetic to fully functional - older age (not clearly shown) - longer time period since acute episode What are the key muscle groups to assess with PPS  What is the management of PPS weakness and the treatment guidelines - determine the function of weak muscles - treatment guidelines - Strengthening - ≥ 3/5 isotonic, isokinetic exs =submaximal, \