PCE 2021 Written Course Manual PDF

WRITTEN COURSE MANUAL  COURSE OUTLINE Session Topics Covered Session 1  Exercise Prescription  Lower Extremity Musculoskeletal Conditions Session 2  Upper...

WRITTEN COURSE MANUAL  COURSE OUTLINE Session Topics Covered Session 1  Exercise Prescription  Lower Extremity Musculoskeletal Conditions Session 2  Upper Extremity Musculoskeletal Conditions  Peripheral Nerve Injuries  Musculoskeletal Special Tests  Posture  Spine Scans  Joint Mobilizations  Myotomes/Dermatomes  Deep Tendon Friction Massage  Neurodynamic Testing  Manual Muscle Testing  Peripheral Nervous System  Range of Motion and Goniometry Session 3  Respiratory Anatomy  IPMA  Lung Volume and Capacity  Breath Sounds  Respiratory Conditions  Critical and Acute Care  Pulmonary Rehabilitation  Cardiovascular System Physiology  Breathing Exercises  Electrocardiogram (EKG/ECG)  Chest PT and Secretion Clearance Techniques  Cardiovascular Conditions  Ventilation/ Perfusion Ratio  Cardiopulmonary Exercise for Cardiac Patients  Arterial Blood Gases  Peripheral Vascular Disease Session 4  Mock Exam Review #1 Session 5  Gait Mechanics  Traumatic Brain Injury  Mobility and Transfers  Non-Traumatic Brain Injury  Joint Replacements  Cerebellar Disorders  Balance  Spinal Cord Injuries  Parts and Functions of the Brain  Neurodegenerative Diseases  Acquired Brain Injury Session 6  Movement Disorders  Arthritis  Inflammatory/Infectious Conditions of the CNS  Bone Conditions  Diseases Affecting the Neuromuscular Junction  Pain Syndromes  Peripheral Neuropathies  Obesity  Vestibular Disorders  Pregnancy and Postpartum Conditions  Cranial Nerves  Pediatrics  Neurological Glossary  Orthotics Session 7  Modalities  Skin Conditions  Cancer  Stress  Liver Conditions  Thyroid Hormonal Dysfunction  Blood Disorders  Adrenal Gland Dysfunction  Metabolic Disorders  Gastrointestinal Disorders  Infection  Temperature Associated Conditions  Infection Transmission  Mood and Mental Disorders  Amputees  Documentation  Connective Tissue Disorders  Outcome Measures  Structural Deformities  Research  Burns  Ethical Considerations  Scars  Canadian Physiotherapy Code of Ethics Session 8  Mock Exam Review #2 1  Session 1 Exercise Prescription Type of Exercise Load (%1-RM) Repetitions Sets Rest Strength >85% 20 mmHg OR DBP >10 mmHg when a person assumes a standing position. Signs and Symptoms:  Dizziness, light headedness, fatigue, blurred vision, muscle weakness, syncope. Treatment:  Optimal position is supine if patient demonstrates signs.  If severe, use tilt table with progressive vertical positioning to assist with standing.  Tolerance can be improved by medications, regular physical activity, being upright and compression stockings. 173  Session 4 Mock Exam #1 You are to complete your first 100 multiple choice mock exam before your next session. We advise you to take the test in a quiet area. Mimic the environment of the exam. E.g. No food, just water, no music or distractions. After you complete the exam, please review the exam #1 feedback which will go through all of the exam questions and the correct answers. 174  Session 5 Gait Mechanics Gait Cycle: Stance and swing phase = heel strike to heel strike on the same leg.  Step: distance between the heel contact point of one foot and that of the other foot (~0.7m). o Example: left step length is measured from right heel to left heel.  Stride: distance between successive points of heel contact of the same foot (double step length) (~1.4m).  Velocity = total distance traveled in a given amount of time; average = ~1.3m/s.  Use this chart to help you understand which muscles are active during gait – try your best to understand which muscles are working eccentrically and concentrically.  Know classic gait terminology as well as Rancho Los Amigos Terminology – know which is included in stance and swing phase. Rancho vs. classic gait classification:  Rancho classification: Initial contact, loading response, mid-stance, terminal stance, pre-swing, initial swing, mid-swing, terminal swing.  Classic: heel strike, foot flat, midstance, heel off, toe off, acceleration, mid-swing, deceleration. 175 Stance Phase  Initial contact (heel strike): o Marks the beginning of the initial double limb stance o Definition: occurs when foot contacts the ground o Muscular contractions  Hip extensors contract to stabilize the hip  Quadriceps contract eccentrically  Tibialis anterior contracts eccentrically  Loading response: o Definition: occurs after initial contact until elevation of opposite limb - bodyweight is transferred on to the supporting limb o Muscular contractions  Ankle dorsiflexors (tibialis anterior) contract eccentrically to control plantar flexion moment  Quadriceps contract eccentrically to stabilize knee and counteract the flexion moment (about the knee)  Mid-stance (single limb support): o Initial period of single leg support o Definition  From elevation of opposite limb until both ankles are aligned in coronal plane o Muscular contractions  Hip extensors and quads undergo concentric contraction  Glute medius contracts eccentrically throughout stance to control pelvic alignment  Terminal stance (single limb support): o Definition: begins when the supporting heel rises from the ground and continues until the opposite heel touches the ground o Muscular contractions  Calf toe flexors contract and are the most active during this phase  Pre-swing (second double limb support): o The start of the second double limb stance in the gait cycle o Definition: from initial contact of opposite limb to just prior to elevation of ipsilateral limb o Muscular contractions  Hip flexors contract to propel advancing limb 176 Swing Phase  Initial swing (toe off): o Start of single limb support for opposite limb o Definition: from elevation of limb to point of maximal knee flexion o Muscular contractions  Hip flexors concentrically contract to advance the swinging leg  Mid-swing (foot clearance): o Definition: following knee flexion to point where tibia is vertical o Muscular contractions  Ankle dorsiflexors contract to ensure foot clearance  Terminal swing (tibia vertical): o Definition: from point where tibia is vertical to just prior to initial contact o Muscular contractions  Eccentric activation of hamstring muscles decelerates forward motion of thigh Four main challenges of gait:  Maintaining upright posture  Maintaining equilibrium  Control of foot trajectory and ground clearance  Control of multiple body segments Three main tasks in gait:  Weight acceptance  Maintenance of stability during single leg support  Limb advancement (swing) Normal wear pattern on shoes:  Increased wear over the lateral portion of the outer sole at the heel.  Even wear along the area corresponding to the 1st, 2nd, and 3rd MTP joints.  Even wear over the 1st, 2nd, and 3rd MT heads. Orthotics:  It is not entry level practice to prescribe orthotics.  Exercise should be your first treatment to correct biomechanical faults. Example: overpronation.  In a scenario where a question states that exercise treatment has not worked, you would want to refer to an orthotist for custom orthotics. 177 Gait Patterns  Antalgic gait: o Antalgic gait is a gait pattern seen when a patient has pain in one of their lower extremities o In order to reduce weight bearing on the affected limb, there will be decreased step length of the unaffected limb resulting in decreased stance time on the affected limb o Cadence is reduced  Steppage gait: o Patient cannot DF, results in excessive hip and knee flexion to clear the foot.  Foot slap: o Patient has a weak or absent dorsiflexors and the foot slap down on the ground  Abducted lurch: o Patient leans over the affected/weak hip to place the center of gravity over the hip. It is a compensatory technique for a gluteus medius muscle weakness  Gluteus maximus gait: o Backward trunk lean or throwing the trunk backward after initial contact may be due to weakness of hip extensors (gluteus maximus)  Parkinsonian gait: o Trunk, head, neck forward and flexed o Narrow base, small shuffling steps o Lack of arm swing and trunk rotation o Tend to fall forward and to increase speed (festination) o Episodes of freezing  Scissoring gait: o Most commonly seen in spastic cerebral palsy o Legs cross midline due to spasticity of adductors  Knee hyperextension o Due to weak knee extensors o Inability to take full weight on limb without hyperextending the knee to prevent buckling  Reminder! Appendix Trendelenburg sign and gait: o Trendelenburg gait: during gait, the weak abductors cause the contralateral side to dip o Compensated Trendelenburg: patient will side flex ipsilaterally over standing leg to compensate for weak glute medius and minimus o Trendelenburg sign: when standing in single leg stance, the opposite pelvis (non- standing leg) drops  E.g. The pelvis dips on the contralateral side o Causes:  Gluteus medius and minimus weakness  Lesion in superior gluteal nerve – common during pregnancy o Refer to video in additional resource list: Trendelenburg Gait 178 Mobility and Transfers When not to Mobilize Dean, et al., 2012 Cardio status Neurological status  Mean Arterial Pressure  Patient status o 110 o Severe agitation, distress, or combative, not able to  BP understand instructions o A drop is systolic pressure >20 mm Hg or below pre-exercise level OR a disproportionate rise (>200mm Hg for systolic or  ICP >110 mm Hg for diastolic) o Increase >20mm Hg  HR o 130  Hemodynamic o Uncontrolled hypertension or active bleeding  Acute or unstable cardiac status o New MI, unstable rhythm  Pulmonary embolus o Discussion with physician required to determine suitability  DVT o May mobilize as tolerated after medication, need mobility order from physician Respiratory status Other  SP02 60 %  Uncleared, unstable SCI or  Ventilator issues head injury  Uncontrolled asthma  Unstable fracture 179 Gait Orders  Non-weight bearing (NWB): weight is entirely on unaffected leg.  Feather weight bearing (FeWB): patient can touch floor with toes to aid in balance, but not for weight bearing.  Partial weight bearing (PWB): affected leg begins to take prescribed amount of weight: o Less than 50% patients body weight o When a weight specification is not provided, minimal weight bearing is taught until medical confirmation of safe weight bearing is confirmed  Weight bearing as tolerated (WBAT): patient bears as much weight as possible on affected leg without undue discomfort.  Full weight bearing (FWB): aid used for balance. Mobility Aids Walker: most stable type of device Fitting: elbow should be in 20-30deg flexion when holding handgrips; measure to wrist crease in standing  CONS: no arm swing and unsafe on stairs.  Used for patient with: generalized weakness, debilitating conditions, poor balance/coordination, unable to use crutches; common in elderly; patient has reasonable UE strength and needs max support/stability o Standard walker  Most stable as it has no wheels  Used for NWB, FeWB situations where maximum support is required  Used for slow walking speeds  Needs to be picked up while walking o 2 wheeled walker:  Used for PWB, WBAT and FWB scenarios  Faster walking speeds  Do not need to pick up back legs when walking o 4 wheeled walker:  Used for WBAT and FWB restrictions  Fastest walking speeds  Can have a basket for carrying items  Brakes on handles  Least stable walker  Patients must have good balance and do not need to put weight through walker 180 Crutches: improves balance and lateral stability  Stairs: good leg up, bad leg down. o Descending stairs: therapist is below patient o Ascending stairs: therapist is beside and slightly behind patient o Railing: if possible, use railing on affected side.  If railing is on unaffected side, teach stairs using rail as it is more stable than 2 crutches alone. o Curb: see stairs. o Turning: turn towards strong side using small steps and avoid pivoting.  Strengthen: latissimus dorsi, trapezius and triceps (key for activating scapular depression and elbow extension). o Weakness in latissimus would make it extremely difficult to ambulate on crutches.  Significant obstacle to independent ambulation with crutches = cognitive impairment  Axillary crutches: potential for injury in axilla due to pressure on brachial plexus; stability maintained by squeezing crutches against thorax o Most commonly prescribed in younger (20mm Hg is dangerous o Head down positioning is contraindicated, head of bed should be elevated 30 degrees Cerebrospinal Fluid (CSF)  Produced by the choroid plexus in the ventricles.  Nourishes and cushions the brain.  CSF is constantly being produced with about 500mL being produced a day.  CSF is constantly being reabsorbed with an average of about 150mL present in the subarachnoid space at a time.  Excessive production, diminished absorption or a blockage in the ventricular system can lead to hydrocephalus and elevated levels of ICP. Basal Skull Fracture  Rare.  Can cause a tear in the meninges resulting in CSF leakage.  Signs are blood or CSF out of nose/ears, raccoon eyes, bruising over mastoid (battle sign).  Contraindication: never do nasal suctioning or put in an NG tube. 198 Coma A state of unconsciousness in which there is neither arousal nor awareness:  No amount of stimulus (or only pain) will cause patient to respond.  It is clinically defined as having a GCS score of 8 or less. Treatment for a patient in a coma:  Suctioning: pre/post oxygenation at 100% O2.  Chest physio.  Positioning: constant changes to help prevent bed sores. Goal of positioning may be to decrease extensor or flexor tone.  PROM, Botox, serial casting, resting splints (6-8 hours per day) to prevent contractures.  Mobilization: dangle, lift to chair.  Aspiration risks: turn feed tube off 20mins prior to treatment. Physiotherapy problem list:  Respiratory complications.  Decreased tidal volumes, atelectasis.  Elevated ICP.  Abnormal posturing.  Decreased mobility causing disuse atrophy.  Contractures.  Skin breakdown.  Confusion/agitation.  Fatigue. Initial medical management:  Prevent hypoxia, maintain adequate BP, adequate fluids to maintain mean arterial pressure, HOB 30 degrees.  Nutrition: Hyper metabolism: o Energy expenditure may be doubled for up to 4 weeks o Brain glucose metabolism rate is increased after TBI due to the metabolic cascade of events happening as a result of the brain damage o Increased muscle tone and issues with temperature regulation also play a role 199 Decorticate and Decerebrate Posturing Involuntary posturing indicating a severe brain injury:  Decorticate posturing o Lower extremities are extended and internally rotated with feet in plantarflexion o Upper extremities positioned in shoulder adduction, elbow flexion, and wrist/finger flexion o Indicates damage above red nucleus (located in midbrain of brainstem)  Damage to areas including cerebral hemisphere, thalamus, internal capsule, and disruption of the corticospinal tract  Decerebrate posturing: o Neck is extended o Lower extremities are internally rotated and extended with ankle plantarflexion o Upper extremities positioned in extension and internal rotation with elbow extension and wrist flexion o Indicated damage at or below the red nucleus  Damage to brain stem or cerebellum Hemorrhage and Hematoma Hemorrhage: bleed. Hematoma: collection of clotting blood  Damage can be from anoxia or pressure. Intracranial hemorrhage: bleeding within the skull  Medical emergency because the buildup of blood within the skull can cause increased ICP  Can be due to traumatic or non- traumatic causes 200 Hemorrhage vs hematoma Type Subarachnoid hemorrhage Sub-dural hematoma Epidural hematoma Location Very high-pressure arterial Low pressure venous Rapid arterial bleed bleed between arachnoid and bleed with blood occurring between cranial pia mater collecting between dura vault and dura and arachnoid mater  90% associated with skull fractures, most often in temporal or temporoparietal region (thin bone) Vessels Arteries Veins Arteries Involved  E.g. Circle of Willis  E.g. Bridging veins  E.g. Middle meningeal artery Symptoms Rapid onset of a severe Onset occurs over hours Classic presentation: “Talk (depending headache, vomiting, confusion, and die” on severity) decreased level of Fluctuating symptoms consciousness Appear drunk Initially patient feels normal, then decline in mental Possible CN III warning signs: status until LOC fixed and dilated pupils  Due to increased pressure on cranial nerve Treatment Requires surgical intervention Often surgical intervention Medical emergency, ensure to stop bleed (Clip, coil) (burr holes or craniotomy) ABC’s, transport to relieve pressure immediately Concussion A complex pathological process affecting the brain induced by traumatic biomechanical forces.  A mild form of traumatic brain injury (most common TBI). Cause:  May be caused by a direct blow to the head, face, neck or elsewhere on the body with an impulsive force transmitted to the head.  Coup contrecoup mechanism.  Results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously (in most cases): o Neurometabolic cascade of events Risks: contact sports, anti-coagulants, prior brain injuries. 201 Diagnoses is through clinical assessment:  Subjective history, clinical symptoms, physical signs, behavioral change, cognitive impairment, sleep disturbance.  Signs and symptoms: may evolve over minutes to hours (they don’t always show up immediately): o Symptoms: drowsiness, headache, confusion, neck pain, dizziness, memory loss, fatigue/low energy, irritability/emotional changes, nausea, vision problems, light/noise sensitivity, tinnitus o Signs: vomiting, poor visual tracking, balance impairment, trouble with memory recall, slurred speech, poor concentration/easily distracted, change in pupil size o Symptoms usually reflect a functional disturbance rather than a structural one resulting in NO abnormalities seen on neuroimaging o May or may not involve a loss of consciousness o Symptoms typically resolve on their own in a sequential manner (80-90% of people) within 7-10 days but in some cases this can be prolonged (>1 month) resulting in post- concussion syndrome (10-20% of people) Review the difference between SIGNS and SYMPTOMS. Sometimes a question will ask for only one or both.  Symptoms: something the patient subjectively reports  Signs: something you can see and objectively measure Baseline testing:  SCAT # (constantly updated versions available): o For individuals 13 years or older o Includes: symptom evaluation, cognitive assessment, balance examination, coordination examination. You do not need to know how to conduct a detailed assessment. Be able to recognize the patient population this would be used with. o Child SCAT: For children 5-12 years old  Immediate post-concussion assessment and cognitive test (ImPACT): o Baseline and post injury testing  King Devick test: o Sideline concussion screening test o Can be administered in less than 2 minutes o Assesses eye movement, attention and language o > 5 sec difference from baseline is predictive of a concussive event Classification of concussions:  Historically, concussions were graded: o Grade 1: Does not lose consciousness, dazed o Grade 2: No LOC, period of confusion, does NOT recall event o Grade 3: Loss of consciousness for short time, no memory of event, requires evaluation asap o Grading classification is no longer used 202 Second impact syndrome:  Extremely rare.  Fatal uncontrolled swelling of the brain.  Occurs when someone suffers a minor second blow before the symptoms of a prior brain injury are resolved.  More common in young males. Post-concussion syndrome:  Persistent concussion symptoms (variable) greater than 1-month post-concussion.  Cumulative effects: 3+ concussions: 5X greater risk Alzheimer’s, 3x memory deficits. Initial treatment:  Physical and cognitive rest.  This does NOT mean sit in a dark room without stimulus.  Education: o Restrict: TV, cell phone, intense physical activity, school, sports, driving, reading o Allow: increased sleep, hydration, proper nutrition, listening to audiobooks/quiet music, slow walks outside, gentle yoga, meditation, relaxing leisure activities (e.g. knitting) o Avoid giving specific timeline for rest period – use patients symptoms to guide o Graduated return to cognitive and physical activity o Educate patients on how they can re-introduce activity by monitoring their symptoms Graduated return to play protocol:  Guided by symptoms.  Physician gives final okay to return to play.  Progression to next step only when symptoms free for 24 hours.  If any symptoms occur, patient must go back to previous asymptomatic level for at least another 24 hours.  Use similar guidelines for integrating clients back into work, school etc. 203 Non-Traumatic Brain Injury Transient Ischemic Attack (TIA) Transient episode of neurological dysfunction.  Sudden onset.  Symptoms last from minutes to up to 24hrs.  A TIA is a warning sign of a potential future stroke. Cerebral Vascular Accident (CVA) 3rd leading cause of death in Canada and 1st leading cause of LT disability. Risk factors:  Non-modifiable: family history, sex: F>M, race, older age, previous stroke or TIA.  Modifiable: hypertension, cardiovascular disease, diabetes, elevated cholesterol, smoking, excess alcohol consumption, poor diet, obesity, stress, inactivity, atrial fibrillation, sickle cell disease. o Atrial fibrillation and sickle cell disease can both be managed with proper medication making these modifiable Signs and symptoms:  Sudden numbness or weakness of the face, arm or leg.  Sudden confusion.  Trouble speaking or understanding speech.  Sudden trouble seeing in one or both eyes.  Sudden trouble walking.  Dizziness, loss of balance, or coordination.  Sudden severe headache with no known cause. Ischemic: 80% of strokes:  Could be due to a thrombus (slower to evolve) or embolism (occurs rapidly without warning).  Most common cause in older adults: thrombosis (blood clot that forms in a blood vessel).  Lacunar strokes: o Subgroup of ischemic strokes o Most common type of stroke o Blockage of small deep penetrating arteries that feed the deep nuclei of the brain o Associated with hypertension and diabetes o Correlation with decreased cognition Hemorrhagic: 20% of strokes:  Due to aneurysms and arteriovenous malformations (AVM), hypertension, head trauma, Illicit drug use, bleeding disorders.  AVM: is a tangle of abnormal and poorly formed blood vessels that have a higher rate of bleeding than normal vessels.  Arterial factors: Atherosclerotic plaques, aneurysms, pressure on artery walls. 204   Venous factors: Tendency for blood to clot quickly, Irritation or inflammation of lining of vein. Penumbra: an area of the brain at risk for dying:  It is located between an area of perfusion and necrosis.  May remain viable for several hours post stroke.  Why early diagnosis of CVA is essential o If the stroke is ischemic in nature, the patient will be eligible for TPA which can save more brain tissue within the penumbra. Prognosis for a stroke: ABCD Score:  Clinical prediction rule used to determine the risk for stroke on the days following a TIA.  Age, blood pressure, clinical features, duration.  Those older than 60 with uncontrolled hypertension who had multiple clinical features and TIA symptoms lasting greater than an hour had increased prognosis for a CVA. Factors that support a good prognosis post CVA:  Younger age.  Ability to mobilize within a couple days.  Ischemic type stroke.  Absence of visuospatial deficits, absence of aphasia, absence of severe cognitive deficits, absence of incontinence, absence of altered LOC, absence of severe co-morbidities.  Early PT on a daily basis to maximize recovery. CVA Medical Treatment:  If thrombotic: o Thrombolytic agents o Tissue Plasminogen Activator (TPA):  Activates plasminogen to digest fibrin which breaks down the clot (for thrombosis only)  Can only be administered within 3 hours of initial symptoms o Within 6 hrs = mechanical thrombectomy o Prevention of recurrent of stroke:  Anticoagulants (aspirin)  Lipid lowering agents  Lifestyle changes (diet and exercise)  Angioplasty/stents to widen artery  If hemorrhagic: o Endovascular procedures: use of a catheter introduced through a major artery in the leg or arm, then guided to the aneurysm or AVM. It then deposits a mechanical agent, such as a coil, to prevent rupture o Surgery to stop the bleed; aneurysm clip 205 Right CVA characteristics Nonverbal/artistic brain  Left sided weakness  Visual agnosia: impairment in recognition of visually presented objects  Prosopagnosia: inability to recognize faces or pictures of familiar people  Anosognosia (denial): they may deny they had a stroke or that their paralyzed arm or leg belongs to them. They look at the paralyzed arm or leg and believe it belongs to someone else  Distorted awareness and impression of self o Neglect: they may ignore the left side of their body or their environment. This means they may not turn to look toward their left side or they may not recognize things that are on their left  Decreased/short attention span o Perseveration: they may have difficulty following instructions or answering many questions asked one right after the other. They may repeat answers or movement even though a new instruction was given or a new question asked  Decreased musical/artistic abilities  Visual/spatial problems o They may have problems judging distance, size, position and rate of movement and how parts relate to a whole  Issues with emotional content of language (speak in monotonous voice), difficulty understanding sarcasm  Issues discriminating smells Left CVA characteristics Verbal/analytical brain  Right sided weakness  Decreased numerical and scientific skills  Diminished functional speech: aphasias (Broca’s and Wernicke’s) o Aphasias affect: speaking, listening, reading, writing, sign language, dealing with numbers, understanding speech, thinking of words when talking or writing 206 Types of Aphasia Type of Aphasia Wernicke’s Broca’s Description Receptive/ fluent Expressive/non-fluent Location Left temporal lobe Left frontal lobe Characteristics Spontaneous speech is Impaired motor production of speech preserved Auditory comprehension is spared Auditory comprehension is impaired Communication Strategies Use demonstration, gesture and Use verbal cues in communication Used pictures (visual modalities) for communicating Note: never speak “loudly” to a patient with aphasia - this does not help them understand you! Some individual’s language centers are in the right hemisphere making this their “dominant” hemisphere. CVA Physiotherapy Treatment General principles  Maintain ROM and prevent deformities through positioning, PROM and mobilization.  General positioning: bed, wheelchair o Support the shoulder (sling, pillows)  Functional mobility: o Transfer practice (rolling, supine to sit, sit to stand, wheelchair to bed)  Promote awareness, active movement and strengthening of affected limbs and trunk.  Hemiplegic shoulder: education (avoid traction), strengthening, positioning, bracing and PROM  Gait re-training with or without gait aids. o Walker, canes, walking sticks o Ankle foot orthosis may be used if patient presents with foot drop  Improve postural control and balance.  Pain management (modalities).  Spasticity management. o Bracing, stretching, splinting  Promote independence in ADL’s.  Functional electric stimulation/NMES for muscle activation.  Cardiovascular endurance (depending on physical level: bike, pool, treadmill). Treating neglect:  Incorporate involved side into crossing midline activities (rolling, using PNF lift pattern).  Teach visual scanning strategies.  Stand and sit on neglect side to encourage attention to that side.  Place nightstand towards neglected side.  Include neglected hand into tasks (e.g. place hand within visual field on table surface).  Stimulate affected side using sensory stimulation. 207 Transfers:  Initially done towards strong side because it is safest  Later in rehab, transferring towards the affected side has the following benefits: o Retrains motor control through weight shift and weight bearing on affected side o Decreases extensor strategy by weight bearing while maintaining knee flexion o Directs attention and vision to affected side Shoulder treatment:  Shoulder subluxation: o Initial position of scapula in flaccid upper extremity = downward rotation and adduction of inferior angle o Subluxation usually caused by traction and gravitational forces acting on a depressed, downwardly rotated scapula o Spasticty (especially in subscapularis and pec major) and loss of external rotation are the most likely causes of hemiplegic painful shoulder  Treatment for flaccid subluxed shoulder: o Weight bearing into affected upper limb for glenohumeral joint loading o Muscle stimulation using NMES o Shoulder positioning (bed, wheelchair)  Glenohumeral joint should always be supported  Avoid positioning shoulder into internal rotation o Education to family, patient and caregivers about handling to avoid further subluxation/shoulder pain:  Do not pull on shoulder  Support shoulder during transfers (e.g. sling) o Safe PROM techniques to avoid impingement/trauma to GH joint:  Clear scapular PROM: elevation, depression, retraction, protraction, upward rotation and shoulder external rotation past neutral prior to shoulder abduction/flexion PROM above 90 degrees to avoid rotator cuff impingement and pain. o Functional shoulder supports (e.g. GivMohr sling), taping o Postural exercise to maximize spinal/scapular alignment Positioning:  If patient shows significant increased extensor spasticity on one side, avoid putting patient in supine (side lying or sitting are better options)  When positioned in supine, ensure a slight bend at hips and knees to avoid mass extension in the lower limb and shoulder is supported in slight abduction/ER; elbow extension; forearm supination (palm up)  If side-lying on good side, position with affected shoulder in protraction and elbow extended forward resting on a pillow - avoid elbow flexion/shoulder adduction/IR of affected upper limb as spasticity typically develops  When a CVA patient lies on the hemiplegic side, the following occurs: o Spasticity is decreased due to elongation of the affected side o Increased physical awareness of the affected side o The hemiplegic side should be extended at the hip and slightly flexed at the knee 208 Question: If patient has left hemiplegia, which side should they lay on (left, right, prone, supine)? Answer: left (as long as they are pain free and left shoulder is positioned carefully to avoid injury). Left side lying will decrease tone on the affected side as well as prevent possible shoulder subluxations and keeps their unaffected arm free to assist in bed mobility. Proprioceptive neuromuscular facilitation (PNF)  An approach to motor retraining that uses synergistic patterns of movement which have been identified as components of normal movement.  Extremity patterns of movement are rotational and diagonal in nature and are referred to as D1 and D2 (Diagonal 1 and 2): o These movement patterns combine motion in all 3 planes (flex/ext, abd/add, and transverse rotation).  Movements between the patterns is stressed to encourage agonist/antagonist muscle activation.  Patterns are varied by changing the action of the intermediate joint (e.g. elbow, knee) or by changing the position of the patient (e.g. standing, sitting, supine). Patterns can also be unilateral or bilateral.  Facilitation is used through cueing, resistance, traction etc. to enhance motor activation.  Used in patients with both neuromuscular or musculoskeletal deficits.  The goal is to improve functional performance and coordinated patterns of movement.  Movement patterns are named according to the action occurring at the proximal joint (shoulder or hip joint). o E.g. The starting position of the proximal joint.  Upper extremity D1 = flexion, adduction, external rotation (D1 flexion) and extension, abduction, internal rotation (D1 extension).  Upper extremity D2 = flexion, abduction, external rotation (D2 flexion) and extension, adduction, internal rotation (D2 extension).  Lower extremity D1 = flexion, adduction, external rotation (D1 flexion) and extension, abduction, internal rotation (D1 extension).  Lower extremity D2 = flexion, abduction, internal rotation (D2 flexion) and extension, adduction, external rotation (D2 extension). Stroke Specific Outcome Measures  Fugl-Meyer and Chedoke McMaster: assessment of post stroke motor function. Other commonly used outcome measures for stroke rehab:  Modified Ashworth Scale (MAS), Functional Indep Measure (FIM), 6MWT, TUG, 10-meter walk test, Box and Block Test (BBT), Berg Balance Scale. 209 Cerebellar Disorders Cerebellar Disorder Presentation May or not present with the following:  Loss of balance: walks with wide base of support, falls toward side of lesion, lurching gait.  Coordination deficits: ataxia, dysmetria, dysdiadochokinesia, dysarthria.  Functional disabilities: intention tremor (tremor during movement).  Motor learning impairments.  Cognitive deficits and emotional dysregulation.  Minimal strength deficits but may have fatigue issues, asthenia (generalized weakness).  May have hypotonia, hyporeflexia due to lack of intensity of input (especially acutely). Therapeutic goals:  Improve coordination: coordination practice, movement patterns (PNF).  Improve postural stability and balance: core stability exercises, static/dynamic balance.  Improve functional mobility: gait aids, gait training.  Improve vestibular functioning: improve gaze stability.  Improve cardiovascular endurance: pool, bike, walking programs. Examples diseases: multiple sclerosis, hereditary ataxia, Friedreich’s ataxia. Coordination Testing Dysdiadochokinesia Testing Dysmetria Testing Upper Extremity Rapid alternating supination and Fingertip to thumb pronation of forearm Finger to nose Opposition Lower Extremity Rapid alternating toe taps Heel slide on shin Non-Cerebellar Coordination Issues  Athetosis: low continuous involuntary movements.  Chorea: rapid repeated jerky coarse movements.  Dystonia: twisting and repetitive movements causing abnormal postures. Caused by simultaneous contractions of opposing muscle groups.  Hemiballismus: sudden stabbing movements of one side of the body. Rhomberg: used to determine the cause of loss of motor coordination (ataxia):  Is a person’s ataxia due to sensory issues or cerebellar issues? 210 Testing procedure:  Patient stands with feet together, arms at their side and eyes open.  Patient is then asked to close their eyes (therapist stays closed for safety): o Positive test if patient loses their balance once eyes are closed o A positive Romberg test suggests that the ataxia is sensory in nature (due to loss of proprioception). If a patient is ataxic and Romberg's test is not positive, it suggests that ataxia is cerebellar in nature. Individual need at least 2 of the 3 following systems intact to maintain balance in standing:  Vestibular  Proprioception  Vision If vision is taken away in standing, there are only 2 systems left to use: vestibular and proprioception. If the patient loses balance once eyes are closed (positive test), we can determine that the sensory system is not working adequately and is contributing to the individual’s ataxia. Note: Romberg can be used with individuals without ataxia and uses the same principles. Patients who lose their balance when their eyes are closed are said to have a positive Romberg. When vision is removed, only 2 of the three systems remain to aid in balance and if there is a vestibular issue or proprioceptive dysfunction, the patient will become unbalanced. A positive Romberg can direct the therapist to look further into the function of the vestibular and proprioceptive systems to see which one is not functioning correctly. Spinal Cord Injuries Spinal Cord Injury Causes of SCI:  Traumatic: 40% are cervical incomplete; tetraplegic and paraplegic common: o Types: Hyperflexion, hyperextension, axial load, rotation, penetrating injury, falls, transportation  Non-traumatic: o Cancer, infection and inflammation, motor neuron disorders, vascular diseases (spinal cord infarcts); most are paraplegic Immediate treatment:  Prevention of edema can prevent some secondary injury (ischemia, hypoxia, necrosis)  direct application of ice.  Spine needs to be immediately immobilized to prevent secondary injury.  Management of airway, breathing, circulation, injuries.  Benefits of Surgery: realignment, stabilization, early mobilization, early rehab, less medical complications, decreased length of stay in hospital: o Goal: spinal stability while maximizing future mobility o Reasons for surgery: unstable fracture or soft tissue injury, neuro symptoms getting worse o Lumbar laminectomy: helps to decompress the cauda equina/roots 211 Spinal Cord Tracts Category Tract Role Where it crosses How to test it Ascending Lateral Pain Within spinal cord, 1-2 Sharp/dull tracts spinothalamic Temperature segments above the Hot/cold (Sensory) point of entry Anterior Crude touch Within spinal cord, 1-2 Light touch spinothalamic Pressure segments above the point of entry Dorsal columns Proprioception Crosses at the Tuning fork (medial Deep touch pyramid motor 2-point discrimination lemniscus) 2-point (medulla) in the brain Stereognosis discrimination stem Kinesthesia Vibration Proprioception Stereognosis Descending Lateral Main motor path Crosses at the No simple clinic test tracts corticospinal (90% of CS tract) pyramid motor can determine (Motor) (medulla) in the brain specific CS tract Motor function of stem function limbs and digit Transcranial cortical musculature stim can be used Injury will result in spastic paralysis (UMNL) presentation of the limb(s) below the level of lesion Anterior 10% of CS tract Within the spinal No specific test corticospinal Motor function of cord at the level of postural and axial innervation musculature 212 213 ASIA Scale  AISA score is comprised of the grade and level of lesion.  Level of lesion: defined as the most caudal segment of the spinal cord with normal sensory and motor function on both sides of the body: o Motor level: most caudal segment with a grade >/= 3 provided all segments above are grade 5  Motor exam looks at 10 bilateral myotomes (always performed in supine)  Note: C5 = test elbow flexion (different than standard myotomes)  If an injury is T2-L1, then motor level is determined by intact sensory level (because there is no myotome testing for these levels)  Strength can differ between right and left sides  Overall motor level is based on the uppermost intact level o Sensory level: most caudal segment with bilateral score of 2 for both light touch and pin prick  Key contact points assigned to each dermatome  Sensation is graded as follows: 0= absent; 1= impaired; 2 = Normal ASIA grade (A-E) Grade Findings ASIA A No motor or sensory function is preserved in the sacral segments (S4-5) Complete ASIA B Sensation but NOT motor is preserved below neurological level and Sensory incomplete, motor includes the sacral segments (S4-5) complete ASIA C More than half the key muscles below the neurological level have a muscle Motor incomplete grade less than 3 ASIA D More than half the key muscles below the neurological level have a muscle Motor incomplete grade greater or equal to 3 ASIA E Normal motor and sensory function Normal Used with patient having a history of prior SCI deficits Deep anal pressure (DAP): if present, indicates sensory incomplete injury (ASIA B) Voluntary anal contraction (VAC): if present, indicates motor incomplete (ASIA C). Zone of partial preservation (ZPP):  There may be dermatomes below the sensory level and myotomes below the motor level that remain partially innervated which is known as the Zone of Partial Preservation (ZPP).  The most caudal segment with some sensory defines extent of ZPP.  ZPP is ONLY ever referenced when describing a complete (ASIA A) injury. Prognosis for spinal cord injuries: pinprick preservation (LE and sacral) within 72hrs is good prognostic indicator of motor function and ability to walk to return. 214  Clinical syndrome Characteristics Central cord syndrome  Most common syndrome seen and can be very disabling  Damage to the central portion of the cord and an incomplete lesion  Caused by hyperextension injury of neck, usually an elderly person who falls  Presents with greater loss of UE function compared to LE (will lose most ADL function, have no mechanism to save self when falling)  Often associated with spinal canal stenosis Here is a tip to help you remember central code syndrome: MUDE Motor > Sensory Upper extremity > Lower extremity Distal > Proximal Extension injury Why is the upper extremity more affected than the lower extremity? The cervical spine is the most central tract in the corticospinal tract, followed by the thoracic, lumbar and sacral tracts. Since only the central portion of the corticospinal tract is affected with this injury, the upper extremities are more affected. Brown sequard  Traumatic neurological disorder resulting from compression of one side of the syndrome spinal cord or hemisection, typically seen after a penetrating/knife-type injury; asymmetrical damage to cord  Ipsilateral loss of proprioception/vibration sense and motor control at/below level of lesion  Contralateral loss of pain and temperature sensation a few levels below the lesion Tip for remembering the spinothalamic tract: Pain and temperature sPinoThalamic, P = Pain and T= Temperature Anterior cord syndrome  Relatively rare, but can happen from occlusion of blood supply to anterior cord  Bilateral loss of motor function, pain and temperature (anterior tracts) below injury level  Preservation of discriminative touch, vibration, proprioception (dorsal columns) Conus medullaris  Spinal cord terminates at L1-L2 syndrome  Conus lies in close proximity to nerve roots and injury to this region can result in combined UMN and LMN features (e.g. spasticity)  May be sparing of sacral reflexes Cauda equina syndrome  Damage to lumbar and sacral nerve roots (L2 and below)  Lower motor neuron type injury  Variable loss, areflexic (flaccid) bowel and bladder  Affects more than one nerve root, surgical emergency  Usually presents with: bilateral leg pain/numbness/weakness, sacral root problems, urinary retention, stool incontinence, absent reflexes 215 Neurogenic Bladder Spastic bladder: injuries ABOVE the conus medullaris:  Messages will continue to travel between bladder and spinal cord since reflex arc is still intact.  Bladder can be trained to empty on its own. o May trigger emptying by “tapping”  Bladder management is either intermittent catheters or condom/Foley drainage. Flaccid bladder: injuries in conus and/or cauda equina:  Messages don’t travel between spinal cord and bladder since the reflex center is damaged.  Bladder loses ability to empty reflexively and will continue to fill.  Bladder must be catheterized. Autonomic System Sympathetic nervous system: “fight or flight”:  Prepares body for an emergency.  Fibers arise from thoracic and lumbar portions of spinal cord: T1-L1.  Short pre-ganglionic fibers and long post-ganglionic fibers.  Actions: o Arteries to skin and intestines are constricted and those to skeletal muscle are dilated o Increases HR and BP o Relaxes bronchial muscles to allow for increased O2 supply Parasympathetic nervous system: “rest and digest”  Fibers arise from cranial nerves III, VII, IX, X and Sacral nerve roots 2-4.  Conserves and restores energy, maintains bodily functions.  Long pre-ganglionic fibers and short post-ganglionic fibers.  Actions: o Primary interest is the vagus nerve which decreases HR and contractility o Increases blood flow to smooth muscle to aid in reproduction, digestion o Contracts bronchial muscles 216 Autonomic nervous system dysfunction in SCI The amount of sympathetic influence occurring is dependent on the level of injury. In higher level lesions, T6 and above, a significant portion of the sympathetic nervous system has been disconnected from normal communication along the spinal cord which can have the following effects: Decreased heart rate:  Sympathetic innervation to heart is T1-4. o Injuries above T4 will directly impact heart rate  Parasympathetic influence remains intact and unopposed via the vagus nerve.  Causes decreased HR and limits cardiac output.  HR response to exercise is blunted with a max of only 110-120bpm.  Heart response is due to vagal withdrawal rather than sympathetic drive.  HR is not a good indicator of exercise intensity with these individuals - use RPE, dyspnea, sing/talk/gasp scales instead. Decreased blood pressure:  With decreased HR, cardiac output is limited.  Decreased cardiac output = blood pressure response to exercise will also be limited (unless they are having an episode of AD).  Do not let BP fall below 70/40.  A combination of altered autonomic HR control and decreased muscle tone in the lower body (venous pooling) contribute to decreased BP in this population. Poor regulation of body temp (will go up and down with environment temperature):  Body temperature regulation via autonomic nervous system: o Normal increase in body temperature: vasoconstriction of blood vessels in skin to maintain heat in the core of the body; shivering to create heat through muscle activation. o Normal decrease in body temperature: vasodilation of blood vessels in skin to bring heat to surface for heat loss/cooling; sweating for increased heat loss through evaporation.  Messages sent to increase or decrease body temperature are blocked due to the spinal lesion.  This can lead to increases in body temperature with exercise and risk of hypothermia when in a cold setting.  Prevent overheating during exercise by: o Ensuring adequate hydration pre-exercise, appropriate light clothing, cooling with fans, close monitoring for signs of over-heating, avoid exercising in heat Reasons for dizziness in SCI patient: autonomic dysreflexia, orthostatic hypotension, hypoglycemia  Ensure you understand why your patient is feeling dizzy.  Example: patient with a SCI is elevated on a tilt table to 60 degrees and begins to feel nauseous and dizzy - always monitor vitals: o If BP is elevated, could be an episode of autonomic dysreflexia – keep patient upright and look for source of noxious stimulus and monitor vital signs o If BP has dropped, it is an episode of orthostatic hypotension - most immediate response is to lower the tilt table to horizontal and monitor vital signs 217 Autonomic Dysreflexia In lesions above or equal to T6:  A noxious stimulus below level of lesion causes a reflexive sympathetic response that causes blood vessels to constrict.  Vasoconstriction causes a sharp rise in BP (increase of >20-30mmHg).  The baroreceptors in the carotid sinus and aortic arch detect the hypertension and stimulate the parasympathetic nervous to decrease BP by decreasing HR (via vagus nerve).  Because of the spinal cord lesion, the descending inhibitory response (via the parasympathetic system) only travel as far as the level of injury and do not cause the desired response in the sympathetic fibers below the injury allowing the hypertension to remain uncontrolled. Above the injury there is parasympathetic dominance resulting in: flushing and sweating above the level of injury, bradycardia, pupillary constriction, and nasal congestion (unopposed parasympathetic responses). Below the level of injury there is a sympathetic dominance resulting in: chills, pale, cool/clammy skin (vasoconstriction to blood vessels of skin).  Patient will have a sudden significant increase in BP (>200/100), may feel dizzy, nauseated and have a headache. Why is this more common in lesions above T6?  The splanchnic vascular bed is one of the body’s largest reserves of circulatory volume and is controlled primarily by the greater splanchnic nerve. This important nerve derives its innervation from T5-T9. Lesions to the spinal cord at or above T6 allow the strong and uninhibited sympathetic tone to constrict the splanchnic vascular bed, causing systemic hypertension. Lesions below T6 generally allow enough descending inhibitory parasympathetic control to modulate the splanchnic tone and prevent hypertension. Physiotherapist’s immediate response:  If standing, sit patient down for safety. If patient is sitting, keep them in sitting.  Keep head elevated – do not lie patient flat.  Find the source of the noxious stimulus - check bladder/catheter and bowel for impairment. Bladder distension or irritation is responsible for 75-85% of the cases.  Monitor BP.  If BP remains >150 mmHg for adults, despite removal of noxious stimuli, then pharmacological management of hypertension should be initiated  send to emergency for assessment and management.  If severe, complications include: uncontrolled hypertension that can result in intracranial hemorrhage, retinal detachment, seizure, or death. 218 Spinal Shock and Neurogenic Shock Spinal shock Neurogenic shock Cause Due to an acute spinal cord Due to an acute spinal cord injury: level T6 and above only injury Signs and Temporary suppression of Hemodynamic phenomenon due to loss of sympathetic symptoms all reflex activity below the vascular tone and unopposed parasympathetic response level of injury: Decreased reflexes Occurs only after a significant proportion of the sympathetic Loss of sensation nervous system has been damaged – lesions at T6 level or Flaccid paralysis higher 3 clinical signs are Bradycardia – due to unopposed parasympathetic stimulation Hypotension – due to massive vasodilation Hypothermia – unable to regulate temperature due to vasodilation of blood vessels in skin Time frame Can last days to months Occurs within 30 minutes of cord injury levels T6 and above (transient) and can last up to 6 weeks Extra info: Spinal shock does not refer Can be life threatening if not treated to circulatory collapse and Treatment for hypotension: volume resuscitation (saline), should not be confused vasopressors (to counter loss of sympathetic tone) with neurogenic shock SCI Health Risks  Pressure sores/wounds.  Poor secretion clearance.  DVT and PE due to: o Venous stasis (lack of muscle pump action) o Transient hypercoagulable state (warfarin causes initial increased risk of clot formation which goes down after weeks to months of taking medications)  DVT signs: sudden lower extremity pain, redness, swelling and increased temperature. Positive Homan’s.  Prevention: anticoagulation meds, compression stockings, sequential compression devices, PROM/AROM, early mobilization  Note: for PE  tachycardia may be masked by parasympathetic dominance  Heterotrophic ossification  2 main contraindications for treatment are forced PROM and serial casting o Signs and symptoms: pain (if sensory sparing), increased spasticity, warmth, low grade fever, erythema, local swelling, sudden decreased ROM with an abnormal firm or hard end-feel o Treatment: PROM within tolerable range  mobilize as able, medications and surgery iflong standing 219   Osteoporosis: o Due to rapid increase calcium excretion within few days of SCI o Decreased bone loading post injury o Large incidence of fracture, especially LE  Post traumatic syringomyelia: o Formation of an abnormal tubular cavity in the spinal cord o Dura tethers/scars to the arachnoid blocking CSF flow o CSF is forced into the spinal cord progressively enlarging the cyst o Leads to compression of cord and vascular supply o Cyst develops below level of lesion  Can occur years after the original injury o Signs and symptoms  Looking for differences or increase in presentation of the injury (presenting like a higher level), pain at level and spreading upwards, sensory changes, motor weakness, increased spasticity, bladder and bowel dysfunction, increased episodes of autonomic dysreflexia, hyperhidrosis o Treatment and prevention  surgery  decompression or shunt  Multisystem: o Individuals with SCI tend to have lower BP, have decreased lean muscle mass and increased adipose tissue which can lead to impaired glucose uptake, glucose homeostasis and abnormalities in lipid metabolism. o Cardiovascular disease is major cause of death in people surviving 30+ years post SCI. o Left ventricular myocardial atrophy seen in SCI. o 100x higher rate of bladder cancer in people with SCI. o In supine, area most susceptible to pressure is the coccyx. SCI and Exercise Adapted from website: http://sci.washington.edu/info/forums/reports/exercise_2013.asp Benefits of exercise in SCI population:  Reduce risk of heart disease;  Improve respiration;  Increase muscle strength;  Improve circulation;  Improve mental health;  Increase independence with functional mobility and ADL’s;  Prevent secondary complications (such as urinary tract infections, pressure ulcers, and respiratory infections);  Reduce the risk for diabetes;  Improve immune system function;  Reduce constipation. Every SCI is unique based on level and grade of the injury. 220 Special exercise precautions for people with SCI: Blood pressure  Individuals with SCI have low blood pressure due to blood pooling in legs resulting in light- headedness: o The higher and more complete the lesion, the more problematic. o Ways to manage this include:  Compression stockings  Medications  Start slow and progress gradually when exercising Temperature  For injuries at T6 or above temperature regulation is affected: o Decreased temperature regulation = increased risk of overheating  Exercise environment should be cool  Dress in loose clothing  Stay hydrated Heart rate  For injuries at T4 or above, heart rate is affected: o Results in difficulty gauging exercise effort using HR o Use of alternative options for monitoring exercise intensity  BORG  Moderate intensity  11-13 on BORG; 3-5 on modified BORG  Sing Talk Gasp Scale  Should exercise hard enough to be breathing heavily but not so hard that they can’t carry on a conversation without gasping for air. Skin breakdown  Protect and monitor skin during exercise. Autonomic dysreflexia  Know signs and symptoms of AD.  Empty catheter bag before starting exercise activity. Overuse injuries  Maintaining good exercise technique.  Avoid repetitive motion injuries.  Choose exercises that do not overuse muscles already used a lot during daily activities (e.g. muscles used to push a manual wheelchair). Medications  Make note if patient is on a pain medication or has sensory loss.  Pain medication and/or sensory loss may decrease pain threshold and make it difficult to know if an exercise is causing injury. 221 Frequency: 5x/week  Cardiovascular conditioning: 3-5x/week.  Strength training: 2-3x/week.  Stretching: daily. Intensity  Cardiovascular conditioning: moderate (see above).  Strength training: start with low weight and gradually work to heavier loads, pain free.  Stretching: gentle, pain free. Time  Cardiovascular conditioning: 30-60 mins.  Strength training: 3-5 sets; 10-15 reps.  Stretching: ~1min hold; 3 sets. Type  Cardiovascular conditioning: o Wheelchair pushing o Seated aerobics o Arm ergometer o Swimming o Rowing o Cycling o Circuit training o Adapted sports o Walking (if applicable)  Strength training: free weights, body weight, elastics, machines etc.: o Focus on back muscles, scapular stabilizers, rotator cuff muscles, triceps Levels of Injury and Functional Expectations 222 Levels - cough Injury Level Cough C1-3 Absent C4-T4 Non-functional T5-T10 Weak Functional: Able to clear normal daily secretions. May have difficulty with abnormal secretions (e.g. pneumonia) T11 - below Normal Levels - respiratory status Injury Level Respiratory Status C1-3 Ventilator dependent Vital capacity is 5-10% C4 Phrenic nerve (C3-5): diaphragm innervation (main muscle of inspiration) C4: enough innervation to diaphragm to breath independently Without full diaphragm innervation, patient may need to use ventilator at night C2-C7 Innervation of accessory muscles of inspiration: SCM, scalenes, pectoralis minor Vital capacity is 20% T1-T11 Intercostals (external intercostals = inspiration; internal intercostal = expiration) Vital capacity 30-50% in higher t-spine lesions T6-L1 Abdominals (aid in active expiration via rectus abdominus, obliques, TA) T11- below Normal vital capacity Levels – functional expectations C1-C4 Patterns of weakness: Paralysis of trunk, UE and probably diaphragm Muscles innervated fully: SCM (CN XI), neck extensors, neck flexors, trapezius (CN XI) Partial: Levator scapulae (C3-C5), diaphragm (C3-C5), rhomboids (C4-C5) Possible movements: Neck movements, slight shoulder retraction, adduction and elevation Functional outcomes: Independent use of power wheelchair with sip and puff or head controls (C4) PT role: ROM, spasticity management (prevent contractures), neck strengthening, inspiratory muscle training, chest physiotherapy 223  C5 Patterns of weakness: Paralysis of trunk, significant imbalance around shoulder girdles, absence of elbow extension, forearm pronation, wrist extension/flexion and all hand movements Muscles innervated fully: Levator scapulae (C3-C5), diaphragm (C3-C5), rhomboids (C4-C5) Partial: Deltoids (C5-6), biceps (C5-6), brachioradialis, teres minor (C5-6), teres major (C5-7), serratus anterior (C5-7), supraspinatus/infraspinatus (C5-6), pectoralis major/minor (C5-T1) Possible movements: Shoulder abduction, flexion and extension (weak), scapular adduction and abduction, elbow flexion, forearm supination Functional outcomes:  Independent use of power wheelchair with modified hand controls  Potential for independent use of manual wheelchair with projection rims (flat surfaces indoors, w/c setup is essential for success)  Able to maintain propped sitting position (locked elbows) but stand by assist necessary at all times and assist needed to get into this position  Independent hand to mouth for feeding with adapted gripping aids (universal cuff)  Potential independent grooming with adapted gripping aids  Able to assist with bed mobility, transfers PT role: As above plus…. Shoulder strengthening/ shoulder health education Wheelchair skills 224  C6 Patterns of weakness: No wrist flexion, elbow extension, hand movement Muscles innervated fully: Deltoids (C5-6), biceps (C5-6), brachioradialis (C5-6), teres minor (C5-6), supraspinatus/infraspinatus (C5-6) Partial: Serratus anterior (C5-7), triceps (C6-8), teres major (C5-7) Pectoralis major/minor (C5-T1), ECRL (C6-7), ECRB (C6-C8), Latissimus dorsi (C6-8) Possible movements: Horizontal adduction, wrist extension Functional outcomes:  Independent use of manual wheelchair with projection rims on indoors and outdoors on relatively flat surfaces (e.g. may be able to move over grass)  Power wheelchair for distance  Independent bed mobility is possible  Independent with pressure relief  Independent transfer with slide board is possible  Maintain propped sitting using shoulder ER (teres minor) and locked elbows  Independent upper body dressing  Assist with LE dressing  Assisted self-care  Independent LE PROM program possible  Tenodesis grip - able to grab light objects  First level of SCI to have potential to function independent without a care assistant (but this is very rare)  Driving with hand controls  Limited participation in wheelchair sports PT role: As above plus… Propped sitting practice Transfer practice with slide board Functional strengthening Teach independent PROM program for LE Wheelchair practice Teach “trick” movement strategies (e.g. tenodesis) Education on avoiding stretching long finger flexors in order to maintain functional tenodesis (only stretch finger flex when wrist is flexed) 225  C7 Patterns of weakness: Limited grasp and release due to limited finger flexion/extension Muscles innervated fully: Serratus anterior (C5-7), teres major (C5-7), pectoralis major (clavicular head), ECRL (C6-7) Partial: Triceps (C6-8), latissimus dorsi (C6-8), ECRB (C6-C8), ED (C7-C8), FDS (C7- T1), FDP (C7-T1), FCR (C6-8), intrinsic hand muscles Possible movements: Elbow extension, wrist flexion, finger flexion/extension (very weak) Functional outcomes:  First level of SCI to have potential to live independently in community without aid  Seat lifts for independent pressure relief in manual w/c  Independent transfers without slide board due to tricep function  Independent with manual wheelchair outdoors with potential to maneuver over slightly uneven terrain (e.g. small curb)  May still use power wheelchair for longer distances  Independent with most/all ADL’s  Stronger tenodesis grip  Strong stable shoulder girdle enabling better control over maneuvering body PT role: As above plus… Transfer training on uneven heights Manual wheelchair training outdoors on uneven terrain C8-T1 Patterns of weakness: C8 level: still have diff with fine motor skills because intrinsics are not fully innervated Muscles innervated fully: Triceps (C6-8), latissimus dorsi (C6-8), FDS (C7-T1), FDP (C7-T1), FCR (C6- 8), ED (C7-C8), interossei (C8-T1), lumbricals (C8-T1) Possible movements: Improved grasp and release due to intrinsic finger flexor activation (C8), selective PIP/DIP flexion/extension and MCP flexion/extension (C8), normal fine motor hand control: opposition, pincer grip (T1) Functional outcomes:  Potential to primarily/solely be a manual wheelchair user  May still use power wheelchair for longer distances  Independent with all ADL’s PT role: As above plus…. W/c endurance training Hand and fine motor strengthening 226  T2-T6 Patterns of weakness: Trunk weakness Muscles innervated fully: Full innervation of upper limb Partial: Intercostals, erector spinae Functional outcomes:  Independent sit balance with adequate righting and protective reactions  Manual wheelchair propulsion outdoors on uneven terrain, negotiating 4-8” curbs, steep ramps, hills, gravel, sand, ascend/descend stairs becomes possible  Uneven transfers e.g. floor to/from w/c transfers  Brace walking with HKAFOs and parallel bars (non-functional) PT role: As above plus…. Standing and gait in parallel bars T7-T12 Patterns of weakness: Trunk weakness Muscles innervated fully: Full innervation of upper limb and upper trunk musculature Partial: Intercostals, erector spinae, abdominals (rectus, obliques, TA) Functional outcomes:  Potential to be an indoor ambulator with bilateral KAFO’s and appropriate assistive device (walker, forearm crutches)  “non-functional” because using trunk to throw legs forward which is very energy consuming  Will use wheelchair for primary means of community mobility PT role: As above plus… Core strengthening Indoor ambulation with KAFO’s and appropriate assistive device (walker, forearm crutches) L1 - L2 Patterns of weakness: Lower limb weakness Muscles innervated fully: Intercostals, erector spinae, abdominals (rectus, obliques, TA) Partial: Iliopsoas, quadratus lumborum Functional outcomes:  Hip flexion during the swing phase of gait allows for a swing through gait pattern or a 4-point gait pattern with bilateral KAFO’s and assistive device (walker or forearm crutches) = functional ambulation  Indoor/outdoor ambulation with orthoses and devices  Will still use wheelchair for primary means of community mobility PT role: As above plus… Functional ambulation training and balance work 227  L3 - L5 Patterns of weakness: Ankle weakness - no gastrocs/soleus (S1-S2), no intrinsic foot activation Muscles innervated fully: Intercostals, erector spinae, abdominals (rectus, obliques, TA), iliopsoas, quadratus lumborum Partial: Quadriceps (L2, L3, L4), adductors, abductors (L4-S1), hamstrings (L5-S2), external rotators, tibialis ant/post (L4-L5), EHL, EDL/B (L5, S1), peroneals (L5-S1) Functional outcomes:  Transition to AFO’s at L3 level due to quadriceps strength  L4/5 = walking is primary means of community ambulation with bilat AFOs and aid (cane, walking poles)  Decreased standing balance due to PF weakness = AFO’s required for balance PT role: As above plus… Functional ambulation training and balance work UMNL vs LMNL SIGNS LMNL UMNL Type of paralysis Reflex response: types of reflexes elicited Response in muscle Early, marked atrophy (total absence Limited and delayed atrophy of any muscle activity) (muscles still receive some Muscle fasciculations stimulation) Conduction velocity of Reduced (if compressed) OR absent Unchanged nerve (if severed) Spasticity A velocity-dependent increase in stretch reflexes with exaggerated tendon jerks, resulting from hyper- excitability of the stretch reflex, as one component of the upper motor neuron syndrome:  Velocity dependent resistance to passive stretch.  Clinical characteristics: increased muscle tone/firmness; increased stretch reflexes, uncontrolled movements. Spasticity Pros and Cons Pros Cons  Maintain muscle bulk, venous return, useful for  Leads to contractures transfers and moving limbs  Possibly painful  Reflex erection can be achieved  Positioning difficulties  Acts as warning sign  Fatigue 228 Treatment:  Medications: o Intrathecal baclofen: is not selective and makes muscles weak as well o Botox: local injections for specific muscles  Therapeutic exercise. Outcome measures specifically used for spasticity: Modified Ashworth, Tardieu. Normal Minimal, if any resistance to passive movement is encountered Findings Abnormal Hypertonia: increased resting tone of a Increased resistance due to spasticity Findings muscle Rigidity: a continuous resistance to passive movement in either joint direction regardless of speed Hypotonia: decreased resting tone Lower than normal resting tone or flaccidity 229 Neurodegenerative Diseases ALS, Parkinson's and MS Amyotrophic lateral sclerosis (ALS) Parkinson’s disease Multiple Sclerosis (Lou Gehrig’s Disease) Disease process A progressive motor neuron disease A chronic progressive neurodegenerative A chronic, progressive demyelinating disease affecting CNS disease of CNS Gradual deterioration of both UMN (descending spinal tracts) and LMN Degeneration of dopaminergic neurons in Autoimmune (anterior horn cells) substantia nigra (basal ganglia) results in decreased dopamine Myelin sheaths around the axons of M>F the brain and spinal cord are Neurotransmitters exist in balance so when damaged leading to demyelination Amyotrophy: muscle fiber atrophy dopamine becomes increasingly deficient, and scarring = impaired neural excessive acetylcholine (Ach) can accumulate transmission and neural fatigue Lateral: lateral column atrophy  The balance of dopamine and acetylcholine Unpredictable, chronic, debilitating is critical for normal movement Sclerosis: harden/thickening of axons Low levels of dopamine results in akinesia and Typical onset 20-40yo Age of onset is 40-70 (average is 55) bradykinesia Despite MS being classified as a High levels of Ach creates an excessive central nervous system disorder, the excitatory output and the constant excitatory cranial nerves can be involved. The state makes movement difficult resulting in most common cranial nerves tremor and rigidity affected are the optic and trigeminal nerves Etiology Unknown (viral, autoimmune, toxic) Possible causes: No known cause, most likely viral Genetic (5-10%, autosomal dominant) HLA-DR2 - there may be a genetic  Infectious/post encephalitis link  Drug induced  Idiopathic Average lifespan Death within 2-5 years Depends upon age of onset, how symptoms are Variable depending on type and managed, general health severity Death usually occurs due to secondary Life expectancy is on average around complications of PD such as pneumonia due to 5-10 year less than healthy adult swallowing issues, fall due to impaired balance 230 Characteristics