Neuro Rehab 1 - Exam 1 Review

ICF - Health Condition

Disorder, disease, injury

ICF - Body Structure and Function

Integrity of tissues and organs; Physiologic processes (cognition, sensation, strength, coordination, voice and speech, cardiovascular, etc.)

ICF - Activity

Tasks and skills (Moving, communicating, thinking, etc.)

ICF - Participation

Fulfilling roles; Engaging in community and society

ICF - Environmental Factors

Physical, social, and attitudinal barriers or facilitators; Technology, devices, medication, natural environment, support, attitudes, services, policies

ICF - Personal Factors

Individual influences not captured elsewhere; Gender, age, race, lifestyle, habits, education, profession

HOAC II Process

Collect initial data (Subjective and other data sources)

Create PIP list

Examination Strategy using Clinical Hypotheses

Examine Patient and Analyze; Refine Hypotheses

Add NPIPs to Problem List (Existing and anticipated problems)

Refine Problem List (Refer if needed)

Set Goals (based upon refined problem list)

Set Criteria

Set Plan to Reassess Criteria

Plan Interventions (Hypothesize rationale for change)

Plan Tactics (Plan of Care)

PIP

Patient Identified Problem; Chief Complaint (i.e. shoulder pain)

NPIP

Non-Patient Identified Problem; Related to exam findings (i.e. Decreased strength of shoulder musculature)

Movement Pattern Coordination Deficit

Poor timing and sequencing (postural response - anticipatory and reactive; Intersegmental movement during tasks)

Presentation: Signs of hesitancy or delayed movement, loss of balance, may have mild decrease in light touch or increased tone

Origin: CNS or non-CNS; can happen in neuro and non-neuro cases

Practice effect: Improvements in performance, but deficits remain

Force Production Deficit

Weakness: Focal (one joint), Segmental (muscles acting in an extremity or body region), Fatigue, can be at muscle, neuromuscular junction, peripheral nerve, central drive

Origin: CNS or non-CNS

Presentation: Compensatory movements (loading “locked” limbs), uncontrolled eccentric contractions, may have good MMT but easily fatigue

Sensory Detection Deficit

Impaired/Absent Sensation: Difficulty executing postural responses and movement due to impaired or absent sensation

Origin: CNS or non-CNS

Presentation: Inconsistent movement that resembles incoordination AND a sensory loss or impairment

Sensory Selection and Weighting Deficit

Impaired postural stability or orientation: Unable to screen for and attend to appropriate sensory inputs to maintain organized, stable posture

Origin: CNS

Presentation: Postural instability (especially with sensory changes - head turn, limb movement), may be associated with dizziness

Vertical Postural Deficit (Perceptual Deficit)

Impaired postural stability and orientation with resistance to correction: Contraversive pushing, backward disequilibrium

Origin: CNS

Presentation: Postural instability, abnormal alignment - usually to one side (lateral) or backward, resists correction to midline

Fractionated Movement Deficit

Inability to fractionate movement: Actions at one joint result in abnormal synergy at other joint(s)

Origin: CNS

Presentation: Can affect any single limb or multiple limbs, no practice effect

Dysmetria (Hypermetria)

Inability to grade force: Improper force for distance and speed requirements of a task, too much or too little

Origin: CNS - usually cerebellar

Presentation: Clumsy, impaired reciprocal movements, movement path variable and inefficient, poor accuracy - especially at faster and slower movement speeds, Fast: too much & Slow: too little

Hypokinesia

Slowness: Slow in initiation and execution of movement, can be associated with stopped movements

Origin: CNS

Presentation: Long delays with initiation, slow execution, ongoing movements may stop

Cognitive Impairment

Impaired mental function that affects movements: Concentration/attention, communication and language, motivation, judgement, problem solving, planning, etc.

Origin: CNS

Presentation: varies based on nature of impairment; Delay, impulsivity, impaired dual task performance, chooses wrong motor action for situation, altered spatial awareness, etc.

Purpose of Neurological Examination

Obtain information and data regarding the individual’s neurologic status, impairments, and impact on foundational tasks and activities

Primary Impairments

Signs and symptoms directly resulting from the individual’s disease or pathology (i.e. Incoordination of the upper extremity after an MCA Infarct)

Secondary Impairments

Changes in structure or function of a system that occur as a consequence of the patient’s pathology and related impairments OR as a result of some other influence (age, lifestyle) (i.e. Cervical and Upper Trapezius pain after MCA Infarct)

Components of Neurological Examination

Patient Observation, History, Systems Review, and Tests & Measures

Neurological Screening Examination: Mental Status

Alertness, orientation, memory, general cognitive function

FOGS: Family history, Orientation, General Information (current president), Spelling (forward and backward - “world”)

Neurological Screening Examination: Cranial Nerves

Cranial nerve screening examination; smell (CN I) often omitted, gag reflex (CN IX) often omitted

Neurological Screening Examination: Motor

Visual inspection of patient’s movement during encounter

Upper extremities: Pronator drift test, bilateral gross strength

Lower extremities: Unilateral gross strength assessment, Hip extensors and plantar flexors screened in sit-to-stand transfer and hell raise

Neurological Screening Examination: Reflexes

Deep Tendon Reflex (DTR) testing

DTR: Biceps

Nerve root: C5-6

DTR: Brachioradialis

Nerve root: C6

DTR: Triceps

Nerve root: C7

DTR: Finger Flexors

Nerve Root: C8

DTR: Quads

Nerve root: L3-4

DTR: Achilles

Nerve root: S1-2

Neurological Screening Examination: Sensory

Bilateral, simultaneous light touch

Proprioception (UE = Pronator drift test, LE = gait/stance observation; walk, rise on toes, tandem walking, wheelchair mobility)

Stereognosis (Impairment = Secondary Somatosensory Cortex damage)

Neurological Screening Examination: Movement Screen

Qualities to Observe = Speed, Amount, Symmetry, Control, Symptom Alteration

Speed

Time to complete task

Amount

Amplitude, excursion, ROM required

Symmetry

Some tasks have natural asymmetries

Control

Smoothness, coordination, stability, sequencing, timing, initiation

Symptom Alteration

Guarding, shortness of breath, pain alteration

Decerebrate Rigidity

LE: Extended, PF

UE: Shoulder ADD, Elbow Ext, Forearm Pronation, Wrist & Finger Flexion

Decorticate Rigidity

LE: Hip Extended and Internally Rotated, Knee Extended, Foot PF
UE: Shoulder ADD, Elbow Flexed, Wrist & Finger Flexion

Dystonia

Basal ganglia disorder/damage

Persistent muscle contraction and unintended repetitive movements and distorted positions of the body

Hypertonia

Increased muscle tone with resistance to elongation at rest

Spasticity

Velocity dependent resistance to externally imposed lengthening; typically on one side of the joint (one direction of motion)

Rigidity

Resistance to movements present at low and high speeds, detected throughout range, typically in a simultaneous co-contraction (both sides of joint)

Any CNS damage, but particularly the substantia nigra

Cogwheel rigidity

Muscular rigidity in which passive movements of the limbs through the available range elicits ratchet-like start and stop movements

Lead pipe rigidity

Muscular rigidity associated with stiffness and inflexibility in which passive movements elicit a uniform resistance throughout the range

Lesion Location and Effect on Muscle Tone: Brainstem - Cortical motor center loss

Spasticity

Lesion Location and Effect on Muscle Tone: Brainstem - Supraspinal motor center loss

Severe Spasticity

Lesion Location and Effect on Muscle Tone: Subcortical White Matter - Internal Capsule and Corona Radiata

Spasticity

Lesion Location and Effect on Muscle Tone: Basal Ganglia

Rigidity

Lesion Location and Effect on Muscle Tone: Cerebellum

Hypotonia

Tests for Hypertonicity

General resistance to lengthening & Deep Tendon Reflexes

Modified Ashworth Scale: Magnitude and point of onset of spasticity

Modified Tardieu Scale: Compares slow and fast speeds —> spasticity/rigidity

Unified Parkinson Disease Rating Scale: Rates severity of rigidity of body regions

Baclofen

GABA B antagonist at the spinal cord level

Side effects: drowsiness, weakness (mostly head and trunk), seizure risk, withdrawal if stopped suddenly

Benzodiazepine (Diazepam/Valium; Clonazepam/Klonopin)

GABA A complex of the CNS causing presynaptic reduction of reflex motor responses

Side Effects: Sedation, increased weakness and incoordination, hypotension, addition potential, withdrawal if stopped suddenly

Calcium Channel Blockers (Dantrium)

GABA B agonist at spinal cord level

Drowsiness, weakness (mostly head and trunk), seizure risk, withdrawal

Imidazolenes (Zanaflex)

Reduces spasms & clonus

Sedation, dizziness, orthostatic hypotension, dry mouth, bradycardia; hypotoxicity in a small proportion

Chemodenervation (Botox, Myobloc, Phenol, Alcohol)

Impairs action of motor unit

Cannabis

Neurotransmitter effect changes: Decreases glutamate (excitatory) and increases GABA (inhibitory)

Side effects: Drowsiness, balance impairments

Hypertonia Rehab: Positioning and PROM

Prolonged Static Stretch - Can elongate shortened muscles over time

PROM

Serial Casting - Progressive casts applied every 1-2 weeks, common in pediatrics

Orthotics - maintain muscle and capsule length

Positioning - to reduce spasticity

Augmented Feedback: Inhibition - When to use

Prior to other active or passive mobilization interventions

Prior to voluntary movement using antagonists of spastic muscles

Augmented Feedback: Inhibition - Deep Tendon Pressure

Firm, non-noxious, sustained pressure

More effective at attachment than at myotendon

Augmented Feedback: Inhibition - Joint Distraction

Stabilize with proximal hand, apply traction with distal

Contraindication: Hypermobility

Augmented Feedback: Inhibition - Sustained Stretch

Maximal elongation to activate GTO

Augmented Feedback: Inhibition - Cold

Prolonged ice/cold pact or immersion of distal limb in chilled water may decrease spasticity

Contraindications: Sensory impairment, poor cognition, cold intolerance

Augmented Feedback: Inhibition - Neutral Warmth

Warm pool, neoprene compression garment, air splint

10-minute application may have effects lasting up to 30 minutes

Contraindications: Sensory impairment, poor cognition, heat intolerance

Augmented Feedback: Inhibition - Rhythmic Rotation

Slow, low amplitude, rhythmic rotary movement

Lengthen involved trunk muscles

UEs go right, LEs bend left

Functional Activities: Aquatic Exercise Temp

84-94 degrees F

Functional Activities: Quadruped Exercises

Prolonged hip and knee flexion

Functional position for floor transitions

Motor control, core strength, balance

Functional Activities: Rolling

Basis for more complex transitional movements, including pivot transfer

Functional Activities: Weight-Bearing Activities

Joints aligned properly

Half kneel, tall kneel, modified plantigrade, standing

Incorporate dissociation (one limb flexed, other extended)

Flaccidity

Complete absence of muscle tone

Absent resistance to passive movement

Hypotonia

Abnormal decrease in muscle tone

Decreased resistance to passive muscle tone

Cerebral Shock

Temporary occurrence of flaccidity early after upper motor neuron lesions of cerebrum and brainstem following stroke that can last days to weeks

Flaccidity & Hypotonia: Findings

“Floppy” limbs

Abnormal posture

Muscle soft with palpation

Increased PROM, joint mobility/laxity

Decreased motor control, postural stability, DTRs, force production, sensation

Neglect

Flaccidity & Hypotonia: Central Causes

Spinal cord, cortex, basal ganglia, cerebellum

Flaccidity & Hypotonia: Peripheral causes

Muscle, neuromuscular junction, alpha motoneuron, anterior horn cell

Aging and Hypotonia

Decreased muscle activation

Decreased motor unit recruitment speed

Decreased ability of muscle fibers to initiate, sustain, and scale movement

Increased recovery time after injury or pathology

Safety Considerations for Hypotonia

Joint subluxation & dislocation

Likely to have difficulty swallowing if they can’t speak - don’t give fluids

Passive and Active Movement Scale - Use

Common in pediatric practice, measure to (try to) grade hypotonia

Passive and Active Movement Scale - Scores of +1 - +3

Hypertonia

Passive and Active Movement Scale - Score of 0

Normal muscle tone

Passive and Active Movement Scale - Score of -1

Mild Hypotonia

AROM: Decreased ability to cocontract axial muscles, slowed postural adjustements

PROM: Mild resistance, full PROM, hyperextensibility of hand, ankle, and foot

Passive and Active Movement Scale - Score of -2

Moderate hypotonia

AROM: Decreased tone in trunk and proximal limbs, limited ability to sustain postures

PROM: Little resistance to passive movements (especially at proximal joints), knee and ankle hyperextensibility when WB

Passive and Active Movement Scale - Score of -3

Severe hypotonia

AROM: Unable to move through gravity, absent co-contraction at proximal joints, weakness

PROM: No resistance, full or excessive ROM, joint hyperextension

Positioning: Supine

UE: non-abnormal flexion synergistic position

Elevate limbs to decrease effusion and edema

Ankle support to prevent foot drop if necessary (don’t place towels on heel - pressure injury)

Pillow support to prevent ER of LE

Head, neck, and trunk in midline

Positioning: Sidelying

Scapular protraction

Shoulder ER, flexion and ABD

Elbow extension and neutral supination

Wrist neutral

Hip neutral rotation & ABD or ADD as necessary

Knee flexion

Ankle neutral

Intervention: Weight Bearing

Benefits: muscle activation, bone loading, local circulation, postural alignment

Precautions: Prevent hyperextension & subluxation

Interventions for Trace Voluntary Movement

Augmented feedback to facilitate

NMES to increase muscle activity, especially supraspinatus and deltoid

Interventions for Flaccidity - mild Hypotonia

Compensation approach to protect joints and aid function in distal segments

Interventions for Severe-Mild Hypotonia

Functional approach: FES, BION to improve selective muscle activation, task-specific practice to incorporate or protect hypotonic segment

Wrist and Hand Splints

Maintain ROM, prevent joint laxity, wrist stability aids functional finger movement

Wrist slightly extended, fingers flexed

Sling

Protects shoulder soft tissue

Decreases subluxation risk

Decreased pressure on neurovascular structures

Tabletop/Wheelchair Support

Decrease postural asymmetries, support flaccid UE in sitting

Lateral Wheelchair Guard

Protects arm from falling off wheelchair

Protects elbow when maneuvering through doorway

Compression Glove

Decreases edema in UE, compensates for lost skeletal muscle pump

Can examine digits (coloration)

AFO & KAFO

Prevents knee hyperextension (KAFO), maintains ROM, aids swing limb advancement

Swedish knee brace

NOT a KAFO

Prevents knee hyperextension

Abdominal Binder

Provides trunk support in sitting

Decreases postural hypotension

Improves respiratory function

Assistive devices for Gait

Provides WB support, Improves postural alignment, May improve independence and safety