spasticity management, a rehab art. hatem s. shehata

HATEM SAMIR M. SHEHATA, M.D PROFESSOR OF NEUROLOGY

CAIRO UNIVERSITY

SPASTICITY MANAGEMENT. REHABILITATION ART

FIRST ANNOUNCEMENT

Movement Disorders And Spasticity

Workshop

TOPICS Dystonias. Diagnosis and Management. Prof M. Eltamawy

Hemifacial Spasms. Prof Amr Hassan

Tremor. What Is New ?. Prof Hanan Amer

Spasticity Assessment. The Art Of Neurorehabilitation. Prof Hatem S. Shehata

Hands-on: Ultrasound-Guided BTX-A Injection. Didactic Approach. All faculty members (moderators: Dr. Hatem S. Shehata, Dr. Sandra Ahmad)

Faculty:

Prof. M Eltamawy

Prof. Hanan Amer

Prof Hatem Shehata

Prof. Nevin Shalaby

Prof. Amr Hassan

Prof. Sandra Ahmad

Dr. Shaimaa Al-Jaafary

Dr. Wael Ezzat

Dr. Haidy Shebawy

7 December, 2016VENUE: LRC-Kasr

Alaini

HATEM SAMIR MOHAMMED, M.D

OBJECTIVES

• Rehabilitation Process • Spasticity – Definition – Pathophysiology – Impact • Assessment of spasticity and ADL • Spasticity management options • Outcome measures – BTX injection sheet • Clinical cases – video

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OBJECTIVES


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HATEM SAMIR MOHAMMED, M.D 4

GOALS 1. Optimizing social participation (considering persons’ wishes) 2. Minimizing distress of both patients and caregivers 3. Help patients to maximize behavioral repertoire

SPASTICITY. “HABILITATION/REHABILITATION”

• Rehabilitation is a long-term (may be life-long), problem-solving process of recovery from an injury to obtain ‘optimum function’ despite of residual disability

• It is the process by which physical, sensory, and mental capacities are RESTORED or DEVELOPED in disabled patients

Change/abnormalities (molecular/cellular) - - organ (e.g., (cord malacia, hemorrhage, infarction, TBIDisease Pathology

(Change/abnormalities of whole body set (functional loss S. & S.((functional loss Impairment

How impairment restricts the social tasks (roles). It is the expression of the gap between a person's capabilities and(the demands of the environment (environment interaction

Social Roles((participation

Activity((disability

TERMINOLOGIES SHOULD BE CHANGED

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REHABILITATION MODEL (ICF-WHO)


REAL CASE SCENARIO . . .• 56 male patient, married (3 daughters), Banker ,

HTN, non diabetic • 1 month ago right sided hemiplegia and dysphasia • Assessment now: hemiparesis (G2 D, 3 P), mild

dysphasia • Pathology: ICH • Impairment: weakness +/- spasticity,

communication disorders • Disability: toilet, dressing, hygiene, chocking,

decision making etc… • Handicap: work / family / carer

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What is the concern of hisprimary physician ?



NEUROLOGICAL REHABILITATION

• Acute onset disability, with a phase of improvement followed by relative stability: CVS, traumatic insults, infections, etc..

• Fluctuating and/or unpredictable disability, often with some progression: M.S

• Progressive, relatively predictable disability: MND

• Stable diseases present from childhood: C.P

– Categories of Neurological Conditions

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• A comprehensive service with a multidisciplinary team who should be involved in an integrated program

• This team includes ‘a list of related specialties‘: Neurologist/Neurosurgeons/ Orthopedics/PMR/Therapists/ Occupational and Speech therapy/ Psychologists/Support workers

• Target: increase patients activities and reduce burden of the patient and carers

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STRATEGIES FOR NEURO-REHABILITATION


Assessment (to collect data) Identify problem Genesis of problem Prognostic factors Expectations (patients / others)

Goals Setting (PLANNING) Short term actions Middle term directions Long term goals

Interventons Deliver treatment (alter natural Hx.) Health education and support Collect further data

Evaluations Compare Goals vs. Set Identify resolvable problems remain

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REHABILITATION PROCESS

More Actions Needed

No Actions Needed


OBJECTIVES


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HATEM SAMIR MOHAMMED, M.D 26/01/2016

SPASTICITY . . . DEFINITION

• One of the most specific impairment that results in muscle over activity resultingfrom UMNL (++ tonic SR)

• It is one of positive UMNL signsthat involves a long-term monitoring

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Mild weakness, loss of ‘precision grip’ which involves opposition


• Spasticity is distinct from other motor disturbances: • Sensori-motor disorder • Velocity-dependent increase in tonic stretch reflex activity • Length-dependent (clasp knife) • State-dependent (variables) • Usually seen in the anti-gravity muscles like the arm flexors and the leg

extensors • Associated with high tone spasms and soft tissues changes

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Pandyan et al., Disabil and Rehab, 2005

SPASTICITY . . . DEFINITION


(1) Disability: weakness / dexterity

(2) Mask actions of antagonists

(3) Seating and postural problems

(4) Pains, stiffness and spasms (discomfort–contractures–deformities)

(5) Hygiene and self care problems

(6) Mood changes and loss of self-esteem (disfigurement–sexuality problems)

(7) Fatigue – Sleep disruption

Disability

Complicatio

ns

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SPASTICITY . . . CONSEQUENCES


Loss of cortical drive after cerebral or above lesion spinal insults

Loss of descending inhibitory spinal circuits (Dorsal RST)

Increase muscle SR by intact Medial reticulospinal and vestibulospinal tracts

Spastic hypertonia, spasms, and clonus

Greenwood, 1998

INCREASE MUSCLE STRETCH REFLEX

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SPASTICITY . . . PATHOPHYSIOLOGY


• As a result neural pathways show changes in their level of excitability:

• Altered α-motoneuron excitability

• Altered Ia and Ib inhibition

• Some studies also report changes in the γ-motoneuron excitability (not commonly accepted)

Voerman and Hermens, Disabil and Rehab, 2005

Spasticity (Pathophysiology)

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NEURAL AND NON-NEURAL COMPONENTS OF SPASTIC LIMB DYSFUNCTION

• These two mechanisms are responsible for the clinically observed resistance to passive movement associated with spasticity

• Muscle hyperactivity (muscle contraction and shortening)

• Bio mechanical changes (soft tissues; tendons, ligaments, joints): thixotropy, intra-articular adhesions

(Gracies, 2005)

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PRO / CONS POSSIBLE BENEFITS OF SPASTICITY

• A common argument

• > 38% of stroke survivors affected by spasticity

☞ May help patients to walk, stand or transfer (e.g., stand pivot transfers)

☞ May assist in maintaining muscle bulk (inherently prevents atrophy)

☞ May assist in preventing DVTs

☞ May assist in preventing pressure ulcer formation over bony prominences

• No positive overall benefit to spasticity in an individual at any stage of life

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OBJECTIVES


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ASSESSMENT TOOLS

• Clinical Assessment: subjectivity - inter-rater variability

• Neurophysiological

Voerman et al., 2005

Neurophysiological response to electric stimulation •(H / M reflex)

Evoked potentials •(motor and sensory evoked potentials)

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Muscle Tone

ADL Barthel index, Others QoL tests

Sensory

Gait assessment

Other tools

MAS, Tardeau scale, Bilateral adductor tone

VAS: for pain and dyasthesia Cramps (Spasms)– Spasms Frequency Scale

Gait analysis laboratory Timed-TMWT

Goal Attainment Scale ‘the most difficult’ ROM ‘the easiest – don’t forget’

Assessment Axes


Q: WHICH TOOL WILL YOU USE ??A: THAT HELPS TO ASSESS THE TARGETED OUT COME

Impairment related measures Spasticity Range of movement

Functional measures Reduction of pain Ease of applying splint/orthosis Ease of maintaining hygiene Ease of dressing Improved seating position Improved gait pattern Improved gait efficiency

MAS / Tardeu scale / dynamic EMG Goniometry

Suggested outcome measure Visual analogue scale/Spasm Frequency Scale Timing of tasks/number of helpers/carer rating scale Timing of tasks/number of helpers/carer rating scale Timing of tasks/number of helpers/carer rating scale Photographic record/measurement i.e. pelvis level Video analysis/10 meter walk test Video analysis/patient rating/energy cost assessment

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CLINICAL SCALES

It measures Stiffness not Spasticity – No Speed of Movement is Specified

Modified Ashworth Scale

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Measurements take place at 3 velocities

Responses are recorded at each velocity as X/Y, with X indicating the 0 to 5 rating, and Y indicating the degree of angle at which the muscle reaction occurs.

Patient position: supine, with head in midlineTardieu Scale

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HOW TO CALCULATE‘Tardieu Scale’

24HATEM SAMIR MOHAMMED, M.D


(1, 2) Bowels and Bladder: 0: incontinent, 1: occasional, 2: continent

(3) Grooming: 0: needs help, 1: independent

(4) Toilet use: 0: dependent, 1: need help, 2: independent

(5) Feeding: 0: unable, 1: need help, 2: independent

(6) Transfer: 0: unable, 1: major help, 2: minor help, 3: independent

(7) Mobility: 0: immobile, 1: wheelchair, 2: walk with help, 3: independent

(8) Dressing: 0: dependent, 1: need help, 2: independent

(9) Stair: 0: unable, 1: need help, 2: independent

(10) Bathing: 0 : dependent, 1: independent

Barthel index, ADL

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Clinical Scales (Cont’d)


VAS: a subjective pain measure, ranged from 0 (no pain) to 10 (unbearable pain). The patients mark the point that represents their perception of the current status

Horizontal line 100 mm in length

Visual Analogue Scale (VAS)

No spasms0

One spasm or less a day1

One to five spasms a day2

Five to nine spasms a day3

Ten or more a day4

Spasm Frequency Scale

How many spasms occurred in the affected muscles or extremities during the last 24 hours ?

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Clinical Scales (Cont’d)


TIMED 10-METER WALKING TEST (TMWT)

• Patient walks with/without assistance 10 meters (32.8 feet) and the time is measured for the intermediate 6 meters (19.7 feet)

• Start timing when the toes of the leading foot crosses the 2-meter mark

• Stop timing when the toes of the leading foot crosses the 8-meter mark

• It can be performed at preferred walking speed or fastest speed possible (preferred vs. fast)

• Collect 3 trials and calculate the average of the three trials

Acceleration Deceleration

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• 3 components:

• Kinematics: analysis of body positions, angles, velocities, accelerations of body segments and joints during motion)

• Kinetics: analysis of forces

• EMG

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Gait Analysis

Assessment Tools (Cont’d)


STANCE-PHASE KINEMATICS

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Heel-strike ----------------------> Mid-stance --------------------------> Toe-off Contact - - - - - Loading - - - - - Midstance - - - - - - Terminal stance - - - - - - Preswing

Pelvic Angle

Knee Angle

Muscle Activity

60% of gait cycle


PATHOMECHANICS OF HEMIPLEGIC GAIT

• Reduced knee flexion in swing phase (stiff-legged gait)

• Equinus (excessive ankle plantar flexion) which leads to: increase energy required to initiate swing period of gait cycle

• Gait asymmetry, short step length, speed reduction and longer gait cycle

• Mass limb movement pattern: on the paretic side requiring compensatory pelvic adjustment in non-paretic side

• Defective “body image”

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OBJECTIVES


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GOALS OF THERAPY

• Increase functionality (improve QoL): ROM, ambulation

• Postural benefits: modify body image

• Ease pain – Decrease spasms

• Prevent or decrease contractures

• Facilitate Rehab/Orthosis

• Hygiene

INDIVIDUALIZE /

AVOID GESTALT

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SPASTICITY MANAGEMENT OPTIONS

Physical therapy

Regular exercises Physiotherapy

Surgery

Severe spasticity

Medical therapy

Generalized Oral agents

Regional Intra-thecal baclofen

Focal BTX-A injection

Phenol blockade

Consider each in combination with others

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PHARMACOLOGIC MANAGEMENT

• Systemic

• Baclofen (30-90 mg/d), diazepam (5-15 mg/d), dantrolene sodium (100-400 mg/d), clonidine (0.3-0.9 mg/d), tizanidine (< 36 mg/d), carbamates (methocarbamol 3–6 g, carisoprodol), endocannabinoids (Sativex)

• Limitations: non-selective; large dosages often required which may result in intolerable side effects (sedation, weakness, GIT disturbances and hepatotoxicity)

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ECB. ‘Retrograde’ inhibition of nerve impulse transmission1. Action potential at the presynaptic

2. Neurotransmitter (NT) release

3. Glutamate and GABA

4. Binding to GABA-R and iGlu-R

5. Inhibitory …………… Excitatory

6. Activated Glu

7. Increase Calcium

8. ECBs bind to pre-synaptic cannabinoid receptors (CB1-R)

9. Net result is inhibition of further Ca

influx, and so inhibition of NT release

stimulates

endocannabinoid

(ECB) synthesis


• Local treatment options. • Motor point and nerve blocks: aqueous phenol (Neurolysis by coagulate

proteins)

Limitations: tissue necrosis, pain and dysesthesia; variable duration of effect; often irreversible

• Local injections of BTX-A

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Pharmacologic Management (Cont’d)

Indications: generalized moderately severe spasticity (not adequately treated with oral medications and BTX).

The spasticity reduction in LL (+/-) UL depends on the catheter position in the spinal fluid.

Low catheters (T 10-12): improve mainly the legs. Higher catheters (T 1-2): arm spasticity is targeted.

■ Regional treatment options. Intra-thecal Baclofen (ITB)

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Test dose: 50 ug baclofen injection in spinal fluid. Then evaluate for 4-8 hours (response)

Pump is inserted under abdominal muscles

A catheter is inserted through a needle intrathecally and is threaded upward

Catheter is tunneled under the skin to the abdomen and is connected to the pump

The pump filled with baclofen is programmed by a computer to continuously release a specified dose

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SURGICAL MANAGEMENT

• Selective dorsal rhizotomy

• Selective Neurotomy: partial section of motor nerve branches

• Orthopedic surgery as tendon release (depending on age of patient)

Limitations: invasive; irreversible; parathesia; effectiveness varies

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Selective Dorsal Rhizotomy (SDR)

1. Exposing LL nerve roots through a midline lumbar incision.

2. Sensory roots are divided into 3 – 5 rootles, that are electrically stimulated to identify and cut nerves with abnormal responses.

Commonly in young patients with LL spasticity (with relative good strength and good back extensors power) or (to improve hygiene).

Prerequisites: No contractures.

Complications rate: 5 – 10% PT should start after a month (1-2 times/wk) if the goal is to improve ROM; and (4-5/wk) if the goal is to improve strength

40HATEM SAMIR MOHAMMED, M.D


Orthopedic Surgery

• Indications: (1) ease care, (2) improve function, (3) cosmetics

• Both bony and soft tissue surgeries

• The major soft tissue procedure involves lengthening the muscle-tendon unit (tenotomy) – and (tendon transfer)

• Other surgeries include: • Capsulotomy

• Fascial arthroplasty

• Removal of excessive callus formation

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OVERVIEW OF REHABILITATION INTERVENTION

• Early start – better outcome.

• Positioning ‘bed, wheelchair, splinting, casting, AFO)

• Joints stretching and PROM to prevent contractures or shortening • Full stretch for 2 hours / 24 hours (Medical Disability Society, 1988)

• Re-educate ‘Relearning’ and facilitate balance/equilibrium

• Gait training

• In advanced spasticity, (Biomechanical hypertonia) resistant disability ▪ Not velocity-dependent and poor response to antispastic agents.

▪ The only treatment: stretching, positioning, splinting and casting

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DOES REHABILITATION WORK ??? ROLE OF NEURONAL PLASTICITY

• Late recovery (neuronal plasticity) is proposed to underlie cortical map reorganization following neurological insults

• The undamaged regions of the brain can progressively adopt the function of the lesioned area by neuronal sprouting and synaptogensis leading to change in cortical representations (maps)

This can be enhanced by enriched environment, structured physiotherapy and TMS

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OBJECTIVES


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NOW . . . I DECIDED TO INJECT BTXWHY ?? HOW ??

• Selection criteria for injection (identify the problem precisely): (1) Preserved functionality (type of spasticity) , (2) Others

• Understanding and expectations of treatment by patient and caregiver

• Dosage and site of injection

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PREPARATORY STEPS

• Before injection: Checklist • Complete examination

• Goal determined: a contract with patient

• Take into account patients on anti-coagulants

• Muscles to inject

• Muscle localization

• Techniques of injection

• Evaluation after 2-4-6 weeks

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PROBLEM DISTRIBUTION GOAL SETTING

RegionalMultifocal (generalized with focal problems)Focal

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COMMON CLINICAL PATTERNS – UPPER LIMB

Adducted/internally rotated shoulder

Flexed wrist Pronated forearm

Clenched fist Flexed elbow Thumb in palm

Courtesy WE MOVE, 2006

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IRO/retrovIRO/ADDIRO/ADDIRO/ADDIRO/ADDSHOULDER

ExtensionFlexionFlexionFlexionFlexionELBOW

Pronated Pronated Neutral SupinatedSupinatedFOREARM

Flexion Flexion Neutral ExtensionFlexionWRIST

28% 8% 86% 27% 6%


COMMON CLINICAL PATTERNS – LOWER LIMB

Equinovarus

Striatal toe

Stiff knee Flexed knee Adducted thighs

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Courtesy WE MOVE, 2006


WHICH MUSCLES TO TREAT ?• Elbow flexion:

• Biceps brachii, brachialis, brachioradialis, pronator teres • Spastic hand:

• FCR, FCU, FDS, FDP, FPL, interosseii, opponens • Stiff knee gait:

• Rectus femoris, hamstrings

• Equinovarus: • Triceps sure, tibialis posterior

• Toe flexion: • Flexor digitorum longus and brevis, FHL

• Muscle treated frequently depends on patient condition and practitioner personal experience,

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WHAT IS THE BEST DILUTION ?• 1 or 2, or 5 ml / 100 U BOTOX ®

• High volume dilution and end-plate targeting achieve greater muscle blockade

• Low volume for small muscles - - - Large volume for large muscles

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WHAT IS THE BEST INJECTION TECHNIQUE AND SITE?

• The best technique is the one you feel confident with • Blind technique:

• Poor accuracy / not to recommend • Risk to inject ‘between’ muscles • Unrelated to injector experience • In one study assessed 121 practitioners injected cadaver muscles, 43%

succeeded and 57% failed

• EMG if large and superficial • ES if small and deep • U/S-guided: if deep or failed to be stimulated

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BTX INJECTION SHEET . . . . • Signed consent: information – patient and caregivers • Agent used: . . . . . Dilution: (. . . units / ml saline) • Muscle identification: palpation / EMG / Others • Muscle injected Units: ………………… …….. • Appointment date for splinting (type, method of applications, review appointment) • Appointment date for further review (2-4-6 wks):

• Response to injection ? • Has functional goal been achieved ? • Is further injection needed at current time ?

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INJECTION RECORD

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DIAGNOSTIC NERVE BLOCK WITH ANAESTHETICS

• Lidocaine injection (1 ml) at the level of motor nerve branches innervating spastic muscles

• Immediate and transient spasticity reduction

• Determine the respective responsibility of spasticity, contracture and weakness

• Evaluation of function without spasticity

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ULTRASOUND - GUIDED INJECTION “UL”


OBJECTIVES


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HATEM SAMIR MOHAMMED, M.D 28/01/2016 59

Target muscle:Extensor Hallucis Longus

DEMO (1) STRIATAL TOE (HITCH-HIKER’S BIG TOE)


Tibialis Posterior

DEMO (2) INJECTION SITE OF TIBIALIS POST.


20 years oldpost-encephalitic Left spastic hemiplegia (2yrs)

Assessment of LL1. Big toe clawing(talipes cavus)2. Spastic Talipus Equinus Target Muscles:1. Triceps surae2. Flexor hallucis longus 3. Quadratus plantae

DEMO (3) (A) CASE SCENARIO


DEMO (3) (B) CASE SCENARIO

Assessment of UL

Fixed elbow flexion deformity (with calcification)


DEMO (3) (C) CASE SCENARIO

Eight days after injection


DEMO (4) UL (ONLY 5 DAYS)


DEMONSTRATION

28/01/2016 66

Pronator teres FDP


DEMO

28/01/2016 67

FDS

CASE VIDEOS Disability: (1) weak back extensors(2) flexed posture (overacting leftiliopsoas) – left loin pain(3) overacting adductors(4) co-contraction (hamstrings/quadriceps F)(5) left talipus eq varus (6) disabling spontaneous clonus Plan: (1) BoNT injection: Iliopsoas (left): 50. Quadriceps (rectus femoris – vastus medialis): 25 X 2 (small doses to minimize clonus). Hamstrings: 50 X 2. Adductors (bilateral), left gracilis: 50 X 2. Left Gastromedialis & lateralis: 30. Left tibialis posterior: 50 (2) Stretching of injected muscles (3) Strengthening of back extensors (4) Then gait and balance ex

A.S, 36-yr, SPMS. Diagnosed 10 yr ago Wheel-chair: 18 mo On CPM (9 mo)This patient was subjected to 3 injection sessions4 mo apart

18 Sep 2011

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3 WEEKS AFTER 1ST INJECTION

(DECREASED HAMSTRINGS OVERACTIVITY– KNEE EXTENDED)

STILL BACK EXTENSORS (WEAK)LEFT LOIN PAIN DISAPPEARED

8 weeks after 2nd injection

(Back extensors can support walking)

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20 Mar 2012

16 Oct 2011

THANK YOU

spasticity management, a rehab art. hatem s. shehata

Health & Medicine