Spasticity Management

2010 Provincial Long Term & Continuing Care

Conference “Respect and Protect”

May 18, 2010

Karen Ethans, MD, FRCPC

Physical Medicine and Rehabilitation

Health Sciences Centre

University of Manitoba

Objectives

By the end of this presentation, the attendee will:

Understand what spasticity is as part of the upper motor neuron syndrome

Be able to assess if spasticity is problematic

Know the array of therapies available in Canada for focal and generalized spasticity

Know what spasticity goals are possibly treated with Botulinium toxin

Understand how the team can help in the treatment of a person with spasticity in the long-term care setting

Spasticity

“a motor disorder characterized by a velocity-

dependent increase in tonic stretch reflexes

(muscle tone) with exaggerated tendon

reflexes resulting from hyperexcitability of

the stretch reflex as one component of the

upper motor neuron syndrome”Lance, 1980

English?

Spasticity array of signs/symptoms:

“jumping” of the limb involuntarily

Involuntary spasm of limb with painful sudden

movement

Tightening up of limbs/muscles – can be

painful or cause abnormal body position

Can lead to contractures, can make it very

difficult to get into areas to clean dress etc

Upper motor neuron syndrome

Refers to different types of motor dysfunction produced in those with lesions of the descending corticospinal tract and other tract systems (brain and spinal cord).

Stroke

Cerebral palsy

Traumatic brain injury

Anoxic brain injury

Spinal cord injury

Multiple sclerosis

Neurodegenerative diseases

Positive Signs

Increased muscle tone

Exaggerated tendon reflexes

Stretch reflexes spread to

extensors

Repetitive stretch reflex –

clonus (bouncing)

Exagerated withdrawal to

light touch

Mass synergy patterns

Negative Signs

Decreased dexterity

Paresis / weakness

Inadequate force

generation

Slow movements

Fatigability

Slowness of movement

Problems with Spasticity MAY:

cause impaired active or passive functions

interfere with mobility (eg walking, transfers), exercise, joint range of motion

interfere with independence in activities of daily living (reaching, grasping, hitting switches)

cause pain and sleep disturbance

make patient care more difficult (eg hygiene problems, dressing, toileting, donning splints)**

cause seating problems/positioning difficulty

Who identifies these problems?

Patient

Nurses, care-givers, attendants

Therapists

Family, especially those involved with

giving care

in long term care BEST people for history

of problematic spasticity is caregivers!

Benefits of Spasticity

maintains muscle mass

?prevent DVT

can be a functional aid

warning signal to secondary complications

Goal oriented questions to

consider Impaired active function

How do muscle overactivity and contracture impair voluntary functions

eg reaching, transfers, and ambulation

tight biceps make it impossible to reach to push elevator button

Can performance of muscles improve if free of antagonist muscle co-contraction?

Eg if loosen biceps would triceps work better

Impaired passive function

When there is little or no active movement

how does muscle overactivity and contracture interfere with passive joint movement needed

hygiene, grooming, and other care activities?

perineal/palmar/axillary hygeine

dressing lower body with knees clamped together

Clinical assessment toolsLimb use Assessment

Skin integrity/hygiene Number, degrees of pressure sores

hygiene-photos/malodor/maceration

Pain Global pain scale

Transfers Level of assistance, aids

Gait Assistance, device, bracing, speed,

endurance, stability, effort, video

Upper limb use Reach distance, object size for grasp

and release, performance time, object

transport, number of tasks for which

limb is used as an assist

Modified Ashworth Scale

0 = No increase in tone

1 = Slight increase in tone, giving a “catch”

1+ = Slight increase throughout less than half range

2 = More marked increase in tone through more than half range but limb easily moved

3 = Considerable increase in tone - passive movement difficult

4 = Limb rigid in flexion or extension

(Just so you know what I‟m talking about in my correspondence!)

Indications for treating spasticity

When spasms or muscle tightness:

interferes with ADL function, mobility, or nursing care/hygiene

interferes with proper wheelchair seating

causes pain

wakening at night

causing contractures

Patient/family/caregivers feels benefits outweigh side effects

Role of care-givers in deciding

indications - KEY take-home message!

Physician CANNOT decide whether spasticity needs treating based on physical exam (doctor does not “know best”!

Communication from patient and care-givers extremely important re need for treating certain goals and effectiveness of particular treatment!

Without this goal directed therapy impossible and treating based on static physical exam findings useless

Thus PLEASE communicate with us re areas that are problems and what you need us to treat!!!

Adult spasticity clinic

Physiatry run, access to interdisciplinary tx

Assess spasticity due to any upper motor neuron cause, effect on function, ADL‟s, pain etc

Assess for causes/triggering factors

Assess re referral to physical/occupational tx, rehab engineering

Rx oral meds, intrathecal pumps, botulinum toxin

Referral for ablative surgeries

Goal oriented

Spectrum of care

Injection

Therapy

Neurosurgeries

Orthopedic

Treatments

Rehabilitation

Therapy

Prevent

Nociception

Intrathecal

Baclofen

(ITB™)

Therapy

Oral

Drugs

Patient

Treat nociceptive factors

Identify the “triggering” stimulus

IE factors that increase sensory input to the

spinal cord

UTI

Fracture

Impaction

Pressure sore

Physical/occupational therapy

Range of motion and stretching exercises

Positioning and frequent repositioning

Serial casting/ splinting/bracing (dynamic/functional etc)

Task practice etc

Physiotherapy per sae NOT needed long-term

Either self-stretches or stretches by attendant/ward - aid are key on regular basis long-term –these need to be done by ward long-term!

Oral Medications At CNS level:

Baclofen – first line, careful of withdrawal (signs?), no real evidence of “weakness”, ++drowsiness.

Tizanidine – drowsiness major issue

Clonidine – hypotension may be issue

Diazepam – tolerance/dependence/cognitive s/e

Cyproheptadine (historical)

Cannabinoids – THC – more evidence needed but empiric/pilots encouraging

Peripherally:

Dantrolene sodium – drowsiness/liver function/myositis

Intrathecal pump

baclofen

For severe, intractable spasticity not

amenable to tolerated doses of oral

medication

Lower extremity spasticity predominantly

affected

Intrathecal pumps -

complications

Pump failure

Battery failure

Catheter breakage, blockage, kink, separation

Pump site infection, seroma, extravasation

Meningitis

Overdose/underdose (ie human error)

Avoid withdrawal! (seizures, coma, death)- if suspect

failure, provide high dose po baclofen!

Neuromuscular junction blocks

Botulinum toxin

Pros

Effective

Little pain (the medication itself doesn‟t hurt, but needle of course does!)

Technically easy

Few side effects/safe +++

Cons

Expensive

Need to repeat in 3-8 months

Ablative surgery

Soft Tissue Procedures

Tenotomy – depending on location may be difficult to access – VERY difficult to get done in Winnipeg

Tendon lengthening - in children

Tendon transfers – children mostly

Neurosurgical Procedures

Dorsal root rhizotomies – effective only at level of rhizotomy – rarely done now

Neurectomy – motor nerves only, rarely done

Botulinum toxin

Botulinum Toxin Injections

Inhibits release of acetylcholine into

neuromuscular junction

Peripheral nerves eventually re-sprout thus

effect 3-6 months (longer?)

Local effect - local spasticity

Clostridium botulinum

Gram +ve bacteria, spore-forming, anaerobe

Toxin 7 antigenic forms (A-G)

Blocks NMJ transmission

In acute botulism death w/ respiratory paralysis

In clinical use, focal miniscule doses for blocking local NMJ

Type A only type available in Canada for clinical use

The craze• 2.8 million injections/year for wrinkles

in USA

• 1/10,000 pics on Google

Botulin Toxin Type A Approved

uses in Canada

Focal Spasticity

Dynamic equinus foot in CP

Cervical Dystonia

Hyperhydrosis of Axilla

Strabismus

Blepherospasm

Hemifacial Spasm

Cosmetic (wrinkles – specifically for glabellar lines)

Reported Clinical Use of BoNTA (BOTOX®) Is

Diverse and Expanding

Siallorhea

Hyperhidrosis*

Migraine

Cervical Dystonia

Cerebral

Palsy

Blepharospasm*

Neuromuscular Autonomic Sensory

Bladder

Aesthetics*

Achalasia

Strabismus*

HFS

RESPROUTING

Chemical denervation of neuromuscular junction stimulates nerve sprouting.

RE-ESTABLISHING

Nerve sprout establishes new neuromuscular

junction. Muscle tone is

restored + spasms return

Injection

Use Teflon coated hollow needle

EMG audio guidance

Stimulator

Injection with stimulator

BOTOX: Safety

Botulinum toxin used clinically for decades

Rare, if any, anaphylactic reactions

Side effects are temporary:

Site specific, e.g.. Weakness in injected and neighbouring muscles

Subjective weakness and fatigue („flu-like‟ syndrome) last less than 4 days

Reported deaths likely due to ++ excessive dose or aspiration pneumonia that patient high risk of already, etc

BoNT: Clinical Effects on

Muscle Overactivity

Onset usually within 3–7 days; maximum effect at

approximately 4 weeks

Clinical benefit usually >12 weeks; may be

extended with adjunctive therapy1

Can be used in conjunction with oral medications

and intrathecal baclofen

1. Brin MF, the Spasticity Study Group. Muscle Nerve. 1997;20(suppl 6):S208-S220..

When do we use it?

Sex: Female

Age: 44

Type of injury: Motor Vehicle Accident, resulting in severe brain damage.

BOTOX® injections received to date: 4

Sex: Female

Age: 43

Type of injury: Motor Vehicle Accident

BOTOX® injections received to date: 2

BOTOX for Spasticity: Patient

Selection No fixed joint deformity*

Obtainable goals present! Do not just do it because the joint/muscle is tight or spastic Pain

Hygiene

ADL (dressing etc by patient or caregiver)

Uncovering antagonist power

Gait

Positioning

Botulinum toxin effectiveness

Reduces muscle tone PLUS:

pain relief

improved hand/axillary/perineal hygiene

improved walking

improved positioning for function

reduce/eliminate clonus -not always needed

Botulinum toxin for Upper Extremity

Post CVA

Double blind, RCT, multicenter, 126 post

CVA

Wrist/finger flexor spasticity

50 u/muscle X 4 +/- thumb muscles

Brashear A et al, the Botox Post-Stroke Spasticity Study Group NEJM 2002

Outcomes:

Functional disability – DAS – hygiene,

dressing, limb posture, pain 0-3 (1

picked)

Muscle tone (Ashworth)

Global Assessment Scale –4 to 4

Assessed at 1, 4, 6*, 8, and 12 weeks

Brashear A et al, the Botox Post-Stroke Spasticity Study Group NEJM 2002

Results

Significantly more reduction in wrist and

finger flex tone @ all visits with Botox

(p<0.001)

Greater improved principal target on DAS

(p<0.001 @6 weeks)

Global assessments better with Botox

(p<0.001)

Brashear A et al, the Botox Post-Stroke Spasticity Study Group NEJM 2002

Summary - Treating Spasticity

with BOTOX

Safe

Minimal side effects

If too much weakness, reversible

Effective

Facilitates rehabilitation goals, e.g.. Increased

ROM, ease of hygiene, positioning

Improves quality of life for patient and caregivers

Summary - Treating Spasticity

with BOTOX

Can be used in conjunction with other

therapies

Spasticity common problem, with increased

awareness likely increase in use

$$$ -covered by pharmacare for spasticity

but in nursing homes?

Conclusions

Spasticity can be problematic, interfere with quality of life

However, don‟t just treat spasticity because it‟s there. Treat for reaching obtainable goals – need team input!!!

Combination of therapies best, with an interdisciplinary approach that involves patient and care-givers

Spasticity Clinic

Fax 7871476

Dr. K. Ethans

Dr. A. Casey