spasticity management · 2011-09-08 · objectives by the end of this presentation, the attendee...
TRANSCRIPT
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