SPASTICITY Pathophysiology and Treatment after a Brain Injury

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1 SPASTICITY Pathophysiology and Treatment after a Brain Injury Kenneth A. Mook, MD, PhD Gateway Rehabilitation Hospital At Florence

2 DISCLOSURE STATEMENT I have nothing to disclose I am the Medical Director at Gateway Rehabilitation Hospital at Florence

3 Types of Brain Injury Traumatic Brain Injury brain injury from an external force to the skull and brain. Congenital - Genetic, Chromosomal, Multifactorial Acquired Brain Injury - damage to the brain that occurs after birth and is not related to a congenital disorder or a degenerative disease, and occurs between perinatal and geriatric. Excludes Cerebral Palsy, Alzheimer s disease, Multiple Sclerosis, Parkinson s Disease.

4 Objectives Understand Basic Neuroanatomy to Understand Spasticity Understand Clinic Evaluation and Treatment Options for Spasticity Understand Medication Management of Spasticity Understand Invasive Options to inhibit spasticity locally or at the CNS

Brain Functions Brain has millions of neurons and connections or synapses Different areas of the brain control specific body functions and other

5 Brain Functions Brain has millions of neurons and connections or synapses Different areas of the brain control specific body functions and other areas are connectors or regulators between brain function and information sent to the spinal cord to the lower motor neurons and back from sensory neurons.

6 How does Traumatic Brain Damage Occur? Focal Damage - contusion or trauma to the location of a particular area of impact: coup-countercoup effects resulting in Fronto-temporal contusions Diffuse axonal injury shifting or rotation of brain inside the skull causing shearing and tearing injuries of neurons/axons These injuries result in hematoma, brain edema, and/or increased intracranial pressure.

Physical Effects of acquired brain injuries Motor weakness or paralysis Extrapyramidal effects on balance, ataxia, uncoordinated movement patterns Sensory impairments to vision,

7 Physical Effects of acquired brain injuries Motor weakness or paralysis Extrapyramidal effects on balance, ataxia, uncoordinated movement patterns Sensory impairments to vision, sensation, and hearing Seizures Hearing, speech (dysarthria), taste, smell, and swallow deficiencies High fatigability Sleep disturbances Increased sensitivity to caffeine, alcohol and drugs

8 Physiology of Spasticity Spasticity = Motor disorder characterized by: velocity dependent increase in muscle tone, involuntary muscle contractions hyperexcitability of tonic stretch reflexes Tone = resistance to passive movement. Rigidity = hyperactivity from prolonged discharge of alpha motor neurons.

Paralysis Later: Hypertonicity Hyperactive reflexes, Babinski sign Atrophy Segmental reflex arc intact CVA, Cerebral Injury, Spina Cord

9 Upper Motor Neuron Cerebral Cortex Corticospinal tracts Upper Motor Neuron vs. Lower Motor Neuron Injuries Definition Lower Motor Neuron Anterior Horn Cell Ventral root axon to striated muscle Initial: Paresis or Paralysis Later: Hypertonicity Hyperactive reflexes, Babinski sign Atrophy Segmental reflex arc intact CVA, Cerebral Injury, Spina Cord Injury Injury Neurology Examples Initial: Loss of tone Rapid atrophy Loss of myotactic reflexes Later: same, no significant changes Reflex arc broken Poliomyelitis, SMA, Root injury, Cauda equina

UMN Syndrome Muscle Softening Initially Weakness Fatigability Slow initiation Reduced motor unit recruitment Reduced dexterity Muscle Tightening Subsequently

10 UMN Syndrome Muscle Softening Initially Weakness Fatigability Slow initiation Reduced motor unit recruitment Reduced dexterity Muscle Tightening Subsequently Velocity-dependent tone increases Abnormal relaxation phase Clonus Rigidity Dystonia Flexor/Extensor spasms Stretch/cutaneous hyperreflexia Autonomic hyperreflexia Babinski reflex

11 Cerebral Cortex NeuroScience Online UTHealth & McGovern Medical School

12 Cerebral Cortex NeuroScience Online UTHealth & McGovern Medical School

13 Cerebral Cortex

14 Motor Unit and Motor Neuron Pools Motor Unit: Individual muscle fibers are innervated by an individual alpha motor neuron. Motor Neuron Pool: Groups of muscle fibers are innervated by a series of motor neuron nuclei clustered in columns in the anterior horn of the spinal cord which is called a motor neuron pool. Innervation Ratio: Light force muscle have a small number of muscle fibers innervated by a each motor neuron while gross, large force muscles have a large number of muscle fibers innervated by each motor neuron. Muscle Force: Muscle force production is determined by how fast a motor neuron fires (Rate code), as well as how many motor neurons are recruited to fire their respective muscle fibers ( Size Principle)

15 Muscle Spindles Muscle Spindles and Golgi signal the LENGTH of a muscle and the RATE OF CHANGE in length of a muscle. specialized muscle fibers within a skeletal muscle itself that consists of Intrafusal fibers and Extrafusal fibers. Golgi Tendon Organ Signal the FORCE applied to a muscle Tendon Organs NeuroScience Online UTHealth & McGovern Medical School

Muscle Spindle Fibers Dynamic Nuclear Bag Fibers bundled nuclei that signal information about the DYNAMIC rate of change (velocity) of muscle length Static Nuclear Bag Fibers bundled

16 Muscle Spindle Fibers Dynamic Nuclear Bag Fibers bundled nuclei that signal information about the DYNAMIC rate of change (velocity) of muscle length Static Nuclear Bag Fibers bundled nuclei that signal information about the STATIC length of a muscle Nuclear Chain Fibers single row nuclei that signal information about the STATIC length of a muscle Muscle Spindle Fibers

Muscle Spindle Innervation Ia, II = Sensory Innervation Group Ia afferents - form annulospiral endings around the intrafusal fibers and signal LENGTH and VELOCITY.

17 Muscle Spindle Innervation Ia, II = Sensory Innervation Group Ia afferents - form annulospiral endings around the intrafusal fibers and signal LENGTH and VELOCITY. Group II afferents form flower spray endings that innervate the ends of nuclear chain and static nuclear bag fibers and signal only about LENGTH. Gamma = Motor innervation Gamma Motor Neurons innervate Intrafusal fibers to keep muscle spindles taut and sensitive to further stretch.

18 Golgi Tendon Organ Located between the muscle fibers and tendon. Signals information about the FORCE applied to the muscle. Group Ib fiber afferent innervation increases firing rate as the force on the muscle increases.

19 Spinal Reflexes Myotatic Reflex (Monosynaptic) Sudden stretch of muscle spindles stimulates Ia afferent firing which has a monosynaptic innervation on the alpha motor neuron that results in muscle contraction to shorten the muscle. Role in maintaining POSTURE. Reciprocal Inhibition The myotatic reflex occurs as the Ia afferent bifurcates and innervates the alpha motor neuron, but also innervates a Ia inhibitory interneuron on the alpha motor neuron of the opposing muscle group.

Spinal Reflexes Autogenic Inhibition Reflex GOLGI TENDON ORGAN Ib afferents fibers innervate a Renshaw inhibitory interneuron to inhibit the alpha motor neuron to the contracting muscle resulting in

20 Spinal Reflexes Autogenic Inhibition Reflex GOLGI TENDON ORGAN Ib afferents fibers innervate a Renshaw inhibitory interneuron to inhibit the alpha motor neuron to the contracting muscle resulting in ceasing muscle fiber firing. Not a complete safety mechanism from a heavy weight. Helps to spread the work more evenly throughout a muscle via recruiting some fibers and allowing inhibition of other muscle fibers.

Spinal Reflexes Reciprocal Excitation in the Golgi tendon organ s autogenic inhibition reflex Ib afferent fibers innervate an excitatory interneuron on the alpha motor

21 Spinal Reflexes Reciprocal Excitation in the Golgi tendon organ s autogenic inhibition reflex Ib afferent fibers innervate an excitatory interneuron on the alpha motor neuron of the antagonist muscle, while via an inhibitory interneuron, inhibiting the alpha motor neuron of the agonist muscle, and allowing relaxation of the agonist muscle.

Descending Motor Pathways Descending pathways from the brain regions send nerve axons down the spinal cord to innervate alpha motor neurons, gamma motor neurons, and interneurons through several

22 Descending Motor Pathways Descending pathways from the brain regions send nerve axons down the spinal cord to innervate alpha motor neurons, gamma motor neurons, and interneurons through several tracts. Flexor-Extensor rule: flexor muscle motor neurons are located posteriorly to the extensor muscle motor neurons. Proximal-Distal rule: distal muscle motor neurons are located lateral to proximal muscle motor neurons. NeuroScience Online UTHealth & McGovern Medical School

23 Descending Motor Pathways Lateral Pathways Control proximal and distal muscles Voluntary movement of arms and legs Tracts: Lateral corticospinal tract Rubrospinal tract Medial Pathways Control muscles of posture, balance, coarse control of axial and proximal muscles Tracts: Vestibulospinal tracts Reticulospinal tracts Tectospinal tract Anterior corticospinal tract

24 Descending Motor Pathways Lateral Pathway: Pyramidal System Corticospinal Tracts Sensori/Premotor Cortex -> motor cortex -> internal capsule -> cerebral peduncle in midbrain -> medullary pyramids (brainstem) -> splits into two branches 90% cross over to lateral corticospinal tract 10% do not cross over and form the anterior corticospinal tract but cross over at their respective spinal cord level of innervation) CONTROL VOLUNTARY MOVEMENT Lateral corticospinal tract distal muscle fine motor control. Anterior corticospinal tract proximal muscle gross motor control.

Descending Motor Pathways Lateral Pathway: ExtraPyramidal System Rubrospinal tract Red Nucleus (Midbrain) -> cross over -> lateral funiculus of spinal cord Minor pathway in humans Purpose: Excitation

25 Descending Motor Pathways Lateral Pathway: ExtraPyramidal System Rubrospinal tract Red Nucleus (Midbrain) -> cross over -> lateral funiculus of spinal cord Minor pathway in humans Purpose: Excitation of flexor muscles and inhibition of extensor muscles. Role in MOVEMENT VELOCITY (Cerebellum innervates the Red nucleus resulting in LEARNED MOTOR COMMANDS) Some innervation from the Motor Cortex (allows some recovery after corticospinal tract damage).

26 Descending Motor Pathways Medial Pathway: ExtraPyramidal System Vestibulospinal Tracts Lateral Vestibulospinal tract antigravity muscles for balance during tilting. Medial Vestibulospinal tract stimulates neck muscles to stabilize the head position and eyes movements Mediate: POSTURAL ADJUSTMENTS HEAD MOVEMENTS BALANCE

27 Descending Motor Pathways Medial Pathway: ExtraPyramidal System Reticulospinal tract Alternative to corticospinal tract where cortical input via the BRAINSTEM RETICULAR FORMATION can excite alpha motor neurons. Regulate flexor responses to only noxious stimuli Also control orientation, stretching, and maintaining complex postures. Integration of sensory input to guide motor output. Pontine Reticulospinal tract Medullary Reticulospinal tract

28 Neurotransmitters Nerves talk to each other through NEUROTRANSMITTERS. These chemicals are released from one nerve terminal when an action potential arrives and they cross over a synaptic cleft to bind to RECEPTORS on the nerve or muscle or terminal organ to pass on information. Neurotransmitters are then taken back up by the nerve terminal and stored until another action potential wave comes and tells them to release again.

29 Neurotransmitters Cerebral Neurotransmitters Glutamate excitatory to next neuron. GABA inhibitory Dopamine excitatory Serotonin Excitatory/Inhibitory Spinal Cord Neurotransmitters Acetylcholine excitatory Glycine inhibitory

30 So How Does All this Relate to Spasticity?

31 Pathophysiology of Spasticity Loss of Inhibitory influence on segmental reflexes from suprasegmental pathways Imbalance between inhibitory and excitatory neural input Spinal reflex excitability from denervation or collateral sprouting Gamma motor neuron hyperexcitability

early ROM and sudden release with sustained tension

32 Clinical Evaluation of Spasticity Physical Evaluation Velocity-dependent UE flexors, LE extensors Occurs at early ROM and sudden release with sustained tension Clonus vs. spasms Upper Motor Neuron signs (Babinski)

33 Modified Ashworth Scale Modified Ashworth 0 = no increased tone 1 = Light increase in tone, manifested by a catch and release, minimal resistance at end of range of motion 1+ = slight increase in tone, followed by a catch, with minimal resistance through the entire ROM 2 = more marked increase in tone but easily flexed 3 = considerable increase in tone, PROM difficult 4 = Affected part rigid in flexion and extension Bohannon, R. and Smith, M. (1987). "Interrater reliability of a modified Ashworth scale of muscle spasticity." Physical Therapy 67(2): 206.

34 Clinical Evaluation of Spasticity Functional Capacity Evaluation ADLs Transfers Resting Position ROM Balance Endurance Orthoses Sleep patterns Gait analysis

35 Common Clinical Conditions with Spasticity Traumatic Brain Injury Stroke Cerebral Palsy Multiple Sclerosis Anoxic Encephalopathy Spinal Cord Injury Developmental Abnormalities

Initial Approach to Spasticity Functional impairment from spasticity? Gait disturbance? Is hypertonicity needed for standing? Flexor spasms? Painful spasms?

36 Initial Approach to Spasticity Functional impairment from spasticity? Gait disturbance? Is hypertonicity needed for standing? Flexor spasms? Painful spasms? Basic Management Proper bed positioning Avoid noxious stimuli Daily stretching program Physical Measures Therapeutic facilitation Topical Cold/anesthesia Casting/Splinting

37 Care of Spasticity Initiate with Conservative measures and progress to more invasive procedures as needed

$Step 1 Prevention of noxious stimuli UTI Bowel impaction pressure ulcers fractures paronychia acute abdomen Patient education Use$

38 Step 1 Prevention of noxious stimuli UTI Bowel impaction pressure ulcers fractures paronychia acute abdomen Patient education Use slow movements Use foot protection Skin inspection Avoid stimulus for spasticity Teach proper body mechanics for lifting, pushing, pulling

and Stretching Program Static stretch to prevent contractures,

39 Step 2 Proper positioning Check W/C, Bed, Chair for proper positioning to prevent contractures and pressure ulcers Daily ROM and Stretching Program Static stretch to prevent contractures, capsule tightness, reduce stretch reflex hyperactivity, and improve motor control

40 Step 3 Physical Modalities Muscle cooling Heat Therapeutic exercises Biofeedback Peripheral Electrical Stimulation Splinting/Orthotics

Spasticity: Modalities Cold (Cryotherapy) decrease myotatic stretch reflex activity decreases Golgi Tendon Organ firing slows NCV decreases sensitivity of cutaneous

41 Spasticity: Modalities Cold (Cryotherapy) decrease myotatic stretch reflex activity decreases Golgi Tendon Organ firing slows NCV decreases sensitivity of cutaneous afferents min, temp < 32C duration of effect = hrs Heat physiology less clear increases Ia afferent firing decreases II afferent firing increase Golgi tendon firing

Spasticity: Modalities Electrical Stimulation increase Ia afferent firing and inhibitory neuron firing neurotransmitter modulation duration = few hrs

42 Spasticity: Modalities Electrical Stimulation increase Ia afferent firing and inhibitory neuron firing neurotransmitter modulation duration = few hrs Casting/Splinting cutaneous stimuli to extremity - decreases tone elongates elastic component increases number of muscle fiber sarcomeres serial casting q 2-5 days

43 Step 4 Antispasticity Medications Zanaflex (Tizanidine) Catapres (Clonidine) Valium (Diazepam) Baclofen (Lioresal) Dantrium (Dantrolene Sodium)

Tizanidine and Clonidine Alpha-2 adrenergic agonist Inhibit presynaptic release of norepinephrine from the presynaptic terminal, as well as decreases postsynaptic adrenergic neuron.

1mg as tolerated Side Effects: Hypotension Hepatotoxicity Toxicity if combined with Cipro, Levaquin, Amiodarone Dizziness, drowsiness, weakness, nervousness, hallucinations, depression, vomiting, dry

44 Tizanidine and Clonidine Alpha-2 adrenergic agonist Inhibit presynaptic release of norepinephrine from the presynaptic terminal, as well as decreases postsynaptic adrenergic neuron. Start Tizanidine 2mg BID and increase as tolerated Start Clonidine 0.1mg daily and increase 0.1mg as tolerated Side Effects: Hypotension Hepatotoxicity Toxicity if combined with Cipro, Levaquin, Amiodarone Dizziness, drowsiness, weakness, nervousness, hallucinations, depression, vomiting, dry mouth, constipation, GERD, rash Kamen, L.; Henney, HR.; Runyan, JD. (Feb 2008). "A practical overview of tizanidine use for spasticity secondary to multiple sclerosis, stroke, and spinal cord injury.". Curr Med Res Opin. 24 (2): Ahlquist RP (Jun 1948). "A study of the adrenotropic receptors". The American Journal of Physiology. 153 (3):

Valium and Baclofen Gamma-aminobutyric acid (GABA) Valium GABA-A receptor GABA receptor increases Chloride influx to hyperpolarize neuron and inhibit firing.

"Mechanism of gamma aminobutyric acid (GABA) action and its relation to synaptic inhibition". J. Neurophysiol.

45 Valium and Baclofen Gamma-aminobutyric acid (GABA) Valium GABA-A receptor GABA receptor increases Chloride influx to hyperpolarize neuron and inhibit firing. Unsuitable for TBI SE: sedation, dependence, depression, impotence, ataxia Dose: 4-60 mg. Start 2 mg bid, increase by 2mg qwk Kuffler SW, Edwards C (November 1958). "Mechanism of gamma aminobutyric acid (GABA) action and its relation to synaptic inhibition". J. Neurophysiol. 21 (6): Baclofen GABA-B receptor Drug of choice for SCI, CP, MS, not cerebral forms Less sedating than Valium Sudden withdrawal - seizures SE: weakness, sedation, respiratory depression, seizures, itching, bradycardia, hypertension, incontinence, hallucinations Dose:10-80 mg. Start 5 mg bid, increase by 5 mg qwk

Peripheral Acting Agents Dantrolene Sodium: (Ca ++ inhibition) Works at the muscle level Reduces Ca release from sarcoplasmic reticulum Reduces phasic > tonic stretch reflexes Effects fast twitch >

46 Peripheral Acting Agents Dantrolene Sodium: (Ca ++ inhibition) Works at the muscle level Reduces Ca release from sarcoplasmic reticulum Reduces phasic > tonic stretch reflexes Effects fast twitch > slow twitch muscle fibers Preferred for cerebral source of spasticity SE: liver toxicity (1%), weakness, sedation, dizziness, paresthesias Dose: mg. Start 25 mg bid, increase 25-50mg qwk Krause T, Gerbershagen MU, Fiege M, Weisshorn R, Wappler F (2004). "Dantrolene a review of its pharmacology, therapeutic use and new developments". Anaesthesia. 59 (4):

47 Step 5 Invasive Treatments Motor point blocks Peripheral Nerve blocks Intrathecal Baclofen Pump Neurolysis/Neurectomy Selective Dorsal Rhizotomy Botox Injections

48 Chemical Neurolysis

Chemical Nerve Blocks Blocks the alpha motor neuron to muscle fibers Decreases clonus Increase speed and dexterity of movement Improved positioning

49 Chemical Nerve Blocks Blocks the alpha motor neuron to muscle fibers Decreases clonus Increase speed and dexterity of movement Improved positioning and ROM Prevent joint contractures Increase tolerance to splinting Local Anesthetics Neurolytic Agents Phenol Ethyl Alcohol Neurotoxins Botox A Myobloc B

50 Chemical Nerve Blocks Peripheral Nerve Blocks Lumbar Spinal Nerves Obturator Nerve Femoral Nerve Perineal Nerve Sciatic Nerve Tibial Nerve Musculocutaneous Nerve Median Nerve

51 Botulinum Toxins Produced by Clostridium botulinum bacteria Seven distinct serotypes (A, B, C1, D, E, F, G) Type A (Botox, Allergan; Dysport, Ipsen Ltd.) is a vacuum-dried form of purified toxin Botox is FDA-approved for the treatment of cervical dystonia, strabismus, blepharospasm, severe glabellar lines, and severe primary axillary hyperhidrosis that is inadequately managed with topical agents Type B (Myobloc /NeuroBloc ) is a sterile liquid formulation of purified neurotoxin Myobloc/NeuroBloc is approved in the United States, Canada, and Europe for the treatment of patients with cervical dystonia to reduce the severity of abnormal head position and neck pain associated with cervical dystonia Simpson LL, et al. J Pharmacol Exp Ther. 2004;308: Fernandez-Salas E, et al. Proc Natl Acad Sci U S A. 2004;101: Data on file, Allergan Pharmaceuticals: Prescribing Information, October Data on file, Solstice Neurosciences Inc.: Prescribing Information, July 2005.

52 Botulinum Toxin Effective in 4-7 days, peaks in 4-6 weeks and lasts 3-4 months Immunologic development with multiple injections (no earlier than 12 weeks)

53 Acetycholine Vesicle Fusion Complex

54 Development of Extrajunctional Acetylcholine Receptors

Disrupts spinal reflex arcs, not supraspinal pathways

55 Step 6 Surgical Intervention Intrathecal Medications Intrathecal Baclofen Rhizotomy Selective Dorsal Rhizotomy Disrupts spinal reflex arcs, not supraspinal pathways Young children with spastic CP Percutaneous radiofrequency rhizotomies

56 Step 6 Surgical Intervention Orthopedic Surgery tenotomy tendon lengthening tendon transfers myotomy arthrodesis neurectomy

57 Step 6 Surgical Intervention Myelotomy - severing tracts of spinal cord Cordectomy - excision of portions of the spinal cord. Leads to severe muscle atrophy, bowel and bladder dysfunction, loss of erectile function

58 CONCLUSION Understand Basic Neuroanatomy to Understand Spasticity Understand Clinic Evaluation and Treatment Options for Spasticity Understand Medication Management of Spacticity Understand Invasive Options to inhibit spasticity locally or at the CNS

59 Thank You

Reflexes. Dr. Baizer

Reflexes. Dr. Baizer Reflexes Dr. Baizer 1 Learning objectives: reflexes Students will be able to describe: 1. The clinical importance of testing reflexes. 2. The essential components of spinal reflexes. 3.The stretch reflex.