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Muscle Tone and Spasticity:

Muscle Tone and Spasticity


MUSCLE TONE A state of partial contraction that is characteristic of normal muscle, is maintained at least in part by a continuous bombardment of motor impulses originating reflexively, and serves to maintain body posture


MUSCLE TONE Slight constant tension characteristic of healthy muscle owing to which the limbs,when handled or moved passively,offer a definite resistance.

Organization of the Spinal Cord for Motor Functions:

Organization of the Spinal Cord for Motor Functions The Sensory signals enter the cord almost entirely through the sensory (posterior)roots. After entering the cord, every sensory signal travels to two separate destinations: (1) One branch of the sensory nerve ter-minates almost immediately in the gray matter of thecord and elicits local segmental cord reflexes and otherlocal effects. 2) Another branch transmits signals to higher levels of the nervou(s system—to higher levelsin the cord itself, to the brain stem, or even to the cere-bral cortex. Each segment of the spinal cord (at the level ofeach spinal nerve) has several million neurons in its gray matter. Aside from the sensory neurons, the other neuronsare of two types: (1) anterior motor neurons (2)interneurons. .

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Anterior Motor Neurons. Located in each segment of the anterior horns of the cord gray matter are several thousand neurons that are 50 to 100 per cent larger than most of the others and are called anterior motor neurons. They give rise to the nerve fibers that leave the cord by way of the anterior roots and directly innervate the skeletal muscle fibers. The neurons are of two types, 1.alpha motor neurons 2.gamma motorneurons

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Alpha Motor Neurons. The alpha motor neurons give rise to large type A alpha (Aa) motor nerve fibers,averaging 14 micrometers in diameter; these fibers innervate large skeletal muscle fibers. Stimulation of a single alpha nerve fiber excites anywhere from three to several hundred skeletal muscle fibers, whichare collectively called the motor unit .   Gamma Motor Neurons. Along with the alpha motor neurons, which excite contraction of the skeletal muscle fibers, about one half as many much smaller gamma motor neurons are located in the spinal cord anterior horns. These gamma motor neurons transmit impulses through much smaller type A gamma (Ag)motor nerve fibers, averaging 5 micrometers in diameter, which go to small, special skeletal muscle fibers called intrafusal fibers, These fibers constitute the middle of the muscle spindle,which helps control basic muscle “tone ,”  

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Interneurons. Interneurons are present in all areas of the cord gray matter—in the dorsal horns, the anterior horns, and the intermediate areas between them, These cells are about 30 times as numerous as the anterior motor neurons. They are small and highly excitable, often exhibiting spontaneous activity and capable of firing as rapidly as 1500 times per second. They have many interconnections with one another, and many of them also synapse directly with the anterior motor neurons. The interconnections among the interneurons and anterior motor neurons are responsible for most of the integrative functions of the spinal cord. Only a few incoming sensory signals from the spinal nerves or signals from the brain terminate directly on the anterior motor neurons. Instead, almost all these signals are transmitted first through interneurons, where they are appropriately processed. Thus, the corticospinal tract from the brain is terminate almost entirely on spinal interneurons, where the signals from this tract are combinedwith signals from other spinal tracts or spinal nerves before finally converging on the anterior motorneurons to control muscle function .

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Renshaw Cell Inhibitory System. Also located in the anterior horns of the spinal cord, in close association with the motor neurons, are a large number of small neurons called Renshaw cells. Almost immediately after the anterior motor neuron axon leaves the body of the neuron, collateral branches from the axon pass to adjacent Renshaw cells. These are inhibitory cells that transmit inhibitory signals to the surrounding motor neurons. Thus, stimulation of each motor neuron tends to inhibit adjacent motor neurons, an effect called lateral inhibition. This effect is important for the following majorreason: The motor system uses this lateral inhibition to, or sharpen, its signals in the same way that the sensory system uses the same principle—that is, to allow unabated transmission of the primary signal in the desired direction while suppressing the tendency forsignals to spread laterally.  

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Muscle Sensory Receptors—Muscle Spindles and Golgi Tendon Organs—And Their Roles in Muscle Control Proper control of muscle function requires not only excitation of the muscle by spinal cord anterior motor neurons but also continuous feedback of sensory information from each muscle to the spinal cord, indicating the functional status of each muscle at each instant. That is, what is the length of the muscle, What is its instantaneous tension, and How rapidly is its length or tension changing? To provide this informa-tion , the muscles and their tendons are supplied abun-dantly with two special types of sensory receptors: (1)muscle spindles , which are distributed throughout the belly of the muscle and send information to the nervous system about musclelength or rate of change of length, and Golgitendon organs , which are located in the muscle tendons and transmit information about tendon tension or rate of change of tension. The signals from these two receptors are either entirely or almost entirely for the purpose of intrinsic muscle control. They operate almost completely at a subconscious level. Even so, they transmit tremendous amounts of information not only to the spinal cord butalso to the cerebellum and even to the cerebral cortex,helping each of these portions of the nervous system function to control muscle contraction.

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Receptor Function of the Muscle Spindle Structure and Motor Innervation of the Muscle Spindle. Each spindle is 3 to 10 millimeters long. It is built around 3 to 12 very small intrafusal muscle fibers that are pointed at their ends and attached to the glycocalyx of the surrounding large extrafusal skeletal musclefibers. Each intrafusal muscle fiber is a very small skeletal muscle fiber. However, the central region of each of these fibers—that is, the area midway between its two ends—has few or no actin and myosin filaments.Therefore, this central portion does not contract when the ends do. Instead, it functions as a sensory receptor . The end portions that do contract are excited by small gamma motor nerve fibers that originate from small type A gamma motorneurons in the anterior horns of the spinal cord. Sensory Innervation of the Muscle Spindle. The receptor portion of the muscle spindle is its central portion. In this area, the intrafusal muscle fibers do not have myosin and actin contractile elements. Sensory fibers originate in this area. They are stimulated by stretching of this midportion of the spindle.   the muscle spindle receptor can be excited in two ways: 1. Lengthening the whole muscle stretches the midportion of the spindle and, therefore, excites the receptor. 2. Even if the length of the entire muscle does not change, contraction of the end portions of the spindle’s intrafusal fibers stretches the midportion of the spindle and therefore excites the receptor.

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Two types of sensory endings are found in this central receptor area of the muscle spindle. They are the primary ending and the secondary ending. Primary Ending. In the center of the receptor area, a large sensory nerve fiber encircles the central portion of each intrafusal fiber, forming the so-called primary ending or annulospiral ending.This nerve fiber is a type Ia fiber averaging 17 micrometers in diameter,and it transmits sensory signals to the spinal cord at a velocity of 70 to 120 m/sec, as rapidly as any type ofnerve fiber in the entire body. Secondary Ending. Usually one but sometimes two smaller sensory nerve fibers—type II fibers with an average diameter of 8 micrometers—innervate thereceptor region on one or both sides of the primary ending, as shown in Figures 54–2 and 54–3. This sensory ending is called the secondary ending; sometimes it encircles the intrafusal fibers in the same way that the type Ia fiber does, but often it spreads like branches on a bush.

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Division of the Intrafusal Fibers into Nuclear Bag and Nuclear Chain Fibers—Dynamic and Static Responses of the Muscle Spindle. There are also two types of muscle spindle intrafusal fibers: (1) nuclear bag muscle fibers (one to three in each spindle), in which several muscle fiber nuclei are congregated in expanded “bags” in the central portion of the receptor area (2) nuclear chain fibers(three to nine), which are about half as large in diam-eter and half as long as the nuclear bag fibers and have nuclei aligned in a chain throughout the receptor area,   The primary sensory nerve ending (the 17-micrometer sensory fiber) is excited by both the nuclear bag intrafusal fibers and the nuclear chain fibers. Conversely, the secondary ending (the 8-micrometer sensory fiber) isusually excited only by nuclear chain fibers.

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  Response of Both the Primary and the Secondary Endings to the Length of the Receptor—“Static”Response. When the receptor portion of the muscle spindle is stretched slowly, the number of impulses transmitted from both the primary and the secondary endings increases almost directly in proportion to the degree of stretching, and the endings continue to transmit these impulses for several minutes. This effect is called the static response of the spindle receptor,meaning simply that both the primary and secondary endings continue to transmit their signals for at least several minutes if the muscle spindle itself remains stretched.   Response of the Primary Ending to Rate of Change of ReceptorLength—“Dynamic” Response. When the length of the spindle receptor increases suddenly, the primary ending is stimulated especially powerfully. This excess stimulus of the primary ending is called the dynamic response, which means that the primary ending responds extremely actively to a rapid rate of change in spindle length.Even when the length of a spindle receptor increases only a fraction of a micrometer, if this increase occurs in a fraction of a second, the primary receptor transmits tremendous numbers of excess impulses to the large 17-micrometer sensory nerve fiber, but only while the length is actually increasing. As soon as the length stops increasing, this extra rate of impulse discharge returns to the level of the much smaller static response that is still present in the signal. Conversely, when the spindle receptor shortens, exactly opposite sensory signals occur. Thus, the primary ending sends extremely strong, either positive or negative, signals to the spinal cord to apprise it of any change in length of the spindle receptor.  

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Control of Intensity of the Static and Dynamic Responses by the Gamma Motor Nerves. The gamma motor nerves to the muscle spindle can be divided into two types: gammadynamic (gamma-d) and gamma-static (gamma-s). Thefirst of these excites mainly the nuclear bag intrafusalfibers, and the second excites mainly the nuclear chainintrafusal fibers.When the gamma-d fibers excite the nuclear bag fibers, the dynamic response of the musclespindle becomes tremendously enhanced, whereas the static response is hardly affected. Conversely, stimulation of the gamma-s fibers, which excite the nuclear chain fibers, enhances the static response while havinglittle influence on the dynamic response. Subsequent paragraphs illustrate that these two types of muscle spindle responses are important in different types of muscle control. Continuous Discharge of the Muscle Spindles Under Normal Conditions. Normally, particularly when there is some degree of gamma nerve excitation, the muscle spindles emit sensory nerve impulses continuously. Stretching the muscle spindles increases the rate of firing,whereas shortening the spindle decreases the rate of firing. Thus, the spindles can send to the spinal cord either positive signals—that is, increased numbers of impulses to indicate stretch of a muscle—or negative signals—below-normal numbers of impulses to indicate that the muscle is unstretched.

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Reciprocal Innervation When a stretch reflex occurs, the muscles that antagonize the action of the muscle involved (antagonists) relax. This phenomenon is said to be due to reciprocal innervation. Impulses in the Ia fibers from the muscle spindles of the protagonist muscle cause postsynaptic inhibition of the motor neurons to the antagonists. The pathway mediating this effect is bisynaptic. A collateral from each Ia fiber passes in the spinal cord to an inhibitory interneuron that synapses on a motor neuron supplying the antagonist muscles.


MOTOR UNIT Basic unit of contraction in skeletal muscle Composed of one or more muscle fibers and the motor neuron that controls them AP in motor neuron results in contraction

Physiology of movement :

Physiology of movement Afferent input from the internal organs, the musculoskeletal system, and the skin converge on the medulla spinalis . This afferent input activates the stretch reflex, both directly and throughthe interneuron , and results in a reflex motor response [A]. The same afferent information goes to the cerebellum and the somatosensory cortex. It is processed in those centers as well as in the basal ganglia. The resulting motor response is relayed to the lower motor neuron through the pyramidal and extrapyramidal system tracts. The pyramidal tracts go directly to the lower motor neuron whereas the extrapyramidal tracts end at the interneuron. The cerebellum, basal ganglia, and extrapyramidal system nuclei modify the motor response as it goes to the medulla spinalis . In this way all motor output is influenced by the incoming sensory input and converges on the lower motor neuron. The interneurons in the medulla spinalis regulate the activity of the motor neuron.

Role of the Muscle Spindle in Voluntary Motor Activity:

Role of the Muscle Spindle in Voluntary Motor Activity 31 per cent of all the motor nerve fibers to the muscle are the small typeA gamma efferent fibers Whenever signals are transmitted from the motor cortex or from any other area of the brain to the alpha motor neurons, the gamma motor neurons are stimulated simultaneously, an effect called coactivation of the alpha and gamma motor neurons. This causes both the extrafusal skeletal muscle fibers andthemuscle spindle intrafusalmuscle fibers to contract at the same time. The purpose of contracting the muscle spindle intra-fusal fibers at the same time that the large skeletalmuscle fibers contract is twofold:

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First, it keeps the length of the receptor portion of the muscle spindle from changing during the course of the whole muscle contraction. Therefore, coactivation keeps the muscle spindle reflex from opposing the muscle contraction. Second, it maintains the proper damping function of the muscle spindle, regardless of any change in musclelength. For instance, if the muscle spindle did not con-tract and relax along with the large muscle fibers,the receptor portion of the spindle would sometimes be flail and sometimes be overstretched, in neitherinstance operating under optimal conditions forspindle function .

Coactivation of Gamma Efferents:

Coactivation of Gamma Efferents

Control of Muscle Tone:

Control of Muscle Tone

Cerebellar ‘Awareness':

Cerebellar ‘Awareness'

The Golgi Tendon Organ:

The Golgi Tendon Organ The Golgi tendon organ is a receptor found within the tendons of muscle. It detects tension >100 grams in the tendon. It is innervated with a 1b afferent fiber.

The Golgi Tendon Organ:

The Golgi Tendon Organ


Summary Golgi tendon organs detects tension in the tendon. Afferent neurons conduct action potentials to the spinal cord. Afferent neurons synapse with inhibitory (inter) association neurons (secretes GABA) which in turn synapse with alpha motor neurons. Inhibition of the alpha motor neurons causes muscle relaxation , relieving the tension in the muscle.

Control of Skeletal Muscle:

Control of Skeletal Muscle The prefrontal area has association areas for the motivation and foresight to plan and initiate movements . In the premotor area motor functions are organized before they are initiated in the Motor Cortex. The motor cortex (primary motor cortex) is found on the precentral gyrus.

The Somatic Motor System:

The Somatic Motor System The Somatic motor system (SMS) can be divided roughly into 3 components: The Pyramidal System Extrapyramidal System Cerebellar System      

The Pyramidal System (direct system):

The Pyramidal System (direct system) Involved with fine, discrete and precise voluntary control of movement. The command arises from the precentral gyrus (where the somatic motor cortex resides). Fibers from the cortex descend to the spinal cord where they synapse on the anterior horn motor neurons (alpha and gamma).

Descending Spinal Pathways:

Descending Spinal Pathways Direct Control muscle tone and conscious skilled movements Direct synapse of upper motor neurons of cerebral cortex with lower motor neurons in brainstem or spinal cord Tracts Corticospinal Lateral Anterior corticobulbar

The Extrapyramidal System (indirect system):

The Extrapyramidal System (indirect system) Its main function is to provide course background voluntary movement . Arises from various sites on the cerebral cortex. Interconnected with the pyramidal system. The EPS is directly connected to the Basal Ganglia

Descending Spinal Pathways:

Descending Spinal Pathways Indirect Synapse in some intermediate nucleus rather than directly with lower motor neurons EPS Tracts Rubrospinal Vestibulospinal Reticulospinal Testospinal tract

The Cerebellar Component:

The Cerebellar Component Function: To enable smooth coordinated movement plays an important role in the maintenance of posture and equilibrium. Sends fibers via the cerebellar-spinal tract to modulate the activity of the alpha (lower motor neurons) as well as the gamma motor neurons.

Cerebellar ‘Awareness':

Cerebellar ‘Awareness' After MS stimulation (stretch) APs are conducted along the afferent fiber (Ia) It enters into the spinal cord and divides into several collaterals. Some of these collaterals synapse on the cell bodies of neurons which ascend to the cerebellum (anterior and posterior spinocerebellar tracts). Thus, at all times the cerebellum is aware of the state of stretch in muscles, in other words the TONE of muscles.

The Cerebellar Functions:

The Cerebellar Functions The cerebellum receives information from a wide array of senses: Pressure and touch Positional receptors: Spindle and Golgi tendon organs Eyes and ears A copy of the command signal is sent from the cerebral cortex to the cerebellum, where it acts as a comparator.

Cerebellar Comparator Function:

Cerebellar Comparator Function

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Spasticity: Etiology, Pathophysiology, and Associated Features

Definition of Spasticity:

Definition of Spasticity The word “spasticity” is derived from the Greek word “ spasticus ”, which means “To pull or To Tug “ Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.” -- Lance, 1980 Tonic Stretch Reflex Tonic muscle response to vibratory stretch Tonic response to a phasic stimulus Thus spasticity = velocity-dependent increase of muscle response to phasic stretch, routinely tested by tendon taps or passive mobilization Simply stated, spasticity is stiffness of muscles that occurs after injury to the spinal cord or brain.

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Characteristics of spasticity: Clasp-knife reflex: an initial high resistance followed by a sudden relaxation or letting go of a spastic muscle in response to a stretch reflex When the muscles are hypertonic, the sequence of moderate stretch muscle contraction, strong stretch muscle relaxation is clearly seen. Passive flexion of the elbow, for example, meets immediate resistance as a result of the stretch reflex in the triceps muscle. Further stretch activates the inverse stretch reflex. The resistance to flexion suddenly collapses, and the arm flexes. Continued passive flexion stretches the muscle again, and the sequence may be repeated. This sequence of resistance followed by give when a limb is moved passively is known as the clasp-knife effect because of its resemblance to the closing of a pocket knife. It is also known as the lengthening reaction because it is the response of a spastic muscle to lengthening.

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Clonus: cyclic hyperactivity of antagonistic muscles occurring at a regular frequency in response to sustained stretch to a spastic muscle


Etiologies Cerebral palsy Stroke Multiple sclerosis Traumatic brain injury Spinal cord injury Anoxia Neurodegenerative disease

Pathophysiology of Impairment After a Central Nervous System Lesion:

Pathophysiology of Impairment After a Central Nervous System Lesion

Pathophysiology of Spasticity:

Pathophysiology of Spasticity Not completely understood, despite considerable investigation Interruption of descending inhibitory pathways Rearrangement of spinal circuitry

Stretch Reflex Pathway:

Stretch Reflex Pathway

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Spasticity has been described in its individual components: intrinsic tonic spasticity, intrinsic phasic spasticity, and extrinsic spasticity. Intrinsic tonic spasticity refers to the increased tone or hyperexcitability state that results from the lower threshold and increased gain of the stretch refex. Intrinsic phasic spasticity (tendon hyperrefexia and clonus) is thought to be due to inhibition of group Ia fbers, leading to excitability of tendon refexes and coactivation of antagonistic muscles. The exact mechanism behind clonus is not clearly understood. extrinsic spasticity . This component results in involuntary muscle spasms that mimic a refex that occurs in response to noxious stimuli. The mostcommon spasms are fexion spasms

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For a short time following injury, there is faccid paralysis and loss of deep tendon refexes. Over time, changes occur which lead to spasticity. Hyperactivity of gamma motor creates hypersensitivity of the stretch refex. Following an injury, there is an initial period of down-regulation of neuronal membrane receptors. This is followed by up-regulation of receptors, which leads to hypersensitivity. Axonal sprouting occurs over time, explaining the temporal changes that occur with spasticity. This mechanism contributes to prolongation of the time-to-peak for excitatory postsynaptic potentials (EPSPs) and the disruption of balancebetween excitatory and inhibitory input. Alterations occur in the excitatory and inhibitory pathways. A phenomenon known as postactivation depression occurs normally as neurotransmit- ters become depleted. There is a reduction of postactivation depression as well as presynaptic inhibition following SCI.

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Normally Ia-reciprocal inhibition prevents simultaneous fring of antagonistic muscles. In SCI, this inhibition is reduced, leading to coactivation of antagonistic muscles. Other well-documented mechanisms that play a large role in spasticity include enhancement in the excitability of motor neurons and interneurons. Motor neuronal excitability arises from activation of persistent inward currents and alternations in the monoaminergic drive from the brainstem to the spinal cord. Altered muscular properties also lead to increased tone. Muscle fbers change, along with accumulation of connective tissue and fbrosis, which decreases the elastic properties of muscle. There is also atrophy and loss of muscle fbers and sarcomeres. Alterations in the contractile properties thus become evident.

Pathophysiology of Spasticity: Established Mechanisms:

Pathophysiology of Spasticity: Established Mechanisms Alterations within the reflex arc Change in muscle active properties (increased ratio torque/EMG) Change in muscle passive properties (decreased extensibility) Decreased pre-synaptic inhibition, at least in paraplegics Increased fusimotor activity and increased excitability of the alpha motor neuron have not been established

Pathophysiology of Spasticity: Established Mechanisms, cont’d:

Pathophysiology of Spasticity: Established Mechanisms, cont’d Mechanisms affecting the reflex arc Decreased reciprocal Ia inhibition on extensors Decreased non-reciprocal Ib inhibition Decreased inhibition from flexor reflex afferents

Phenomena Commonly Associated with Spasticity:

Phenomena Commonly Associated with Spasticity Abnormal cutaneous reflexes (Babinski sign) Spastic dystonia muscle contraction present at rest, dependent on tonic stretch significant contribution to deformity Spastic co-contraction abnormal antagonist contraction present during voluntary agonist effort, dependent on tonic stretch on antagonist Extra-segmental co-contraction abnormal contraction distant from the muscles involved in a voluntary effort

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The Ashworth scale The Ashworth scale is by far the most commonly used evaluation method for spasticity. Always test the patient while he or she is in a relaxed supine position. Passively move the joint rapidly and repeatedly through the available range of motion and grade the resistance using the definitions

Impact of Spasticity:

Impact of Spasticity

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Spasticity Pharmacological Treatment


Benzodiazepines Long- and short-acting formulations diazepam clonazepam clorazepate ketazolam tetrazepam Mechanism of action (CNS) brain stem and spinal cord post-synaptic site of action potentiates presynaptic inhibitory effect of GABA

Benzodiazepines, cont’d:

Benzodiazepines, cont’d Clinical indications: spinal cord injury, multiple sclerosis Possible applications: traumatic brain injury, cerebral palsy, cardiovascular accident Clinical effects: decreased resistance to passive ROM decrease in hyperreflexia reduction in painful spasms sedation and reduced anxiety

Diazepam :

Diazepam Initial adult dosing: 2 mg twice daily Slow titration to maximum of 60 mg/day Bedtime dosing for nocturnal spasms: 5-10 mg Pediatric dosing: 0.12-0.8 mg/(kg day) Adverse effects: sedation, weakness, hypotension, GI symptoms, memory impairment, incoordination, confusion, depression, ataxia Intoxication uncommon at recommended dosing; dependency and withdrawal possible

Oral Baclofen (Liofen):

Oral Baclofen (Liofen) Mechanism of action GABA B selective agonist pre- and post-synaptic actions mono- and polysynaptic pathways

Oral Baclofen, cont’d:

Oral Baclofen, cont’d Clinical indications spasticity of spinal origin (intrathecal baclofen approved for spinal and cerebral spasticity) Clinical effects: decreased resistance to passive ROM decrease in hyperreflexia reduction in painful spasms reduced anxiety

Oral Baclofen, cont’d:

Oral Baclofen, cont’d Initial dose: 5 mg 3x daily Slow titration to 20 mg 4x day (higher doses have been reported) Adverse effects: weakness, sedation, hypotonia , ataxia, confusion, fatigue, nausea, dizziness, lower seizure threshold May potentiate antihypertensives Sudden withdrawal may cause seizures, hallucinations, rebound spasticity

Dantrolene Sodium:

Dantrolene Sodium Mechanism of action: reduces calcium release from sarcoplasmic reticulum uncouples excitation and contraction Clinical indications: cardiovascular accident, multiple sclerosis, spinal cord injury, cerebral palsy Possible applications: traumatic brain injury Clinical effects: decreased resistance to passive range of motion decreased hyperreflexia and muscle tone reduction in spasms and clonus

Dantrolene Sodium, cont’d:

Dantrolene Sodium, cont’d Obtain baseline serum liver function tests Hepatotoxicity associated with long-term maximum dose, especially in women >30 Recommended dosing: initial dose 25 mg 2x day typical maintenance dose 100-200 mg/day (max. 400 mg/day) Adverse effects: weakness (including ventilatory muscles), drowsiness, lethargy, nausea, diarrhea

Tizanidine :

Tizanidine Mechanism of action: alpha-2 noradrenergic agonist blocks release of excitatory amino acids from spinal interneurons inhibition of facilitory coeruleospinal pathways Clinical indications: multiple sclerosis, spinal cord injury; possibly cerebral spasticity Clinical effects: reduced tone, spasm frequency, hyperreflexia no decrease in strength antinociceptive in animal studies

Tizanidine, cont’d:

Tizanidine, cont’d Obtain liver function tests at baseline and months 1, 3, and 6 Initial dose: 2-4 mg at bedtime Titrate in 2-4 mg steps Maintenance dose 12-36 mg/day (max. 36 mg/day) Adverse effects: drowsiness, dizziness, dry mouth, orthostatic hypotension

Other Oral Antispasmodics (I):

Other Oral Antispasmodics (I) Clonidine alpha-2 agonist may allow decreased baclofen dose limited tolerability available as a patch

Other Oral Antispasmodics (II):

Other Oral Antispasmodics (II) Cyproheptadine (Periactin ® ) histamine and serotonin antagonist limited experience; well tolerated in open trials

Other Oral Antispasmodics (III):

Other Oral Antispasmodics (III) Cannabinoids ( Cesamet ® , Marinol ® ) placebo? general relaxation effect? specific antispastic ? limited experience; anecdotal efficacy, 1 single-patient double-blind trial effective in multiple sclerosis mouse for spasticity and tremor Orphenadrine citrate ( Norflex ® ) NMDA antagonist fast-acting, short duration possibly useful as preparation for physical therapy session

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Intrathecal Baclofen (ITB) Baclofen is one of the most potent antispastic drugs. It cannot easily cross the blood brain barrier because of its poor lipid solubility. ITB is useful for the severely involved spastic, dystonic or mixed child [A].

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Eperisone (formulated as the eperisone hydrochloride salt) is an antispasmodic drug . centrally-acting muscle relaxant Eperisone acts by relaxing both skeletal muscles and vascular smooth muscles , and demonstrates a variety of effects such as reduction of myotonia , improvement of circulation , and suppression of the pain reflex. The drug inhibits the vicious cycle of myotonia by decreasing pain, ischaemia , and hypertonia in skeletal muscles, thus alleviating stiffness and spasticity , and facilitating muscle movement [1] Eperisone also improves dizziness and tinnitus associated with cerebrovascular disorders or cervical spondylosis . Eperisone has a relatively low incidence of sedation when compared with other antispasmodic drugs; this simplifies the clinical application of the drug and makes it an attractive choice for patients who require antispasmodic therapy without a reduction in alertness .

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Dosage and administration In adults, the usual dose of eperisone is 50–150 mg per day, in divided doses, Eperisone has not been established as definitely safe for paediatric use, therefore its use in paediatrics cannot be recommended without further study. [6] ] Safety during pregnancy and breast-feeding Eperisone has not been established to be safe for use by pregnant women; therefore the drug should only be used in pregnant women, or women who may be pregnant, if the expected therapeutic benefits will outweigh the possible risks associated with treatment. The manufacturers of Myonal recommend the drug not be used during lactation ( breast-feeding ). If eperisone must be used, the patient is advised to stop breast-feeding for the duration of treatment. Eperisone has beed reported to be excreted in breast milk in an animal study (in rats).

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Pharmacology Skeletal muscle relaxation Relaxation of hypertonic skeletal muscles Improves intramuscular blood flow Suppression of spinal reflex potentials Reduction of muscle spindle sensitivity via motor neurons Vasodilatation and augmentation of blood flow Analgesic action and inhibition of the pain reflex in the spinal cord Contraindications Eperisone is contraindicated in patients with known hypersensitivity to the drug. [8] Side effects: 'very rare' excessive relaxation, stomachache, nausea, vertigo, anorexia, drowsiness, skin rashes, diarrhoea, vomiting, indigestion, GI disturbances, insomnia, headache, constipation etc. [9] Cautions Eperisone should be administered with care in patients with a history of hypersensitivity to any medication, or with disorders of liver function (it may aggravate hepatic dysfunction).

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Weakness , light-headedness , sleepiness or other symptoms may occur. In the event of such symptoms, the dosage should be reduced or treatment discontinued. Patients should be cautioned against engaging in potentially hazardous activities requiring alertness, such as operating machinery or driving a car. [6] Side effects Shock and anaphylactoid reactions: In the event of symptoms such as redness, itching , urticaria , oedema of the face [10] and other parts of the body, dyspnoea , etc., treatment should be discontinued and appropriate measues taken. Oculomucocutaneous syndrome and toxic epidermal necrolysis: [11] Serious dermatopathy such as oculomucocutaneous syndrome ( Stevens–Johnson syndrome ) or toxic epidermal necrolysis may occur. [ citation needed ] Patients should be carefully observed, treatment discontinued and appropriate measures taken, in the event of symptoms such as fever , erythema , blistering, itching , ocular congestion or stomatitis , etc. [10] CNS side effects: depletion of myelin sheath of nerves [ citation needed ] Other side effects: anaemia , rash , pruritus , sleepiness, insomnia , headache , nausea and vomiting , anorexia , abdominal pain, diarrhoea , constipation , urinary retention or incontinence . [ citation needed ] Drug interactions There have been reports of disturbances in ocular accommodation occurring after the concomitant use of the related drug tolperisone hydrochloride and methocarbamol .  

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