Mkgrady8 Neuro 3 Spinal Reflexes

Front 1

definition of a spinal reflex

Back 1

an immediate and involuntary response to a stimulus; all reflexes when reduced tot heir simplest level are SENSORIMOTOR ARCS; the REFLEX ARC governs the operation of reflexes; reflexes whose arc passes through the spinal cord are called spinal reflexes

Front 2

what is an autonomic reflex

Back 2

automatic subconscious response to changes within or outside the body (e.g. BP or HR)

Front 3

what is a spinal reflex and what is it concerned with

Back 3

maintaining muscle tone, aid in balance and posture

Front 4

what are cranial reflexes

Back 4

involve reflex centers in the brainstem

Front 5

neurologic exam includes assessment of reflexes through what checks?

Back 5

mental status; cranial nerves; motor system (muscle size, strength, tone); sensory system (superficial pain, light touch and vibration, and positional sense); cerebellar; gait; REFLEXES (deep tendon reflexes (DTRs))

Front 6

the deep tendon reflex exam: grading

Back 6

DTRs are the most objective part of the neurologic exam; 0= absent despite reinforcement; 1= present only with reinforcement; 2= normal; 3= increased but normal; 4= markedly hyperactive with clonus; major part of the exam; sensation or gait may be difficult to discern in a pt with altered mental state

Front 7

the 4 types of spinal reflexes

Back 7

1. stretch or jerk or myotatic or "deep tendon" reflexes (DTRs); 2. withdrawal reflexes; 3. superficial reflexes; 4. primitive (infant) reflexes

Front 8

the sensorimotor arc of the stretch reflex

Back 8

when a muscle lengthens the MUSCLE SPINDLE within the HOMONYMOUS or AGONIST muscle senses stretch and its afferent nerve firing frequency increases; the homonymous muscle is the one associated with the sensory receptor; the agonist muscle is the 'prime mover' that provides force to complete a specified motion; the sensory signal is transmitted via the Ia AFFERENT making a MONOSYNAPTIC contact onto the alpha motor neuron; increased firing of the alpha motor neuron causes the EXTRAFUSAL FIBERS to contract and thus oppose the stretching of the muscle

Front 9

reciprocal innervation during the stretch reflex

Back 9

joints are controlled by 2 opposing sets of muscles= EXTENSORS AND FLEXORS; when the stretch reflex is activated the opposing (ANTAGONIST) muscle group is inhibited to prevent it from working against the contraction of the AGONIST muscle; a branch of the Ia AFFERENT innervated the Ia INHIBITORY INTERNUEORN which projects to the alpha mn of the ANTAGONIST MUSCLE mediating RECIPROCAL INHIBITION; dysfunction of the RECIPROCAL INHIBITION may cause both groups of muscles to contract simultaneously and work against each other

Front 10

the renshaw cell during the stretch reflex

Back 10

RENSHAW CELLS are inhibitory interneurons found in the gray matter of the spinal cord; when a motoneuron fires an action potential it excites a RENSHAW CELL that contributes to RECURRENT INHIBITION of the same motoneuron as well as surrounding motonuerons thereby terminating the stretch reflex and sharpening and focusing the motor activity; renshaw release GABA or gkycine

Front 11

inhibition of spinal cord interneuron mediated inhibition

Back 11

reciprocal inhibition failure with strychnine poisoning or tetanus toxin; strychnine poisoning= inhibits competitively and reversibly the inhibitory neurotransmitter glycine at postsynaptic neuronal sites, results in unchecked reflex stimulation of motor neurons affecting all the striated muscles; tetanus toxin (lockjaw)= blocks release of inhibitory neurotransmitters causing generalized muscle stiffness, characterized by persistent tonic spasm with violent brief exacerbations in response to sensory stimuli

Front 12

summary: stretch reflex

Back 12

the stretch reflex involves an involuntary muscle contraction in response to muscle stretch; the MUSCLE SPINDLE is the proprioceptor of the stretch reflex; the stretch reflex involves MONOSYNAPTIC (THE ONLY ONE THAT IS= TEST QUESTION) activation of the alpha motor neuron projecting to the HOMONYMOUS OR AGONIST (prime mover) muscle; RECIPROCAL INHIBITION is the inhibition of the ANTAGONIST muscle via the Ia INHIBITORY INTERNEURON; RECURRENT INHIBITION by the RENSHAW CELL inhibits the same motor neuron that excited it; loss of GABAergic or glycine inhibition results in skeletal muscle spasms

Front 13

what are muscle spindles?

Back 13

composed of sensory receptors called INTRAFUSAL FIBERS; lie parallel to the much larger muscle fibers called EXTRAFUSAL fibers; respond to change in muscle length and rate of change in length

Front 14

dynamic (phasic) and static (tonic) stretch receptors

Back 14

the typical muscle spindle contains 2 types of intrafusal muscle fibers (intrafusal= inside the fusiform spindle)= the NUCLEAR BAG FIBERS and the NUCLEAR CHAIN FIBERS; the nuclear bag fibers are thicker and longer than the nuclear chain fibers and they receive their name from the accumulation of their nuclei in the expanded bag like equatorial region (the nuclear bag), measure rate of change in muscle length; the nuclear chain fibers have no equatorial bulge rather their nuclei are lined up in the equatorial region (the nuclear chain), measure change in muscle length; nuclear bag fibers are innervated by type Ia afferent axons, the nuclear chain fibers are innervated by type II afferent axons

Front 15

responses of dynamic and static stretch fibers

Back 15

TYPE Ia AFFERENTS respond to the rate of length changes, a rapidly adapting sensory receptor (from bag fibers); TYPE II AFFERENTS response to muscle length (from chain fibers), a non adapting sensory receptor

Front 16

the muscle spindle is a principal regulatory of muscle tone and stretch reflex amplitude

Back 16

DYNAMIC INTRAFUSAL FIBERS and TYPE Ia AFFERENTS respond primarily to the rate of change in muscle stretch= they work to oppose sudden changes in muscle length, the DYNAMIC INTRAFUSAL FIBER and Ia AFFERENT carry the sensory component of the CLINICAL STRETCH REFLEX; STATIC INTRAFUSAL FIBERS AND TYPE II AFFERENTS respond to the level of sustained change in muscle length and play a principal role in MUSCLE TONE= muscle tone is a state of partial contraction maintained in part by a continuous bombardment of motor impulses originating from the non adapting receptors, STATIC INTRAFUSAL FIBERS are important in maintaining the POSTURE of the body

Front 17

The main function of muscle spindles is to:a. pass neural information evenly to all parts of themuscleb. enable contraction of the musclesc. generate the force of contractiond. act as stretch receptors

Back 17

d act as stretch receptors

Front 18

The clinical stretch reflex is elicited by abrief sharp tap to a muscle tendon that results in sudden small lengthening ofthe muscle. This action strongly:a. excited muscle spindle type Ia afferentsb. inhibits muscle spindle type Ia afferentsc. excites muscle spindle type II afferentsd. inhibits muscle spindle type II afferents

Back 18

A

Front 19

After 180 days at the international spacestation, astronauts return with muscle tone that resembles that of the average80 y/o. A reasonable hypothesis is that astronautmuscle tone is lost due to:a. reduced load on anti-gravity skeletal muscleb. increased load on anti-gravity skeletal musclec. reduced stimulation of alpha-motor neurons bystatic intrafusal fiber activationd. reduced stimulation of alpha motor neurons bydynamic intrafusal fiber activation

Back 19

C

Front 20

dynamic and static gamma motor neurons innervate dynamic and static intrafusal fibers respectively

Back 20

gamma motor neurons are 1/2 as numerous as alpha motoneurons but are about 1/3 of fibers in nerve; gamma motor neurons innervate contractile elements at the poles of the muscle spindles; activation of these contractile elements causes the central (equatorial) region of the muscle spindle to stretch like a rubber band which in turn stretches sensory endings increasing sensitivity to stretch associated with muscle lengthening

Front 21

gamma motor neuron regulation of the stretch reflex and muscle tone

Back 21

gamma motor neuron input to dynamic intrafusal fibers modulates the stretch reflex amplitude so if it is active it causes the stretch reflex to be more exagerated; gamma motor neuron input to static intrafusal fibers modulates muscle tone, so when it is active it has greater tone; thus the CNS can independently adjust the dynamic and static sensitivity of muscle spindles

Front 22

Gamma motor neuron activity is increased byelectrical stimulation of specific areas of the brainstem containing decreasingmotor pathways. Stimulation of these brainstemsites is expected to:a. cause tendons to contractb. transmit action potentials from gamma motorneuron to skeletal musclec. increase the response of the muscle spindle tostretchd. enable the brain to perceive that a muscle hasbeen stretched

Back 22

C

Front 23

the 2 roles for gamma motor neurons

Back 23

COACTIVATION of alpha and gamma motor neurons prevents UNLOADING of the muscle spindle; PREACTIVATION of gamma motor neurons by descending motor projections increases muscle stiffness and improves joint control

Front 24

coactivation of alpha and gamma motor neurons

Back 24

allows spindles to function at all muscle lengths during movements and postural adjustments; cerebellum via bulboreticular pathway modulates alpha and gamma motor neuron gain; allows for increased gamma motor neuron stimulation results in fin increased feedback to the intrafusal fibers which resist the shortening increasing the simulation of the alpha motor neurons again creating the feedback loop which allows the muscle to accomdate the load

Front 25

summary: physiological roles of gamma motor neurons

Back 25

dynamic and static gamma motor neurons contribute to the gain (aka sensitivity) of the stretch reflex circuit modulating stretch reflex amplitude and muscle tone respectively; COACTIVATION of alpha and gamma motor neurons prevents UNLOADING of the muscle spindle; PREACTIVATION of gamma motor neurons descending motor projections increases muscle stiffness and improves joint control

Front 26

why is it important to understand how motor neurons affect muscle tone and the stretch reflex

Back 26

pathologically modification of central drive to spinal motor neurons results in alterations in spinal motor control; since muscles are always under some degree of stretch the gain (or sensitivity) of the stretch reflex circuit contributes to the steady state level of muscle tone; in an upper motor neuron lesion where supraspinal pathways are interrupted the GAIN (or sensitivity) of the stretch reflex circuit may change contributing to SPASTICITY which is characterized by signs of HYPERTONIA AND HYPERREFLEXIA

Front 27

gamma versus alpha spasticity

Back 27

gamma spasticity= characterized by increased central excitatory drive converging onto gamma motor neurons; alpha spasticity= occurs when the alpha motor neuron is hyperexcitable, alpha motor neurons develop plateau potentials in SCI

Front 28

what is the golgi tendon organ and where is it

Back 28

a proprioceptor sensitive to muscle tension; it is in the tendon right when muscle becomes tendon

Front 29

golgi tendon organ (GTO) reflex

Back 29

inverse (bc alpha responds to length so smaler length means less firing whereas decreased length means contraction means increase in tension means increase in firing of golgi tendon) myotatic reflex= golgi tendon organ repsonds to muscle tension, transmits input to cord via Ib AFFERENT, activation inhibits the homonymous muscle via Ib INHIBITORY INTERNEURON, example of a DISYNAPTIC INHIBITION; the tricky part= in the GTP reflex the agonist muscle relaxes while the antagonist muscle contracts while in DTR the agonist muscle contracts while the antagonist muscle relaxes

Front 30

changes in spinal inhibitory mechanisms and its relation to spasticity

Back 30

SPASTICITY broadly refers to the increased muscle tone and reflexes typically seen with an UMN LESION; reduction of spinal inhibitory mechanisms is involved in spasticity; it seems highly likely that multiple mechanisms are operative in causation of human spasticity many of which still remain to be fully elucidated in brain or spinal lesion

Front 31

withdrawal reflexes: flexion, crossed extension

Back 31

polysynaptic and multisegmental; appropriate sensory stimulus= most forcefully elicited by pain stimulus, following damage to descending pathways non noxious stimuli may produce the same response; clinical significance= positive sign, increased responsiveness --> UMN lesion; FLEXION REFLEX is a polysynaptic WITHDRAWAL REFLEX initiated by nociceptors (Adelta or IV fibers); CROSSED EXTENSION provides postural support form extension of the contralateral limb; withdrawal reflexes are exaggerated after a UMN lesion and may contribute to muscle spasms after several spinal cord injury; FLEXION RESPONSE OF UPPER EXTREMITIES WITH EXTENSION OF LOWER EXTREMITIES IN RESPONSE TO PAIN is part of glasgow comma scale scoring

Front 32

superficial reflexes: what are they, grading, path, clinical significance, 3 classic examples

Back 32

polysynaptic reflexes; appropriate sensory stimulus 'cutaneous reflexes' evokes by gentle scraping of the skin; graded simply as present or absent; sensory signal must ascend the cord to reach the brain, the motor limb then has to descend the spinal cord to reach the motor neurons; clinical significance= absent --> UMN lesion; classic examples of superficial reflexes include= ABDOMINAL REFLEXES, CREMASTER REFLEX, AND NORMAL PLANTAR RESPONSE

Front 33

superficial reflexes: abdominal reflexes= how to test, what do you see, requires what, if it is absent what does this mean

Back 33

test by lightly but briskly stroking each side of the abdomen above (T8, T9, T10) and below (T10, T11, T12) the umbilicus; contraction of the abdominal muscles and deviation of the umbilicus toward the stimulus; requires descending long tract facilitation; absent --> UMN lesion

Front 34

primitive (infant reflexes): when, clinical significance, 3 classic examples

Back 34

underlying movements form the last 4 months of prenatal life and first 4 months after birth; suppressed by supraspinal activity sometime before 6 months of age; clinical significance= in adult presence indicates UMN lesion; classic examples of primitive (pathological) reflexes include= MORO (STARTLE) REFLEX, ASYMMETRIC TONIC REFLEX, AND BABINSKI REFLEX

Front 35

primitive reflexes: moro (startle) reflex= how to test, what do you see, clinical significance

Back 35

suddenly but gently lower baby's head, hit surface beside baby (loud noise), arms and legs extend; prenatal= disappearance 4-6 months postpartum; in adult indicative of lesion in corticospinal tract; early excessive startle response to sound is pathognomic for Tay-Sachs

Front 36

primitive reflexes: asymmetric tonic neck= how to test, what do you see, clinical significance

Back 36

prone/suprine position, turn head to one side, limbs flex on one side, extend on other side called fencer's position; seen after birth to 3 months; in adult indicative of lesion in corticospinal tract

Front 37

postural reflexes: landau

Back 37

if you suspend the infant (superman style) and then push their head down, the lest of their limbs will instinctively drop downwards as well

Front 38

primitive reflexes: babinski sign= how to test, what do you see, when do you see it, clinical significance

Back 38

stroke bottom or lateral portion of foot, extensor plantar response in infant; see from birth to 4 months; in adult indicative of lesion in corticospinal tract

Front 39

summary types of reflexes: stretch of myotatic or deep tendon reflexes (DTRs)

Back 39

monosynaptic; appropriate sensory stimulus is muscle stretch; clinical significance= brisk DTRs --> UMN lesion, decreased/absent DTRs --> LMN lesion, myopathy

Front 40

summary types of reflexes: flexor, crossed extension

Back 40

polysynaptic multisegmental; appropriate sensory stimulus= most forcefully elicited by painful stimulus following damage to descending pathways non noxious stimuli may produce the same response; clinical significance= increased responsiveness --> UMN lesion

Front 41

summary types of reflexes: superficial reflexes

Back 41

polysynaptic reflexes, signal must ascend and then descend the cord; appropriate sensory stimulus= 'cutaneous reflexes' evoked by gentle cutaneous stimulation; clinical significance= absence --> used primarily to detect UMN lesion

Front 42

summary types of reflexes: primitive (infant) reflexes

Back 42

normally suppressed by supraspinal pathways; clinical significance= presence --> UMN lesion

Front 43

reflex evaluation: DTRs and superficial spinal nerve correlations

Back 43

DTRs= biceps C5-6, triceps C7-8, brachioradialis C5-6, quadriceps (patellar) L2-4, achilles L5-S2; superficial reflexes= plantar reflex/babinski L4-S2, abdominal reflexes upper T8-10 and lower T10-12, cremasteric reflex L1-S2

Front 44

spinal cord injury

Back 44

spinal shock; neurogenic shock; autonomic dysreflexia; upper motor neuron (UMN) syndrome= negative and positive signs, spasticity, clonus, clasp knife response, exaggerated flexor/withdrawal reflex

Front 45

spinal shock: characterized by what which reflects what, associated with what, full expression can take how long

Back 45

characterized by the loss of reflexes, muscle tone,and sensation below the level of traumatic injury; reflexes the decreased activity of spinal circuits suddenly deprived of input from the motor cortex and brainstem; associated with hyperpolarization of alpha MNs; full expression may take several hrs and lasts for approximately 4-6 weeks; ventilatory assistance needed if lesion is above C3 (diaphragm is innervated by C3-5 levels); absent sphincteric reflexes lead to urinary and fecal retention

Front 46

recovery from spinal sock: bulcovavernosus

Back 46

aka clitoral sacral reflex in female; refers to external anal sphincter contraction in response to squeezing the glans penis or tugging on the foley (involves S2-4); early signal of recovery from spinal shock

Front 47

neurogenic shock: signs at different levels

Back 47

1. SCI above T6= loss of sympathetic vasoconstrictor outflow --> HYPOTENSION; 2. disruption of sympathetic cardiac nerve outflow results in unopposed vagal tone -->BRADYCARDIA; 3. interrupting the descending pathway of the baroreflex results in lack of compensation for hypotension from the loss of sympathetic vasomotor tone

Front 48

autonomic dysreflexia (AD): occurs when, what is it

Back 48

occurs as spinal shock is resolved and reflexes return; occurs in pts with SCI above the splanchnic sympathetic outflow (T5-6); occurs when the inhibitory outflow above the SCI from cerebral vasomotor centers is unable to pass below the block of the SCI; acute AD is a reaction of the autonomic nervous system to overstimulation (e.g. bladder distension is most common in up to 85% of cases, bowel distension, constrictive clothing, pain); morbidity associated with HYPERTENSION

Front 49

upper motor neuron (UMN) syndrome: what is it

Back 49

damage to the descending motor pathways anywhere along their trajectory gives rise to a set of symptoms called the UPPER MOTOR NEURON (UMN) SYNDROME

Front 50

UMN versus LMN clinical manifestations

Back 50

UMN= spasticity and associated hyperreflexia and hypertonia are hallmarks (stoke, ischemic or traumatic injury to brain stem or spinal cord); LMN= flaccid paralysis, areflexia, atrophy, fasiculations, and fibrillations of the muscle fibers (polio, werdnig-hoffman disease (floppy baby))

Front 51

UMN negative and positive signs

Back 51

negative signs= muscle weakness, impaired coordination, impaired motor motor control, impaired motor planning, fatigue; positive signs= spasticity, clonus, clasp knife response, flexor/withdrawal reflex, babinski

Front 52

what is spasticity

Back 52

velocity dependent increase in muscle tone caused by the increase in muscle tone caused by the increased excitability of the muscle stretch reflex; increased resistance to passive movement due to a lowered threshold of tonic and phasic stretch reflexes; associated with other POSITIVE SIGNS such as clonus, clasp knife response, exaggerated flexor/withdrawal reflex, and babinski sign

Front 53

what is clonus and what is its scale

Back 53

3-7 Hz oscillatory motor response to sustained muscle stretch; strong deep tendon reflex (DTR) that occurs associated with loss of descending inhibition; sustained CLONUS 5+, very brisk hyperreflexia with nonsustained clonus 4+, brisker than normal 3+, normal 2+, low normal diminished 1+, 0 no response

Front 54

clasp knife response: what is it

Back 54

an abnormal sign in which a spastic limb resists passive motion and then suddenly gives away similarly to the motion of the blade of a jackknife; the initial intense resistance is due to an exaggerated stretch reflex; the sudden give away is due to AUTOGENIC INHIBITION via Ib INHIBITORY INTERNEURON innervated by GOLGI TENDON ORGAN (GTO) and Ib AFFERENT

Front 55

clinical pearl: lower MN and upper MN

Back 55

lower MN= everything lowered (less muscle mass, decreased muscle tone, lowered reflexes, down going toes); upper MN= everything up (increased tone, increased DTRs, up going toes)

Front 56

The anatomical location of a lesion is established by determining whether the weakness is spastic or flaccid. Spastic weakness is characterized by increased muscle stretch reflexes, sustained ankle clonus, and excessive resistance by decreased or absent muscle stretch reflexes and no resistance to passive movement. It is most accurate to state that flaccid weakness occurs with: a. upper motor neuron lesion b. lower motor neuron lesion c. upper and lower motor neuron lesions

Back 56

C upper and lower motor neuron lesions because of spinal shock; otherwise you would think only lower motor neuron lesions

Front 57

the 4 types of myelopathy to know

Back 57

brown sequard syndrome; vascular myelopathies (anterior spinal artery syndrome); central cord syndrome (syringomyelia); cauda equina syndrome

Front 58

brown sequard syndrome: motor signs, sensory signs

Back 58

motor signs= UMN signs (ipsilateral SPASTIC PARALYSIS below the level of the lesion), LMN signs (FLACCID PARALYSIS at the level of the lesion); sensory signs= loss of ipsilateral proprioception and light touch below the lesion, loss of ipsilateral pain and temp for 2 segments below lesion, loss of contralateral pain and temp from 2 segments below the lesion

Front 59

anterior cord syndrome: what does it involve, motor signs, sensory signs

Back 59

often involves THORACIC "CRITICAL WATERCHED ZONE" that is particularly vulnerable to HYPOPERFUSION because of sparse collaterals; ARTERY OF ADAMKIEWICZ (T10-L2) provides the major blood supply to the lumbar and sacral cord via the anterior spinal artery; motor signs= UMN signs (complete spastic paralysis), LMN signs (flaccid paralysis at lesion level), greater motor loss in the legs than arms; sensory signs= sparing of the dorsal column, sensory anesthesia (spinothalamic function)

Front 60

central cord syndrome: motor signs and sensory signs

Back 60

most common incomplete SCI syndrome; motor signs= UMN signs (spastic paralysis of lower extremities (indicative of involvement of upper motor neurons), LMN signs (bilateral flaccid paralysis of upper extremities especially intrinsic muscle of the hands), muscle stretch reflexes may initially be absent but will eventually return along with variable degrees of spasticity in affected muscles; sensory signs= cape like bilateral loss of pain and temp as second order neurons are damaged bilaterally as they cross in the anterior commissure, usually sparing of light touch and proprioception; KNOW THAT 2 CAUSES OF THIS ARE SYRINGOMYELIA AND CHIARI MALFORMATION (ON TEST)

Front 61

syringomyelia: can cause what, what is it, motor sings, sensory signs

Back 61

THERE WILL BE A QUESTION ON THIS ON THE EXAM; one cause of central cord syndrome; an accumulation of CSF forms within the spinal cord called a SYRINX that can expand over time; motor signs= LMN signs (weakness, atrophy, and fasciculation i.e. anterior horn cells in both hands), UMN signs (hyperreflexia and babinski sign indicating some involvement of the lateral white funiculus containing the lateral corticospinal tract); sensory signs= cape like loss of pain and temp sensation along the back and arms, often antecedent history of spinal cord injury

Front 62

chiari type I malformation: what is it, type I and type II

Back 62

a number of pathological conditions can cause an obstruction of the normal cerebrospinal fluid spaces including the chiari malformation; type I= the most common form of chiari malformation, signs and symptoms DO NOT APPEAR UNTIL LATE CHILDHOOD OR EARLY ADULTHOOD, develops as the skull and brain are growing, HEADACHE often severe classic symptom at the skull base, neck, and shoulder and associated with exertion such as couching or sneezing; type II= the most common is present at birth (congenital)

Front 63

cauda equina syndrome: what is it, where is it, symptoms

Back 63

conus equina contains L1/2-5, S1-5; affects saddle area (buttocks, genitalia, and thighs); bowel and bladder dysfunction; sacral sensory loss; cauda equina syndrome is a nerve root injury so it exhibits primarily LMN sings; considered a surgical emergency because it left untreated it can lead to permanent loss of bowel and bladder control and paralysis of the legs

Front 64

cauda equina versus conus medullaris syndrome

Back 64

cauda equina syndrome= classically gradual and unilateral, nearly all pts complain of sciatica (pain radiating from the buttocks down the posterior or lateral aspects of the lower limb below the knee most often due to disk herniation between L4-5, UNILATERAL MUSCLE ATROPHY AND ABSENT REFLEXES (HYPOREFLEXIA) (patellar (L4) and ankle (S1) jerks), may progress to foot drop and loss of control of bowel and bladder, loss of sensation in unilateral saddle shaped area; conus medullaris syndrome= bilateral, mild pain, HYPERACTIVE STRETCH REFLEXES, increased anal tone, babinski reflex may affect the extensors, hypertonia (i.e. SPASTICITY), loss of sensation in bilateral saddle shaped area