Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
36 Cards in this Set
- Front
- Back
|
ALS destroys what kinds of motor neurons?
|
upper and lower
|
|
|
spastic paralysis is associated with what kind of motor neuron lesion?
|
upper motor neurons
|
|
|
what are the four levels of motor control?
|
upper motor neuron pathways, limbic pathways, supraspinal reflexes, segmental and intersegmental reflexes
|
|
|
all motor pathways in the spinal cord are located where?
|
in the lateral and anterior funiculi
|
|
|
tectospinal and tectobulbar tracts are tracts for what type of message? What type of path do they have?
|
supraspinal reflex for movement of head and eyes in response to auditory and visual stimuli. The cross to contralateral side
|
|
|
the lateral vestibulospinal tract descends from what nucleus? Controls what movements?
|
It descends uncrossed from the vestibular nuclei in the rostral medulla. It controls posture, equilibrium, and balance via strong excitatory input to lower motor neurons innervating antigravity (axial and extensor) muscles
|
|
|
the medial vestibulospinal and bulbar tracts control what?
|
posture and equilibrium of head and coordinates head and eye movement (dowel's eye effect)
|
|
|
what are the two main descending limbic motor pathways? what do they control? What NT do each use?
|
the ceruleospinal and bulbar tracts use NE from the locus ceruleus while the raphespinal and bulbar tracts use serotonin from the raphe nu. They regulate muscular strength and responsiveness in accordance with varying emotional states.
|
|
|
what are the two pathways for upper motor neuron descent? What part of the cortex do they descend from?
|
pyramidal and extrapyramidal pathways. The motor cortex (precentral gyrus) and premotor cortex (a bit more anterior on the cortex).
|
|
|
most upper motor neurons control the lower motor neurons via what? What do the upper motor neurons that control the intrinsic muscles of the hand do differently?
|
most use interneurons while the lower motor neurons that control the hands have direct connections with large upper motor neurons from the pyramid called betz cells.
|
|
|
the major motor pathway in humans for precise, skilled movements is via what tract? What is the general path on the descent down?
|
the pyramidal tract (corticobulbar and corticospinal tracts), they arise from the motor cortex in somatotopic organization through the internal capsule to the cerebral peduncle in the brain. About 90% of the fibers cross at the pyramidal decussation
|
|
|
what tract in the pyramidal tract is the major pathway for voluntary movement? what is the descending path of this tract? What body part does this tract have exclusive control over (characterize the neurons that control this body part and what percentage of the neurons in the tract control this body part)?
|
lateral corticospinal tract. From the primary motor cortex nuclei that control arms, trunk, and leg movement to the cerebral peduncle on down, then all fibers dessucate in the pyramidal decussation. This tract has exclusive control over the intrinsic hand muscles by 50% of its neurons, and these muscles are innervated by the two neuron hookup: 1 UMN and 1 LMN (the UMN is the betz cell).
|
|
|
What tract in the pyramidal tract is a small crossed and uncrossed pathway that controls proximal musculature on each side, chiefly in the upper body region?
|
the anterior corticospinal tract
|
|
|
what pyramidal tract controls the LMN's mediated by the cranial nerves? Describe the pathway from the motor cortex and the major exception.
|
corticobulbar tract. From the cortex (nuclei that control the face movement) then to the cerebral peduncle and through the pyramid to the level of the brainstem that contains the desired cranial nerve nuclei. Some fibers cross and some do not cross to get to the desired nuclei; however, most of the fibers do cross to the contralateral side. The exception is the lower half of the face (facial nerve); the portions of the facial nerve nuclei that control the lower half of the face ONLY receive fibers of this tract from the contralateral side of the body.
|
|
|
this tract is an extrapyramidal tract that is a crossed pathway which has strong excitatory effects on proximal flexors of the upper extremity. what nucleus does it use?
|
the rubrospinal tract which uses the red nucleus in the midbrain
|
|
|
this extrapyramidal tract is the major alternate pathway for the control of axial and proximal musculature as well as a strong excitatory effect on antigravity muscles. crossed or uncrossed? what nucleus?
|
the medial reticulospinal tract which is crossed and uncrossed and uses the pontine reticular nucleus.
|
|
|
this extrapyramidal tract is crossed and uncrossed to give rise to excitatory and inhibitory actions on axial and proximal limb muscles. what nucleus does it use?
|
the lateral reticulospinal tract which uses the medullary reticular nuclei
|
|
|
why are the rubro and reticulospinal tracts called corticorubro and corticoreticular in humans?
|
BC the premotor cortex AKA M2 AKA brodmans #6 controls these tracts.
|
|
|
the motor cortex has what kind of threshold for stimulation thus evoking what kind of muscles? the premotor cortex?
|
a low threshold for evoking movement of individual muscles. M2 has a higher threshold for more mass movements like postural adjustment.
|
|
|
what is cerebral shock?
|
the period after a stroke in which complete paralysis may exist as well as other extreme symptoms, but some function may return over time. All this is due to UMN
|
|
|
define spasticity.
|
increased resistance to passive movement with associated hypertonia.
|
|
|
What are the major signs and symptoms of upper motor neuron lesions?
|
spastic paralysis, muscular weakness on paretic sign with pronator drift, complete loss of control of distal muscles, and abnormal reflexes
|
|
|
what are the abnormal reflexes seen in upper motor neuron lesions?
|
increased DTR's (they have a lower threshold for excitation), clonus, clasp knife reflex (lowered threshold for DTR AND golgi), babinski sign (most characteristic of UMN lesion in these reflexes), hoffman sign, and raised threshold of superficial reflexes (include abdominal and cremasteric reflexes)
|
|
|
characteristics seen in the LE with upper motor neuron lesions are what?
|
extensor hypertonia and a stiff , spastic gait with circumduction at the hip joint
|
|
|
UMN lesions usually cause what caharacteristic signs in the UE?
|
flewor hypertonia, paralysis of intrinsic muscles of hand (thus no skilled movements), but grasping movement maybe seen.
|
|
|
in a spastic muscle, the more rapid the manipulation...
|
the greater the resistance quickly followed by the collapse of resistance (clasp-knife phenom)
|
|
|
what is the grading scale of DTR reflexes?
|
0 is no response (LMN)
1 is diminshed (LMN or cerebellar) 2 is normal 3 is hyperactive (UMN) 4 is hyperactive with clonus (UMN) |
|
|
what is the normal response to stroking the sole of the foot? abnormal and what does it indicate?
|
normal is plantar flexion of all toes; abnormal is the babinski sign which is dorsiflexion of the big toe and fanning of the little toes, babinski's sign, thus indicating a pyramidal lesion specefically the lateral corticospinal tract
|
|
|
what are three causes of spasticity, hpertonia, and hyperreflexia?
|
loss of cortical inhibition to the medial reticulospinal and rubrospinal tracts especially to gamma motor neurons which mediate muscle tone; loss of UMN control of renshaw cells reflex activity; lateral vestibulospinal tract left unchecked
|
|
|
loss of cortical control and thus cortical inhibition of brainstem results in what happeneing to the gamma motor neurons?
|
there is a constant release of excitatory messages from the medial reticulospinal, rubrospinal, and vestibulospinal tracts on the gamma motor neurons thus resulting in hypertonia
|
|
|
UE flexor hypertonia is do to constant excitatory stimulus from what?
|
rubrospinal tract
|
|
|
LE extensor hypertonia is due to constant excitatory stimulus from what?
|
the medial reticulospinal tract
|
|
|
this syndrome is produced by bilateral damage of the cortex and thalamus resulting in coma, bilateral UMN spasticity including UE flexion and LE extension via loss of input to brainstem motor centers.
|
decorticate rigidity
|
|
|
this syndrome is usually produced by bilateral damage to the rostral brainstem (midbrain) and characterized by bilateral UMN spasticity and coma. hypertonia is seen in extensors of neck, LE, and proximal extensors of UE. What tract is believed to be lost in this rigidity that is still functioning in the other common rigidity coma?
|
this is decerebrate rigidity. It is believed that loss of the rubrospinal tract (gives strong excitatory input to the proximal flexors)
|
|
|
what are alternating hemiplegias? how do they occur and what common cranial nerves are involved?
|
they are brainstem lesions involving motor cranial nerves and the pyramidal tract. The LMN of the cranial nerves on the ipsilateral side are affected and the UMN on the contralateral side are affected on body parts bellow the medullary decussation. Common nerves include III (superior alternating hemiplegia), VI (middle alternating...), and XII (inferior alternating...)
|
|
|
what are the three effects of corticobulbar tract lesions?
|
complete volitional paralysis of contralateral lower face muscles, paritial paresis of contralateral muscles innervated by CN V, VII (upper), IX, X, and XII, and NO spasticity present in unilateral corticobulbar lesions
|
