Motor Systems, Pyramidal Pathway & Basal Gang. Flashcards
where are the motor cortices and what is their specific functions
Primary Motor Cortex: exisits within the frontal lobe at the precentral gyrus
- resonsible for the motor function
the Pre-Motor Cortex: exisits just anterior to the primary motor cortex: responsible for planning based on externally driven movements
the Supplementary Premotor area: just superior to the premotor cortex: responsible for motor planning when the signal is originated from internally driven movements
the reason the motor control also includes the parietal and temporal lobes to some extent is because multiple pathways are involved with motor movements = need sensory input, visual, audiotry and tactile stimuli to assist in the plan!
additional input comes from the cerebellum and basal ganglia
What is the Internal Capsule
what is its function
3 parts
fibers within each part
Internal Capsule
- connects the Cortex to the Brainstem
Anterior Limb
Genu
Posterior Limb
Anterior Limb
- carries decending fibers from the NON MOTOR areas of the frontal, parietal, temporal and occiptal cortex to the same side pons
Genu
- carries decending fibers from the PRIMARY MOTOR CORTEX to the brainstem with targets at the cell bodies of the crainal nerve motor nuclei
Posterior Limb
- carries decending fibers from the PRIMARY MOTOR CORTEX to the cell bodies of CONTRALATERAL anterior (ventral) horn of their target SC level
Describe the Somatotopy of the Motor Tracts from the SC and teh corticospinal tracts
Corticospinal tracts: carry motor neruonal signals from teh cortex to the spine and to the target organ
it travels via UMN and LMN: so the UMN from the motor cortex travels down through the brainstem to the medulla
- at the pyramids of the medulla, the motor neruon (UMN) CROSSES but does not synapse
- it now travels down the contrallateral side of the SC
- once it gets to its level of the spinal cord: it synpases (LMN) and leaves
the Somatotopy
- the lateral corticospinal tract: carries voluntary motor signals: medial centers are for UE andn lateral centers are for the LE
- the ventral corticospinal tract also carries voluntary motor neruons
UMN v LMN Lesions
how do thye present differently
UMN Lesions
- lesions of the UMN: thus anything that is lesioned prior to the SC level of action
- result = muslce weakness
- will have hyperreflexive states = hyperreflexive DTR
- hypertonia = increased muscle tone
LMN Lesions
- the lesions of the LMN: thus anything after the synpase at the level of the SC where the action is to occur all the way to the NM junction
- muscle weakness
- hypotonia = decreased muscle tone
- hypoactive deep tendon reflex
what is specific to the anterior corticospinal tract (motor) that is different than the lateral corticospinal tract
- they both transmit voluntary motor neruons
- the ANTERIOR corticospinal tract transmits voluntary motor of trunk pathway
the PATHWAY is different
- the motor nerves cross over at the SPINAL CORD LEVEL AND SYNPASE (instead of crossing at the medulla)
What is the corticobulbar tract
voluntary pathway of motor neurons which go to the cranial nerve nuclei
Pathway
- from the lateral ednge of the primary motor cortex
- leave the genu of the internal capsule
- CROSS OVER at the level of their target nuclei in the brainstem (lower number CN cross higher up in brainstem)
- then SYNPASE on the CONTRALATERAL nucleus
(so lesions from the brain and above the nuclei will have contralateral effects, but lesions below the nuclei (like from peripheral lesions) will have ipsalateral effects
** all CN aslo have same sided innervation EXCEPT CN7 and CN12** they ony have contrallater innervation
what are the vestibulospinal tracts
lateral v medial
vestibulospinal tract
Lateral: compensates for tiliting (like a boat over waves) via postural changes
Medial: compensates for head position as we move; cooridnates eyes with head movements
what is the VOR (vestibular occular reflex)
what is the VOR- cancellation reflex
VOR
- the trat reflex that allows the head to move and the eyes will then move at the same speed in the opposite direction
- think: you keep your eyes locked on something as your head moves
- this is medicated in the semicircular canals of the ears
- Gain: is the measurement to determine if its right
- a gain normally should be 1
- + test = hypofunction, usually a peripheral issue
VOR cancellation reflex
- when the head moves, the eyes move with it
- so when they focus on one thing in front of them, the head and eyes move TOGETHER as the object moves
Myotomes
what are they
what muslces are associated with the C5-S1 spinal nerves
Myotomes: muslce groups which are coordinated and respons to a specific nerve stimuli
good tool for assessing integritiy of spinal nerves
C5 = elbow flexion
C6 = wrist extension
C7 = elbow extension
C8 = finger flextion (fist)
T1 = finger ABDuction
L2 = hip flexion
L3 = knee extension
L4 = ankle dorsiflexion
L5 = big toe extension
S1 = ankle plantarflexion
Define the following
hemiplegia
hemiparesis
mono v tetra v para plegia
Hemiplegia: parlysis to one half of the body
hemiparesis: weakness to one half of the body
Mono = one limb parlysis
tetra/quad = all limbs
para = only lower limbs affected
Spastic v Flaccid Paralysis
UMN lesion v LMN lesions
what will you see
UMN lesions = will have spastic paralysis
LMN lesions = will have flaccid paralysis
SO
- at the LEVEL of the lesion: there will be flaccid paralysis (since thats a LMN) BUT UMN signs (spastic) anywhere below the lesion
sometimes, UMN can have periods of flacidy that transitions to spasticity
define and explain the different types of atrophy
deinnervation atrophy
disuse atrophy
age related atrophy
disease-related atrophy
deinnervation: complete lesion to the nerve innervating that muslcce: rapid atropy
disuse: low mechanical load (bed bound, etc.) results in lack of muscle fiber use and atrophy
age-related: sarcopenia: lack of sarcomeres as you age, atrophy happens (exercise can help slow this!)
disease-related: a profound muslce mass loss secondary to canecr, HIV, etc. which atrophy the body
Brown- Sequard Lesion
- what is it
- how does it occur
- what is the following losses to the tracts
- motor? sensory pain? sensory vibration?
Brown-Sequard Lesion
- a lesion which results in 1/2 of lateral disruption of the SC: think either the left side is knocked out, or the right side is knocked out
usually a result of a GSW impacting a localized region
so the follow results will occur
Motor (corticospinal tract): loss of motor function on the SAME SIDE at the level of the lesion and below the lesion
Sensory (spinothalmic pain/temp) : loss of pain/temp at the level of the lesion AND the CONTRALATERAL SIDE below the lesion (since these fibers cross immediately at the level they are, they wont be able to travel up)
Sensory (dorsal: vibration, proprioception) : lost on the SAME SIDE at the lesion and the SAME SIDE BELOW (since these travel up the same side of the SC)
poliomyelitis
how does it happen
lesions results in what losses
recovery?
Poliomylelitis
viral (polio): orcal/fecal transmission
symptoms: mild flu-like to motor loss (varies)
prefers to be in LMN, destroys LMN bilaterally or unilaterally
deficts see more proximally (trunk) over the extremities
- flaccid paralysis, hyporeflexia and hypotonia (since its LMN)
some pts. recover; others have respitory invovemen and disability
Post-polio syndreom: some neurons take over the areas where the dead neruosn were supposed to work: but overtime this can become atrophied as they cant do it forever
Syringomyelia
what is it & how does it occur
treated how
symptoms and deficts include what
Syringomyleia: a congential abnormality which results in an expansion of the central canal in teh cervical spinal cord
(essentially: too much expansion of the central canal destorys the tracts nearby)
the lateral spinothalamic tract sits closest = thus you get loss of pain and temperatrue at the level of the lesion Bilaterally and below since its knocking out both the left and right tracts on eitehr side
- as it expands can get UE muscle atrophy (since the corticospinal tract is the next to get impacted, and the UE are more medial than the LE somatotopographic)
VP shunt and surgery can fix this
