Motor Tracks (Stephens) Flashcards
- condition that may result from a disruption of the system that relates stored tool use and gesture info w/ the holistic sensory body scheme to produce the appropriate motor output
- for example, inability to correctly imitate hand gestures and voluntarily mime tool use (pretend to brush hair)
- frequent sites of lesions that result in this condition are the left parietal lobe and premotor cortex
- in the dominant hemisphere, aphasia is often present, and must be assessed by the physician
ideomotor apraxia (IMA)
A 67 y/o male is seen in acute rehabilitation after the inability to demonstrate how to produce a voluntary cough is called:
a) agnosia
b) agraphia
c) apraxia
d) aphonia
e) automatic-voluntary dissociation
c) apraxia
(reflex cough may be unaffected)
A lesion in the dominant hemisphere resulting apraxia is frequently a/w which of the following?
a) agnosia
b) agraphia
c) apraxia
d) aphasia
e) alexia
d) aphasia
(makes it hard for a person to understand spoken or written language)
The motor subcortical loops are subserviant to the:
a) supplemental motor cortex
b) parieto-occipito-temporal cortex
c) frontal lobe
d) primary motor cortex
e) premotor cortex
d) primary motor cortex
- 40-60% of corticospinal fibers originate from this area (also called the precentral gyrus)
- this area controls precise and individual movements of the digits and distal extremities
primary motor cortex
- located anterior to primary motor cortex (precentral gyrus)
- includes Broca’s speech area and frontal eye field
- involved in the ideation and programming of movement patterns
- receives input from the cerebellum via the ventral anterior nucleus of the thalamus
premotor cortex
- gives rise to 20-40% of the corticospinal fibers
- most of these fibers convey holographic somatosensory info to motor cortices
primary somesthetic cortex
- contributes 10-20% of its fibers to motor tracts
- involved in guiding task-oriented movements toward their goals
posterior parietal lobe
- located near the paracentral lobule and primarily influences proximal limb musculature and simultaneous movements of the limb
- receives input from basal ganglia via the ventral lateral nucleus of the thalamus
supplementary motor cortex
- results from ischemia within the territory supplied by perforating branches of the MCA or ICA
- usually secondary to cardiac embolisms
- prognosis dependent on degree of infarction of posterior limb of IC
- clinical signs: motor and/or sensory deficits and cognitive dysfunction
lenticulostriate infarcts
(usually supply blood to part of the basal ganglia and posterior limb of the internal capsule)
What is the general pathway of the lateral corticospinal tract?
fibers arise from pyramidal neurons (cells of Betz) in laminae V of the primary motor and premotor cortices (upper motor neurons)
↓
CST sends radiating fibers (corona radiata) and converges at the posterior 1/3 of IC
↓
fibers descend through midbrain, move through crus cerebri of the cerebral peduncles and enter the pons
↓
pontine nuclei relay signals to contralateral cerebellum through the middle cerebellar peduncles
↓
fibers scatter around pontine nuclei and condense again when descending into medulla
↓
in the medulla, fibers condense into pyramids and 85-90% of fibers cross over at the pyramidal decussation, forming the lateral corticospinal tract (LCST)
↓
the remaining uncrossed fibers (ipsilateral) continue as the anterior corticospinal tract (ACST)
↓
the LCST descends into the lateral funiculus (lateral white columns)
↓
most of the fibers terminate in lower motor neuron pools (intermediate gray matter), which activate α and γ motor neurons
↓
α neurons activate extrafusal (contractile) fibers in muscles and γ neurons activate intrafusal (muscle spindle) fibers in muscles
What is the general pathway of the anterior corticospinal tract?
ACST follows the same pathway as the LCST throughout the brainstem
↓
once the fibers reach the lower medulla, they remain ipsilateral (instead of crossing over w/ the LCST fibers at the pyramidal decussation)
↓
fibers continue to descend uncrossed in the anterior funiculus (anterior white column)
↓
once the fibers reach the segment they will exit the SC, they cross over to the contralateral gray horn
↓
they then go on to activate motor neurons for axial, gross movements
(unilateral lesions of the ACST have minimal clinical effect)
- groups of highly interconnected interneurons in the base of the intermediate gray matter of SC
- this is where most descending motor fibers of the CST terminate
- play an important role in processing and intergrating descending motor info w/ the incoming “current status” sensory information
lower motor neuron pools
lesion that results in contralateral spastic hemiplegia or spastic hemiparesis
unilateral lesion of the CST
lesion that results in ipsilateral paralysis or paresis of the distal limb musculature innervated by those spinal segments below the level of the lesion
unilateral lesion of the LCST
- neurons that directly innervate striated or intrafusal muscle cells
- two different types: α neurons (innervates extrafusal/contractory tissue) and γ neurons (innervate intrafusal/muscle spindle tissue)
- a single axon from one of these α neurons may innervate a variable number of muscle cells
- the neuron and the myofibers it innervates is the motor unit
lower motor neurons
What conditions/symptoms would a LMN lesion elecit?
- flaccid paralysis: muscle is completely limp and there is no resistance to passive movement
- areflexia: loss of efferent component of the reflex arc to a muscle, results in the absence of the associted muscle reflex
- atonia: destruction of gamma motor neurons or their axons results in absence of muscle tone
- atrophy: denervated muscle atrophies due to the loss of stimulation from motor neurons
- fasciculations: twitching of the denervated muscle, probably due to hypersensitivity of the motor end plate
- condition that is commonly due to interruption of the motor cortex, corticospinal and/or corticobulbar tracts
- other tracts and nuclei may be involved and produce some of the associated sxs
- condition usually referred to as spastic paralysis of the antigravity muscles
- signs and sx: spastic paresis of axial and proximal limb musculature; spastic paralysis of distal limb musculature, especially UE’s; hypertonia, hyperreflexia, Babinski sign, clonus, rigidity, and disuse atrophy
- rare sx: isolated lesions of CST result in paresis and incoordination of primarily the distal musculature of the extremities
upper motor neuron paralysis
- inability to perform certain complex learned motor acts in absence of any paralysis, ataxia, sensory changes, or deficiencies of understanding
- usually due to a lesion in the superior parietal lobe of the dominant hemisphere (usually left in most ppl)
- two types: ideomotor and ideational
apraxia
- inability to perform a given act correctly although old, habitual motor acts can be performed spontaneously or repetitiously
- specifically a/w lesions of the supramarginal gyrus of the dominant hemisphere
ideomotor apraxia
- loss of ability to formulate the thoughts necessary to perform a motor activity
- affected individuals can perform isolated tasks, but not a series of related tasks
- occurs as a manifestation of brain disorders such as cerebral arteriosclerosis
- not seen in isolation, but conjunction w/ widespread intellectual deterioration
- sequential motor events may be laden w/ errors in method and procedure, or completely impossible
ideational apraxia
A unilateral lesion of the lateral corticospinal tract would result in which of the following?
a) bilateral flaccid paralysis
b) contralateral spastic hemiplegia
c) ipsilateral hemiplegia
d) no motor deficits
c) ipsilateral hemiplegia
A lesion of the corticospinal tract would result in which of the following?
a) areflexia
b) flaccid hemiplegia
c) hypertonia
d) spastic hemiplegia
a) areflexia (LMN paralysis)
b) flaccid hemiplegia (LMN paralysis)
c) hypertonia (could exist in this case but less likely)
d) spastic hemiplegia
A lesion of the anterior horn neurons at C7 would result in which of the following?
a) flaccid paralysis
b) hemiparesis
c) hypertonia in the hand
d) spastic paralysis
a) flaccid paralysis
b) hemiparesis
c) hypertonia in the hand
d) spastic paralysis
Which of the following is an upper motor neuron?
a) facial motor nucleus
b) trigeminal motor nucleus
c) dorsal motor nucleus of CN X
d) corticobulbar fibers
a) facial motor nucleus
b) trigeminal motor nucleus
c) dorsal motor nucleus of CN X
d) corticobulbar fibers (other name for these is corticonuclear fibers)
How is the level of a lesion determined based upon a patient’s symptoms, if the patient has multiple descending symptoms that would involve more than one cranial nerve?
(level is NOT determined by corticobulbar fibers)
level is determined by deficits a/w most superior cranial nerve and the side of those deficits
case example:
- patient presents w/ right external strabismus, pupillary dilation and complete ptosis, inability to smile on the left, uvula deviates to the right, protruded tongue deviates right, left spastic hemiplegia
- level of lesion is oculomotor nerve on the right (mesencephalon)
- lesion is located in CNS because of the deficits (spastic hemiplegia) that can only occur w/ a CNS lesion
- the other cranial nerve deficits are due to involvement of corticobulbar fibers, which are damaged at CN III nerve, and therefore do not descend to other somatic motor CN nuclei
- some of the CN below the level of lesion may recover spontaneously or w/ PT
What is the general pathway of the corticobulbar fibers?
fibers descend from head region of primary motor cortex (precentral gyrus)
↓
course through genu of IC and cerebral peduncles
↓
uncrossed CBT are at/above the level of the trigeminal N. (unilateral lesions of uncrossed CBT result in contralateral facial palsy
↓
fibers decussate in lower pons (between CN V and CN VI)
↓
crossed CBT (unilateral lesions below the decussation may result in some ipsilateral cranial nerve palsies
↓
fibers innervate somatic motor nuclei of the brainstem
- fibers that course bilaterally and terminate in reticular formation surrounding brainstem motor nuclei
- do not affect LMN’s as strongly as direct corticobulbar fibers, but play a role in recovery from lesions involving the direct fibers (neuronal plasticity of the RF)
corticoreticulobulbar fibers (indirect corticobulbar fibers)
- fibers that originate in the frontal and occipital eye fields and descend in the dorsal aspect of the midbrain adjacent to central gray matter
- these fibers terminate in superior colliculus and PPRF as part of the oculomotor system
- drive volitional and nonvolitional eye movements
- separation of these fibers from corticospinal and corticobulbar makes it difficult to destroy all 3 in same lesion
corticomesencephalic fibers
Corticobulbar Tracts
- indirect CBT fibers
- other name for them:
- location:
- function:
- aberrant corticobulbar fibers
- other name for them:
- location:
- function:
- direct fibers
- cortical rep: none
- nuclei:
- muscle groups:
- cortical rep: contralateral
- nuclei:
- muscle groups:
- cortical rep: some bilateral
- nuclei:
- muscle groups:
- cortical rep: bilateral
- nuclei:
- muscle groups:
- cortical rep: none
Corticobulbar Tracts
- indirect CBT fibers
- other name for them: corticoreticulobulbar fibers
- location: RF
- function: ameliorate s/s of CBT lesions
- aberrant corticobulbar fibers
- other name for them: corticomesencephalic fibers
- location: OEF and FEF of oculomotor sys
- function: eye movements
- direct fibers
- cortical rep: none
- nuclei: MMCC
- muscle groups: axial musculature
- cortical rep: contralateral
- nuclei: facial, LMCC
- muscle groups: lower 1/2 facial muscles, limb musculature
- cortical rep: some bilateral
- nuclei: trigeminal motor, hypoglossal, accessory
- muscle groups: mastication, tongue muscles, SCM and trapezius
- cortical rep: bilateral
- nuclei: facial, N. to ambiguus, phrenic
- muscle groups: upper 1/2 facial Ms., larynx and pharynx, diaphragm
- cortical rep: none
*MMCC=medial motor cell column; LMCC=lateral motor cell column
What would lesions above CBT decussate (at/above trigeminal) result in? What would lesions below (at/below abducens) result in?
- above: contralateral cranial nerve palsies (supranuclear facial palsy)
- below: ipsilateral cranial nerve palsies
What is the association between the structure of the facial motor nucleus (CN VII) and CBT fibers?
- facial motor nucleus is divided into 2 parts: anterior and posterior
- anterior: receives CBT fibers from contralateral cortex and innervates muscles of lower quadrant of face
- posterior: receives CBT fibers from both hemispheres and innervates muscles of upper quadrant of the face
- condition caused by unilateral lesions of CBT fibers above level of facial motor nucleus
- contralateral mimetic muscles on lower quadrant of face are paralyzed
- upper quadrant facial muscles are unaffected due to the bilateral innervation of the posterior portion of the facial motor nucleus
- most common sites of lesions causing condition: facial region of motor cortex and genu of the IC
- differs from central lesion of facial N., which results in Bell’s palsy
supranuclear facial palsy
