Test 3 Motor Systems CC Flashcards
Damage to LMN- what type of neuron, 4 signs?
LMN= alpha motor neurons
- Flaccid paralysis==> atrophy
- Fibrillations or fasciculations
- Hypotonia
- Hyporeflexia or areflexia
Areflexia
Loss of reflexes, from damage to LMN
Myasthenia Gravis
Autoimmune disease of neuromuscular junction. Form Ab to AchR. Ocular muscles first affected (sometimes limited to extraocular muscles)
Myasthenia Crisis
Weakness of respiratory muscles==requires rapid intervention
Muscle stretch reflex
Ia spindle afferent==> excitatory connection with alpha motor neurons
Reciprocal Inhibition
Ia fibers (afferent stretch) activate Ia interneurons= inhibition of antagonistic muscles
Crossed Extensor Reflex
Interneurons activate extensors and inhibit flexors on opposite side so that when you withdraw the limb, the opposite side is ready for it.
Blocking AchR
Causes: myasthenia gravis, curare, alpha bungaro toxin, curare, Treatment: Achesterase inhibitors= neostigmine
According to Dr. Bridges…drooping eyelids is characteristic of?
Myasthenia gravis
+ babinksi sign
corticospinal tract problem
Apraxia
inability to preform complex motor tasks (ex: dressing). Damage to motor or association cortex.
Blocking cholinesterase
Nerve gases: Saran, Soman, Tabun, VX- death by asphyxiation
Blocking Ach Release
Botulinum toxin
Explosive Ach Release
Black widow= alpha-latrotoxin Convulsion–> paralysis (when run out of Ach) 1) Prevents fusion at synaptic vesicle followed by 2) triggered Ach Release.
Rubrospinal system
UE, no influence on LE
Supratentorial lesions
=central/transtentorial lesions Unopposed hyperactivity of extensor muscles= decerebrate rigidity
Noxious stimulus to decerebrate patient
exacerbate decerebrate rigidity or evoke it if it isn’t apparent
Diencephalic stage=
during central herniation (transtentorial), before herniation through notch Sx= decreased level of consciousness, lethargy, small and poorly reactive pupils. Withdraw reflex is intact. Bilateral babinski response. Weak extremeties==>decorticate on ipsilateral side then both sides.
Part 2 of central herniation
=herniation through tentorial notch Sx: decerebrate, comotose, dilated fixed puils without light reaction. No eye movement. As it reaches midbrain, respiration stops
Cheyne Stokes
Damage to brain stem during central/transtentorial herniation:
abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea.
Decerebrate condition
=gamma rigidity. flexor muscles are inactive (corticospinal and corticorubrospinal input) Extensor muscle tracts not effected
Extensor muscle tracts
reticulospinal (gamma motor neurons) and vestibulospinal
Flexor muscle tracts
corticospinal and corticorubrospinal tracts
Decerebrate condition
=gamma rigidity (mostly reticulospinal) flexor muscles are inactive (corticospinal and corticorubrospinal input) Extensor muscle tracts not effected
Flexor muscle tracts
corticospinal and corticorubrospinal tracts
Decerebellate rigidity
=alpha rigidity (mostly vestibulospinal) loss cerebellar anterior lobe= no purkinje cell inhibition to vestibular nuclei and of fastigial neurons.
Decorticate rigidity- Symptoms?
Sx:
- flexion of upper extremities (intact rubrospinal);
- extensor hypertonus (intact reticulospinal);
- altered state of consciousness, respiration, oculomotor deficits, weakness
Upper Motor neuron damage- Symptoms? do they change ove time?
5 total
- Initially weak and flaccid
- Become spastic
- Hypertonia- resistance to passive movement
- hyprereflexia
- Babinksi sign=dorsiflexion of great toe (normal is plantar)
Spasticity- clinical symptoms? Most obvious muscles?
Spasticity
Increased resistance to passive movement or manipulation. Velocity dependent: increased resistance the faster the examiner moves the extremity.
- upper extremitiy: proximal flexors
- Lower extremity: extensors
Clasp Knife Effect
Clasp Knife Effect
After brief period of applied force (during exam for spasticity), the increased resistance collapses. –the spasticity stops
Clonus
Clonus: Observed in UMN lesion
- Repetitive sequential contractions of flexors and extensors following flexion/extension.
- Usually accompanied by spasticity
Corticospinal lesions cause ipsilateral/contralateral deficits?
Corticospinal tract lesions
Ipsilateral= below motor decussaiton
Cotralateral deficit= above decussation
Infarction of primary motor cortex=
infaction of MI (= primary motor cortex)= usually paralysis
- Infarction of premotor cortex=
- Infarction of supplementary motor cortex
- Lesion to premotor cortex= Contralateral apraxia
- normal strenght and tone
- Inability to perform voluntary action (ex: picking up pencil)
- Lesion to supplementary motor cortex= ability to corrdinate actions on both sides of the body
- normal strength and tone
Posterior limb of internal capsule
- Blood supply
- Damage causes
Posterior limb of internal capsule- has corticospinal fibers
- Blood= Lenticulostriate branches of M1
- Symptoms: Transient flaccid paralysis followed by spastic paralysis in contralateral UE/LE. never resolves.
Fiber bundles found in posterior limb of internal capsule
- Posterior limb of internal capsule:
- Corticospinal= motor loss
- thalamocortical= hemisensory loss, homonymous hemianopia
Corticospinal fibers in the midbrain are found?
Midbrain corticospinal fibers are found in the middle third of the crus cerebri.
UE= medial; LE=lateral
Weber’s Syndrome
Weber’s Syndrome= Damage to medial 2/3 of crus cerebri-
- Causes: Hemorrhage of posterior communicating artery and paramedial branches of P1
-
Symptoms: superior alternating hemiplegia, crossed deficit
- Corticospinal fibers-contralateral hemiparesis
- Frontopontine/corticobulbar fibers-deviation of ipsilateral eye (down and out); possible loss of direct, consensual light reflex and loss of accomodation
Corticospinal fibers in pons are supplied by ____ a.
Symptoms of occlusion to the artery? What is the general condition called? what is the specific name for it?
FOVILLE SYNDROME
Blood supply: Paramedian branches of the basilar a
Symptoms: MIDDLE alternating hemiplegia, crossed deficit
- Hemiplegia, UMN sign
- Damage to abducens fibers=ipsilateral lateral rectus paralysis
- possible damage to medial lemniscus
Corticospinal fibers in the medulla
-
Blood supply
- What else is supplied by this artery-sx if occluded?
- Symptoms if occluded?
- Name of syndrome?
-
Blood supply in Medulla= Anterior spinal artery
- hypoglossal nerve=ipsilateral flaccid paralysis of tongue (LMN); deviation to side when protruded
- medial lemniscus=contralateral loss of two point discriminations
- pyramids= Contralateral hemiparesis
- Dejerine Syndrome= inferior alternating hemiplegia
Damage to ROSTRAL half of motor decussation=
Damage to ROSTRAL half of motor decussation=
- Ipsilateral hemiparesis in UPPPER extremity
- Contralateral hemiparesis in LOWER extremity
Anterior vs lateral corticospinal tract
Anterior corticospinal tract= does not decussate
Lateral corticospinal tract- decussates in pyramids
Damage to corticospinal tract in upper cervical cord
Corticospinal tract damage in cervical part=
- hyperreflexia
- Babinski sign
- spastic hemiplegia in ipsilateral LE and UE
Lesion of cervical enlargement
Lesion of cervical enlargement
- LMN signs in ipsilateral UE
- UMN signs in ipsilateral LE
Clinical symptoms if patient has corticospinal damage AND damage to anterior horn?
Clinical symptoms if patient has corticospinal damage AND damage to anterior horn?
LMN signs
Central Cord Syndrome
Central Cord Syndrome- hyperextension of the neck-can damage cord or occlude sulcal branches of ASA.
- bilateral hemiparesis of UE (medial region of both lateral corticospinal tracts)
- urinary retention
- bilateral patchy loss of pain and temp below injury
Blood supply to
- Medial part of lateral corticospinal tract
- Lateral part of lateral corticospinal tract
Blood supply to
- Sulcal branches of ASA=Medial part of lateral corticospinal tract=UE
- Penetrating branches of ASA= Lateral part of lateral corticospinal tract= LE
Brown Sequard Syndrome
Brown Sequard Syndrome=hemisection of spinal cord
- Ipsilateral loss of two point discrimination (posterior columns)
- Contralateral loss of pain, temp, crude tough (ALS)
- Ipsilateral paralysis (corticospinal tract)
Corticonuclear fibers course (start in cortex)- blood supply in each region? –list nuclei it innervates in order
Innervates 5 nuclei
- Start in Layer V of face part of motor cortex= MCA
- Go through genu of internal capsule= lenticulostriate arteries
- Midbrain: medial part of crus cerebri=paramedian branch of basilar a.
- Pons: trigeminal ==>facial motor nuclei
- Medulla: Hypoglossal, nucleus ambiguous==> Accessory motor nucleus
Unilateral damage to corticonucluear fibers?
Equal innervation from both sides to motor V and upper muscles of motor VII.
- No visisble weakness of muscles of mastication
- No visisble weakness of upper facial muscles
- contralateral weakness of lower facial muscles (if rsotral to motor nucleus)
Central facial paralysis
Central facial paralysis: Lesion of corticonulcear fibers rostral to facial motor nucleus=
- CONTRALATERAL drooping of muscles at corner of the mouth and lower portion of face on the side opposite to the lesion
Bell’s Palsy
Damage to ROOT of facial nerve= flaccid paralysis of all muscles on IPSILATERAL side
Corticonuclear fiber damage at mid-medullary levels
contralateral weakness to palatal arch muscles (nucleus ambiguous), failure to elevate on weak side and deviation of uvula to side of lesion
Damage to root of vagus nerve
- what can cause this?
- clinical manifestations
Root=LMN lesion
- can happen in jugular foramen syndromes
- weakness and slight drooping of the arch on same side, deviation of uvula to contralateral side of lesion
- (uvula deviates to STRONG side)
Hypoglossal muscles- damage to fibers before vs after nucleus
damaged corticonuclear fibers= UMN, deviation of tongue during protrusion to opposite side of lesion (to weak side). May also have symptoms associated with damaged genu of internal capsule (central seven, uvula deviation)
damaged hypoglossal nerve- LMN= atrophy of tongue, deviates to side of lesion.
Damage to corticonuclear fibers to accessory nucleus
IPSilateral weakness. Cannot shruf or elevate shoulder on side of lesion, cannot turn head away from lesion
Lenticulostriate A hemorrhage=
Lenticulostraite artery= genu and posterior limb of internal capsuel
Corticospinal damage=contralateral spastic hemiparesis
Corticonuclear damage= contralateral central facial paralysis, deviation of uvula to side of lesion, deviation of tongue to contralalteral side of lesion, inability to turn head away from lesion, raise shoulders on side of lesion
Uncal herniation
Damage to occulomotor nerve and crus cerebri on side of herniation
CN III= ipsilateral paralysis of eye movement, diplopia, dilated pubul
Corticospinal= contralateral hemiplegia
Kernohan Syndrome
Kernohan Syndrome=midbrain displaced against edge of tentorium on side CONTRALATERAL to the herniation
- IPSilateral occulomotor nerve palsy (expected)
- IPSilateral hemiplegia (false localizing sign, caused by compression of crus CONTRAlateral to herniation)
Corticorubral system
- where does it start?
- function?
Corticorubral system
- From area 4 and 6 of cortex
- can partially compensate for loss of corticospinal tract
- flexion of upper extremity
