Cerebellum and Cranial Nerves Flashcards
What is the Cerebellum used for?
What do lesions to the cerebellum lead to?
UMN syndrome or LMN syndrome?
motor output
lesions lead to deficits in motor output and mobility
lesions to cerebellum do not result in UMN syndrome (does not cause spasticity, hyper, pathological reflexes)
Does lesion to cerebellum cause UMN syndrome?
NO
lesions to cerebellum do not result in UMN syndrome (does not cause spasticity, hyper, pathological reflexes)
Cerebellum: motor or sensory?
not only a motor effector but takes sensory input
Cerebellum Function (5)
- coordinates activity, fluid movement and postures
- comparison of motor activities to intend plan and modify it if not achieved (continual loop)
- modification of motor output based on sensory input and motor output: continuous loop
- compensation for motor tasks: predictive / anticipatory
big role in predictive movement: feed forward, anticipatory *if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance - major role in learning new motor programs because of its modifying function
If Cerebellum Damaged
learning new motor programs is limited: challenge in PT because we depend on motor learning – here plasticity cannot occur
*if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance
depending on where lesion is in the cerebellum can change deficits
Vestibulocerebellum
another name
receives input from _____ and outflow to ________
lesions result in _________
what happens in lesion?
archicerebellum
receives input from and outflow to the vestibular nuclei
lesions result in inability to use vestibular inputs (even though vestibular input comes in)
luckily the pons can help to some extent
if lesion to vestibulocerebellum can vestibular input still come in?
YES
Spinocerebelleum
another name
role
receives input from _____ and outflow to ________
lesions result in _________
what happens in lesion?
paleocerebellum
input: from spinocerebellar tracts (alot from spinal cord)
outflow to:
movement completion: termination of movement
muscle tone: initiate–>accelerete –>peak –>deccelerate –>terminate
lesion of the spinocerebellum results in overshooting when reaching for something reach past object: abnormality in maintaining the muscle tone (ie in a rebound test)
big effect on muscle tone–spasticity is excessive tone
if i hold my arm out, agonists and antagonsits are being used to keep my arm in this position
(regulating muscle tone and in adapting the body to changing circumstances. )
Rebound Test
hold arm straight, ability to maintain tone because firing of muscles is equal and opposite on all sides maintaining muscle tone
What does lesion to spinocerebellum cause?
abnormality in maintaining the muscle tone (ie in a rebound test)
NOT IN FLACCIDITY
NOT IN RIGIDITY
but ability to maintain an EVEN tone
ie doorbell: lesion to spinocerebellum- amount of pressure put onto the doorbell did not stay the same because could not maintain an even pressure/tone
Cerebrocerebellum
- another name
- role
- receives input from _____ and outflow to ________
- lesions result in _________
what happens in lesion?
- neocerebellum
- control of rapid movements, sudden movements (throw a ball and he quickly reacts to catch it)
precise movement control
motor planning - lateral cerebral hemispheres recieve input from pontine nuclei and has output to the thalamus, motor cortex, and premotor cortex
- dysmetria
disdiadokinesia
Vestibulocerebellum (online)
input/output
function
damage
The vestibulocerebellum,receives a substantial amount of its input from the vestibular nerve. This is unique since no other portion of the cerebellum receives direct input from a sensory nerve.
Additionally, there are connections from the vestibular nuclei to the vestibulocerebellum.
The vestibulocerebellum is an important regulator of the vestibular system.
Most important function of this is to allow adaptation to vestibular damage.
Damage to this region will result in vertigo and nystagmus.
Spinocerebellum (online)
input/output
function
damage
important in regulating muscle tone and in adapting the body to changing circumstances.
receives extensive input from the spinal cord. several direct and indirect spinocerebellar pathways terminate in the spinocerebellum
The input from muscles and the spinal cord reflex pathways are necessary for proper regulation of muscle tone and movement.
Since the spinocerebellum includes both vermal and paravermal zones of the cerebellum, there are connections with both the fastigeal nuclei and the interposed nuclei.
The fastigeal nuclei, in turn, connect to the reticular formation can affect muscle tone and crude movements via the reticulospinal tracts.
The interposed nuclei connect predominantly to the contralateral red nucleus through the superior cerebellar peduncle, origin for the rubrospinal tract that mainly influences limb flexor muscles.
-Therefore, the spinocerebellum can influence both muscle tone and coordination of the extremities.
-cerebellum is important in determining the appropriate response to changing situations.
For example, when attempting to resist a force on the extremities, a sudden release of force would result in a rebound of the the limb. The ability to rapidly check this motion requires feedback from muscle stretch and tension receptors.
Neocerebellum (online)
input/output
function
damage
The neocerebellum receives the vast majority of its input from the pontine nuclei. The pontine nuclei receive input from the majority of the cerebral cortex via corticopontine fibers. The pontine nuclei project exclusively through the middle cerebellar peduncles to the cerebellum, where these axons terminate as mossy fibers. It is the largest input to the cerebellum and almost exclusive input to the neocerebellum (which comprises most of the lateral hemispheres of the cerebellum).
involved in regulating the cerebral cortical motor output. The best-known effect of this is in procedural learning. —Activities such as riding a bike or learning to ski involve activity of the cerebellar hemispheres.
Damage to the lateral hemispheres results in lack of coordination of limb movement, with overshoot and undershoot (intention tremor).
The discussion to this point has largely focused on control of balance and of skilled voluntary movements. In addition to these functions. the cerebellar vermis receives visual input from the superior colliculus and is involved in coordinating eye movements. It also coordinates speech. Drunken speech, for example, derives from the effect of alcohol on the vermal portions of the cerebellum.
Signs of Cerebellar Dysfunction
5 traits
- Dysmetria
- Asynergia/dysnergia
- Rebound phenomena
- Tremor
- Hypotonia
Dysmetria
what is it
word root
what happens as a result
inability to accurately judge speed (of movement), force (of movement), or distance needed for task
“difficulty” + “measurement”
miss the target, too much force, too little force, cannot grade the amount of force needed for the task
Asynergia/Dysnergia
what is it
movement decomposition
lack movement fluidity
parts of the body working together in a particular/effective way to accomplish a task in synergy
motor planning that needs cerebellum to function normally is not occurring
movement is fractionated
decomposition: movement is less fluid, more robotic, less smooth movement. broken into short static components, because amount of control to make it fluid is gone and the nervous system reconstructs the movement to accomplish the task
Rebound Phenomena
- instructions
- normal result
- abnormal result
hold arm out in front of you
do not let me push you down
when PT removes hand, pt should have only one upswing–but in a cerebellar issue it swings around
Tremor
what is cerebellar tremor due to?
why is cerebellar tremor different than PD tremor?
cerebellar tremor is due to not maintaining stable tone
-need equal and opposite tone of flexors and extensors, adductors and abductors, agonists and antagonists
different from tremor seen in PD that is due to almost the opposite
Hypotonia
amount of tone that normally goes through the arm is lower rather than higher
Signs of Cerebellar Dysfunction (6)
findings
- findings usually ipsi-lateral (different than the contra-lateral in stroke or spinal cord lesion)
- ataxic gait: wide BOS, tremor and shaking
- dysarthria: cerebellar speech
—-need motor control of mouth/lips/tongue/ lower jaw/ and soft palate
—-sounds myffy
if diaphragm involved, not able to control pitch and volume - Nystagmus: rapid involuntary beating of eye in specific direction (direction indicates location of lesion) and impaired extra-occular movements
- loss of motor learning: feet forward loss, makes therapy difficult
- inability to learn from movement errors-may be aware made error but cannot correct it
are cerebellar dysfunctions contralateral or ipsilateral?
ipsilateral
What type of gait from cerebellar dysfunction?
- ataxic gait: wide BOS, tremor and shaking
dysarthria
what is it
cerebellar speech
—-need motor control of mouth/lips/tongue/ lower jaw/ and soft palate
—-sounds myffy
if diaphragm involved, not able to control pitch and volume
Nystagmus
apid involuntary beating of eye in specific direction (direction indicates location of lesion) and impaired extra-occular movements
What aspect of cerebellar dysfunciton makes PT difficult?
loss of motor learning: feet forward loss, makes therapy difficult
ataxia
lack of order (in their movements), better to say nystagmus, rebound, tremor, dysmetria etc because ataxia can be about a lot of things
coordination assessment
Dysmetria: Finger Nose Finger
Disdiachokinesia: difficulty in moving in two opposite directions
eye movements
part of vestibular exam
VOR1, VOR2
Tracking, sacaads
Dysmetria Assessment
Finger nose Finger
patient touches your finger and then your nose
different ranges, speeds, locations: i move my finger side to side/across midline/ speeds range/ location
note accuracy under different conditions (more than speed)
heel to shin test: slide heel of one foot across the shin of the other leg (may be too weak to do that, and get a false positive)
do not mistake weakness, spasticity, sensory loss for dysmetria!
Not Cerebellar findings, do not make this mistake!
- -LMN lesion in arm is a weakness
- -spasticity: cannot do the full movements
- -visual loss
- -sensory loss
what may be mistaken for dysmetria?
do not mistake weakness, spasticity, sensory loss for dysmetria!
Which are cerebellar findings?
- -LMN lesion in arm is a weakness
- -spasticity: cannot do the full movements
- -visual loss
- -sensory loss
Not Cerebellar findings, do not make this mistake!
Disdiadochokinesia
- what is it
- how is it tested
- what mistakes made
- what needs this
- False positive
1) “difficulty” “two”
difficulty moving in two opposite directions
two opposite movements, rapid and alternating movements
tested at different speeds
rapid and alternating movements
hands or feet
2) sit with hands on knees with palms up switch to palms down now as fast as you can–provocative, fast
can also do heel-toe: alternate heel/toe touching the ground
3) do not mistake weakness, spasticity, contracture, or sensation for a positive test result
4) what needs it:
1. all functional movements require combinations: flexors/extensors, IR/ER, AD/ABductors
- lengthening, shortening, correct force, correct timing, correct speed (accelerate, deccelerate), correct “choice”
- speaking requires rapid alternating movements: tongue and lips in rapid speech and therapists test for this
5) false positive: spasticity, contracture, sensory loss, visually dominant (cannot do it with eyes closed)
Mistaken test result for disdiadochokinesia
do not mistake weakness, spasticity, contracture, or sensation for a positive test result
alse positive: spasticity, contracture, sensory loss, visually dominant (cannot do it with eyes closed)
when is disdiadochokinesia relevant that we need it fore
- all functional movements require combinations: flexors/extensors, IR/ER, AD/ABductors
- lengthening, shortening, correct force, correct timing, correct speed (accelerate, deccelerate), correct “choice”
- speaking requires rapid alternating movements: tongue and lips in rapid speech and therapists test for this
Testing on practical (4)
Dysmetria: Finger Nose Finger or
heel to shin test: slide heel of one foot across the shin of the other leg (may be too weak to do that, and get a false positive)
Disdiachokinesia: difficulty in moving in two opposite directions
finger-nose-finger:
patient touches your finger and then your nose
different ranges, speeds, locations: i move my finger side to side/across midline/ speeds range/ location. note accuracy under different conditions (more than speed)
do not mistake weakness, spasticity, sensory loss for dysmetria!
rebounding: hold arm straight, ability to maintain tone because firing of muscles is equal and opposite on all sides maintaining muscle tone
Cranial Nerves
Motor or Sensory?
Peripheral or Central?
peripheral nerves mediate motor and sensory function
transmit impulses to the CNS–not purely peripheral structures because have central component
Sensory Motor and reflex functions
Cranial Nerve lesion abnormalities:
where can they be (4)
lesion at any of these areas can qualify as cranial nerve abnormality
- Nerves
- Nucleus
- Pathways to/from cortex, diencephalon, cerebellum,
- brainstem
- receptor (muscle, reflex, etc)
Effects of Cranial Nerve Lesion
Nagi model application
examine the impairment, functional limitation, and disability level
ie vestibulochochlear nerve lesion
- impair: nystagmus and vertigo
- functional limitation: disequilibrium
- disability: cannot work
Olfactory Nerve
- seonsory or motor
- why is it unique
- where do olfactory tracts project to location and lobe
only sensory afferent impulses of sense of smell
only sensory modality with direct access to cerebral cortex without going through the thalamus (relay station for senses)
the olfactory tracts project mainly to the UNCUS of the TEMPORAL LOBE (near hippocampus)
–projections to hippocampus suggests role in memory
CN1 Lesion
name 2 pathologies
disable?
classical pathology: olfactory groove meningioma
basal skull fractures another potential cause (unilateral or bilateral)
can be part of a larger pathology
not disabling but can affect QOL
CN1 Testing
what is more important in smell?
what is used in testing?
how is it done?
detection of the smell is more important than the actual identification
the non-noxious odors are used in tests
noxious odors may be used in sensory stimulation
test unilaterally and bilaterally
CN1 Pathology
loss of ____
Anosmia: loss of smell (unilateral vs bilateral)
- sudden loss: infarct, trauma
- gradual loss: tumor
olfactory hallucinations: associated with seizure disorders (auro smell often before seeizure comes) or limbic system lesion
CN2
- sensory or motor
- pathway
Optic Nerve
arise from RETINA of the eye
optic nerves pass through the optic CANALS and converge at the optic CHIASM
they continue to the THALAMUS where they synapse
from there optic RADIATION FIBERS run to the visual cortex in the occipital lobe
functions solely by carrying SENSORY afferent impulses for vision to the occipital lobe
Function of CN2 (4)
acuity: central vision (focus on something directly)
fields: peripheral vision
pupillary dilation and contraction (light reflex)
accommodation reflex [eyes converge together to focus on moving subject nearer or farther]
CN2 Lesion
monocular blindness: associated with optic neuritis of Multiple Sclerosis
Bitemporal hemionopsia: loss of vision in temporal fields, associated with pituitary tumors
Homonymous Hemianopsia: loss of vision in temporal fields of one eye and nasal fields of the other. Associated with optic tract lesions-CVA
Homonymous Quadrantanopsia: defect in SAME quadrant of each eye (such as left and right superior temporal)
Bitemporal hemionopsia:
casue
loss of vision in temporal fields
associated with pituitary tumors
Homonymous Hemianopsia:
cause
loss of vision in temporal fields of one eye and nasal fields of the other.
Associated with optic tract lesions-CVA
Homonymous Quadrantanopsia:
case
defect in SAME quadrant of each eye (such as left and right superior temporal)
upper: temporal lobe lesion
lower: parietal lobe lesion
visual confronting testing
patient covers one eye, looks at examiners nose
examiner brings fingers from behind patients eyes in all four quadrants
patient should signal awareness of object a few cm past the plane of their eyes
(ie R eye: right side move finger, left side move finger covering left eye)
record normal vs restricted in each quadrant for each eye
CNII and CNIII Pupillary Light Reflex
stimulus
direct reflex
consensual reflex
document as
stimulus: penlight into eye
Direct Reflex: constriction in primary eye (shining light into)
Consensual reflex: constriction in opposite eye
Document as present, absent, diminished
Pupillary light reflex interpretation
Sensory input: CNII afferent impulses from retina
Motor output: CNIII oculomotor nerve
stimulate R eye and neither pupil constricts
stimulate L eye and both pupils constrict
problem:
Sensory input: CNII afferent impulses from retina
or
RIGHT retina
stimulate R eye and right pupil does not constrict but left does
stimulate L eye and right pupil does not constrict left pupil does
Right occulomotor nerve
Motor output: CNIII oculomotor nerve
sensory paths in are intact but motor response impaired
stimulate R eye and right pupil constricts but left does not
stimulate L eye and right pupil constricts but left does not
problem with occulomotor nerve
or
left retina
CNII Accommodation
bring object 1-2 feet away from patients face towards nose as patient stares at object
NORMAL: constriction and convergence of both eyes
ABNORMAL: lack of constriction and/or convergence of both eyes
Pupillary light reflex documentation
PERLA: pupils equal, round, light reactive, accommodating
Anisocoria : unequal pupil diameter
Argyll Robertson Pupil: pupil small and doesnt react to light but accommodates
Fixed pupil: non reactive to light, or accommodating
Anisocoria
unequal pupil diameter (on pupil wider)
Argyll Robertson Pupil:
pupil small and doesnt react to light but accomodates
Fixed pupil:
non reactive to light, or accommodating (brainstem damage or damage to CN 2 or 3)
CN 3, 4, 6
occulomotor
trochlear
abducens
pursuit: slow eye movements used to maintain vision on moving target
H test
H TEST
inferior oblique(3) _________________superior rectus(3)
medial rectus(3) _____________________lateral rectus (5)
superior oblique(4)_________________inferior rectus (3)
Testing Pursuit
test unilaterally and bilaterally
follow my finger
common complaints: diplopia, blurred vision, unequal tracking
document areas of mac and minimal diplopia
EOMI-extra ocular muscles intact
Saccades
rapid movement of the eye from one point of fixation to another
ie looking up from a page to someone walking accros the room with or without moving your head
Testing Saccades
instructions
what we look for (9)
patient seated
have patient look from one finger to another without moving head
test in all 4 planes to assess extraocular ms
note deviations in for each eye, each movement, smoothness, speed, do both eyes move at similar speeds, nystagmus, vertigo, diplopia, blurring
CN3
role
what innervates
role
Oculomotor nerve
responsible for 73% of eye movements
tested along with CN4 and CN6
TEst all movements in order:
SR: superior movement IR: inferior movement Medial Rectus: nasal movement Inferior oblique: superior nasal Levator palperbrae-open eyes wide (if not, ptosis)
Trochlear Nerve
superior oblique–inferior nasal motion
with lesion, eye cannot track past midline
consistent with midbrain lesion
CN 6
Abducens:
single function
lateral rectus: abduct they eye past midline
with lesion unable to move eye laterally past midline
common injury due to length of nerve and increased susceptibility to ICP
(teach to move head and body to see)
EOM
extra ocular movement intact
strabismus
weakness/paralysis of the EOM (extra ocular movement)
Lateral Strabismus
wall eyed. loss of medial rectus
Medial Strabismus
cross eyed, loss of lateral rectus
Hypertropia
eyes turned upward, loss of downward gaze
Hypotropia
eyes turned downwards, loss of upward gaze
CN5
trigeminal nerve
primary sensory, some motor
3 sensory to face from pons
- optic (sensory)
- maxillary (sensory)
- mandibular (sensory and motor)-muscles of mastication
Trigeminal Neuralgia
Trigeminal Neuralgia
also called tic douloureux, the trigeminal nerve’s function is disrupted.
dental, MS, brainstem nucleus of trigeminal nerve, or ideopathic
pain
Testing CN7
squeeze eyes shut-obicularis oris
zygomaticus: smile wide
frontalis: wrinkle forehead
frown
purse lips
Grimace: tighten neck
Facial Nerve Lesions
CN7
central corticobulbar droop of lower contralateral face
peripheral droop of entire ipsilateral face
CN7
role
motor: muscles of facial expression
sensory-to stapes, hyperaccusis
taste: anterior 2/3 of tongue
tearing, unilateral
2 types of bells pasley
PNS lesion: ipsilateral droop of full side of face
CNS facial droop: lower contralateral face
CN 8
vestibulocochlear nerve
vestibular component-balance, stable eye and head poisiton
cochlear component: hearing
Vestibular Ocular Reflex
VOR
primary output of vestibular nerve
allows eyes to track a moving object regardless of head position or movement
deficits can be peripheral or central
Testing VOR
- patient sitting
- examiner places finger arms length from patients eyes
- patient moves head from side to side keeping eyes focused on a finger
- test vertically and horizontally, diagonally, in different positions
VOR1: person moves head, object stable
VOR2 testing: finger moves in opposite directions to head movement
Abnormal VOR findings
- loss of focus
- nystagmus
- vertigo
- imbalance
- disequilibrium
- nausea
Nystagmus
oscillating eye movement
slow phase and fast phase, named for FAST phase
Torsional and linear components
Type of nystagmus can be diagnostic
Hallpike Dix +
To complete the test, the patient is brought back to the seated position, and the eyes are examined again to see if reversal occurs
Vertigo
Hallucination of movement
usually spinning, can be jumping, telescoping, pulsing
vertigo is NOT dizziness
differentiate from lightheadedness (hypotension)
Central vs Peripheral Vestibular Findings
Central Lesion in pons, cerebellum, parietal cortex
-MS parietal, cerebellum, or brainstem strokes, TBI, tumor
Peripheral Lesion of the nerve itself or supporting structures
-BPPV, vestibular neuritis, labyrinthis, meniers, otoxicity, accoustic neuroma
Central vs Peripheral Vestibular Nystagmus
Central: Nystagmus Direction changes Rotary or linear nystagmus and not both nystagmus can be seperate from vertigo unable to suppress with fixation
Peripheral unidirectional nystagmus rotary AND linear components nystagmus nystagmus matches with vertigo suppresses with fixation
BPPV: Benign Paroxysmal Positional Vertigo
calcium carbonate crystals (autoconia) in SEMICIRCULAR CANALS
most common vestibular complaint
tx relatively simple
dx with hallpike dix test
Hallpike Dix Manouver
- pt in long sitting
- look up and over LEFT shoulder
- brought rapidly into head hanging position, neck extended about 20 degrees
- wait 20-60 seconds for nystagmus (torsional/horizontal)
- nystagmus clears
- return to sitting position
- reversal of nystagmus
CNIX, CNX
glossopharyngeal (9) and vagus (10)
posterior 1/3 of tongue
gag reflex
all parasympathetic
recurrent laryngeal nerve to vocal cords
Test CN9 and 10
Dysphagia: difficulty swallowing
Dysphonia: hoarseness or quietness of voice
Absent gag reflex
deviation of soft palate to normal side (CN IX and X are damaged on one side (not uncommon), stimulation of the normal side elicits only a unilateral response, with deviation of the soft palate to that side; no consensual response is seen. Touching the damaged side produces no response at all.)
CN11
Spinal Accessory
trapezius: shrug shoulders
SCM: rotate head to left and right
CN 12
hypoglossal
motor to tongue
CENTRAL lesion-tongue deviation away from side of lesion without atrophy of fibrillations
PERIPHERAL Lesions: tongue deviate toward side of lesion with atrophy and fibrillations
component of dysphagia (difficulty with swallowing. )and dysarthria (inability to speak clearly due to problems with control of the motor apparatus of speech)