Cerebellar Pathways, Function, and Dysfunction Flashcards
Last 4 cards cover areas of the lecture we're not responsible for. Oops.
For the paravermis region of the spinocerebellum, name the: Inputs, deep nuclei, outputs, and functions.
Inputs: Spinal afferents
Deep nuclei: Interposed nuclei
Outputs: Lateral descending system
Function: Smoothing/correction of limb movement
For the vermis region of the spinocerebellum, name the: Inputs, deep nuclei, outputs, and functions
Inputs: Spinal afferents, and facial/visual/auditory/vestibular inputs
Deep nuclei: Fastigial nuclei.
Outputs: Medial descending systems
Function: Smoothing/correction of axial movements
What are the inputs to the corticopontine cerebellum (aka cerebrocerebellum)? Deep nuclei? Outputs?
Cortical afferents (Frontal pontine and POTpontine).
Dentate nuclei.
Sends info to motor and premotor cortex
What are the outputs of the vestibulocerebellum? Functions
Vestibulospinal, MLF (for eye movements)
Posture, balance, and coordination of head and eye movements.
Where do the two inputs to the cerebrocerebellum first synapse?
Where do their axons cross the midline?
Through which peduncle do they enter the cerebellum
Frontopontine and Parietal-Occipital-Temporal(POT)pontine fibers both synapse in the pontine nuclei.
They cross immediately in the crossing fibers of the pons.
They enter the cerebellum through the MCP.
Does ataxia involve weakness or involuntary movement?
Nope.
What will a midline cerebellar lesion lead to?
Truncal and proximal limb dysfunction.
What is titubation?
Aka. truncal ataxia. When person trying to sit still, trunk shakes all over due to lots of overcorrections to maintain posture (it’s like oversteering a car)
For our purposes dysmetria and intention tremor are the same… but what is the difference?
Dysmetria: Initiation of a complex movement is delayed, muscles at different joints are often desynchronized, pathy is erratic and jerky.
Intention tremor: oscillations from over-correcting for error when
What is dysdiadochokinesis?
Problems with rapidly alternating movements.
What is nystagmus?
Jerky eye movments,
“Gaze-evoked” nystagmus vs. “occular dysmetria”?
“Gaze evoked” when moving eyes horizontally. Occular dysmetria occurs when trying to fixate on still object. Eyes overshoot, then oscillate until obtaining fixation.
What is ataxic dysarthria? How do you test for it?
Disruption of metrical nature of speech. Can’t say “ka-ka-ka-ka-ka” etc. at constant rhythm or volume.
How much cerebellum function must you lose before you start having signs/symptoms? Is recovery rapid or slow?
“A large volume,” obviously, depending on the area. Recovery can be rapid.
Are isolated cerebellar symptoms common or uncommon? Why or why not?
Uncommon. Structures in brain stem are right nearby and share blood supply with the cerebellum.
How does tone change in cerebellar damage? (note acute vs. chronic effects)
Acute: transient hypotonia
Chronic: normal or hypotonia
If you have truncal or limb ataxia,. what part of the cerebellum might be damaged?
Midline cerebellar regions.
What parts of the body are affected when there’s damage to a cerebellar hemisphere?
Ipsilateral limb dysfunction.
Where is appendicular ataxia most evident?
Distal from the body, when the limb is fully extended away from the body.
Cerebellar lesions: ipsilateral or contralateral deficits?
ipsilateral, ipsilateral, ipsilateral
What kind of lesion might produce a contralateral ataxia?
Lesion in the pontine nuclei… theoretically, but since there are pretty much always crossing fibers there that have come over from the other side, that would more likely have bilateral effects.
How can sensory ataxia be distinguished clinically from cerebellar ataxia?
Sensory ataxia will have a positive Romberg sign. Additionally, would expect mechanoreception (esp vibration) to be impaired.
How can vestibular function be distinguished from cerebellar dysfunction?
Vertigo will occur in vestibular dysfunction… *I’m trying to resolve this contradiction with the previous lecture
How can pseudoataxia from corticospinal (UMN) disease be distinguished from cerebellar dysfunction?
UMN lesions will have UMN signs, such as hyperreflexia.
How can proximal muscle weakness (say in muscular dystrophy) be distinguished from cerebellar dysfunction?
Both will cause a wobbly gait, but cerebellum things don’t cause weakness.
What might a big mass in the midline cerebellum cause? (3 things)
Truncal titubations
Unsteady gait
Inability to do tandem (heel-to-toe) gait
A patient has lots of atrophy of the right cerebellar hemisphere. What might you expect to see? (3 things)
Abnormal rebound (when you push held out arm down)
Dysmetria of finger-to-nose
Dysdiadochokinesia
all on the right side
What causes “dysarthria-clumsy hand” syndrome?
Infarct of right SCA superior cerebellar artery.
(can also occur with right pontine a. infarct)
(this is probably too much detail…)
What structures in the cerebellum does the SCA supply? (5 things)
Superior areas… Fastigial, interposed, and (some of) dentate nuclei.
SCP, and MCP
(… this is definitely too much detail….)
What areas of the cerebellum does the AICA supply? (3 things)
Lateral regions of inferior surface…
flocculus, some of MCP, some of dentate nucleus
What areas of the cerebellum does the PICA supply? (1 structure…)
Medial inferior surface of cerebellum…
nodulus
