Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

22 Cards in this Set

  • Front
  • Back
Compare the structure of the cerebellum with that of the cerebrum in terms of its mass, number of neurons, and surface area.
*cerebellum has 1/10 the mass of the cerebrum
*cerebellum has the same number of neurons as the cerebrum
*due to extensive folding, cerebellum has 20 times the surface area of the cerebrum
What structures make up the spinocerebellum?
The vermis and the intermediate hemispheres.
Where does the spinocerebellum receive input from?
Spinal cord and muscle and joint afferent fibers.
Which of the cardinal symptoms is due to a lesion in the spinocerebellum?
What structures make up the cerebrocerebellum?
The lateral hemispheres.
Where does the cerebrocerebellum receive input from?
The primary motor and somatosensory cortices (as well as association areas in the cortex) send fibers that synapse in the pontine nuclei. Second order fibers decussate and enter the cerebellum through the contralateral middle cerebellar peduncle.
Which of the cardinal symptoms is caused a lesion in the cerebrocerebellum or any of its inputs or outputs?
Intention tremor.
What structures make up the vestibulocerebellum?
The flocculus and nodulus.
Where does the vestibulocerebellum receive input from? What effects will a lesion in this structure have?
*vestibular apparatus and nucleus
*vertigo and nystagmus
What kind of neurons make up most of the cerebellar cortex? Where do these neurons synapse? What kind of signals do they send?
Purkinje cells make up most of the cerebellar cortex. They synapse on the deep nuclei of the cerebellum, and provide inhibitory signals only.
Describe the two paths mossy fibers take.
*they can make excitatory synapses directly on the deep nuclei
*they can synapse on granule cells in the cortex which give rise to parallel fibers, each of which will synapse on hundreds of Purkinje cells
Where do climbing fibers arise from?
*inferior olivary nucleus
What are two paths that a climbing fiber may take into the cerebellum?
*it may make direct excitatory synapses on deep nuclei
*it may make a 1:1 synapse on a Purkinje cell which then makes an inhibitory synapse on the deep nuclei
How does output from the deep nuclei leave the cerebellum? To what two destinations does most of the output go?
*most leaves through the superior cerebellar peduncle (some leaves through the ICP)
*the majority synapses on either the red nucleus or the VL region of the thalamus
What are four cardinal signs of cerebellar damage? What other deficits give credence to the idea that the cerebellum is involved in higher functions?
4.Intention tremor
*deficits in non-declarative learning, language, and sequence learning
How is the cerebellum organized - ipsilaterally or contralaterally?
How is Friedrich's ataxia inherited? What neurons are affected in this disorder?
*autosomal recessive
*large diameter neurons in the dorsal root ganglia, as well as spinocerebellar and corticospinal tracts
When is the onset of Friedrich's ataxia? How long is average survival after onset of symptoms? What is the most common cause of death?
Onset is at puberty, and survival is thirty years. Cardiomyopathy is the most common cause of death.
What symptoms are seen in Friedrich's ataxia?
*progressive ataxia
*spasticity with decreased deep tendon reflexes
What is the molecular defect in Friedrich's ataxia?
There is an expansion of a GAA triplet in the gene that codes for frataxin. This adds glutamate residues and reduces the cell's ability to deal with oxidative stress.
How are spinocerebellar atrophies inherited? What cellular effects are seen?
They are usually autosomal dominant. There is loss of Purkinje cells and tissue in the brainstem and spinal cord.
What is the most common genetic defect seen in the spinocerebellar atrophies?
They are usually associated with ustable CAG triplets in one of several ataxin genes.