Anatomy: Exam 1, Case Study 2

- The basal ganglia are a cluster or nuclei deeply embedded in each hemisphere.

- There are 3 major components: caudate nucleus, putamen and Globus pallidus .

- There is also a functional connection with substantia and the subthalamic nucleus.

- Plays an essential role in the control of movement. Organise highly learned/autonomic movements.

1) Corpus Striatum:

- Consists of the caudate nucleus and putamen.

- Collectively located in the medial aspect of each hemisphere

- Partially separated by anterior limb of internal capsule.

2) Lentiform nucleus:

- Consists of putamen and Globus pallidus and they lie close together.

- separated by a thin, lateral medullary laminar

Aim: take away inhibition on thalamus

1) Motor cortex excites the striatum which synapses with an inhibitory neuron of GPm . The GPm is inhibited as the inhibitory neurons of G.P become more active.

2) When the GPm is inhibited by striatal neurons , activity is turned down --> it can't inhibit thalamus as it normally would --> Thalamus becomes more active --> sends excitatory neurons to the motor cortex which becomes more active --> sends excitatory messages to the muscles we want to move

The substantia nigra sends dopamine neurons to synapse with D1 receptors of the inhibitory neurons of the striatum going to the GPm which causes more inhibition of GPm = less activity = thalamus even more excited.

Aim: stop movements. GPl keeps thalamus on a

leash'

1) Message gets sent from motor cortex --> striatum and excites the striatum --> excites inhibitory neurons going to GPl --> inhibitory neurons turn down activity in GPl.

2) Because activity is turned down in GPl, it can't talk to the sub thalamus as much --> sub thalamus gets more excited --> sends excitatory message to GPm.

3) Exciting the GPm leads to 'leash' tightening = neurons will inhibit thalamus --> less 'chatting' with cortex --> no/less muscle movement.

- Loss of dopamine neurons in the substantia nigra, decreasing the amount of dopamine used as a neurotransmitter.

1) In idiopathic form dopamine depletion results from degeneration of the nigrostriatal pathway.

2) Dopamine is usually excitatory to the direct pathway and inhibitory to the indirect pathway. Decreased muscle movements due to the fact that they can't initiate more movement in direct pathway and can't prevent excessive reduction of movement in indirect pathway.

1) Resting tremor: often begins in a finger or hand, can be subtle at first. It is involuntary at rest and stops when not at rest. Shaking is caused by muscle relaxation/contraction.

2) Rigidity: Stiff muscles when bending. Loss of smooth movements, become more 'jerky'. Become 'stooped' in posture and can lose ability for facial expression as facial muscles become rigid.

3) Bradykinesia/ slowess of movement: weakness/fatigue. Slowness in initiating movement and difficulty in sudden, unexpected stopping of movement. Change the way they walk, begin to shuffle.

4) Postural instability: Postural reflexes stop working. Become unbalanced on their feet, gets worse and can lose ability to walk.

5) ANS involvement: sweating, salivation, hypotension, temperature regulation.

- Smooth, coordinated, skillful movement

- influences voluntary and automatic response

- Affects flocculonodular lobe

- Difficulty/ inability to maintain a steady posture of trunk, off balance, walks on a wide base.

- Can't fix eyes on target, involuntary rapid eye movement

- Succeeding components of a complex movement occur separately instead of being blended into a smooth action

- Movements are intermittent/jerky

- Rapidly alternating movements are performed slowly/ in a clumsy manner

- hypotonia (floppy) + muscles tire easily

- Rhythmic back-and-forth movement of a finger that worsens as the target is approached with over correction

- Over and under reaching, unable to touch a target the first time

** Can also affect motor skills such as chewing/swallowing and speech can be slow/slurred with varying loudness