Neuro 62: Basal Ganglia

Question 1

How do the basal ganglia affect mvmnt?

Answer 1

• play a role in starting mvmnt, not active during rest
• enhance cortical motor activity
• FACILITATE mvmnt –> provide a boost, since the UMN activity in the cortical motor areas is not enough to cause mvmnt
• involved in positive feedback loop with cortical motor areas
• use both excitation and inhibition in pathways

Question 2

Extrapyramidal

Answer 2

-another term for the corticospinal tract

Question 3

5 components of the basal ganglia & locations

Answer 3

1. caudate
   - cerebral hemisphere
2. putamen
   - cerebral hemisphere
3. globus pallidus- has 2 parts = internal (GPi) and external (GPe)
   - cerebral hemisphere
4. substantia nigra- has 2 parts = pars compacta and pars reticulata
   - midbrain
5. subthalamic nucleus
   - midbrain

Question 4

The 2 different pathways of the BG

Answer 4

1. Motor
2. Association/cognitive loop
   - both pthwys have similar organization & utilize parallel circuits
   - why parkinsons and huntington pts can have cognitive and emotional deficits

Question 5

Role of subthalamic nucleus (STN)

Answer 5

-STN neurons have excitatory (glutamatergic) synapses on the GPi

Question 6

Role of substantia nigra

Answer 6

• pars compacta (SNc) = dopaminergic part

- releases dopamine which will bind to D1 and D2 receptors in the putamen

Question 7

Dopamine receptors in the putamen

Answer 7

• D1 = excited by dopamine via opening of Na channels –> depolarization and excitation
• D2 = inhibited by dopamine via K+ channels opening
• so dopamine turns the “accelerator” on and the “brakes” off and causes the VL to be active = +cortex

Question 8

Tonic activity in the BG

Answer 8

• many components in the pathway are tonically active = activity is normally ON
• the circuit can influence cortical motor areas even when there is no input to the putamen
• so when there is damage to any component of the pathway the system does not turn off, it just gets out of control

Question 9

Excitatory NTs

Answer 9

1. Ach
2. glutamate
3. dopamine

Question 10

Inhibitory NTs

Answer 10

1. GABA

2. dopamine

Question 11

Parkinson’s disease

Answer 11

• loss of substantia nigra’s dopamine effects:
  1. direct pathway = less activity of D1 receptors –> GP1 more active –> VL less active –> decrease in voluntary mvmnt = bradykinesia/akineasia
  2. Indirect pathway = more activity of GPi –> less VL activity –> decrease in voluntary mvmnt = bradykineasia/akineasia
• *get abnormal rhythmic activity in basal ganglia neurons = tremor that decreases during voluntary mvmnt and increases with stress

Question 12

Effect of too little dopamine

Answer 12

• decrease in accelerator pathway & increase in break pthwy –> decrease mvmnt

Question 13

Effect of too much dopamine

Answer 13

• increase in accelerator & decrease in break –> spontaneous mvmnt
• caused by too much meds

Question 14

Role of Ach

Answer 14

• Ach and dopamine have antagonistic effects in the BG circuit
• when there is a loss of dopamine the release of Ach increases –> this worsens the effects of the dopamine loss
• balance of Ach and dopamine can be corrected through the use of anticholinergics

Question 15

Huntington disease

Answer 15

• D2 receptors degenerate –> decrease in STN activity –> decreases GPi activity –> increase in VL activity –> increase in motor cortex excitability = spontaneous mvmnt
• autosomal dominant
• sx usually appear in adulthood

Question 16

4 Sx of Basal ganglia dysfunction

Answer 16

1. involuntary mvmnts
2. decreased overall mvmnt
3. changes in posture and muscle tone
4. changes in mood - b/c of interaction btwn BG and cortical association areas

Question 17

Dyskinesias

Answer 17

-abnormal mvmnts

Question 18

Hemiballismus

Answer 18

• flailing mvmnts of one or both limbs

- type of dyskinesia

Question 19

Chorea

Answer 19

• involuntary, jerky mvmnts of face, body, or extremities

- type of dyskinesia

Question 20

Dystonia

Answer 20

• prolonged contractions of axial or extremity muscles, affects posture
• type of dyskinesia

Question 21

Athetosis

Answer 21

• slow, twisting mvmnts of distal extremities

- type of dyskinesia

Question 22

Resting tremor

Answer 22

• involuntary tremor that is not associated with voluntary mvmnt
• can be a sx of BG disease

Question 23

Hypokinesia

Answer 23

• decreased mvmnt

- can be a sx of BG disease

Question 24

Bradykinesia

Answer 24

• slow mvmnt

- can be a sx of BG disease

Question 25

Rigidity

Answer 25

• increased muscle tone in both the extensors and flexors –> resistance to passive mvmnts in all directions (unlike spasticity) = “lead pipe” rigidity
• can have cogwheel rigidity too = “catch and give” b/c of underlying tremor

Question 26

Ballism

Answer 26

• BG disease
• cased by lesion in the STN –> increased VL activity –> + mvmnt
• sx: wld flailing mvmnts contralateral to the lesion

Question 27

Tardive dyskinesia

Answer 27

• lesion = dopamine and other receptors
• sx = facial chorea/athetosis
• usually caused by prolonged antipsychotic use which are D2 receptor blockers
• can be irreversible if not caught soon enough
• probably caused by D2 upregulation and supersensitivity
• affects the indirect circuit by lowering the inhib output of the putamen

Question 28

Tourette’s

Answer 28

• BG disease
• lesion site is unknown
• sx = motor and verbal tics

Question 29

Parkinson’s Sx

Answer 29

1. postural instability
2. autonomic dysfunction = drooling, sweating, orthostatic hypotension, urinary disturbance
3. psychiatric problems = depression, dementia

Question 30

4 Major tx for parkinson’s

Answer 30

1. increase dopamine effectivness via meds that:
   a. increase L-dopa
   b. decrease dopamine metabolism
2. pallidotomy = surgical lesion of the GPi
3. Deep brain stimulation
4. implanting dopamine secreting cells into the BG

Question 31

Pallidotomy

Answer 31

• parkinsons tx
• surgical lesion of the GPo
• reduces GPi’s inhibition of VL
• this is risky b/c the internal capsule is near by

Question 32

Deep brain stimulation

Answer 32

• parkinsons tx
• stimulator is placed into the STN or GP
• decreases the tremor via an unknown mechanism
• the bradykinesia will still be present and is treated with meds

Question 33

Wilson’s disease

Answer 33

• caused by deficit in copper metabolism that results in serum copper levels
• cause widspread changes throughout the body and nervous system
• effects caudate, putamen, cerebral cortex, and cerebellum –> sx: resting tremor, chorea, rigidity, hypokinesia, etc.

Question 34

CO intoxication

Answer 34

• the BG are sensitive to CO exposure

- CO destroys neurons in the putamen and globus pallidus