Basil Ganglia

Question 1

The basil ganglia (BG) has 2 definitions:

Answer 1

1. the deep grey matter structures that develop from the embryological division – telencephalon.
2. a systems definition and is defined by a series of grey matter structures that are interconnected and serve a common function.

Question 2

What are the 3 devisions of the corpus striatium?

Answer 2

1. caudate nucleus (striatum)
2. putamen (striatum)
3. globus pallidus

Question 3

What divides the two nucleus of the striatum (caudate nucleus & globus pallidus)?

Answer 3

anterior limb of the internal capsule

Question 4

What are the 3 parts of the caudate nucleus?

Answer 4

head, body and tail

Question 5

What are the two divisions of the globus pallidus (GP) or pallidum?

Answer 5

external (GPe - lateral)
internal (GPi - medial)

seperated by internal medullary lamina

Question 6

What does the amygdaloid nuclear complex develop from?

Answer 6

telencephalon

BUT functionally, associated with the limbic system

Question 7

What are 4 additional structures related to BG?

Answer 7

1. subthalamic nucleus (ST nuc.)
2. Substantia nigra (SN): 2 parts
3. Thalamic nuclei
4. Pedunculopontine nucleus

Question 8

What are the two parts of the substantia nigra?

Answer 8

1. zona or pars compacta (SNc) = dopamine neurons with black pigment, neuromelanin
2. zona or pars reticulata (SNr) = GABA neurons, no neuromelanin it is functionally similar to the medial GP (GPi)

Question 9

Thalamic nuclei of the BG are:

Answer 9

VA, VL, DM, CM

Question 10

What is the pedunculopontine nucleus?

Answer 10

• reticular formation nucleus that sets up a rhythmic cholinergic input to the striatum.
• plays a role in the coordination of synergistic movement

Question 11

Lenticular nucleus =

Answer 11

name given to GP + putamen

Question 12

Claustrum =

Answer 12

bounded by external and extreme capsules

Question 13

What is the basic schema of the BG?

Answer 13

It is a collection of sub-cortical (suprasegmental) masses of gray matter that serve to modulate cortical control of motor function, cognition and motivation

Question 14

New research suggest that basal ganglia pathways form several circuits or loops that start in widespread areas of cortex and end where?

Answer 14

in more circumscribed parts of motor cortex, limbic cortex or frontal lobe association cortex.
* these circuits have number of effects on motor control and cognition

Question 15

From a functional point of view, the BG (and related nuclei) have been divided into a dorsal and ventral striatum. The dorsal consists of:
The ventral striatum consists of:

Answer 15

The dorsal consists of: pathways involving the caudate and putamen. The caudate is involved more with cognitive processing, while the putamen is involved more with sensorimotor processing.
The ventral striatum consists of: a preferential involvement with the limbic system and emotion.

Question 16

The dorsal striatum has 4 afferent pathways:

Answer 16

1. Widespread cortex (glutemate) projects to striatum; smaller inputs to SNr and ST nuc
2. Intralaminar nucleus of thalamus (centromedian thalamic nucleus; CM) projects to striatum
3. Serotonin-containing fibers from raphe nuclei of RF to all parts of basal ganglia
4. Acetylcholine-containing fibers from pedunculopontine nuc. of RF to SNr and GP [This was one of those “extra” reticular formation nuclei)

Question 17

The dorsal striatum has 3 interconnections: Direct and indirect pathway.
Direct =
Indirect =
third?

Answer 17

1. direct = extensive interconnections that can be categorized as direct or main circuit
2. indirect = or auxilary circuit and
3. = nigro-striatal-nigral pathway

Question 18

How does the direct circuit travel?

Answer 18

from widespread areas of cortex (Glutamate) –> striatum –> (GABA and substance P) –> GPi and SNr (GABA) –> thalamic nuclei (glutamate) –> frontal lobe cortex

Question 19

How does the indirect circuit travel?

Answer 19

from widespread areas of cortex –> striatum –> GPe (GABA) –> subthalamic nuc. (glutamate) –> SNr and GPi (GABA) –> thalamic nuclei –> frontal lobe cortex

Question 20

Nigrostriatal pathway =

Answer 20

dopamine containing fibers from SNc to striatum and GABA fibers from striatum back to SNc

Question 21

Are there direct outputs from the BG?

Answer 21

efferents - No direct output of BG to brainstem or spinal cord lower motor neurons

Question 22

Describe the major efferents of the BG

Answer 22

Major efferents are from GPi (largest number) and SNr to the VA and VL (motor function), DM (cognitive function) and CM of the thalamus.

Question 23

Subsequently relayed to frontal lobe cortex, supplementary motor cortices (cerebellar connections running through the thalamus end primarily in lateral premotor cortex), as part of the direct and indirect circuits; fiber bundles connect to what?

Answer 23

connect to GPi to the thalamus

Question 24

Other efferents of the BG include:

Answer 24

SNr to tectum (modalities tectospinal path) and GPe to the pedunculopontine nuc. (RF nucleus)

Question 25

What is the primary underlying function of the basal ganglia?

Answer 25

“disinhibition” (inhibition of a toncially active inhibitory pathway; an inhibitory neuron inhibiting a tonically active inhibitory neuron)

Question 26

How is the disinhibition of the BG accomplished?

Answer 26

Through a balance of signals from the direct and indirect loops converging on the output nuceli, GPi and SNr.

*Groups of cells in the GPi are strongly linked to remembered motor tasks coupling them to an internally generated initiation of movement.

Question 27

Is the initiation from sensory cued stimuli?

Answer 27

NO, the initiation is not from sensory cued stimuli such as vision or proprioception.

Question 28

Some groups of GPi cells are associated with specific phases of complex movements, active only during a portion (single joint) of a complex activity, while others, what?

Answer 28

while other groups of cells are active throughout the entire sequence of the movement, programming sequential multi-joint activity.

Question 29

What are cells of the GP controlled by?

Answer 29

The cells of the GP are spontaneously active and are controlled by cortical or nigral activation of the relatively quiet striatal cells (caudate and putamen)

Question 30

Cellular activity and abnormal movement and posture noted following changes (lesions in basal ganglia) in this circuitry demonstrate what?

Answer 30

the importance in the control of movement and posture. This is achieved by coupling BG activity to areas of the cortex that are involved in planning and execution of motor activity.

Question 31

What is a second proposed function?

Answer 31

Noted in procedural learning of motor activity.
Procedural learning is different from declarative (facts) learning. Procedural memory is more task oriented, i.e., the ability to learn and replicate automatic motor skills. Alzheimer’s patients can learn new motor tasks, but not new facts.

Question 32

Recent evidence suggests that BG are also involved in cognitive function, such that:

Answer 32

the head of the caudate nucleus receives a large projection from frontal lobe association cortex and projects back to the same cortical area via VA and DM thalamic nuclei.
** The putamen is primarily a motor function nucleus and functions more in habit formation and procedural or implicit memory.

Question 33

What is the blood supply of the BG?

Answer 33

from Striatal or Ganglionic arteries, small deeply penetrating branches of Circle of Willis, They supply the bulk of caudate nuc., anterior globus pallidus, putamen and internal capsule. A specific branch, the Thalamo-geniculate branch of posterior cerebral artery supplies the subthalamic nucleus (plus thalamus and adjacent posterior limb of internal capsule).

Question 34

Diffuse disease of the CNS with multiple sites of damage (e.g. encephalitis and cerebral palsy) produce a variety of dyskinesias (disorders of movement) making localization of lesions difficult. However, the idea that individual components of the BG and related motor areas do have certain distinct functions is based on observations of 2 types of dyskinesias:

Answer 34

1. hyperkinetic

2. hypokinetic in nature

Question 35

List 3 hyperkinetic disorders:

Answer 35

1. athetoses
2. choreas
3. ballismus

Question 36

athetoses =

Answer 36

involuntary, ceaseless, slow, writhing movements (like an “oriental dancer”), often seen in cerebral palsy. Lesion location is unclear but probably involves striatum.

Question 37

choreas =

Answer 37

• involuntary, jerking, dancing, grimacing movements of varying duration and latency - frequently appear “purposive”. Lesions are typically in striatum or VL of thalamus. When not moving, patients’ muscles exhibit hypotonia.

Question 38

Ballismus =

Answer 38

• violent flinging movements due to involuntary contractions, esp. of proximal limp muscles; usually on one side only = hemiballism. Caused by localized lesion of subthalamic nucleus contralateral to affected limb. WHY is it contralateral???

Question 39

In hypokinetic disorders, the lesion is usually in the striatum and SN; primary example is parkinsonism. Describe PD:

Answer 39

caused by degeneration of nigrostriatal neurons that use dopamine as their neurotransmitter. Deficit may be worse on one side than the other in which case dopamine loss is greater on the side contralateral to the worst deficits.

Question 40

Hypothesized mechanism of hyperkinesias =

Answer 40

best interpretation from clinical observations and primate research: the basal ganglia normally have an inhibitory influence on upper motor neurons through the indirect circuit and an excitatory influence through the direct circuit. Lesions of the subthalamic nucleus would cut the indirect circuit and permit the direct circuit to drive movements unopposed. The explanation for choreas and athetoses is still unknown but may involve selective loss of striatal GABA neurons that normally inhibit motor activity

Question 41

Hypothesized mechanism of hypokinesia with rigidity =

Answer 41

Current hypothesis is that dopamine normally enhances the direct (excitatory) circuit and inhibits the indirect (inhibitory) circuit. Loss of SNc dopaminergic neurons results in a much reduced ability of the cortex to initiate movement through the activation of cortical upper motor neurons. Loss of control over upper motor neurons results in loss of voluntary control of alpha lower motor neurons (akinesia) and decreased inhibition of the gamma loop reflex (rigidity).