Chapter 19, Basal Ganglia (基底神經核)

Chapter 19, Basal Ganglia (基底神經核)
In Telencephalon In Telencephalon ((端,終腦)
Subcortical nuclei near the base of each hemisphere.
(1) Five major nuclei
(2) Circuitry (3) Movement disorders 1
Basal Ganglia in the Head
2
(I) Terminology of CNS in development
The end of the 4th week in embryo:
3 Primary brain vesicles
3
(菱形腦)
2
(中腦)
1
(前腦)
3
(II) Prosencephalon Telencephalon + Diencephalon
The 6th week: 5 Secondary brain vesicles
3
(後腦)
(延髓,末腦)
2
(中腦)
(間腦)
(端,終腦)
1
4
(III) Developmental Division of the Brain
Primary vesicle
1. Prosencephalon
(Cerebrum, 大腦)
Secondary vesicle
Telencephalon
Derivatives
Cerebral cortex
(Cerebral hemisphere) White matter
Basal ganglia
Diencephalon
Thalamus,
Hypothalamus
Subthalamus
Epithalamus
2. Mesencephalon
Mesencephalon
Midbrain
3. Rhombencephalon
(菱形腦)
Metencephalon
Cerebellum
Pons
Myelencephalon
Medulla oblongata
5
(IV) Human brain and animal brain
CNS=Brain +Spinal Cord
Brain= Cerebrum ((telen+dien
telen+dien))
+ Brain stem + Cerebellum
Brain of J. Nolte and
Brain of Rhinoceros
Human: 2~3%
Rhino: 0.05%
(brain/body weight)
6
(e) Basal ganglia in the brain
Left
side
Above
(19--5)
(19
Front
Behind
7
(A) Components of Basal Ganglia (BG)
★Five major nuclei
1. Caudate nucleus (尾核)
2. Putamen (外殼)
3. Globus pallidus (蒼白球)
4. Subthalamic nucleus (底丘腦)
5. Substantia nigra (黑質)
(伏核)
http://cnsvp.stanford.edu/atlas/basal_ganglia.html
BG functions:
‐‐Motor control
‐‐Cognition: learning
‐‐Emotion and motivation
http://3d‐brain.ki.se/atlas/window/ http://3d‐
pathways/3dBrain.html
8
(a)
(紋狀體)
(伏核)
Head, body, tail
--head bulges into anterior horn of
lateral ventricle (LV).
--head of caudate continues with
anterior part of putamen via
nucleus accumbens
(豆狀核)
LV
(19--3)
(19
http://www.neuroanatomy.ca/anima
tions/animations.html
9
The compact and reticular parts of SN
SNc: dopaminergic neurons
(19--6)
(19
10
Mesostriatal Dopamine System: Dopaminergic neurons of Substantia Nigra compacta project to the Caudate and Putamen
Dopamine pathways
11
Parkinson’s Disease (PD) (1817)
Disease of mesostriatal dopaminergic system
PD
Degeneration of the dopaminergic neurons in SNc
Damage is characterized by tremors or twitches
Normal
Midbrain
12
(b) Relations of Basal ganglia, thalamus & lateral ventricle ★
★
Basal ganglia is associated with the lateral ventricle. 13
(c) Basal ganglia and Lateral ventricle
Head of
caudate
Lateral
ventricle
Lentiform
nucleus
Amygdala
(杏仁核)
Hippocampus
(海馬)
14
(d) Ventricular
System
Caudal view
15
(e‐1) Putamen: approximately coextensive with insula (腦島). Insula
Horizontal
section
16
(f-1) Basal ganglia and surrounding structures: Extreme capsule;
Claustrum (帶狀核); External capsule; Internal capsule (內囊)
Claustrum:
Integration of motor, auditory, & visual information
(19--1)
(19
17
(f-2) Basal ganglia and surrounding structures
A
(19--2)
(19
18
(f-3) Basal ganglia and surrounding structures
Lateral medullary lamina: separate Putamen from Globus pallidus
Medial medullary lamina: separate external from internal segment (19--2)
(19
19
(f-4) Basal ganglia and thalamic nuclei
(19--2)
(19
20
(f-5) Parasagittal section showing striated striatum
(19--4)
(19
21
(B) Basal Ganglia Pathways +
+
—
+
—
—
+
Spinal Cord
Direct pathway
—
+
+
—
+: Excitatory
glutamate Indirect pathway
—: inhibitory
GABA
22
(a) Direct pathway Indirect pathway
+
Caudate —
Putamen
Thalamus GPi STN GPe GPi STN SNr (19--21)
(19
23
(a‐1) Basal Ganglia circuitry involves multiple parallel loops that modulate cortical output Principle inputs to and outputs from basal ganglia
Inputs (excitatory, green)
from cerebral cortex
caudate, putamen,
nucleus accumbens &
subthalamic nucleus (STN).
Outputs:
From globus pallidus
internal segment (GPi),
and SNr (inhibitory, red)
 thalamus cerebral
cortex
+
Caudate Thalamus Putamen
GPi STN SNr (19--7)
(19
24
3. Limbic areas 
N. accumbens (A)
(a‐2) Parallel loops through basal ganglia
2 1
C
A
P
3
1. Motor & somatosensory
cortices  putamen (P).
2. Association cortex  caudate (C).
C
VA
DM VL
A
GP
GP: globus pallidus
VP: ventral pallidum
A small extension of GP under the ant. commissure.
VP
SNc  to all areas of
caudate and putamen.
(19-8)
25
(a‐3) Cerebral cortex and SNc project to the striatum cerebral cortex
**1. Motor & somatosensory cortices  putamen (P).
 GP VA, VL motor areas: motor functions
2. Association cortex & prefrontal areas‐‐> caudate (C) 
GP DM prefrontal cortex: cognitive functions
3. Limbic areas (Limbic lobe cortex, hippocampus & amygdala)  nucleus accumbens (A) ventral pallidum (VP) DM limbic cortex: drive‐related behavior.
**SNc all areas of caudate & putamen GP thalamus
cortex
★Limbic lobe cortex= cingulate gyrus + isthmus + parahippocampal gyrus
26
★ Limbic lobe= cingulate gyrus + isthmus+ parahippocampal gyrus
27
(a‐4) Cerebral Cortex, Thalamus & SNc projects to the striatum Cerebral cortex, & Thalamus (Intralaminar
n., centromedian & parafascicular n.) the putamen, caudate, & N. accumbens  GPe, GPi, SNr, & SNc
SNccaudate & putamen
(VTAnucleus accumbens)
(a‐5) The Striatum Projects to Globus Pallidus (int. & ext. segments) & SN.
+
-
(19--9)
(19
28
(a‐6) Somatotopic representation of body parts on the left striatum from MRI scans
Medial veiw Lateral view
(19--10)
(19
29
(a‐7) Chemical compartmentalization of the striatum
AChE Enkephalin (腦啡) AChE
*: AChE
*: AChE‐‐free areas, free areas, striosomes
striosomes; Enkephalin in ; Enkephalin in striosomes
striosomes
(AChE= acetylcholinesterase)
(19--11)
(19
30
(a‐8) A case of bilateral damage to the caudate nucleus
(19--12)
(19
Pathology, BBB break
Pathology, BBB break‐‐
down of head of caudate
8 months later, the head of caudate disappeared
31
(b‐1) Major connections of GPe.
GPe distributes inhibitory signals within BG
Striatum, STN GPe
GPe GPi
Striatum STN
SNr
-
(19--13)
(19
32
(b‐2) Major Connections of GPi
Striatum, GPe, STN  GPi
GPi & SNr Provide the Output from BG
GPi
VA/VL, IL, DM, PPN (pedunculo‐
pontine nucleus)
SNr DM, PPN
(19--14)
(19
33
(b‐3) Efferents from GP
(19--15)
(19
GPe subthalamic nucleus & GPi.
GPi  lenticular fasciculus (豆狀束) & ansa lenticularis (豆狀環)join together
thalamic fasciculus to thalamic nuclei.
34
(c‐1) Subthalamic fasciculus STN
STN
(19--16)
(19
GPe GPi
35
(c‐2) Major connections of the subthalamic nucleus (STN)
Cortex, & GPe 
project to STN
STN  projects to GPe, GPi, and SNr
(19--17)
(19
36
(C) Blood supply of brain
(a) Areas of the cerebrum and cerebellum supplied by major arteries and their perforating branches, shown in coronal (A to C) and axial (D to F) sections. Ant. Post. cerebral a. 37
(b) Blood supply of basal ganglia by perforating branches of the anterior and middle cerebral arteries (Circle of Willis)
1. The medial
striate artery (MSA)= a branch of the anterior
cerebral artery. 2. Lenticulostriate
arteries, one of which is seen here (LSA)= branches of the middle
cerebral artery.
C, caudate nucleus; IC, internal capsule; LV, lateral ventricle; P, putamen
38
(D) Many Basal ganglia disorders result in abnormalities of movement
(a) Huntington’s disease
• Degeneration of neurons in the striatum, frontal and temporal cortices.
• Inherited disease (顯性遺傳疾病, 1/1000): Huntington gene
• Uncoordinated, jerky body movements and a decline in some mental abilities (cognitive and psychiatric). 39
(a‐1) MRI scans of a man with Huntington’s disease
Diseased
brain
Normal
brain
(19--18)
(19
Degeneration of caudate and putamen
40
(a‐2) Degeneration of the striatum in Huntington’s disease
Red: most degeneration
Blue: least degeneration
Ventral striatum
(19--18)
(19
41
(b) Hemiballismus (單側抽搐)
(19--19)
(19
A 65 year old HIV positive man developed unintentional forceful
flinging of his right arm and leg over several months. – MRI reveals a rim‐enhancing mass (abscess) in the subthalamic n.
‐‐Anti‐toxoplasmosis (弓漿蟲) treatment relieved the symptom. 42
(b‐1) Loss of excitatory subthalamic projections
+
-
(19--21)
(19
Disinhibit thalamus  a failure to suppress some cortical outputs
involuntary movements (hemiballismus)
43
(c) Parkinson’s Disease
1/800, 1/100 (>60 yr old)
‐‐Motor symptoms: tremor, rigidity... ‐‐Non‐motor symptoms: Disorders of mood, behavior, thinking, and sensation. Cause of primary symptoms of PD: ‐‐Degeneration of dopaminergic neurons in substantia nigra compacta.
‐‐Decreased stimulation of the motor cortex by the basal ganglia.
44
(c-1) Parkinson’s disease
Midbrain of a patient: Loss of pigmentation in SNc
(19--20)
(19
DSCP: decussation of superior
cerebellar peduncle
45
(B) Basal Ganglia Pathways +
+
—
+
—
—
+
Spinal Cord
Direct pathway
—
+
+
—
+: Excitatory
glutamate Indirect pathway
—: inhibitory
GABA
46
(c‐2) Striatal neurons of direct and indirect pathways have different dopamine receptors
Direct:
Excitatory receptor (1)
increase suppressing GPi (2)inhibit output of GPi (3)
+
-
(19--21)
(19
Thalamus Indirect:
Inhibitory receptor (4)
increase inhibitory output of GPe to STN (5)decrease excitatory output of STN (6)  inhibit output of GPi (3)
*Dopamine facilitates
movement.
47
(c‐3) Parkinson’s disease: loss of dopamine neurons
Direct: Decreased excitatory DA (1)
decrease inhibitory input to GPi (2)  increase output of GPi (3)
+
-
Indirect:
Decreased Inhibitory DA (4)
Thalamus decrease inhibitory output of GPe to STN (5) increase excitatory output of STN (6) increase
output of GPi (3)
Both Inhibit thalamus output
diminished cortical output
bradykinesia (運動遲緩) and hypokinesia (運動減退)
(19--21)
(19
48
(c‐4) Therapy on Parkinson’s disease (1) Following L‐DOPA treatment: Increased blood flow in supplementary motor area (S) and premotor cortex (P) of Parkinson’s disease patients during movement
(19--22)
(19
49
(2) Following unilateral pallidotomy: Improvement in motor system function of Parkinson’s disease patients
Pallidotomy:
Lesions in GPi or its output pathway
(19--22)
(19
Improvement in bradykinesia (運動遲緩)
& rigidity of 6 patients 3‐
4 months after surgery
50
Summary
(1). Components of basal ganglia (BG)
Striatum, GP, STN, SNc, SNr
(2). Relations of BG to surrounding brain areas
(3). Circuits of BG
Direct: Cortexstriatum GPi  thalamus cortex
Indirect: CortexstriatumGPe
STN GPi thalamuscortex
(4). Parkinson’s disease, Huntington’s disease
Hemiballismus
51