Download Basal Gang Dental 2011

Dental Neuroanatomy
Suzanne S. Stensaas, Ph.D.
Marcjh 8, 2011
Reading: Waxman pp. 141-146 are not very helpful!
Computer Resources: HyperBrain, Chapter 12
THE BASAL GANGLIA
Objectives:
1. What are the main manifestations of Basal Ganglia disease?
2. Be able to contrast signs and symptoms of:
• Basal Ganglia Disease
• Cerebellar Disease
• Corticospinal Tract Disease = Upper motor neuron
• Motor Neuron Disease = Lower Motor neuron
3. Identify the structures involved in:
• Huntington's Disease
• Parkinson's Disease
I. Introduction
A. General features of the basal ganglia, one of our 3 major motor control
centers:
1. Involved in motor, cognitive and affective tasks
2. Do not project directly to targets below the midbrain
3. Act mainly on the premotor cortex via the thalamus, similar to cerebellum.
B. What Do the Basal Ganglia Do?
1. We are beginning to understand that there are more than 3 different loops
or parallel circuits and functions (motor, cognitive and affective) all
influenced by a dopaminergic mesencephalic system.
2. The only one we will focus on is the motor loop. Motor pattern generators
permit voluntary movements to take place in what seems like an automatic
manor.
3. Normally the BG are the “brakes” on the voluntary motor system.
4. Selectively facilitate some movements and inhibit others, and/or
compare commands for movement from the precentral motor cortex with
proprioceptive feedback from the movement in progress.
5. Play a role in initiating internally generated movements
C. Definitions
1. Basal ganglia
a. Corpus striatum
1. Caudate \ = the striatum
2. Putamen /
3. Globus pallidus = the pallidum
b. Though technically not part of the basal ganglia, the subthalamic
nucleus and substantia nigra are presented with the basal ganglia
because of their connections and involvement in disease.
1
2. Lenticular nucleus is an old descriptive term for the lens-shaped gray matter
just lateral to the internal capsule; it includes both the globus pallidus and
putamen. Another term is lentiform, even more confusing. Avoid using
either term.
2
From The Digital Anatomist Interactive Brain Syllabus. John Sundsten and Kate Mulligan, Univ.
Washington School of Medicine. 1998 ©
Source: Kandel?
3
II. Connections of Basal Ganglia
A. The caudate and putamen are a single entity that is divided by the anterior
limb of the internal capsule. Both have similar connections, cell types
and neurotransmitters. There is evidence that the caudate is more
involved in cognitive functions and the putamen more with motor
functions
B. Striatal Afferents
1. From the Cerebral CORTEX: Corticostriate afferents
Nearly every region of the cerebral cortex sends axons to the ipsilateral
caudate and putamen. See diagram by Dr. Voron next page
(a. Visual cortex projects to the tail of the caudate and cells there
respond to complex patterned visual stimuli.)
b. Frontal cortex projects to the head of the caudate; therefore, this
part of the caudate responds to environmental stimuli that are
important in preparing for movement.
2. From the SUBSTANTIA NIGRA: Nigrostriatal afferents. These neurons
use dopamine as their neurotransmitter. See diagram by Dr. Voron next page
C. Striatal Efferents – Globus Pallidus. See diagram by Dr. Voron next page
D. Efferents to Thalamus: The Globus Pallidus –
1. Pallidothalamic axons terminate in thalamic nuclei. In different region
from the axons coming from the cerebellum.
Myelin stained section through thalamus and BG, Stensaas
E. The Thalamic nuclei project to the premotor and supplementary cortex in
front of the precentral gyrus.
4
F. The premotor and supplementary motor cortex is a region important in
planning movements.
1. Premotor cortex is the part of area 6 on the lateral surface of the
hemisphere in front of the precentral gyrus.
2. Supplementary motor cortex is the part of area 6 on the medial surface
of the hemisphere. .
3. These areas then project to area 4 (the precentral gyrus), primary motor
cortex and hence to the corticospinal tract.
III. Striatal Motor Functions
The striatum is thought to link sensory cues to motor behavior integrating nearly all
the activity occurring in the cortex.
1. Many
connections (subthalamus and globus pallidus, substantia
© Stephen C. Voron,
M.D., reciprocal
2004
nigra and striatum).
Excitatory (Glu):
2. A role in initiating internally generated movements like associated
movement when walking.
Cortex, Subth Nuc, VL Thal
3. Interplay
of inhibition and excitation results in normal motor behavior.
Inhibitory
(GABA):
Interruption of either the Direct or Indirect pathways results in decrease
or increase in movement. We call these diseases: Movement disorders
GPe,
Gpi/(SNr)
which
usually occur at rest.
Striatum,
Both inhibitory and excitatory:
SNc: dopamine
Striatum interneurons: ACh
Indirect pathway Inhibits extraneous movement
Direct pathway Facilitates intentional
movement
Excitatory (Glu):
Cortex, Subth Nuc, VL Thal
Inhibitory (GABA):
Striatum, GPe, Gpi/(SNr)
5
IV. Basal Ganglia Diseases-Often called Involuntary Movement Disorders. There
may be an increase or a decrease in movements depending on the disease and
structures involved.
A. Involuntary movements during wakefulness. In general there are
POSITIVE (hyperkinetic) signs such as rigidity, chorea, athetosis, resting
tremor, etc.
In addition there are NEGATIVE (hypokinetic) sympto ms such as akinesia,
bradykinesia, masked face, decreased blinking, loss of associated
movements, difficulty planning movements.
B. Basal ganglia disease is relatively common and results from release (or
disinhibition),
Suzanne Stensaas©
C. Parkinson's disease was the first example of a neurological disorder with a
molecular basis. It is a slowly progressive disorder characterized by
bradykinesia (trouble initiating movement), festinating gait, resting tremor,
lead pipe or cogwheel rigidity, and masked facies.
.
1. Substantia nigra (pars compacta) contains pigmented dopaminergic
neurons that project to the striatum; the dopamine has the general
effect of facilitating movement.
2. In Parkinson's disease, >70% of dopaminergic neurons in the
substantia nigra die. There is also neuronal loss in other monoaminecontaining nuclei, but the nigrostriatal dopamine loss is considered
most important for the movement disorder. This loss in turn affects the
direct pathway
3. L-DOPA therapy increases dopamine and provides significant
improvement in movement in many patients.
6
D. Huntington's disease is an autosomal dominant disorder (CAG repeat)
resulting in degeneration of cholinergic and inhibitory GABAergic neurons in
the striatum and cerebral cortex, probably via glutamate-mediated excitotoxic
mechanisms. Huntington's Disease usually includes choreoathetosis,
dementia, and death within 10-20 years of the onset of symptoms. No
specific treatment is available. Disease is often diagnosed after reproductive
years reached and offspring produced.
7