basal Ganglia & cerebellum Flashcards
Layers of Cerebellum
Molecular
- Superficial
- Low neuron density
- Dendritic arborizations
Purkinje
- Middle Cell bodies of Purkinje neurons (inhibitory via GABA)
- Granular Innermost
- Tightly packed with granule cells
Cerebellar Inputs
Need to put information here.
- Inferior (restiform body)
- Middle (brachium pontis)
- Superior (brachium conjuctivum)
Cerebellar Inputs
•Mossy fibers
–Excitatory
–Most numerous
–Project indirectly through granule cells to the Purkinje neurons
–Originate from vestibular nuclei, spinal cord, and cerebral cortex
•Climbing fibers
–Excitatory
–Most direct to Purkinje neurons
–Originate form contralateral inferior olivary nucleus
Cerebellar Output
•Purkinje neurons
– May project directly to vestibular nuclei
–Or synapse in deep cerebellar nuclei
•Net effect of Purkinje neurons is inhibitory
•Outputs from the cerebellum are modulated by mossy and climbing fibers collaterals to deep cerebellar nuclei, creating an excitatory drive and being sculpted by the inhibitory influence of the Purkinje neurons
Phylogenetic Terminology
•Used to describe components of the cerebellum
•No perfect terminology exists
•Archicerebellum
–Flocculonodular lobe and deep parts of vermis
•Paleocerebellum
–Intermediate zone and most of vermis
•Neocerebellum
–Lateral hemispheres
Archicerebellar Inputs, Outputs, and Function
•Archicerebellum
–Flocculonodular lobe and deep parts of vermis *FASTIGIAL NUCLEI (deep)
INPUTS
•Vestibular afferents project to archicerebellum
–Primary fibers direct from ispilateral CN VIII
–Secondary fibers from ipsilateral vestibular nuclei
–Influence distribution of tone in limbs, trunk, neck, and extraocular eye muscles
•Retina projects indirectly to archicerebellum through climbing fibers of the inferior olivary nucleus –Assist in regulating the VOR
OUTPUTS
•Archicerebellar outputs to the brainstem
–Vestibular nuclei to influence extraocular motor neurons via MLF and to influence body and limb tone and responses via the vestibulospinal tracts
–Reticular formation to influence descending fibers of the reticulospinal tracts
•Central to influencing and maintaining equilibrium
FUNCTION
•Removal of the flocculonodular lobe in monkeys results in
–Disequilibrium, falling, wide base of support
- Ablation of the nodulus and uvula in animals confers immunity to motion sickness
- Removal of the vestibulocerebellum reduces plasticity of the VOR
DAMAGE: Medulloblastoma
- Most common lesion of the archicerebellum
- Highly malignant tumor occurring predominantly in children ages 4–8
- Symptoms of listlessness, vomiting, headaches, and falling
- Increased intracranial pressure causes papilledema
Medulloblastoma
DAMAGE of Archicerebellum: Medulloblastoma
- Most common lesion of the archicerebellum
- Highly malignant tumor occurring predominantly in children ages 4–8
- Symptoms of listlessness, vomiting, headaches, and falling
- Increased intracranial pressure causes papilledema
FUNCTION of Archicerebellum
•Removal of the flocculonodular lobe in monkeys results in
–Disequilibrium, falling, wide base of support
- Ablation of the nodulus and uvula in animals confers immunity to motion sickness
- Removal of the vestibulocerebellum reduces plasticity of the VOR
•Archicerebellum
–Flocculonodular lobe and deep parts of vermis
INPUTS
•Vestibular afferents project to archicerebellum
–Primary fibers direct from ispilateral CN VIII
–Secondary fibers from ipsilateral vestibular nuclei
–Influence distribution of tone in limbs, trunk, neck, and extraocular eye muscles
•Retina projects indirectly to archicerebellum through climbing fibers of the inferior olivary nucleus –Assist in regulating the VOR
OUTPUTS
•Archicerebellar outputs to the brainstem
–Vestibular nuclei to influence extraocular motor neurons via MLF and to influence body and limb tone and responses via the vestibulospinal tracts
–Reticular formation to influence descending fibers of the reticulospinal tracts
•Central to influencing and maintaining equilibrium
Paleocerebellar Connections
and Function
Paleocerebellar Connections
and Function
-outputINTERPOSE NUCLEI RELATED
- Role as comparator
- Information about intended movement is sent to the cerebellum – efference copy
- Patterns of peripheral receptor discharge are also sent to the cerebellum
- Cerebellum constantly updates movement as it is evolving
five tracts
- Dorsal spinocerebellar tract (DSCT) - copy of DCML like FG (proprioception, muscle tension, length) - tells cerebellum “you are standing..”
- Cuneocerebellar tract (CCT) - redundant tract of DCML related to UE, like FC (proprioception, muscle tension, length)
- Ventral spinocerebellar tract (VSCT) - receives excitation based on input to LMNs, tells the cerebellum what the LMNs are doing - tattle take “omg omg”, they are going to kick the soccer ball, I heard it in the ventral grey).
- Rostral spinocerebellar tract (RSCT) - related to tone around control of head (upper cervical segments, GTO about tone of head)
- Trigeminocerebellar projections - (tongue…?)
DAMAGE: Paleocerebellar Syndrome
- Produced in experimental animals, but similar presentation in humans with chronic alcoholism
- Difficulty standing and walking against gravity
- Wide base of support
- Marked incoordination of the lower extremities
Paleocerebellar Syndrome
DAMAGE: Paleocerebellar Syndrome
- Produced in experimental animals, but similar presentation in humans with chronic alcoholism
- Difficulty standing and walking against gravity
- Wide base of support
- Marked incoordination of the lower extremities
Paleocerebellar Connections
and Function
- Role as comparator
- Information about intended movement is sent to the cerebellum – efference copy
- Patterns of peripheral receptor discharge are also sent to the cerebellum
- Cerebellum constantly updates movement as it is evolving
five tracts
- Dorsal spinocerebellar tract (DSCT) - copy of DCML like FG (proprioception, muscle tension, length) - tells cerebellum “you are standing..”
- Cuneocerebellar tract (CCT) - redundant tract of DCML related to UE, like FC (proprioception, muscle tension, length)
- Ventral spinocerebellar tract (VSCT) - receives excitation based on input to LMNs, tells the cerebellum what the LMNs are doing - tattle take “omg omg”, they are going to kick the soccer ball, I heard it in the ventral grey).
- Rostral spinocerebellar tract (RSCT) - related to tone around control of head (upper cervical segments, GTO about tone of head)
- Trigeminocerebellar projections - (tongue…?)
Tracts of paleocerebellum
five tracts of paleocerebellum
- Dorsal spinocerebellar tract (DSCT) - copy of DCML like FG (proprioception, muscle tension, length) - tells cerebellum “you are standing..”
- Cuneocerebellar tract (CCT) - redundant tract of DCML related to UE, like FC (proprioception, muscle tension, length)
- Ventral spinocerebellar tract (VSCT) - receives excitation based on input to LMNs, tells the cerebellum what the LMNs are doing - tattle take “omg omg”, they are going to kick the soccer ball, I heard it in the ventral grey).
- Rostral spinocerebellar tract (RSCT) - related to tone around control of head (upper cervical segments, GTO about tone of head)
- Trigeminocerebellar projections - (tongue…?)
DAMAGE: Paleocerebellar Syndrome
- Produced in experimental animals, but similar presentation in humans with chronic alcoholism
- Difficulty standing and walking against gravity
- Wide base of support
- Marked incoordination of the lower extremities
Paleocerebellar Connections
and Function
- Role as comparator
- Information about intended movement is sent to the cerebellum – efference copy
- Patterns of peripheral receptor discharge are also sent to the cerebellum
- Cerebellum constantly updates movement as it is evolving
Neocerebellar Connections and Function
Neocerebellar Connections and Function
output to dentate
- Role in the governance of voluntary movement and motor learning
- Does not receive projections from peripheral receptors
- Afferent projections to the neocerebellum originate in the motor and association cortices of the cerebrum via corticopontocerebellar projections
Figure 19-6 Afferent projections to the neocerebellum (frontopontine fibers) originate in the motor and association areas of the cortex. These fibers synapse in nuclei in the pons whose neurons decussate and enter the cerebellum by way of the middle cerebellar peduncle. This pathway in its entirety is also referred to as the corticopontocerebellar projection.
Neocerebellar Outputs
- Neocerebellum projects to the dentate nuclei
- Dentate nuclei projections exit by way of the superior cerebellar peduncle to two locations
–Contralateral red nucleus of the midbrain
–Contralateral ventrolateral nucleus of the thalamus
Neocerebellar Connections and Function
- Ablation of the dentate nucleus in monkeys causes deficits in reaching and incoordination of compound finger movements
- In humans damage to the neocerebellum results in deficits in timing of agonist and antagonist muscle contractions
Neocerebellar Syndrome
- Most common encountered type of cerebellar disease in humans
- Causes include cardiovascular pathology, tumors, multiple sclerosis and degenerative diseases
•Characterized by
– intention tremor (a trembling of a part of the body when attempting a precise movement, associated especially with disease of the cerebellum.),
– hypotonia, asthenia (Asthenia: Weakness. Lack of energy and strength. Loss of strength. Myasthenia refers to a loss of muscle strength, as in myasthenia gravis.),
- asynergia (A severe movement disorder due to faulty coordination of groups of musclesnormally acting in conjunction. Asynergia involves the breaking down of movements into theircomponent parts so that movements become jerky and sequential. It is due to dysfunction of theCEREBELLUM.) , and
– ataxia
An inability to coordinate muscle activity during voluntary movement;
Neocerebellar Syndrome
Neocerebellar Syndrome
- Most common encountered type of cerebellar disease in humans
- Causes include cardiovascular pathology, tumors, multiple sclerosis and degenerative diseases
- Characterized by
– intention tremor (a trembling of a part of the body when attempting a precise movement, associated especially with disease of the cerebellum.),
– hypotonia,
– asthenia (Asthenia: Weakness. Lack of energy and strength. Loss of strength. Myasthenia refers to a loss of muscle strength, as in myasthenia gravis.),
- asynergia (A severe movement disorder due to faulty coordination of groups of musclesnormally acting in conjunction. Asynergia involves the breaking down of movements into theircomponent parts so that movements become jerky and sequential. It is due to dysfunction of theCEREBELLUM.) , and
– ataxia
An inability to coordinate muscle activity during voluntary movement;
Neocerebellar Connections and Function
- Role in the governance of voluntary movement and motor learning
- Does not receive projections from peripheral receptors
- Afferent projections to the neocerebellum originate in the motor and association cortices of the cerebrum via corticopontocerebellar projections
Figure 19-6 Afferent projections to the neocerebellum (frontopontine fibers) originate in the motor and association areas of the cortex. These fibers synapse in nuclei in the pons whose neurons decussate and enter the cerebellum by way of the middle cerebellar peduncle. This pathway in its entirety is also referred to as the corticopontocerebellar projection.
Neocerebellar Outputs
- Neocerebellum projects to the dentate nuclei
- Dentate nuclei projections exit by way of the superior cerebellar peduncle to two locations
–Contralateral red nucleus of the midbrain
–Contralateral ventrolateral nucleus of the thalamus
Neocerebellar Connections and Function
- Ablation of the dentate nucleus in monkeys causes deficits in reaching and incoordination of compound finger movements
- In humans damage to the neocerebellum results in deficits in timing of agonist and antagonist muscle contractions
Cerebellar Damage: general characteristics, examination, and intervention
- Severity of cerebellar deficits may not reflect the magnitude of damage
- Due to small and compact space
- Difficult to determine location of a focal lesion
- Cerebellar hemispheres are likely to become involved, even with lesions of the vermis
- Unilateral lesions produce ipsilateral deficits
Examination of Coordination: for Cerebellar problems
- Finger-to-nose and heel-to-shin
- Observation for dysmetria, intention tremor, and decomposition of movement during voluntary movement
- Pronation – supination to observe for dysdiochokinesis
- Romberg test
- Observation of gait
Intervention for cerebellar problems
•In general intervention is complicated and prognosis of restoration of normal function is poor
Basal Ganglia
General
&
Nuclei
- Distinct, parallel operating circuits or loops run through specific parts of the basal ganglia, each with a relationship to specific part of the cerebral cortex
- Naturally occurring disorders of the basal ganglia such as Parkinson’s disease (PD) or Huntington’s disease (HD) may affect multiple loops and therefore present with motor, cognitive, and emotional symptoms
NUCLEI
Caudate Nucleus/Putamen: striatum
Putamen & Globus Pallidus: lentiform
Globus Pallidus internus: holds VA/VL in inhibition in everyday life
Subthalamic Nucleus: located at junction of thalamus and midbrain
Substantia Niagra: located inside midbrain, largest of BG
====
Basal Ganglia Disorders: you see a lot of random, burst, movements/thoughts that get released because there is no way for them to “turn them off”
Thalamic Syndrome: damage to thalamus causes intense neurogenic pain
Huntington’s Disease: degeneration of caudate nucleus and putamen (striatum), rapid cognitive and physical decline
Hemiballism: damage to subthalamic nucleus, violent flinging movements
Diabetes: problems regulating body temp, hunger thirst (hypothalamus)
Parkinson’s: degeneration of substantia niagra, dopamine no longer produced, cognitive decline as well
Concept of Disinhibition of BASAL GANGLIA
CONCEPT OF DISINHIBITION OF BG
Thalamus (VA/VL) excites cortex
BG tonically inhibits VA/VL
- Thalamocortical (VA/VL) projections are excitatory
- VA/VL are tonically inhibited by output nuclei of the basal ganglia
- In order for thalamus to excite cortex, must phasically disinhibit the motor nuclei of the thalamus (VA/VL)
BASAL GANGLIA
- Distinct, parallel operating circuits or loops run through specific parts of the basal ganglia, each with a relationship to specific part of the cerebral cortex
- Naturally occurring disorders of the basal ganglia such as Parkinson’s disease (PD) or Huntington’s disease (HD) may affect multiple loops and therefore present with motor, cognitive, and emotional symptoms
NUCLEI
Caudate Nucleus/Putamen: striatum
Putamen & Globus Pallidus: lentiform
Globus Pallidus internus: holds VA/VL in inhibition in everyday life
Subthalamic Nucleus: located at junction of thalamus and midbrain
Substantia Niagra: located inside midbrain, largest of BG
====
Basal Ganglia Disorders: you see a lot of random, burst, movements/thoughts that get released because there is no way for them to “turn them off”
Thalamic Syndrome: damage to thalamus causes intense neurogenic pain
Huntington’s Disease: degeneration of caudate nucleus and putamen (striatum), rapid cognitive and physical decline
Hemiballism: damage to subthalamic nucleus, violent flinging movements
Diabetes: problems regulating body temp, hunger thirst (hypothalamus)
Parkinson’s: degeneration of substantia niagra, dopamine no longer produced, cognitive decline as well
Parkinson’s Disease (PD)
Parkinson’s Disease (PD)
- PD is a progressive degenerative disease caused by death of neurons primarily in the SNpr
- Loss of dopaminergic projections
Cardinal signs include
–Tremor
–Bradykinesia - slowness of movement and is one of the cardinal manifestations of Parkinson’s disease
–Rigidity
–Postural instability
•Nonmotor impairments occur including cognitive decline, autonomic changes, pain, and fatigue
ETIOLOGY OF PD
- In most cases no known cause of degeneration of dopaminergic neurons; however, in some cases environmental or genetic causes are known
- Combination of factors
–Age, genetic susceptibility, environmental factors
•Signal-mediated cell death, apoptosis
BRAIN DISORDER IN PD
- Loss of SNpr neurons that synthesize and release dopamine (DA)
- Also loss of neurons and neurotransmitters in other areas
–The ventral tegmental area (VTA) produces DA
–Locus coerulus produces norepinephrine
–Dorsal motor nucleus of the vagus produces norepinephrine
•Disease affects many areas
–Basal ganglia
–Mesocortical projections
–Mesolimbic projections
Pharmacological Management of PD
- Dopamine replacement
- Dopamine agonists
- Inhibitors of dopamine metabolism
- Anticholinergic agents
SURGICAL INTERVENTION
- Pallidotomy
- Ventrolateral thalamotomy
- Deep brain stimulation
- Fetal nigral transplantation
PHYSICAL REHABILITATION IN PD
- Assessment of the cardinal signs
- Rating scales
–United Parkinson’s Disease Rating Scale (UPDRS)
–Profile PD
- Response to mediation
- History of falls
- Assessment of nonmotor signs
INTERVENTION IN PD
- Possible to facilitate movement through auditory, visual, or tactile stimuli
- Remediation of the musculoskeletal and cardiovascular sequelae that accompany the disease due to loss of activity
- Animal studies suggest high-intensity exercise may actually protect against the degeneration associated with PD
