Flashcards in 09 09 2014 Basal Ganglion Deck (33):
What is the basal Ganglia
cluster of nuclei in the cerebrum, diencephalon, and midbrain that function together to facilitate or inhibit behaviors and actions.
-play large role in movement (also play a role in emotion and cognition and eye movement)
Basal Ganglia loops
- What does it help in?
--Motor cortex sends signal to striatum.
-Striatum sends output to Globus pallidus.
-Internal Globus pallidus sends signal to VA/VL
-VA/VL (thalamus) sends signal back to cortex
Facilitates motor cortical areas -- turns up excitability
1. initiates movement
2. sequencing movement
What happens when there is a lesion in the basal ganglia
Increase or decrease in movement
Dopamine modulates actions in the basal ganglia, limbic system and prefrontal cortex through which pathways?
1. Nigrostriatal pathway (aka mesostriatal) -- dopaminergic neurons that control of movements. Projects to caudate and putamen. Defect = parkinson's disease ( Basal ganglia)
2. Mesolimbic pathwy -- dopminergic neurons that regulate the reward pathway. Defects = schizophrenia (positive symptoms) and/or depression
3. Mesocortical pathway- working memory. Defects may play a role in Schizophrenia (negative symptoms), hypokinesia seen in Parkinson's.
Mechanisms of VA/VL
Excites motor complex by increasing motor output
Internal Global Pallidus
provides tonic inhibition to VA/VL
Disinhibition vs. Excitation
Disinhibition: inhibition of internal globes pallid us cause more excitation of VA/VL to cortex
Excitation: Internal Globus Pallidus gets excited via input. It leads to more inhibition of VA/VL --> less signals sent to motor cortex
Who excites GPi and who inhibits GPi?
-Subthalamic nucleus excites GPi -- causing inhibition of cortex and movement
-Striatum inhibits GPi -- causing more excitation of cortex and movement.
What would happen to the frequency of movement if there was a lesion in the sub thalamic nucleus?
produce too much movement (contralateral hemiballismus -- wild flinging movement)
-Subthalamic nucleus excites GPi -- causes damping of VA/VL and cortex signals.
Direct pathway (loop)
-disinhibition of GPi (from striatum) that increases activation of VA/VL
Indirect pathway (loop)
Inhibits unwanted movement
-disinhibition of subthalamic nucleus -- increases GPi = decrease VA/VL signaling
The effect of dopamine to both the direct and indirect pathway ( general)
Dopamine facilities movement! Increase signaling from VA/VL to motor cortex
How/ what is the mechanism by which dopamine increases signaling to motor cortex (via VA/VL) via direct ?
- dopamine from substance nigra pars compactus binds to DA1 receptors in Striatum (excitatory). They inhibit GPi (downstream)
How/ what is the mechanism by which dopamine increases signaling to motor cortex (via VA/VL) via the indirect pathway?
Dopamine neurons from substance nigra target D2 receptors (inhibitory) on striatum (putamen) . Inhibits sub thalamic nucleus which therefore also inhibits GPi stimulation.
Releases VA/VL from inhibition
Acetylcholine is present in the striatum. In what pathway does it have an effect and what is the effect?
ACh is in striatum and is most effective in indirect pathway.
It excites the indirect pathway --> tends to inhibit movement.
Anticholinergics are effective if you want more movement in Parkinson's disease
too little movement
too much movement
If there is a lesion in basal ganglia, where will the effects be seen-- ipsilateral or contralateral?
-basal ganglia is sitting right next to motor complex.
--regulates pathway on same side so of course it affects the opposite side of the body.
Negative symptoms of Basal Ganglia disease
-Akinesia (no movement)
-Bradykinesia (slow movement)
-Decreased postural adjustments
-Hypokinesai (decreased amplitude of movements
-handwriting gets smaller
Positive symptoms of Basal Ganglia disease
-dystonia-increased muscle tone in isolated muscles
-limbs to bend/twist
- head turned to one side (CN 11)
-athetosis: slow, writhe ring movements in lips, hands, and fingers. Patients cannot maintain fixed position.
-chorea: continuous rapid movements of face, tonuge, and limbs. Most common with Huntingont's
-Hemiballismus -- violent, involuntary flailing movements
-Tardive dyskinesia : from antipsychotic or antiemetic drugs- causes dyskinesia
-Prakinson's: 3-5 hz at rest: hands and arms. beginning unilaterally.
-Essential tremor:5-8 Hz : everywhere. Usually bilaterally.-- basal ganglia
-Myoclonus: sudden rapid muscular jerks -- whole body. damage = basal ganglia, cerebellum and cortex.
what are the 4 parallel basal ganglia pathways
2. Oculomotor -- abnormal eye movements
3. Cognition (prefrontal)
4. Emotions (limbic)
What are two diseases that result from damage to basal ganglia
1. Huntington's Chorea
2. Parkinson's disease
what is it?
Autosomal dominant neurodegenerative disorder with cell loss in caudate and putamen.
onset = 40s-50s
progressive and degenerative
Median survival = 15 years
treated with drugs that decrease dopamine.
Major symptoms with huntington's chorea
1. chorea: rapid movements of face, tongue, limbs.
2. dementia (cognitive impairment)
3. psychiatric manifestations
What basal ganglia pathway does Huntington's disease affect?
-cell death of caudate and putamen causes loss of inhibition of sub thalamus. Subthalamus is inhibited so stimulation of GPi is lost.
VA/VL is released from inhibition
= increase in movement
Cardinal symptoms of PD
-resting tumor (pill rolling motion)
Other motor symptoms of parkinson's
-Masked facies (hypomimia)-- no emotional feeback.
-Festination gait -- a shuffle that starts out slowly and then increases in speed.
-difficulty turing in bed.
What are some non-motor symptoms?
symptoms can spread across systems. May develop dementias and other cognitive/behavioral disorders
what are some treatment options of PD
1. pharmaceutical (look at pharm lecture for PD)
2. Surgical lesions
-Thalamus : young unilateral tremor and no rigidity or bradykinesai.
-Globus pallidus (internal) for tremor and rigidity
3. Deep-brain stimulation
How does deep brain stimulation work?
1. normalizes outputs
2. blocks action potential
What is the more common neuroprotective treatment?
-neuroprotective AND neurorestorative (after lesions)